Chapter 5 from Yanof Ophthalmology. LENS by Agustin Carron

PART 5 THE LENS Uploaded at issuu by dragustincarron.blogspot.com

5.1

Basic Science of the Lens Eric Dai and Michael E Boulton

Definition: The lens is a highly organized transparent structure that

GROSS ANATOMY OF THE ADULT HUMAN LENS

has evolved to alter the refractive index of light entering the eye.

Key features n�� n�� n�� n��

n�� n�� n��

T he lens comprises three parts: (1) the capsule, (2) the lens epithelium, and (3) the lens fibers. α-, β- and γ-crystallins constitute 90% of the total protein content of the lens. Lens function is dependent on the metabolism of glucose to produce energy, protein synthesis, and a complex antioxidant system. Lens transparency is dependent on the highly organized structure of the lens, the dense packing of crystallin, and the supply of appropriate nutrients. The ability to change its focusing power occurs by a process called accommodation. The lens exhibits age-related changes in structure, light transmission, metabolic capacity, and enzyme activity. Secondary cataract occurs when remnant lens cells following cataract extraction cause opacification in the visual axis.

INTRODUCTION

proliferative capacity increases

anterior pregerminative zone germinative zone

epithelial central zone cells

cortex

pregerminative zone germinative zone

equator

transitional zone embryonic nucleus fetal nucleus infantile nucleus adult nucleus

transitional zone

posterior

capsule

bow

Fig. 5-1-1 Gross anatomy of the adult human lens. Note the different regions are not drawn to scale.

The lens is a vital refractive element of the human eye. In 2002, the World Health Organization estimated that lens pathology (cataract) was the most common cause of blindness worldwide, affecting over 17 million people across the globe.1 Not surprisingly, cataract surgery is the most common surgical procedure performed in the developed world.2 An understanding of the basic science of the lens provides valuable insight into the various pathologies involving the lens, as well as the continually evolving techniques used to treat them.

of the capsule depends upon the region of the capsule being measured (Fig. 5-1-2) and, except for the posterior capsule, increases with the age of the individual.4–6 The lens capsule is composed of a number of lamellae stacked on top of each other. The lamellae are narrowest near the outside of the capsule and widest near the cell mass.7 Major structural proteins and a small amount of fibronectin are found within the lamellae.8 This structure is continuously synthesized and represents one of the thickest basement membranes in the body. The capsule is produced anteriorly by the lens epithelium and posteriorly by the elongating fiber cells.

ANATOMY OF THE LENS

Epithelial Cells

The adult human lens is an asymmetric oblate spheroid that does not possess nerves, blood vessels, or connective tissue.3 The lens is located behind the iris and pupil in the anterior compartment of the eye. The anterior surface is in contact with the aqueous on the corneal side; the posterior surface is in contact with the vitreous. The anterior pole of the lens and the front of the cornea are separated by approximately 3.5 mm.4 The lens is held in place by the zonular fibers (suspensory ligaments), which run between the lens and the ciliary body. These zonular fibers, which originate from the region of the ciliary epithelium, are a series of fibrillin-rich fibers that converge in a circular zone on the lens. Both an anterior and a posterior sheet meet the capsule 1–2 mm from the equator and are embedded into the outer part of the capsule (1–2 μm deep). It also is thought that a series of fibers meets the capsule at the equator.5, 6 Histologically the lens consists of three major components – capsule, epithelium, and lens substance (Fig. 5-1-1).

Capsule

The lens is ensheathed by an elastic acellular envelope, which serves to contain the epithelial cells and fibers as a structural unit and allows the passage of small molecules both into and out of the lens. The thickness

The lens epithelium arises as a single layer of cells beneath the anterior capsule and extends to the equatorial lens bow. These cells have a cuboidal shape, being approximately 10 μm high and 15 μm wide. Their basal surface adheres to the capsule, whereas their anterior surface abuts the newly formed elongating lens fibers. Lens epithelial cells have large, indented nuclei and a normal array of organelles. They also contain dense bodies and glycogen particles. The lateral membranes of epithelial cells (membranes in contact with the adjacent epithelial cells) are highly tortuous and attachment to adjacent cells occurs by adhesion complexes located in the lateral membranes that include both desmosomes and tight junctions.3, 8–10 Lens epithelial cells contain the three main groups of cytoskeletal elements, which are microfilaments (actin), intermediate filaments (vimentin), and microtubules (tubulin). These cytoskeletal elements form a network that provides structural support, controls cell shape and volume, ensures intracellular compartmentalization and movement of organelles, enables cell movement, distributes mechanical stress, and mediates chromosome movement during cell division. Epithelial cell density is greatest in the central zone, a region in which cells normally do not proliferate. Cells in this zone are the largest epithelial cells found in the lens. The proliferative capacity of epithelial

381

THICKNESS OF THE LENS CAPSULE

THE LENS

21�m

LENS WEIGHT AND CELL NUMBERS WITH AGE

anterior pole 14�m

21�m

weight 250 (mg)

c. 761,184 epithelial cells c. 3,045,100 fibers

17�m

200 23�m

c. 1,009,312 epithelial cells c. 3,546,100 fibers

23�m 150

4�m posterior pole

100

Fig. 5-1-2 Changes in thickness of the adult lens capsule with location.

birth c. 402,595 epithelial cells c. 1,662,010 fibers

cells is greatest at the equator (see Fig. 5-1-1). Cells in the germinative equatorial zone are dividing constantly; newly formed cells are forced into the transitional zone where they elongate and differentiate to form the fiber mass of the lens.3, 11

Lens Substance

The lens substance, which constitutes the main mass of the lens, is composed of densely packed lens cell cytoplasm (fibers) with very little extracellular space. The adult lens substance consists of the nucleus and the cortex, two regions that often are histologically indistinct. Although the size of these two regions is age dependent, studies of lenses with an average age of 61 years indicate that the nucleus accounts for approximately 84% of the diameter and thickness of the lens and the cortex for the remaining 16%.12 The nucleus is further subdivided into embryonic, fetal, infantile, and adult nuclei (see Fig. 5-1-1). The embryonic nucleus contains the original primary lens fiber cells that are formed in the lens vesicle. The rest of the nuclei are composed of secondary fibers, which are added concentrically at the different stages of growth by encircling the previously formed nucleus. The cortex, which is located peripherally, is composed of all the secondary fibers continuously formed after sexual maturation. The region between the hardened embryonic and fetal nuclear core and the soft cortex (i.e., the fibers added to form the infantile and adult nuclei) sometimes is referred to as the epinucleus. Fibers are formed constantly throughout life by the elongation of lens epithelial cells at the equator. Initially, transitional columnar cells are formed but, once long enough, the anterior end moves forward beneath the anterior epithelial cell layer and the posterior end is pushed backward along the posterior capsule. The ends of this U-shaped fiber run toward the poles of both capsular surfaces.3–6 Once fully matured, the fiber detaches from the anterior epithelium and the posterior capsule. Each new layer of secondary fibers formed at the periphery of the lens constitutes a new growth shell. Lens fibers are held together by the interlocking of the lateral plasma membranes of adjacent fibers to form ball-and-socket and tongue-andgroove joints. These joints, which are found at regular intervals along the length of their membranes, are characterized by square array membranes. Both desmosomes and tight junctions are absent from mature lens fibers, although desmosomes are found between elongating fibers.3, 8, 9

Sutures

Sutures are found at both the anterior and the posterior poles. They are formed by the overlap of ends of secondary fibers in each growth shell. No sutures are found between the primary fibers in the embryonic nucleus. Each growth shell of secondary fibers formed before birth has an anterior suture shaped as an “erect Y” and a posterior suture shaped as an “inverted Y.” The formation of sutures enables the shape of the lens to change from spherical to that of a flattened biconvex sphere.3, 9, 13

Growth

382

The growth of the lens throughout life is a unique characteristic not shared with any other internal organ. The growth rate, which is greatest in the young, diminishes with increasing age. During an average life span the surface area of the lens capsule increases from 80 mm2 at birth to 180 mm2 by the seventh decade.5, 7 The rate of increase in cell numbers parallels the increase in both mass and dimensions of the lens, and therefore decreases dramatically after the second decade. Numbers of

80 age (years)

Fig. 5-1-3 Increase in lens weight and cell numbers with age. Note the correlation between these two parameters. (Lens weight data from Phelps Brown N, Bron AJ. Lens growth. In: Phelps Brown N, Bron AJ, Phelps Brown NA, eds. Lens disorders. A clinical manual of cataract diagnosis. Oxford: ButterworthHeinemann; 1996:17–31. Cell number data from Kuszak JR, Brown HG. Embryology and anatomy of the lens. In: Albert DM, Jakobiec FA, eds. Principles and practices of ophthalmology. Basic sciences. Philadelphia: WB Saunders; 1994:82–96.)

both epithelial cells and fibers increase by approximately 45–50% during the first two decades (Fig. 5-1-3). After this, the increase in cell numbers is reduced, with the proportional increase in fibers being very small.3

Mass

The weight of the lens rapidly increases from 65 mg at birth to 125 mg by the end of the first year. Lens weight then increases at approximately 2.8 mg/year until the end of the first decade, by which time the lens has reached 150 mg. Thereafter, the mass of the lens increases at a slower rate (1.4 mg/year) to reach about 260 mg by the age of 90 years (see Fig. 5-1-3).14 The lenses of men are heavier than those of women of the same age, the mean difference being 7.9 ± 2.47 mg (once adjusted for age).15

Dimensions

The equatorial diameter of the human lens increases throughout life, although the rate of increase is reduced significantly after the second decade. The diameter increases from approximately 5 mm at birth to 9–10 mm in a 20-year-old. The thickness of the lens increases at a much slower rate than does the equatorial diameter. The distance from the anterior to the posterior poles, which is 3.5–4 mm at birth, increases throughout life, reaching up to 4.75–5 mm (unaccommodated).4, 14 The thickness of the nucleus decreases with age, as the result of compaction, whereas cortical thickness increases as more fibers are added at the periphery. Because the increase in cortical thickness is greater than the decrease in size of the nucleus, the polar axis of the lens increases with age.16 The radius of curvature of the anterior surface decreases from 16 mm at the age of 10 years to 8 mm by the age of 80 years as this surface becomes more curved. There is very little change in the radius of curvature of the posterior surface, which remains at approximately 8 mm.

PHYSIOLOGY OF THE LENS Permeability, Diffusion, and Transport

After involution of the hyaloid blood supply to the lens (tunica vasculosa lentis), the metabolic needs of the lens are met by the aqueous and the vitreous humors. The capsule is freely permeable to water, ions, other small molecules, and proteins with a molecular weight up to 70 kDa. The tight junctions between the epithelial cells do not restrict greatly the

SODIUM AND POTASSIUM CURRENT LOOPS

5.1

TRANSMITTANCE OF THE LENS

Basic Science of the Lens

transmittance 100 (%) 80

K+

Na+

lens transmittance: total, 4½ years direct, 4½ years direct, 53 years direct, 75 years

60 40 20

Fig. 5-1-4 Sodium and potassium current loops. (Adapted from Patterson JW. Characterization of the equational current of the lens. Ophthalmic Res. 1998;20:139–42.)

movement of molecules into the fiber mass. Epithelial cells and fibers possess a number of different channels, pumps, and transporters that enable transepithelial movement to and from the extracellular milieu.

Transport of ions

Fiber cells contain large concentrations of negatively charged crystallins. As a result, a large number of positively charged cations enter the lens cell to maintain electrical neutrality, and therefore the osmolarity of the intracellular fluid becomes greater than that of the extracellular fluid. Fluid flow and swelling is minimized by the resting potential of the plasma membrane being set at a negative voltage using, principally, potassium (K+)-selective channels. An equilibrium is reached when the electrical force that attracts these ions is balanced by the outward leak of K+ down its concentration gradient. The Na+ ions that leak into the cells are exchanged actively for K+ ions, which diffuse through the lens down their concentration gradient and leave through ion channels in both the epithelial cells and surface fibers. There is a net movement of Na+ ions from posterior to anterior and of K+ ions from anterior to posterior (Fig. 5-1-4).17 Although a pH gradient exists, which increases from the central nucleus to the peripheral layers, the intracellular pH of the lens is approximately 7.0. Lens cells need to continually extrude intracellular protons that are generated from lactic acid, as a result of anaerobic glycolysis, and by the continuous inward movement of positive ions from the extracellular space. The pH is regulated by mechanisms capable of increasing and decreasing intracellular acid levels. Molecules, especially proteins, with the capacity to act as buffers also play a role.

Amino acid and sugar transport

Although amino acids can enter the lens across both the anterior and posterior surfaces, most amino acids are transported into the lens from the aqueous. The lens contains most, if not all, amino acids and also can convert keto acids into amino acids. The lens acts as a “pump–leak” system: amino acids are “pumped” into the lens through the anterior capsule and passively “leak” out through the posterior capsule. Although glucose has the capacity to enter via both the anterior and the posterior surfaces, most enters from the aqueous humor.

BIOPHYSICS Light Transmission

The cornea and lens act as spectral filters absorbing the more energetic wavelengths of the electromagnetic spectrum (i.e., ultraviolet (UV) radiation) that have the potential to damage the retina. The cornea absorbs wavelengths below 295 nm while the lens absorbs strongly in the long UV-B (300–315 nm) and most of the UV-A (315–400 nm) wavelengths. However, in children under 10 years there is a transmission band centered around 320 nm of about 8% which is reduced to 0.1% by age 22 years and by age 60 years no UV radiation transmits across the lens. The total transmittance of the young lens begins increasing rapidly at about 310 nm and reaches 90% at 450 nm, compared with the older lens (e.g., 63 years), which begins transmitting at 400 nm but

300

400 500 600

800 1000 1200

1600 2000

wavelength (nm)

Fig. 5-1-5 Changes in transmission (UV and visible) of the normal aging human lens. (From Boettner and Wolter. Transmission of the ocular media. Invest Ophthalmol Vis Sci. 1962;1:776–83.)

does not reach 90% total transmittance until 540 nm (Fig. 5-1-5). The overall transmission of visible light decreases with increasing age, a feature that arises largely from age-related changes and brunescence in the lens (see Fig. 5-1-5).18, 19

Transparency

During the early stages of embryonic development the lens is opaque, but as development continues and the hyaloid vascular supply is lost the lens becomes transparent. The young lens is transparent because of the absence of chromophores able to absorb visible light and the presence of a highly organized structure that gives minimal light scatter (less than 5% in the normal human lens). The amount of light scatter is minimized in fiber cells once the fibers have elongated fully and matured and their organelles have degenerated. Although the epithelial cells contain large organelles that scatter light, the combined refractive index of this layer and the capsule is no different from the refractive index of the aqueous, so light scatter in this area is very small.

Refractive Indices

Refractive index increases from 1.386 in the peripheral cortex to 1.41 in the central nucleus of the lens. Because both the curvature and refractive index of the lens increase from the periphery toward the center, each successive layer of fibers has more refractive power and, therefore, can bend light rays to a greater extent.20 The anterior capsular surface of the lens has a greater refractive index than the posterior capsular surface (1.364–1.381 compared with 1.338–1.357). The change in refractive index from the surface of the lens to the center results from changes in protein concentration; the higher the concentration, the greater the refractive power. This increase must occur as a result of both packing and hydration properties, because protein synthesis in the nucleus is minimal.18, 21

Chromatic Aberration

When visible light passes through the lens it is split into all the colors of the spectrum. The different wavelengths of these colors result in different rates of transmission through the lens and some deviation. As a consequence, yellow light (570–595 nm) normally is focused on the retina; light of shorter wavelengths, for example blue (440–500 nm), falls in front because of the slower transmission and increased refraction compared with yellow light; and light of longer wavelengths, for example red (620–770 nm), falls behind because of the faster transmission and less refraction (Fig. 5-1-6). However, although the lens is not designed to correct this chromatic aberration, yellow is normally the ray of greatest intensity. Because the amount of dispersion between the red and the blue images is approximately 1.5–2 D, very little reduction occurs in the clarity of the image that is formed on the retina. As the lens accommodates, refraction increases as a result of the increasing power of the lens and, therefore, the amount of chromatic aberration also increases.20, 22–24

383

PRINCIPAL ABERRATIONS OF THE LENS Sperical aberration

THE LENS Chromatic aberration

Fig. 5-1-6 Principal aberrations of the lens.

Spherical Aberration

Light rays that pass through the periphery of an optical lens have a focal length shorter than that of light rays that pass through the center. This occurs because the refractive power is greater at the periphery, so the light rays are refracted to a greater degree as they pass through this region. The lens of the human eye is designed to minimize this spherical aberration since: (1) refractive index increases from the periphery to the center of the lens; (2) curvature of both the anterior and the posterior capsule increases towards the poles; and (3) curvature of the anterior capsule is greater than that of its posterior counterpart. As a result of these structural features the focal points of the peripheral and central rays are similar, which ensures that the reduction in the quality of the image is minimal (see Fig. 5-1-6). The pupil diameter also affects the amount of spherical aberration, because light rays do not pass through the periphery of the lens (unless the pupil is dilated). The optimal size of the pupil needed to minimize this imperfection is 2–2.5 mm.20, 22–24

Accommodation

384

The lens, through its ability to change shape, has the capacity to change the focusing power of the eye. This process is known as accommodation and enables both distant and close objects to be brought to focus on the retina. At rest the ciliary muscle is relaxed and, therefore, the zonules pull on the lens, which keeps the capsule under tension. In this state the capsule is stretched and the lens flattens, enabling the eye to focus on distant objects. Light rays from close objects are divergent and, therefore, are focused behind the retina with the lens in this shape. The lens accommodates these objects by contraction of the ciliary muscles, which relaxes the zonules thus increasing the curvature of the anterior surface and decreasing the radius of curvature from 10 mm to 6 mm. The increase in curvature of the anterior surface increases the refractive power, so that the light rays from close objects are refracted toward each other to a greater extent and, therefore, converge on the fovea. Because the front of the lens has moved forward, the depth of the anterior chamber decreases from 3.5 mm to 3.2–3.3 mm. Very little change occurs in

Fig. 5-1-7 Change in form of the lens on accommodation in a person of age 29 years. (A) Relaxed. (B) Accommodated. (Grid squares 0.4 mm.) Note the change in curvature of the anterior surface. (From Phelps Brown N, Bron AJ. Accommodation and presbyopia. In: Phelps Brown N, Bron AJ, Phelps Brown NA, eds. Lens disorders. A clinical manual of cataract diagnosis. Oxford: ButterworthHeinemann; 1996:48–52.)

the curvature of the posterior capsule, which remains at approximately 6 mm (Fig. 5-1-7). The distance between the cornea and the posterior surface of the lens, therefore, changes very little or not at all. Accommodation is accompanied by a decrease in pupil size (miosis) and convergence of the two eyes. Light rays can pass only through the thickest central parts of the lens and the two images become fused. The mechanisms of accommodation can be divided into both physical and physiological processes. Physical accommodation, a measure of the change in shape of the lens during the accommodative process, is measured in terms of the amplitude of accommodation using the unit diopter. It represents the difference between the contractility of the eye at rest and when fully accommodated and, therefore, a measure of the extent to which objects close to the eye can be focused. Physiological accommodation, a measure of the force of ciliary muscle contraction per diopter, is measured with the unit myodiopter. The myodiopter increases during the act of accommodation.25, 26

BIOCHEMISTRY The lens, like most tissues, requires energy to drive thermodynamically unfavorable reactions. Adenosine triphosphate (ATP) is the principal source of this energy within the cell. The majority of ATP produced

MAJOR PATHWAYS OF GLUCOSE METABOLISM IN THE LENS

Polyol dehydrogenase

5% Aldose reductase

Sorbitol pathway

Fructose

Glucose

Hexokinase

Gluconic acid

90% 10%

Glucose-6-phosphate Phosphofructokinase

Basic Science of the Lens

Sorbitol

5.1

Glycolysis

6-phosphogluconate

Pentose phosphate pathway

Ribulose-5-phosphate

80% Glyceraldehyde-3-phosphate Glycercaldehyde3-phosphate dehydrogenase

Lactate

Lactate dehydrogenase

Pyruvate kinase Pyruvate

Acetyl CoA

Tricarboxylic acid cycle

3% C4

Fig. 5-1-8 Overview of the major pathways of glucose metabolism in the lens. Percentages represent the estimated amount of glucose used in the different pathways.

within the lens comes from the anaerobic metabolism of glucose. Other important components required by the lens include the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH), which is produced principally by the pentose phosphate pathway and acts as a source of readily available reducing agent used in the biosynthesis of many essential cellular components, such as fatty acids and glutathione. Because the lens is susceptible to oxidative damage, it also must maintain sufficient antioxidant defenses to protect against the accumulation of this damage and the development of cataract.

Sugar Metabolism

Approximately 90–95% of the glucose that enters the normal lens is phosphorylated into glucose-6-phosphate in a reaction catalyzed by hexokinase. Although this enzyme exists as three different isoforms (types I–III), only two have been found in the lens. Because type I has a greater affinity for glucose, it is found in the lens nucleus where glucose levels are low. Type II, which accounts for 70% of the total soluble lens hexokinase but has a lower affinity for glucose, is found predominantly in the epithelium and cortex, where glucose levels are higher. Glucose6-phosphate is used either in the glycolytic pathway (80% of total glucose) or in the pentose phosphate pathway (hexose monophosphate shunt; 10% of total glucose) (Fig. 5-1-8). Because hexokinase is saturated by the normal concentrations of glucose found in the lens, this enzyme is working to maximal capacity and, therefore, limits the rate of both glycolysis and the pentose phosphate pathway. Glycolysis also is regulated by phosphofructokinase and pyruvate kinase.27, 28 Owing to its avascularity and location in the ocular humors, the lens exists in a hypoxic environment. This results in at least 70% of lens ATP being derived from anaerobic glycolysis, a relatively inefficient mechanism for the production of ATP (two net molecules of ATP per molecule of glucose). However, although only a very small amount, approximately 3% of lens glucose, passes into the tricarboxylic acid cycle (see Fig. 5-1-8), this aerobic metabolism generates 25% of lens ATP (36 net molecules of ATP per molecule of glucose). Glycolysis and the tricarboxylic acid cycle generate two energy-rich molecules, the reduced form of nicotinamide adenine dinucleotide (NADH) and the reduced form of flavin adenine dinucleotide (FADH2). These donate their electrons to oxygen, which releases large amounts of free energy that is subsequently used to generate ATP. This cycle, which is restricted to the

epithelial layer, also provides carbon skeleton intermediates for biosynthesis, such as amino acids and porphyrins.27, 29 The bulk of the pyruvate produced by the glycolytic pathway is reduced to lactate in a reaction catalyzed by lactate dehydrogenase (see Fig. 5-1-8), which is concentrated mostly in the cortex. The formation of lactate results in the reoxidation of the cofactor NADH to NAD+. Glyceraldehyde-3-phosphate dehydrogenase, an enzyme used in the glycolytic pathway, regulates the activity of lactate dehydrogenase by controlling the rate of conversion of glyceraldehyde-3-phosphate into 1,3-diphosphoglycerate and, therefore, the availability of NADH.27–29 The 5–10% of glucose that is not phosphorylated into glucose-6phosphate either enters the sorbitol pathway or is converted into gluconic acid (see Fig. 5-1-8). Although the precise function of these pathways is still unknown, the activity of the sorbitol pathway increases if glucose levels are increased above normal. Glucose is converted into sorbitol by aldose reductase, an enzyme localized to the epithelial layer. This enzyme uses NADPH supplied by the pentose phosphate pathway as a cofactor. Sorbitol then is converted by polyol dehydrogenase into fructose, a suboptimal, but usable, substrate for glycolysis. This enzyme is inactive at low concentrations of sorbitol and metabolizes sorbitol into fructose only if sorbitol has accumulated. Because both sorbitol and fructose have the potential to increase osmotic pressure, and so cause water to enter cells, these sugars may help to regulate the volume of the lens.27–29

Protein Metabolism

The protein concentration within the lens is higher than that of any other tissue in the body. Because the lens grows throughout life, protein synthesis also must occur throughout life. Most of this synthesis is concerned with the production of the crystallins and major intrinsic protein 26 (MIP26). It is assumed that protein synthesis occurs only in the epithelial cells and surface cortical fibers, which contain the organelles needed.30 Lens proteins remain stable for long periods because the majority of the degradative enzymes normally are inhibited. The lens controls the breakdown of proteins by marking those to be degraded with a small 8.5 kDa protein called ubiquitin. This system, which is ATP dependent, is most active in the epithelial layer. Lens proteins are broken down into peptides by endopeptidases and then into the constituent amino acids by exopeptidases. Neutral endopeptidase, previously called neutral proteinase,

385

THE �-GLUTAMYL CYCLE Enzymes

THE LENS

1. Membrane-bound �-glutamyltransferase

Amino acid

2. �-glutamylcyclotransferase

�-Glutamyl amino acid

3. 5-oxoprolinase 4. �-glutamylcysteine synthetase

ATP

5-Oxoproline

5. Glutathione synthetase 6. Dipeptidase Amino acid

Cysteinylglycine 1

ADP + Pi

Glycine

Glutamate ATP

Cysteine 4

Glutathione

ADP + Pi

5 �-Glutamyl cysteine

extracellular

intracellular

ADP + Pi

ATP

Fig. 5-1-9 The γ-glutamyl cycle. (From Harding JJ, Crabbe MJC. The lens: development, proteins, metabolism and cataract. In: Davson H, ed. The eye. 3rd ed. London: Academic Press; 1984:207–492.)

is activated by both calcium and magnesium, and is optimally active at pH 7.5 (the pH of the lens is approximately 7.0–7.2). The principal substrate of this enzyme is α-crystallin. The calpains (I and II), which mainly are localized in the epithelial cells and cortex, are used to degrade crystallins and cytoskeletal proteins. They are cysteine endopeptidases, the activities of which are regulated by calcium (Ca2+). These enzymes are inhibited by calpastatin, a natural inhibitor found at higher concentrations than the calpains. The lens also contains a serine proteinase (with trypsin-like activity) and a membrane-bound proteinase.28, 29, 31 The main exopeptidase is leucine aminopeptidase, an enzyme that is optimally active at pH 8.5–9.0, which catalyzes the removal of amino acids from the N-terminal of peptides. Aminopeptidase III, another endopeptidase found in the lens, has an optimal pH of 6.0 and as a result has a greater activity than leucine aminopeptidase in the normal lens.28, 29, 31

Glutathione

Glutathione (L-γ-glutamyl-L-cysteinylglycine) is found at high concentrations in the lens (3.5–5.5 mmol/g wet weight), especially in the epithelial layer (in which levels are higher than in the nucleus; the cortex contains an intermediate concentration). Glutathione has many important roles in the lens, including the following:28, 29, 32 l Maintenance of protein thiols in the reduced state, which helps to maintain lens transparency by preventing the formation of highmolecular-weight crystallin aggregates l Protection of thiol groups critically involved in cation transport and permeability; for example, oxidation of the –SH groups of the Na+,K+ATPase pump, which results in an increased permeability to these ions l Protection against oxidative damage (see below) l Removal of xenobiotics; glutathione-S-transferase catalyzes the conjugation of glutathione to hydrophobic compounds with an electrophilic center

Amino acid transport

386

Glutathione has a half-life of 1–2 days and, therefore, is recycled constantly by the γ-glutamyl cycle; its synthesis and degradation occur at approximately the same rate (Fig. 5-1-9). Glutathione is synthesized from L-glutamate, L-cysteine, and glycine in a two-step process that uses 11–12% of lens ATP.28, 29, 32 Reduced glutathione also can be taken into the lens from the aqueous humor. A reduced glutathione transporter that allows the uptake of glutathione by the lens epithelial cells has been characterized.33 The breakdown of glutathione releases its constituent amino acids, which subsequently are needed to synthesize more glutathione.

Antioxidant Mechanisms

Reactive oxygen species is a collective term for highly reactive oxygen radicals (including free radicals) that have the potential to damage lipids, proteins, carbohydrates, and nucleic acids. Such radicals include the superoxide anion, the hydroxyl free radical, hydroperoxyl radicals, lipid peroxyl radicals, singlet oxygen, and hydrogen peroxide (H2O2). Reactive oxygen species generally have two origins in tissues: cell metabolism and photochemical reactions. Photochemical damage occurs when light is absorbed by a photosensitizer, a chromophore, that upon photoexcitation to photoexcited singlet state undergoes intersystem crossing and forms a transient excited triplet state. The excited triplet state is long lived, allowing for interaction with other molecules producing free radicals via electron (hydrogen) transfer, or singlet oxygen via transfer of excitation energy from the photosensitizer in the triplet state to molecular oxygen. The continuous entry of optical radiation into the lens, in particular the preferential absorption of shorter wavelengths (295–400 nm), makes lens tissue particularly susceptible to photochemical reactions. The major ultraviolet (UV) absorbers in the lens are free or bound aromatic amino acids (e.g., tryptophan), numerous pigments (e.g., 3-hydroxykynurenine), and fluorophores. Reactive oxygen species also can enter the lens from the surrounding milieu (e.g., H2O2 is present at high levels in the aqueous humor (30 mmol/L in humans)).29,34 Highly reactive oxygen species have the capacity to damage the lens in several ways:29, 35 l Peroxidizing membrane lipids results in the formation of malondialdehyde, which in turn can form cross-links between membrane lipids and proteins. l Introducing damage into the bases of the DNA, such as base modifications (8-hydroxyguanosine), plana-lesions (cytosine glycols) and lesions leading to major helical distortions of the DNA (8,5’ cyclo purine deoxyribonucleosides), initiates DNA repair mechanisms. l Polymerizing and cross-linking proteins result in crystallin aggregation and inactivation of many essential enzymes, including those with an antioxidant role (e.g., catalase and glutathione reductase). Although these reactions would result rapidly in lens damage, the presence of a complex antioxidant system offers considerable protection. This system, however, is not 100% efficient and a low level of cumulative damage occurs throughout life. Protection against damage induced by reactive oxygen species in the lens is achieved in a number of ways. The superoxide anion undergoes dismutation by superoxide dismutase or interaction with ascorbate (see below), which results in the formation of H2O2. This, along with the

COUPLING OF THE ASCORBIC ACID AND GLUTATHIONE SYSTEMS

Ascorbate

GSSG Nonenzymatic

H2O2 + O2

Dehydroascorbate

Catalase

H2O + 1/2O2

NAD(P)H2 Glutathione reductase

GSH

NAD(P)

Basic Science of the Lens

–

2O2 + 2H

5.1

Glutathione peroxidase

2H2O + GSSG

Fig. 5-1-10 Coupling of the ascorbic acid and glutathione systems.

high levels of exogenous H2O2, is detoxified by the enzyme catalase or glutathione peroxidase or both (Fig. 5-1-10).36 Catalase is present in epithelial cells but is found at very low levels in fibers. Glutathione peroxidase, however, is found in significant amounts in both epithelial cells and fibers, although the highest levels are found in the epithelial cells. The glutathione system, therefore, is thought to provide the most protection against H2O2. In addition to neutralizing H2O2, the glutathione system provides important protection against the lipid free-radical chain reaction by the neutralization of lipid peroxides.29, 32, 34, 35 Ascorbic acid (vitamin C) appears to play a major role in the antioxidant system in the lens, although this may be species dependent, because the human lens is rich in ascorbate (1.9 mg/kg wet weight or 1.1 mmol/kg), while it is almost absent in the rat lens (0.08 mmol/kg). Ascorbate is present at high levels in the outer layers of the lens and virtually absent from the nucleus. It rapidly reacts with superoxide anions, peroxide radicals, and hydroxyl radicals to give dehydroascorbate. It also scavenges singlet oxygen, reduces thiol radicals, and is important in the prevention of lipid peroxidation. The ascorbic acid and glutathione systems are coupled in that dehydroascorbate reacts with the reduced form of glutathione to generate ascorbate and GSSG (oxidized glutathione).31, 34, 37, 38

LENS CRYSTALLINS Crystallin Structure

Up to 60% of the wet weight and most of the dry weight of the human lens is composed of proteins. These lens proteins can be divided on a laboratory basis into water-soluble (cytoplasmic proteins) and waterinsoluble (cytoskeletal and plasma membrane) fractions. The watersoluble crystallins constitute approximately 90% of the total protein content of the lens.39, 40 The three groups of crystallins found in all vertebrate species can be divided into the α-crystallin family and the β/γ-crystallin superfamily. The properties of these crystallins are summarized in Table 5-1-1. The α-crystallins have the largest molecular size of the crystallins. The β-crystallins are composed of light (βL) (c. 52 kDa) and heavy (βH) (150–210 kDa) fractions, which can be separated by gel chromatography. The light fraction can be further subdivided into two fractions, βL1 and βL2.39–43 The smallest of the crystallins are the γ-crystallins. Six members of this family, known as γA–γF, have a molecular weight of 20 kDa.

Crystallin Gene Expression During Lens Growth

The α-, β-, and γ-crystallins are synthesized in the human lens during gestation, and the absolute quantities of these three families increases during development. The first crystallin to be synthesized is α-crystallin,

which is found in all lens cells. The β- and γ-crystallins are first detected in the elongated cells that emerge from the posterior capsule to fill the center of the lens vesicle.44 Throughout life the same pattern of synthesis is maintained, with the result that the α-crystallins are found in both lens epithelial cells and fibers, whereas the β- and γ-crystallins are found only in the lens fibers. α-Crystallin synthesis is far greater in the lens epithelium than in the fibers. The α-crystallins are found in both dividing and nondividing lens cells, whereas the β- and γ-crystallins are found only in nondividing lens cells. Differentiation of a lens epithelial cell into a fiber, therefore, may be one of the factors that triggers a decrease in translation of the α-crystallin gene and stimulates the synthesis of the β- and γ-crystallins.45

Crystallin Function

The high concentration of crystallins and the gradient of refractive index are responsible for the refractive properties of the lens. The short-range order of these proteins ensures that the lens remains transparent. The crystallins also have other functions within the lens. The α- and βB1crystallins are able to bind to cell membranes and the cytoskeleton. The importance of this binding is not clear, but is thought to be needed for the change in shape observed during the differentiation of an epithelial cell into a lens fiber. α-Crystallins also may be involved in the assembly and disassembly of the lens cytoskeleton. Similarities in structure between the small heat shock proteins (sHSPs) and αB-crystallin suggest that this crystallin family may provide the lens with stress-resistant properties.40, 41, 46 α-Crystallins have chaperone-like functions that enable them to prevent the heat-denatured proteins from becoming insoluble and facilitate the renaturation of proteins that have been denatured chemically.47 They also act as chaperones under conditions of oxidative stress and, therefore, may help to maintain lens transparency.48 Although the function of the β-crystallins is unknown, their structural similarities with the osmotic stress proteins suggests that they also may act as stress proteins in the lens.46 The γ-crystallins (with the exception of γs-crystallin) are found in the regions of low water content and high protein concentration, such as the lens nucleus. The presence of this family of crystallins correlates with the hardness of the lens. Concentrations are higher in those lenses that do not change shape during accommodation, as in fish, than in those that do, as in the human.40

AGE CHANGES Morphology

Increases in both the mass and dimensions of the lens, which occur throughout life, are greatest during the first two decades. These increases result from the proliferation of lens epithelial cells and their

387

5 THE LENS

388

TABLE 5-1-1 PROPERTIES OF DIFFERENT CRYSTALLINS α

γs

Subunits

αA, αAI, αB, αB1, up to nine minor subunits

Basic: βB1, βB2, βB3 Acidic: βA1, βA2, βA3, βA4

γA–γF

γs

Subunit molecular weight

20 kDa

Basic: 26–32 kDa Acidic: 23–25 kDa

20 kDa

24 kDa

Native molecular weight

600–900 kDa

βH: 150–200 kDa βL: c. 50 kDa

20 kDa

24 kDa

Number of subunits

30–45

βH: 0–8 βL: 2

Thiol content

Low

High

N-Terminal amino acid

Masked

Glycine or alanine

Masked

Secondary structure

Predominantly β-pleated sheet

β-pleated sheet

Three-dimensional structure

Unknown

Two domains with four “Greek key” motifs

Chromosome

αA: 21

βB1–βB4: 22

2 αB: 11

3 βA1/βA3: 17 βA2: ?

differentiation into lens fibers. As a consequence of the unique pattern of growth of the lens, it contains cells of all ages. The oldest epithelial cells are found in the middle of the central zone under the anterior pole. Because cells are added to the periphery of this zone throughout life, the age of the cells decreases from the pole toward the outer units of this region so that the newest cells always are found near the pregerminative zone. Because newly formed fibers are internalized as more are added at the periphery of the lens, the oldest fibers are found in the center of the nucleus and the newest fibers in the outer cortex. Each growth shell, therefore, represents a layer of fibers that are younger than those in the shell immediately preceding.49 As the lens ages many morphological changes occur to the epithelial cells, fibers, and capsule. Epithelial cells become flatter, flatten their nuclei, develop electron-dense bodies and vacuoles, and exhibit a dramatic increase in the density of their surface projections and cytoskeletal components. As a result of cellular flattening, the basal surface area of the cell increases; thus the number of cells needed to cover a region of the growing anterior capsule is less than that needed to cover a region of the same size in a younger lens. This, in combination with the decrease in proliferative capacity, means that epithelial cell density decreases as the lens ages.49, 50 Lens fibers show partial degradation or a total loss of a number of plasma membrane and cytoskeletal proteins as the lens ages. The most significant degradation is that of MIP26. Early in life spectrin, vimentin, and actin are present in both the outer cortical fibers and the epithelial layer; however, they are degraded as the fibers age and are further internalized. By 80 years of age expression of these cytoskeletal proteins is restricted to the epithelial cells. The cholesterol-to-phospholipid ratio of fiber cell plasma membranes increases throughout life, and consequently membrane fluidity decreases and structural order increases. These changes, which are known to occur from the second decade, are greatest in the nucleus and are therefore partially responsible for the increase in nuclear sclerosis (hardening).51, 52 Furthermore, it is thought that the changes in structure of the plasma membrane and the degradation of cytoskeletal components may contribute to the increase in the number of furrowed membranes and microvilli found on the fiber surface.49 From the fourth decade onward, ruptures are found in the equatorial region of cortical fiber plasma membranes (Fig. 5-1-11). Reparation of these ruptures often prevents the formation of opacities. Any opacities which do develop become surrounded by deviated membranes and therefore isolated from the remainder of the lens. The lens capsule thickens throughout life. It also increases in surface area as a result of the growth of the lens. Ultrastructural changes include the loss of laminations and an increase in the number of linear densities. Although the young lens capsule is known to contain collagen type IV and the aged capsule collagen types I, III, and IV, the presence of types I and III collagen in the young capsule has yet to be confirmed; however, their synthesis may be age related.53

ant

Fig. 5-1-11 Scanning electron micrograph of equatorial region of cortical fiber plasma membranes. Note the circular shade with the fracture of fibers in the deep equatorial cortex (eq) (arrows) and folding fibers in the anterior deep cortex (ant) (arrowheads). (nu, lens nucleus). (From Vrensen GFJM. Aging of the human eye lens – a morphological point of view. Comp Biochem Physiol A Physiol. 1995;111:519–32.)

Physiological Changes

Changes to the cellular junctions and alterations in cation permeability occur as the lens ages. The major gap junction protein MIP26 loses some of its amino acids to form new variants, which include polypeptides with molecular weights of 15, 20, and 22 kDa.51, 52 The membrane potential of an isolated, perfused human lens may be –50 mV at the age of 20 years, but only –20 mV at the age of 80 years. Although potassium (K+) levels do not alter greatly, remaining at approximately 150 mmol/ L (150 mEq/L), the sodium (Na+) content of the lens increases from 25 mmol/L (25 mEq/L) at the age of 20 years to 40 mmol/L (40 mEq/L) by the age of 70 years. Thus, the Na+:K+ permeability ratio increases approximately sixfold, which results in a proportionately greater increase in the sodium content of the lens.54 The change in the ratio of these two ions correlates with the increase in optical density of the lens.55 This change in ion permeability with increasing fiber age is thought to occur due to a decrease in membrane fluidity as a result of the age-related increase in the cholesterol-to-phospholipid ratio. The lens, therefore, becomes more dependent on the Na+,K+-ATPase in the epithelial cells. The decrease in membrane potential also results from changes in the

MAIN SPECIES IN THE HUMAN LENS WHICH ABSORB LIGHT TRANSMITTAL BY THE CORNEA

PRESBYOPIC CHANGES IN AMPLITUDE OF ACCOMMODATION WITH AGE

5.1 Basic Science of the Lens

amplitude of 14 accommodation (D) 12

relative 1.2 absorbance

0.8

8 6

0.4

4 2

0.0 295

345

395

yellow, aged proteins o-�-glucoside of 3-hydroxykynurenine protein-bound tryptophan

445 495 wavelength (nm)

0 10

60 70 age (years)

Fig. 5-1-12 Main species in the human lens which absorb light transmitted by the cornea. (From Dillon J. The photophysics and photobiology of the eye. J Photochem Photobiol B. 1991;10:23–40.)

Fig. 5-1-13 Presbyopic changes in the amplitude of accommodation with age. The different colored symbols represent the data obtained from different publications. (From Fisher RF. Presbyopia and the changes with age in human crystalline lens. J Physiol. 1973;223:765–79.)

free calcium (Ca2+) levels, which increase from 10 mmol/L (0.04 mg/dL) at the age of 20 years to approximately 15 mmol/L (0.06 mg/dL) by the age of 60 years. It is thought that the Ca2+-ATPase may be inhibited by the decrease in membrane fluidity, which decreases the rate at which calcium is pumped out of the cell. It also is possible that the increase in Na+ and Ca2+ permeability may result from the increased activity of nonspecific cation channels.54

the yellowing of the lens. This reaction is initiated by the attachment of a sugar molecule (e.g., glucose) to an amino acid, normally valine or lysine. In young lenses, 1.3% of lysine residues of human crystallins (both soluble and insoluble) are glycated, but by the age of 50 years this increases to 2.7% and to approximately 4.2% in older lenses.51 Yellow fluorescent photoproducts also are formed in the presence of ascorbic acid. Because ascorbic acid is found in the lens at much higher concentrations than glucose, and because the ascorbic acid reaction is faster, it probably plays a role in the formation of these yellow pigments.59

Biophysical Changes

The absorption of both ultraviolet (UV) and visible light by the lens increases with age. Both free and bound aromatic amino acids (tryptophan, tyrosine, and phenylalanine), fluorophores, yellow pigments, and some endogenous compounds (such as riboflavin) are responsible for the absorption properties of the lens.51 Tryptophan (which absorbs more than 95% of the photon energy absorbed by amino acids) is cleaved in the presence of sunlight and air to form N-formylkynurenine and a series of other metabolic products, which includes 3-hydroxykynurenine glucoside (3-HKG). Because more than 90% of the UV radiation that reaches the lens is UV-A (315–400 nm), and 3-HKG absorbs light between 295 and 445 nm whereas tryptophan only absorbs light between 295 and 340 nm, this glucoside has a relative absorbance greater than that of tryptophan in the young human lens (95% compared with 5%) (Fig. 5-1-12). As the lens ages it changes from colorless or pale yellow to darker yellow in adulthood, and brown or black in old age. These changes in coloration, which are limited to the nucleus, are thought to result from the attachment of 3-HKG and its metabolic derivatives to proteins to produce yellow-pigmented proteins that also absorb light. As the concentration of these pigments increases they compete with 3-HKG, but as the concentration of the kynurenines decreases further the yellow, aged proteins become the major absorbing species of the lens.56, 57 Because these yellow proteins are fluorescent species, the wavelength absorbed increases to approximately 500 nm (see Fig. 5-1-12). A blue fluorophore, which absorbs between 330 and 390 nm and fluoresces between 440 and 466 nm, increases as the lens ages. The autofluorescent properties of the lens also change with age. A green fluorophore, which is excited between 441 and 470 nm and emits between 512 and 528 nm, then is formed by oxygen-dependent photolysis of the blue fluorophore.58 This age-related shift in the spectral transmission of the lens explains the change in an artist’s use of colors throughout a lifetime. The increased capacity of the lens to absorb visible light, in combination with the increased scattering properties of the lens (because of the aggregation of lens proteins and possibly the release of bound water), results in a decrease in transparency.50 The increase in the total number of photons absorbed is accompanied by an age-related loss in antioxidant levels which, therefore, increases the amount of photo-oxidative stress. Nonenzymatic glycation of proteins by the Maillard reaction results in the formation of advanced glycation end products, which also increase

Accommodation Changes

The amplitude of accommodation decreases throughout life from 13– 14 D at the age of 10 years to 6 D at 40 years and almost 0 D by the age of 60 years (Fig. 5-1-13). The older subject, therefore, is unable to focus clearly on near objects and is presbyopic. The change in accommodative power is attributable to a number of factors, including those listed below:60–62 l Young’s modulus of capsular elasticity decreases from 700 N/cm2 at birth to 150 N/cm2 by the age of 80 years. l Stiffness of the lens substance increases, which renders the lens less deformable. l Although the cortex increases in thickness throughout life, very little change occurs in the thickness of the nucleus. The effect of the rounding of the nucleus on the change in curvature of the anterior surface during accommodation, therefore, is reduced with age. l Radius of curvature of the anterior capsule decreases, which renders the lens rounder. Contraction of the ciliary muscle, therefore, does not greatly alter the shape of the lens. l Distance between the anterior surface of the lens and the cornea decreases. l The internal apical region of the ciliary body moves forward and inward with age. The zonules, therefore, no longer put the lens under so much tension in the unaccommodated state. The increases in curvature and thickness of the lens suggest that the refractive power should increase with age, resulting in myopia. This, however, does not happen because these changes are accompanied by small alterations to the gradient of refractive index. This gradient becomes flatter near the center of the lens and steeper near the surface and, therefore, the refractive power of the eye is lowered.63

Biochemical Changes

The overall metabolic activity of the lens, as well as the activity of many glycolytic and oxidative enzymes, decreases with increasing age. This is attributed, in part, to decreasing enzyme activities in the cortex and nucleus. The activity of many enzymes involved in the metabolism of glucose decrease with age. These include glyceraldehyde-3-phosphate dehydrogenase, glucose-6-phosphate dehydrogenase, aldolase, enolase,

389

5 THE LENS

phosphoglycerate kinase, and phosphoglycerate mutase. Although overall metabolic activity decreases, the lens still maintains the capacity to synthesize proteins, fatty acids, and cholesterol at substantial rates. Decreased metabolic activity, therefore, does not serve as a significant limiting factor for the production of new lens fibers.51, 52 A reduction in the activity or levels or both of many antioxidants occurs with increasing age. Because this decrease is greatest in the nucleus, fibers in this region of the lens are more susceptible to oxidative damage and lipid peroxidation. As a result they rely upon the overlying cortical fibers and epithelial layer to protect them. The activity of both catalase and superoxide dismutase decreases with age. A decrease also occurs in the levels of ascorbate and glutathione.50 The reduced activity of both glutathione synthetase and γ-glutamylcysteine synthetase, accompanied by a decrease in the uptake of L-cysteine (an amino acid needed for glutathione synthesis), decreases the rate of synthesis of reduced glutathione (Fig. 5-1-14).64 In the human lens a very slow decrease occurs in the total activity of glutathione reductase (converts oxidized glutathione into reduced glutathione). Glutathione peroxidase, which is involved in the breakdown of lipid peroxides and hydrogen peroxide, levels increase from birth until approximately 15 years of age and then slowly decrease throughout adulthood.51, 52 This decreased antioxidant activity coupled with increased photon absorption with increasing age will advance photoxidative damage in the lens.

Crystallins

With increasing age there is an increase in both the complexity and the number of crystallin fractions found in the lens. Age-related changes in crystallins include accumulation of high molecular weight (HMW) aggregates, partial degradation of crystallin polypeptides, increased crystallin insolubility, photo-oxidation of tryptophan and the production of

EFFECT OF AGE ON THE CAPACITY TO SYNTHESIZE REDUCED GLUTATHIONE GSHg–1 lens 3000 (cpm 10000–1)

2000

1000

data from one lens overlapping data from two lenses

100 age (years)

Fig. 5-1-14 Effect of age on the capacity to synthesize reduced glutathione. (From Rathbun WB, Murray DL. Age-related cysteine uptake as rate-limiting in glutathione synthesis and glutathione half-life in the cultured human lens. Exp Eye Res. 1991;53:205–12.)

photosensitizers, loss of sulfhydryl groups, and nonenzymatic glycation. These changes can alter the short-range spatial order of the crystallins and therefore decrease transparency.50–52,56 Levels of soluble HMW aggregates (greater than 15 × 103 kDa) increase from approximately 0.16 mg in the lenses of donors between the ages of 16 and 19 years to 2.3 mg by the age of 60 years (Table 5-1-2).65 This increase occurs as the result of many factors, which include the inhibition of proteolytic enzymes that have the capacity to degrade these aggregates. Most of these aggregates are localized to the lens nucleus and are, in the majority of the young, principally composed of α-crystallin.50 As the lens ages these aggregates increase in complexity and are composed of a mixture of crystallins. The major subunits thought to be involved are αA-, αB-, and γs-crystallins. Many of these polypeptides undergo post-translational modifications, such as the formation of an intramolecular disulfide bond within αA-crystallin, glycation of lysine residues, cross-linking, deamidation of αA- and γs-crystallins and loss of the C-terminal end of αA-crystallin. Such modifications to α-crystallin result in a decrease in the capacity of this crystallin to act as a chaperone protein.50, 66 Below the age of 20 years, approximately 6% of the HMW protein is composed of degraded polypeptides, but by the age of 60 years this increases to 27% (see Table 5-1-2).65 It is thought that many of the HMW aggregates act as precursors for the accumulation of insoluble proteins. Below the age of 50 years, approximately 4% of lens proteins are insoluble, but by the age of 80 years this increases to 40–50%.67 This increase in insolubility is approximately the same in the cortex and nucleus before age 30 years, but with increasing age insolubility increases to a greater extent in the lens nucleus. Up to 80% of nuclear proteins of an aged lens may be insoluble and most of the nuclear α-crystallin is insoluble by the age of 45 years.51, 52 This will contribute to the loss of lens transparency and the development of senile cataract. Tryptophan residues in the crystallins are photo-oxidized to produce photosensitizers. This results in a decrease in tryptophan fluorescence and an increase in nontryptophan fluorescence throughout life. The oxidation of sulfhydryl groups results in the formation of disulfides, which may be one of the factors responsible for the age-related decrease in solubility of lens proteins. Because the γ-crystallins have sulfhydryl groups that are more exposed, they are more susceptible to this oxidation than are the α- and β-crystallins.52 Increases in the glycation of crystallins in the presence of glucose or ascorbic acid results in protein cross-linking and the resultant formation of HMW proteins. The α- and βH-crystallins rapidly cross-link; βL-crystallins are slower, but no γ-crystallin cross-linking occurs. One of the modifications that occurs most frequently to aging crystallins is deamidation of asparagine residues. This results in the formation of aspartic acid residues, which can alter the structure, destabilize the protein, and increase its susceptibility to proteolytic degradation. These age-related changes can lead to disorganization of lens structure and opacities that develop into cataract, a topic covered elsewhere in this section of the book. While the surgical management of cataract is discussed extensively elsewhere, the histopathology of one common sequela of cataract extraction is covered in the following section.

SECONDARY CATARACT A major complication of extracapsular cataract extraction (ECCE) is secondary cataract (also known as after cataract). Posterior capsule opacification (PCO) is the most clinically significant type of secondary cataract and develops in up to 50% of patients between 2 months and 5 years

TABLE 5-1-2 LEVELS OF DEGRADED POLYPEPTIDES IN WATER-SOLUBLE HIGH-MOLECULAR-WEIGHT PROTEINS OF HUMAN LENSES

390

Donor’s Age (years)

HMW Protein/Lens (mg)

HMW Protein-Associated Degraded Polypeptides/Lens (mg)

HMW Protein as Degraded Polypeptides (%)

16–19

0.16

0.009

5.6

38–39

0.93

0.17

18.2

49–51

2.17

0.255

11.75

55–56

2.2

0.42

19.1

60–80

2.3

0.62

26.9

(Adapted from Srivastava OP, Srivastava K, Silney C. Levels of crystallin fragments and identification of their origin in water soluble high molecular weight (HMW) proteins of human lenses. Curr Eye Res. 1996;15:511–20.)

Fig. 5-1-15 Fibrosis of the posterior capsule. This opacification developed in a 5-year-old child 20 days after extraction of a traumatic cataract (perforation with a knife). No intraocular lens was implanted. (From Rohrbach JM, Knorr M, Weidle EG, Steuhl KP. Nachstar: klinik, therapie, morphologic, and prophylaxe. Akt Augenheilkd. 1995;20:16–23.)

Fig. 5-1-16 Elschnig’s pearls. This opacification developed within 3 years of an extracapsular cataract extraction with implantation of a posterior chamber intraocular lens. (From Rohrbach JM, Knorr M, Weidle EG, Steuhl KP. Nachstar: klinik, therapie, morphologic, and prophylaxe. Akt Augenheilkd. 1995;20:16–23.)

Fibrosis-Type Posterior Capsule Opacification

Residual lens epithelial cells that are still attached to the anterior capsule after ECCE are thought to be the predominant cells involved in the formation of fibrous membranes. Although cases of fibrosis tend to appear within 2–6 months of ECCE, many are clinically insignificant.69 Remnant epithelial cells left on the anterior capsule after surgery differentiate into spindle-shaped, fibroblast-like cells (myofibroblasts), which express α-smooth muscle actin (normally only expressed in smooth muscle cells) and become highly contractile. These fibroblastic cells proliferate and migrate onto the posterior capsule to form a cellular layer that secretes extracellular matrix components and a basal laminalike material. Cellular contraction results in the formation of numerous fine folds and wrinkles in the posterior capsule. At this stage the capsule is only mildly opacified. No significant visual loss occurs until the cells migrate into the visual axis.68, 71 More advanced stages of PCO result from further proliferation and multilayering of cells on the posterior capsule, and are associated with additional extracellular matrix production

5.1 Basic Science of the Lens

after the initial surgery. The frequency of PCO is age related; almost all children develop PCO after ECCE, but in adults the incidence is much lower. This is thought to be because of the higher proliferative capacity of lens epithelial cells in the young compared with the old.68, 69 After ECCE the lens is composed of the remaining capsule and the residual epithelial cells and cortical fibers that were not removed at the time of surgery. The lens epithelial cells still possess the capacity to proliferate, differentiate, and undergo fibrous metaplasia. Migration of these cells toward the center of the previously acellular posterior capsule together with the synthesis of matrix components results in light being scattered, and the associated opacification reduces visual acuity. In the minority of cases, PCO results from the deposition of fibrin and other cell types onto the posterior capsule either at the time of surgery or postoperatively.69 The two morphologically distinct types of PCO are fibrosis and Elschnig’s pearls, which occur independently or in combination. In addition, ECCE procedures may result in the formation of a Soemmering’s ring (Figs 5-1-15–18).69, 70

Fig. 5-1-17 Mixture of Elschnig’s pearls and fibrosis on the posterior capsule. This opacification developed in a 64-year-old woman 2 years after uncomplicated cataract surgery. Note the wrinkling of the posterior capsule. (Courtesy of M Knorr.)

Fig. 5-1-18 Soemmering’s ring. Taken from behind the lens of a human eye obtained postmortem. A three-piece, modified J, polypropylene loop posterior chamber intraocular lens is present. (From Apple DJ, Solomon KD, Tetz MR, et al. Posterior capsule opacification. Surv Ophthalmol. 1992;37:73–116.)

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5 THE LENS

and the appearance of white fibrotic opacities. The majority of the extracellular matrix produced in the fibrosis-type of PCO is composed of types I and III fibrillar collagen with associated proteoglycans (dermatan sulfate and chondroitin sulfate).72 The basal lamina-like material contains both collagen type IV and heparin sulfate proteoglycan.72 In cases in which the cut edge of the anterior capsule rests on the IOL optic, residual anterior capsular cells may proliferate and extend from this cut edge onto the surface of the IOL, which results in the formation of a membranous outgrowth within approximately 1 week postoperatively.73 Detailed studies using polymethylmethacrylate IOLs have shown that cells do not appear to cover the central part of the optic, and migration onto this optic decreases as the cells in the region of the anterior capsule in contact with the optic undergo fibrous metaplasia and begin to opacify. The cells on the IOL completely disappear within 3 months. It is also possible that cells may migrate around onto the posterior surface of the IOL implant and, therefore, contribute to the formation of PCO. Growth factors present in both the aqueous and the vitreous humors have been implicated in the development of fibrosis-type PCO. These include acidic and basic fibroblast growth factors, insulin-like growth factor-I, epidermal growth factor, platelet-derived growth factor, hepatocyte growth factor, and transforming growth factor-β.

Pearl-Type Posterior Capsule Opacification

The pearls formed in this type of PCO are identical in appearance to Wedl (bladder) cells involved in the formation of posterior subcapsular cataracts. Because Wedl cells are known to originate from equatorial lens epithelial cells, it is believed that residual cells in this region of the capsule are the predominant cells involved in the formation of pearls. The possibility that the residual anterior capsular cells also are involved cannot be excluded completely. Clinically, cases of pearl formation occur somewhat later than those of fibrosis (up to 5 years postoperatively).69 Pearls were first observed by Hirschberg74 in 1901 and then by Elschnig75 in 1911; they now are referred to as Elschnig’s pearls. After ECCE the fiber mass of the lens is no longer present and, as a result, no internal pressure exists. Newly formed lens fibers, therefore, are no longer forced in the anterior and posterior directions, which results in the formation of a mass of cells (normally large and globular, but sometimes spindle shaped), loosely connected and piled on top of each other. Each pearl represents the aberrant attempt of one epithelial cell to differentiate into a new lens fiber, possessing characteristics of both epithelial cells and fibers, and may be embedded in an extracellular matrix. Visual acuity is affected only if the pearls protrude into the center of the posterior capsule and therefore into pupillary space.76–78

Soemmerring’s Ring

Soemmerring first noticed PCO in humans in 1828.79 After ECCE, the cut edge of the remaining anterior capsular flap may attach itself to the posterior capsule within approximately 4 weeks postoperatively, through the production of fibrous tissue. Any residual cortical fibers and epithelial cells, therefore, are trapped within this sealed structure. The equatorial cells still retain the capacity to proliferate and differentiate into lens fibers. The increase in the volume of this lenticular material fills the space between the anterior and the posterior capsule, which results in the formation of a ring that often has the appearance of a string of sausages. Proliferating epithelial cells remain attached to the anterior capsule but also are found to a lesser extent on the posterior capsule, where they form small isolated groups. In some cases the epithelial cells escape from the ring and migrate onto the anterior surface of the anterior capsule. Because the ring forms at the periphery of the lens, vision is not affected.76, 80, 81

Fig. 5-1-19 Posterior capsule following a Nd:YAG laser posterior capsulectomy. (From Rohrbach JM, Knorr M, Weidle EG, Steuhl KP. Nachstar: klinik, therapie, morphologic, and prophylaxe. Akt Augenheilkd. 1995;20:16–23.)

Prevention and Treatment of Posterior Capsule Opacification

As yet there is no reliable treatment to prevent PCO and posterior capsulotomy is the treatment of choice when PCO does affect the visual field. A posterior capsulectomy removes the central part of the posterior capsule and therefore instantly improves vision. Although this removal used to be achieved surgically, a neodymium:yttrium–aluminum–garnet (Nd:YAG) laser is now used (Fig. 5-1-19). In a number of patients with posterior segment problems, however, massive proliferation of lens epithelial remnants has been observed within months of the capsulectomy. As a result of this proliferation, the size of the capsulectomy decreases, which may in turn reduce visual acuity. It has been postulated that this occurs because of “activation” of the cells, the release of growth factors from the vitreous humor, the direct stimulation of proliferation, or a combination of these factors.82 Removal of the barrier between the posterior chamber and the vitreous cavity increases the risk of complications such as cystoid macular edema, retinal detachment, uveitis, and secondary glaucoma.69 The implantation of a posterior chamber IOL into the capsular bag after ECCE is known to reduce the likelihood that a patient will develop PCO, because the IOL acts as a barrier to the migration of cells around and into the center of the posterior capsule. Posterior convex or biconvex optics sit in the capsular bag with their posterior surface firmly against the posterior capsule. As a result this capsular surface is stretched radically and flattened, so there should be no room for the cells to pass this mechanical barrier and migrate into the center of the posterior capsule. Barrier-ridge optics have a rim on the posterior surface of the IOL, which also should create a barrier to migrating cells. Migration also has been shown to be dependent on the implant biomaterial. Trials have shown that the posterior capsules of patients who were given polyacrylic (AcrySof) implants were significantly clearer 2 years after implantation than the posterior capsules of those given polymethylmethacrylate or silicone implants. Lens epithelial cells also have been shown to regress in eyes implanted with polyacrylic IOLs.83

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6. Forrester J, Dick A, McMenamin P, Lee W. Anatomy of the eye and orbit. In: Forrester JV, Dick AD, McMenamin P, Lee WR, eds. The eye: Basic sciences in practice, London: WB Saunders; 1996:1–86. 7. Seland JH. The lens capsule and zonulae. Acta Ophthalmol. 1992;70:7–12. 8. Phelps Brown N, Bron AJ. Lens structure. In: Phelps Brown N, Bron AJ, Phelps Brown NA, eds. Lens disorders: a clinical manual of cataract diagnosis, Oxford: ButterworthHeinemann; 1996:32–47. 9. Kuszak JR. The ultrastructure of epithelial and fiber cells in the crystalline lens. Int Rev Cytol. 1995;163:305–50.

10. Lo W, Harding CV. Tight junctions in the lens epithelia of human and frog: freeze-fracture and protein tracer studies. Invest Ophthalmol Vis Sci. 1983;24:396–402. 11. Olivero DK, Furcht LT. Type IV collagen, laminin, and fibronectin promote the adhesion and migration of rabbit lens epithelial cells. Invest Ophthalmol Vis Sci.. 1996;34:2825–34. 12. Taylor VL, Al-Ghoul KJ, Lane CW, et al. Morphology of the normal human lens. Invest Ophthalmol Vis Sci. 1996;37:1396–410. 13. Kuszak JR. The development of lens sutures. Prog Retina Eye Res. 1995;14:567–91.

38. Varma SD, Richards RD. Ascorbic acid and the eye lens. Ophthalmic Res. 1988;20:164–73. 39. Harding J. The normal lens. In: Harding J, ed. Cataract: Biochemistry, epidemiology and pharmacology. London: Chapman & Hall; 1991:1–70. 40. Zigler JS. Lens proteins. In: Albert DM, Jakobiec FA, eds. Principles and practice of ophthalmology. Basic sciences. Philadelphia: WB Saunders; 1994:97–113. 41. de Jong WW, Lubsen NH, Kraft HJ. Molecular evolution of the eye lens. Prog Retina Eye Res. 1994;13:391–442. 42. Harding JJ, Crabbe MJC. The lens: development, proteins, metabolism and cataract. In: Davson H, ed. The eye. vol 1B, 3rd ed. London: Academic Press; 1984:207–492. 43. Berman ER. Lens. In: Blakemore C, ed. Biochemistry of the eye. New York: Plenum Press; 1991:201–90. 44. McAvoy JW. Cell division, cell elongation and the coordination of crystallin gene expression during lens morphogenesis in the rat. J Embryol Exp Morphol. 1978;45:271–81. 45. McAvoy JW. Cell division, cell elongation and the distribution of α-, β- and γ-crystallins in the rat lens. J Embryol Exp Morphol. 1978;44:149–65. 46. Wistow G, Richardson J, Jaworski C, et al. Crystallins: the over-expression of functional enzymes and stress proteins in the eye lens. Biotechnol Genet Eng Rev. 1994;12:1–38. 47. Horwitz J. The function of α-crystallin. Invest Ophthalmol Vis Sci. 1993;34:10–22. 48. Wang K, Spector A. α-Crystallin can act as a chaperone under conditions of oxidative stress. Invest Ophthalmol Vis Sci. 1995;36:311–21. 49. Kuszak JR. The ultrastructure of epithelial and fiber cells in the crystalline lens. Int Rev Cytol. 1995;163:305–50. 50. Chylack LT. Aging changes in the crystalline lens and zonules. In: Albert DM, Jakobiec FA, eds. Principles and practice of ophthalmology. Basic sciences, Philadelphia: WB Saunders; 1994:702–10. 51. Berman ER. Lens. In: Blakemore C, ed. Biochemistry of the eye. New York: Plenum Press; 1991:201–90. 52. Harding J. The aging lens. In: Harding J, ed. Cataract: biochemistry, epidemiology and pharmacology. London: Chapman & Hall; 1991:71–82. 53. Marshall GE, Konstas AGP, Bechrakis NE, Lee WR. An immunoelectron microscope study of the aged human lens capsule. Exp Eye Res. 1992;54:393–401. 54. Duncan G, Hightower KR, Gandolfi SA, et al. Human lens membrane cation permeability increases with age. Invest Ophthalmol Vis Sci. 1989;30:1855–9. 55. Coren S, Girgus JS. Density of human lens pigmentation: in vivo measures over an extended age range. Vision Res. 1972;12:343–6. 56. Vrensen GFJM. Aging of the human eye lens – a morphological point of view. Comp Biochem Physiol. 1995;111A:519–32. 57. Dillon J. The photophysics and photobiology of the eye. J Photochem Photobiol B. 1991;10:23–40. 58. Ellozy AR, Wang RH, Dillon J. Model studies on the photochemical production of lenticular fluorophores. Photochem Photobiol. 1994;59:479–84. 59. Ortwerth BJ, Linetsky M, Olesen PR. Ascorbic acid glycation of lens proteins produces UVA sensitizers similar to those in human lens. Photochem Photobiol. 1995;62:454–62. 60. Fisher RF. Presbyopia and the changes with age in the human crystalline lens. J Physiol. 1973;228:765–79. 61. Koretz JF. Accommodation and presbyopia. In: Albert DM, Jakobiec FA, eds. Principles and practice of ophthalmology. Basic sciences, Philadelphia: WB Saunders; 1994:270–82.

62. Phelps Brown N, Bron AJ. Accommodation and presbyopia. In: Phelps Brown N, Bron AJ, Phelps Brown NA, eds. Lens disorders: a clinical manual of cataract diagnosis, Oxford: Butterworth-Heinemann; 1996:48–52. 63. Hemenger RP, Garner LF, Ooi CS. Change with age of the refractive index gradient of the human ocular lens. Invest Ophthalmol Vis Sci. 1995;36:703–7. 64. Rathbun WB, Murray DL. Age-related cysteine uptake as rate-limiting in glutathione synthesis and glutathione half-life in the cultured human lens. Exp Eye Res. 1991;53:205–12. 65. Srivastava OP, Srivastava K, Silney C. Levels of crystallin fragments and identification of their origin in water soluble high molecular weight (HMW) proteins of human lenses. Curr Eye Res. 1996;15:511–20. 66. Yang Z, Chamorro M, Smith DL, Smith JB. Identification of the major components of the high molecular weight crystallins from old human lenses. Curr Eye Res. 1994;13:415–21. 67. Lerman S. Composition and formation of the insoluble protein fraction in the ocular lens. Can J Ophthalmol. 1970;5:152–9. 68. Green WR, McDonnell PJ. Opacification of the posterior capsule. Trans Ophthalmol Soc UK. 1985;104:727–39. 69. Apple DJ, Solomon KD, Tetz MR, et al. Posterior capsule opacification. Surv Ophthalmol. 1992;37:73–116. 70. Rohrbach JM, Knorr M, Weidle EG, Steuhl KP. Nachstar: klinik, therapie, morphologie und prophylaxe. Akt Augenheilkd. 1995;20:16–23. 71. McDonnell PJ, Stark WJ, Green WR. Posterior capsule opacification: a specular microscopic study. Ophthalmology. 1984;91:853–6. 72. Ishibashi T, Araki H, Sugai S, et al. Detection of proteoglycans in human posterior capsule opacification. Ophthalmic Res. 1995;27:208–13. 73. Pande MV, Spalton DJ, Marshall J. In vivo human lens epithelial cell proliferation on the anterior surface of PMMA intraocular lenses. Br J Ophthalmol. 1996;80:469–74. 74. Hirschberg J. Einführung in die Augenheilkunde. II. Hälkft I Abt. Leipzig: Themie; 1901:159. 75. Elschig A. Klinisch-anatomischer Beitrag zur Kenntnis des Nachstares. Klin Monatsbl Augenkeilkd. 1911;49:444–51. 76. Kappelhof JP, Vrensen GFJM. The pathology of aftercataract. Acta Ophthalmol. 1992;70(Suppl 205):13–24. 77. Sveinsson O. The ultrastructure of Elschnig’s pearls in a pseudophakic eye. Acta Ophthalmol. 1993;71:95–8. 78. Kappelhof JP, Vrensen GFJM, de Jong PTVM, et al. An ultrastructural study of Elschnig’s pearls in the pseudophakic eye. Am J Ophthalmol. 1986;101:58–69. 79. Soemmering DW. Beobachtungen von die organischen Veränderungen in Auge nach Staaroperationen. Frankfurt: Wesche; 1913. 80. Kappelhof JP, Vrensen GFJM, de Jong PTVM, et al. The ring of Soemmering in man: an ultrastructural study. Graefes Arch Klin Exp Ophthalmol. 1987;225:77–83. 81. Jongebloed WL, Dijk F, Kruis J, Worst JGF. Soemmering’s ring, an aspect of secondary cataract: a morphological description by SEM. Doc Ophthalmol. 1988;70:165–74. 82. Jones NP, McLeod D, Boulton ME. Massive proliferation of lens epithelial remnants after Nd-YAG laser capsulotomy. Br J Ophthalmol. 1995;79:261–3. 83. Pande M, Ursell PG, Spalton DJ. Lens epithelial cell regression on the posterior capsule with different intraocular lens materials. Br J Ophthalmol. 1998;82:1182–8.

5.1 Basic Science of the Lens

14. Phelps Brown N, Bron AJ. Lens growth. In: Phelps Brown N, Bron AJ, Phelps Brown NA, eds. Lens disorders. A clinical manual of cataract diagnosis, Oxford: ButterworthHeinemann; 1996:17–31. 15. Harding JJ, Rixon KC, Marriott FHC. Men have heavier lenses than women of the same age. Exp Eye Res. 1977;25:651. 16. Cook CA, Koretz JF, Pfahnl A, et al. Aging of the human crystalline lens and anterior segment. Vision Res. 1994;34:2945–54. 17. Patterson JW. Characterization of the equatorial current of the lens. Ophthalmic Res. 1988;20:139–42. 18. Lerman S. Lens transparency and aging. In: Regnault F, Hockwin O, Courtios Y, eds. Ageing of the lens, Amsterdam: Elsevier/North-Holland Biomedical Press; 1980:263–79. 19. Zigman S. Photochemical mechanisms in cataract formation. In: Duncan G, ed. Mechanisms of cataract formation in the human lens, London: Academic Press; 1981:117–49. 20. Duke-Elder S. The refraction of the eye – physiological optics. In: Abrams D, ed. The practice of refraction, 10th ed. Edinburgh: Churchill Livingstone; 1993:29–41. 21. de Jong WW, Lubsen NH, Kraft HJ. Molecular evolution of the eye lens. Prog Retina Eye Res. 1994;13:391–442. 22. Bennett AG, Rabbetts RB. Ocular aberrations. Clinical visual optics, 2nd ed.. London: Butterworths; 1989:331–57. 23. Elkington AR, Frank HJ. Aberrations of optical systems including the eye. Clinical optics, 2nd ed. Oxford: Blackwell Scientific; 1991:75–82. 24. Moore DC. Geometric optics. In: Coster DJ, ed. Physics for ophthalmologists. Edinburgh: Churchill Livingstone; 1994:29–34. 25. Duke-Elder S. Accommodation. In: Abrams D, ed. The practice of refraction, 10th ed.. Edinburgh: Churchill Livingstone; 1993:85–9. 26. Fisher RF. The ciliary body in accommodation. Trans Ophthalmol Soc UK. 1986;105:208–19. 27. Kador PF. Biochemistry of the lens: intermediary metabolism and sugar cataract formation. In: Albert DM, Jakobiec FA, eds. Principles and practice of ophthalmology. Basic sciences, Philadelphia: WB Saunders; 1994:146–67. 28. Harding JJ, Crabbe MJC. The lens: development, proteins, metabolism and cataract. In: Davson H, ed. The eye. 3rd ed.. London: Academic Press; 1984:207–492. 29. Berman ER. Lens. In: Blakemore C, ed. Biochemistry of the eye. New York: Plenum Press; 1991:201–90. 30. Bassnett S. The fate of the Golgi apparatus and the endoplasmic reticulum during lens fiber cell differentiation. Invest Ophthalmol Vis Sci. 1995;36:1793–803. 31. Harding J. The normal lens. In: Harding J, ed. Cataract: biochemistry, epidemiology and pharmacology, London: Chapman & Hall; 1991:1–70. 32. Reddy VN. Glutathione and its functions in the lens – an overview. Exp Eye Res. 1990;50:771–8. 33. Kannan R, Yi JR, Zlokovic BV, Kaplowitz N. Molecular characterization of a reduced glutathione transporter in the lens. Invest Ophthalmol Vis Sci. 1995;36:1785–92. 34. Augusteyn RC. Protein modification in cataract. In: Duncan G, ed. Mechanisms of cataract formation in the human lens, London: Academic Press; 1981:72–115. 35. Lerman S. Free radical damage and defense mechanisms in the ocular lens. Lens Eye Toxic Res. 1992;9:9–24. 36. Costarides AP, Riley MV, Green K. Roles of catalase and the glutathione redox cycle in the regulation of anterior-chamber hydrogen peroxide. Ophthalmic Res. 1991;23:284–94. 37. Sasaki H, Giblin FJ, Winkler BS, et al. A protective role for glutathione-dependent reduction of dehydroascorbic acid in lens epithelium. Invest Ophthalmol Vis Sci. 1995;36:1804–17.

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PART 5 THE LENS

5.2

Evolution of Intraocular Lens Implantation Liliana Werner, Andrea M. Izak, Robert T. Isaacs, Suresh K. Pandey and David J. Apple

Introduction Cataract is the most prevalent ophthalmic disease. For 1998 the number of persons blind as a result of cataract was estimated to be about 20 million worldwide; this number was expected to double by early in the twenty-first century.1, 2 Although a pharmacological preventive or therapeutic treatment for this blinding disease is being sought actively, the solution still appears to be many years away. Therefore, surgical treatment for cataracts, which increasingly includes intraocular lens (IOL) implantation, remains the only viable alternative. Treatment of cataracts has been practiced for centuries using various surgical and nonsurgical procedures. However, avoidance of complications and attainment of high-quality postoperative visual rehabilitation in the years before the introduction of modern IOLs were difficult problems. Because significant dioptric power resides in the crystalline lens, its removal results in marked visual disability. Aphakic spectacle correction has been prescribed throughout history, but spectacles are less than satisfactory because of the visual distortions inherent in such high-power lenses. It was not until the late 1940s that the tremendous optical advantages that an IOL could provide in visual rehabilitation were understood and acted upon by Harold Ridley.3–7 The implantation of IOLs is now a highly successful operation; the safety and efficacy of the procedure are now well established. For 1998 the number of IOL implants in the United States was estimated to be 1.6 million. Implantation data from other countries are scant, but the total number of implantations per year worldwide is increasing rapidly. Studies are still needed to determine which surgical technique(s) and which IOL design(s) are safest, most practical, and most economic for high-volume use in the less advantaged areas of the world. For general discussions that review the evolution and provide clinicopathologic overviews of IOLs, see Apple et al.7–10 and Binkhorst.11 Posterior chamber IOLs, following a long period of disfavour after the Ridley lens was discontinued, were reintroduced in the mid-1970s and early 1980s. Jaffe and other authors compared posterior chamber lenses with iris-supported lenses and were impressed by the superior results achieved with the former type of lens using an extracapsular cataract extraction technique. The use of posterior chamber IOLs is now clearly the treatment of choice.

Generation I (Original Ridley Posterior Chamber Lens)

A practical application of the concept of IOLs began with Harold Ridley,3–7 and credit for the introduction of lens implants clearly belongs to him. Ridley’s first IOL operation was performed on a 49-year-old woman at St Thomas’ Hospital in London on November 29, 1949. His ori ginal IOL was a biconvex polymethyl methacrylate (PMMA) disc designed to be implanted after extracapsular cataract extraction (ECCE) (Fig. 5-2-1). Ridley’s procedure was initially met with great hostility by several skeptical and critical ophthalmologists. However, good results were attained in enough cases to warrant further implantation of the Ridley IOL, although dislocation of the lens ultimately proved troublesome.

Table 5-2-1 The Evolution of Intraocular Lenses Generation

Date

Description

1949–1954

Original Ridley posterior chamber lens

1952–1962

Early anterior chamber lenses

III

1953–1975

Iris-supported lenses

1963–1990

Intermediate anterior chamber lenses

1975–1990

Improved posterior chamber lenses

1990 to present

Modern capsular posterior chamber lenses and modern anterior chamber lenses

Lens Design and Fixation

394

In 1967 Binkhorst11 proposed a detailed classification of the various means of fixation for each IOL type. In a 1985 update of this classification, Binkhorst12 listed four IOL types according to fixation sites: l Anterior chamber angle-supported lenses; l Iris-supported lenses; l Capsule-supported lenses; and l Posterior chamber angle (ciliary sulcus)-supported lenses. By common agreement, most surgeons today differentiate lens types as follows: l Iris-supported lenses; l Anterior chamber lenses; and l Posterior chamber lenses. From the time of Ridley’s first lens implantation to the present day, the evolution of IOLs can be arbitrarily divided into six generations (Table 5-2-1).

Fig. 5-2-1 Posterior view of an eye (obtained postmortem) showing the implantation site of a Ridley lens. To the time of death, almost 30 years after implantation, the patient’s visual acuity remained 20/20 (6/6) in both eyes. Note the good centration and clarity of the all-polymethyl methacrylate optic in the central visual axis. The lens was implanted by Dr. W. Reese and Dr. T. Hammdi of Philadelphia.

It is gratifying to note that Ridley, who died in 2001, lived long enough to experience the acknowledgment, respect, and honor he so fully deserved for this innovation. As a consequence of the relatively high incidence of dislocations with the Ridley lens, a new implantation site was considered − the anterior chamber, with fixation of the lens in the angle recess. The anterior chamber was chosen because less likelihood existed of dislocation within its narrow confines. In addition, anterior chamber lenses could be implanted after either an intracapsular cataract extraction (ICCE) or an ECCE. Also, anterior chamber placement of the pseudophakos was considered a simpler technical procedure than placement of the lens behind the iris. Although many surgeons worked on the concept of this type of lens, Baron, in France, is generally credited as being the first designer and implanter of an anterior chamber lens (Fig. 5-2-2A).10 He first performed this procedure on May 13, 1952. Late endothelial atrophy, corneal decompensation, and pseudophakic bullous keratopathy were observed with the original Baron lens and also developed with many subsequent anterior chamber lens designs. The entity now termed uveitis−glaucoma−hyphema (UGH) syndrome was described first when ocular tissue damage occurred that was clearly the result of poorly manufactured anterior chamber lenses.13 It took many modifications of the haptic-loop configuration and the lens-vaulting characteristics (see Fig. 5-2-2B) to develop an

Generation III (Iris-Supported Lenses)

Relatively frequent dislocation of the Ridley lens and an unacceptably high rate of corneal decompensation associated with the anterior chamber lenses available in the early 1950s caused some surgeons to discontinue implantation of IOLs entirely.14 However, iris-supported or iris-fixated IOLs were introduced subsequently in an attempt to overcome these problems. Cornelius Binkhorst in The Netherlands was an early advocate of iris-supported IOLs.11, 12 His first lens was a four-loop, iris-clip IOL (Fig. 5-2-3A) design. Although Binkhorst initially believed that IOL contact with the iris would not cause problems, he soon noted that iris chafing, pupillary abnormalities, and dislocation developed with the early irisclip lens. Also, in an effort to circumvent dislocation, Binkhorst made the anterior loops of his four-loop lens longer, but this led to increased corneal decompensation from peripheral touch. His initial implantations were done after ICCE, but occasionally he implanted his four-loop lens following ECCE. His positive experience with this procedure prompted him to modify his iris-clip lens design for implantation following ECCE. Binkhorst’s change from ICCE to ECCE and the introduction of his two-loop iridocapsular IOL (see Fig. 5-2-3B) in 1965 were important advances in both IOL design and mode of

5.2 Evolution of Intraocular Lens Implantation

Generation II (Early Anterior Chamber Lenses)

anterior chamber lens that allowed a reasonable prediction of longterm success. This was achieved largely because of the advances in lens design by Dr. Peter Choyce of England and later by Dr. Charles Kelman of New York.

ANTERIOR CHAMBER LENSES Original 1952 Baron lens

Modern anterior chamber lens

Fig. 5-2-2 Sagittal section of the anterior segment of the eye. (A) The original 1952 Baron anterior chamber lens, with fixation in the angle recess. Because this one-piece lens was rigid, sizing problems were unavoidable. Note the extremely steep anterior curvature of the lens. Such excessive anterior vaulting invariably caused corneal endothelial problems. (B) Placement of a modern anterior chamber lens fixated in the angle recess. Note the more subtle anterior vaulting of the loops and lens optic.

Fig. 5-2-3 Binkhorst iris-clip lenses. (A) A correctly positioned Binkhorst four-loop, iris-clip lens, well centered in an eye that had good visual acuity. Moderate pupillary distortion and sphincter erosion occur. Note the iris-fixation suture superior to the site of the large iridectomy. (B) Posterior view of an autopsy globe that contains a two-loop iridocapsular intraocular lens. Note the rod that helps to secure the lens to the iris through the iridectomy. An outer Soemmering ring is present, but the visual axis remains clear. The optic is well centered.

395

5 THE LENS

fixation.15 His and others’ experiences with the two-loop lens style and its modifications were influential in the development of modern design concepts of IOLs, including capsular-bag fixated, posterior chamber IOLs. Binkhorst’s innovative lens designs and his advocacy of ECCE came at a time when the entire future of IOL implantation was in jeopardy; they provided the major impetus that set the stage for modern posterior chamber lens implantations. During the early years of iris-fixated IOLs, many clinical and subclinical problems emerged, such as dislocation, pupillary deformity and erosion, iris atrophy with transillumination defects, pigment dispersion, uveitis, hemorrhage, and opacification of the media. Many of these complications were the result of chronic rubbing or chafing of the iris by IOL loops or haptics. Problems were especially severe with metal loop IOLs and also occurred frequently with multiple-looped lenses because uveal contact and chafing against the mobile iris tissues were unavoidable with these designs. An increased incidence of corneal edema occurred in association with iris-supported lens designs. Corneal decompensation and pseudophakic bullous keratopathy became major indications for penetrating keratoplasty. The well-known coexistence of pseudophakic bullous keratopathy and cystoid macular edema (CME) has been termed corneal-retinal inflammatory syndrome by Obstbaum and Galin.16 Binkhorst’s return to ECCE, with the introduction of his two-loop iridocapsular lens in 1965 (see Fig. 5-2-3B),17 brought about an almost immediate reduction in the incidence of many of these complications. Most iris-supported lenses were biplanar, with the optic placed in front of the pupil. In general, biplanar IOLs required a larger limbal wound opening for insertion. The change to capsular fixation after ECCE provided better stability for the pseudophakos. This important modification was a forerunner to capsular sac (in-the-bag) fixation of modern posterior chamber IOLs. At the time when iris-supported lenses were in widespread use, and until the mid-1980s in many cases, manufacturing methods and surgical techniques were less sophisticated. It is now clear that most modern, high-quality anterior and posterior chamber IOLs provide better success than the IOLs that depend on the iris for support. At present, it is the consensus of surgeons that when a patient who has an iris-supported IOL develops late complications, such as inflammation or corneal decompensation that does not respond rapidly to conservative therapy, lens explantation and/or exchange is usually the best treatment.

Generation IV (Intermediate Anterior Chamber Lenses)

396

While iris-supported IOLs underwent major modifications in the early 1950s up to the beginning of the 1980s, several designs of anterior chamber IOLs were introduced. The problems of tissue chafing and difficulties in correct sizing associated with rigid IOLs were addressed by the development of anterior chamber lenses with more flexible loops or haptics (Box 5-2-1). Unlike the ill-fated, nylon-looped lenses introduced by Dannheim in the early 1950s, the fixation elements of these anterior chamber IOLs were made from more stable polymers, usually PMMA and polypropylene. The best lenses were the various rigid18 and flexible, open-loop, onepiece PMMA designs, such as the three- and four-point fixation Kelman IOLs.19 Modifications of the latter have been in use since the late 1970s and are the styles most commonly implanted today (Fig. 5-2-4). These lenses now are well designed, correctly vaulted, and properly sized and can provide excellent long-term results. As with the early generation of anterior chamber IOLs, new lens designs included both haptic (footplate) fixation lenses and small-diameter, round-looped IOLs. Although in the 1950s implantations with early anterior chamber IOLs were often disappointing, some models of anterior chamber lenses provided good success, particularly when the lens was properly sized. Two important factors that led to an improved success rate with anterior chamber IOL use are: l Improved lens designs; and l Improved manufacturing techniques. More appropriate lens flexibility has decreased the need for perfect sizing. Increased attention has been given to the anterior-posterior vaulting characteristics of IOLs, which has reduced the incidence of intermittent touch and uveal chafing problems. Design flaws in older lens styles have been identified and these lenses removed from the market in the United States. Tumble polishing of IOLs, particularly one-piece, all-PMMA lenses, produces excellent surfaces

Box 5-2-1 Anterior Chamber Lenses Disadvantages of Closed-Loop Anterior Chamber Lenses Lenses may be difficult to size Lenses may have inappropriate vault–compression ratios; when a lens is compressed, it may vault anteriorly or posteriorly − either type of response can cause deleterious effects Small-diameter loops may cause a “cheese-cutter” effect, particularly if the lens is too large; subsequent erosion and chafing can cause uveitis, including cystoid macular edema and pseudophakic bullous keratopathy Some lenses have a large contact zone over broad areas of the angle with the potential for secondary glaucoma The poorly finished, sharp edges of some lens models can cause chafing, which leads to sequelae such as uveitis or the uveitis– glaucoma–hyphema syndrome Synechiae formation around the small-diameter loops may make the lens difficult to remove when necessary; tearing of ocular tissues, hemorrhage, and iridocyclodialysis are possible complications of intraocular lens removal if correct procedures are not used Advantages of Modern, Open-Loop, One-Piece, All-Pmma Flexible Anterior Chamber Lenses Most modern lenses have an excellent finish with highly polished smooth surfaces and rounded edges from tumble polishing; tissue contact with any component of these intraocular lenses is much less likely to result in chafing damage Sizing is less critical with flexible, open-loop designs In contrast to a closed-loop anterior chamber intraocular lens, the vault (a well-designed, open-loop lens) is maintained even under high compression – this minimizes intraocular lens touch against the cornea anteriorly, or against the iris posteriorly Point fixation is possible, since the haptic may subtend only small areas of the angle outflow structures Most open-loop intraocular lens designs are much easier to remove, when necessary, especially those with Choyce-like haptic or footplate fixation; the well-polished surfaces of these lenses usually do not become completely surrounded by goniosynechiae or cocoon membranes, and, therefore, can usually be removed if necessary without undue difficulty or excessive tissue damage

and edges. The elimination of sharp optic or haptic edges is critical in the production of anterior chamber IOLs. This is true even more so than for posterior chamber IOLs because anterior chamber IOLs are fixated in a confined space directly adjacent to delicate anterior segment tissues. The two major disadvantages of an anterior chamber IOL, as compared with posterior chamber lens styles, are: l The close proximity of the haptics or loops to delicate tissues such as the trabecular meshwork, corneal epithelium, angle recess, and anterior iris surface; and l The difficulty often encountered in IOL sizing, particularly with rigid lens designs. The close proximity of anterior chamber lens components to the corneal endothelium is an obvious disadvantage because of the potential for corneal decompensation and/or pseudophakic bullous keratopathy as a result of contact of the cornea with the IOL. In the past, the most common causes of pseudophakic bullous keratopathy were related to anterior chamber IOLs that were sized incorrectly, vaulted too steeply, or designed with an inappropriate amount of flexibility.20 Haptics or spatula-like footplates are one of the two types of fixation elements used for anterior chamber IOLs. Haptics or footplates, popularized by Peter Choyce, are often likened to the flattened portion of a spatula and were used originally with the more rigid IOL styles. They now are used with both rigid and flexible modern anterior chamber IOLs. When IOL removal is necessary for any reason, the footplate generally slides out of the eye much more easily than does a smalldiameter loop and with minimal tissue damage. Small-diameter lens loops are the second type of fixation element for anterior chamber IOLs. Loops may be of either an open or a closed design. Round, small-diameter, closed loops may cause a “cheese-cutter”

5.2

Fig. 5-2-4 Modern one-piece, all-polymethyl methacrylate, Kelman-style anterior chamber lenses of four-point and three-point fixation designs. Note the excellent polishing and tissue-friendly Choyce-Kelman style footplates. These represent modern, state-of-the-art lenses that should be distinguished clearly from the earlier, unsatisfactory, closed-loop anterior chamber lenses.

effect within the eye and difficulty with removal. A 360° fibrouveal encapsulation, or “cocoon,” often forms around such small-diameter, round loops as the loops become embedded in the tissues of the angle recess. If the correct explantation procedure is not used, these adhesions may result in tissue tears, hemorrhage, and iridocyclodialysis. These anterior chamber IOLs,21–25 often generically classified together as “closed-loop lenses,” do not provide the safety and efficacy achieved by other anterior chamber lens designs, such as finely polished, flexible, one-piece, all-PMMA lenses (see Fig. 5-2-4). By 1987 the Food and Drug Administration had placed IOLs of the closed-loop design on core investigational status. This had the effect of removing them from the market in the United States, although it did not prevent the export of such lenses. The flexible, open-loop designs,24–28 modifications of the original Kelman anterior chamber IOLs (with Choyce-style footplates), can be well finished using tumble polishing, which provides a rounded, “tissue-friendly” surface at points of haptic contact with delicate uveal tissues. One-piece IOLs, particularly those with a footplate design, are usually much easier to explant than IOLs with round, small-diameter loops, of either closed-loop or open-loop design. Iris- or scleral-fixated, sutured posterior chamber IOLs may be used in cases formerly reserved for anterior chamber IOLs. Results are encouraging.29, 30 Uncertainty still exists as to whether a retropupillary lens is superior to a modern, well-manufactured, Kelman-style anterior chamber IOL for cases such as intraoperative capsular rupture or vitreous loss or as a secondary or exchange procedure. The technique is more difficult than insertion of a single anterior chamber lens and should, therefore, be carried out only by an experienced surgeon.

Generation V (Improved Posterior Chamber Lenses)

The return to Harold Ridley’s4–7 original concept of IOL implantation in the posterior chamber occurred after 1975. John Pearce31 of England implanted the first uniplanar posterior chamber lens since Ridley.32 It was a rigid tripod design with the two inferior feet implanted in the capsular bag and the superior foot implanted in front of the anterior capsule and sutured to the iris. Steven Shearing33 of Las Vegas introduced a major lens design breakthrough in early 1977 with his posterior chamber lens. The design consisted of an optic with two flexible J-shaped loops. William Simcoe of Tulsa publicly introduced his C-looped posterior chamber lens shortly after Shearing’s J-loop design appeared. Eric Arnott of London was an early advocate of one-piece, allPMMA posterior chamber IOLs. The flexible open-loop designs (J-loop, modified J-loop, C-loop, or modified C-loop) still account for the largest number of IOL styles available today (Fig. 5-2-5).

Evolution of Intraocular Lens Implantation

Fig. 5-2-5 View from behind of an autopsy eye. (A) A Sinskey-style, J-loop posterior chamber intraocular lens implanted within the lens capsular bag. The optic is well centered, the visual axis is clear, and there is only minimal regeneration of cortex in scattered areas. Moderate haziness or opacity occurs at the margins of the anterior capsulotomy, which does not encroach on the visual axis. (B) The placement of the loop of this modified C-style intraocular lens in the capsular bag.

One obvious major theoretical advantage that a posterior chamber IOL has over an anterior chamber IOL is its position behind the iris, away from the delicate structures of the anterior segment. As posterior chamber lens implantation evolved, the type of fixation achieved in the early years depended largely on chance or on the surgeon’s individual preference. As Figure 5-2-6 illustrates, several loopfixation sites are possible with modern, flexible-loop posterior chamber IOLs. In general, the loops were anchored in one of three ways: l Both loops were placed in the ciliary region; l Both loops were placed within the lens capsular sac; or l O ne loop (usually the leading or inferior loop) was placed in the capsular sac and the other loop (usually the trailing or superior loop) in a variety of locations anterior to the anterior capsular flap. These fixation sites have been confirmed histologically by analyses of postmortem globes implanted with posterior chamber IOLs. The return to posterior chamber lenses coincided with the development of improved ECCE surgery. Shearing33 identified four major milestones that have marked the evolution of ECCE surgery: l Microscopic surgical techniques; l Phacoemulsification; l Iridocapsular fixation; and l Flexible posterior chamber lenses.

397

POSSIBLE PLACEMENT SITES OF POSTERIOR CHAMBER LENS LOOPS

THE LENS 3 5

4 6

8 Site 1: loop in the ciliary sulcus. Site 2: loop after erosion into the ciliary body stroma in the region of the major iris arterial circle. Site 3: loop in contact with the iris root. Site 4: loop attached to a ciliary process. Site 5: loop in aqueous without tissue contact (can result in ‘windshield wiper’ syndrome because of inadequate fixation). Site 6: loop in the lens capsular sac. Site 7: loop ruptured through the lens capsular sac (a rare occurrence). Site 8: loop in the zonular region between the ciliary sulcus and the lens capsular sac. The loop may penetrate the zonules (zonular fixation) or extend as far posteriorly as the pars plana (pars plana fixation).

Fig. 5-2-6 The possible placement sites of posterior chamber lens loops.

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Without microscopic surgery, modern IOL implantation would be far more difficult. Although phacoemulsification was promoted originally because it required only a small wound, it became clear that if an IOL were to be inserted, the wound would have to be enlarged after removal of the cataract, and thus nonultrasonic surgical methods were refined. By 1974, implantation of IOLs again began to achieve significant acceptability. A natural marriage between phacoemulsification and implantation of IOLs occurred. As noted previously, Cornelius Binkhorst11, 12, 17 was one of the pioneers in the return to the ECCE procedure. Binkhorst recognized that an intact posterior capsule enhanced stability, and he also recognized the many advantages of IOL implantation within the capsular sac. Evidence continues to accumulate that CME and retinal detachment occur less frequently with ECCE than with ICCE. The introduction of flexible posterior chamber lenses designed to be implanted following ECCE largely resolved the debate about ECCE versus ICCE clearly in favor of the extracapsular procedure. Securing both loops in the lens capsular sac is the only type of fixation in which IOL contact with uveal tissues is avoided.34 Placement of a lens with one or both loops outside the capsular bag is associated with various potential complications, including decentration and uveal erosion.34, 35 The consequences of uveal touch have been learned after experiences with the earlier iris-fixated IOLs. The excellent success rate now achieved with posterior chamber IOL implantation is associated with improved IOL designs and improved surgical techniques, including the meticulous placement of loops (Box 5-2-2). Posterior capsule opacification (PCO; Elschnig pearls, secondary or after cataract) is a significant postoperative complication in IOL implantation. A well-designed posterior chamber lens in the lens capsular sac provides a gentle but taut radial stretch on the posterior capsule. Of the present open-loop flexible IOLs, the one-piece, all-PMMA posterior chamber designs with posterior convex or biconvex optics appear to be especially effective in providing a symmetrical stretch. Symmetrical stretch may help minimize PCO, as it reduces the folds in the capsular sac and holds the posterior capsule firmly against the posterior surface of the IOL optic. This is sometimes termed the “no space, no cells” concept. The quality of surgery and the accuracy of loop placement are important factors that affect the outcome of the cataract operation. Two very

Box 5-2-2 Advantages of Placing Both Loops in the Lens Capsular Sac Intraocular lens is positioned in the proper anatomical site Both loops can be placed symmetrically in the capsular sac as easily as in the ciliary sulcus Intraoperative stretching or tearing of zonules by loop manipulations in front of the anterior capsular leaflet is avoided Low incidence of lens decentration and dislocation No evidence of spontaneous loop dislocation Intraocular lens is positioned a maximal distance behind the cornea Intraocular lens is positioned a maximal distance from the posterior iris pigment epithelium, iris root, and ciliary processes Iris chafing (caused by postoperative pigment dispersion into the anterior chamber) is reduced No direct contact by, or erosion of, intraocular lens loops or haptics into ciliary body tissues Chronic uveal tissue chafing is avoided, and the probability of long-term blood–aqueous barrier breakdown is reduced Surface alteration of loop material is less likely Intraocular lens implantation is safer for children and young individuals Posterior capsular opacification may be reduced Intraocular lens may be easier to explant, if necessary

helpful tools are available to surgeons that make precise loop or haptic placement possible: l Ophthalmic visco-surgical devices (OVDs); and l New methods to control the size, shape, and quality of the anterior capsulotomy. The intercapsular (envelope) technique and its successor, circular continuous tear capsulorrhexis, greatly increase the ability to achieve accurate and permanent loop placement.

Generation VI (Modern Capsular Lenses − Rigid PMMA, Soft Foldable, and Modern Anterior Chamber)

By the end of the 1980s clinical laboratory studies demonstrated clearly that cataract surgical techniques and IOL design and manufacture had shown remarkable advances.36–40 Surgical technique and IOL design and manufacture had advanced to a point at which the older techniques gave way to more modern ones that allowed consistent, secure, and permanent in-the-bag (capsular) fixation of the pseudophakos. A marriage between IOL design and improved surgical techniques has evolved into capsular surgery. The “capsular” IOLs are fabricated from both rigid and soft biomaterials. The many changes in surgical techniques that occurred after 1980 and into the 1990s include the introduction of OVDs,40–43 increased awareness of the advantages of in-the-bag fixation, the introduction of continuous curvilinear capsulorrhexis (CCC)44–51 (Fig. 5-2-7), hydrodissection52 (Fig. 5-2-8), and the increased use of phacoemulsification. This has allowed not only much safer surgery but also implantation through a smaller incision than was possible in the early days of extracapsular extraction. The evolution from can opener toward capsulorhexis (see Fig. 5-2-7) was initiated by Binkhorst, who developed a two-step (envelope) technique that eventually evolved into the single-step CCC. Two clear advantages of CCC exist over the early can-opener techniques. First, the formation of radial tears (Fig. 5-2-9) is reduced,47 which minimizes radial tears of the anterior capsule; these reduce the stability of the capsular bag and may allow prolapse of haptics out of the capsular bag through the anterior capsular tear. Second, and less commonly recognized, capsulorhexis provides a stable capsular bag that allows copious hydrodissection, which in turn is very helpful in cortical cleanup. With a frayed, emptier capsular edge, such as seen with the can-opener technique, hydrodissection is difficult without forming unwanted radial tears. Hydrodissection (see Fig. 5-2-8) was a term coined by Faust52 in 1984. This technique, and the many variations thereof (e.g., cortical cleavage hydrodissection, hydrodelineation), makes the surgery much simpler in that mobilization and removal of cells and cortical material

5.2

Fig. 5-2-8 Surgeon’s view (cornea and iris removed) of a human eye (obtained postmortem) showing experimental hydrodissection. In this case the cannula is placed immediately under the anterior capsule (cortical cleavage hydrodissection). Hydrodissection is one of the most important maneuvers to help reduce the incidence of posterior capsular opacification.

are rendered much easier. The long-term risk of PCO is, in turn, clearly minimized because of the more thorough removal of cells in cortical material, especially in the region of the equatorial fornix. Modern phacoemulsification, pioneered by Charles Kelman, has now made possible the removal of lens material through small incisions and the implantation of IOLs through incisions down to 3 mm in length, as opposed to incisions of 11–12 mm length in the early days of ECCE. Many real advantages of small-incision cataract surgery exist, including safer healing (with fewer risks of complications such as inflammation), more rapid healing, and rapid recovery of visual rehabilitation (with less postoperative astigmatism). In accompaniment with the developments of surgical techniques that allow secure in-the-bag implantation, IOLs have evolved that work well with these techniques − both rigid PMMA designs (Figs 5-2-10 and 5-2-11) and foldable IOLs.53 Figure 5-2-10 shows an example of a modern, state-of-the-art, one-piece, all-PMMA IOL that is designed for in-the-bag implantation. These can be inserted through incisions as small as 5.5–6 mm in length and provide an excellent alternative for the surgeon who finds the almost 50-year history of PMMA as a lens biomaterial of comfort. Long-term results with these IOLs are excellent and, indeed, these lenses provide slightly better centration than do some of the more modern foldable lenses at the present time. The ideal diameter for a one-piece IOL design such as that in Fig. 5-2-10 is 12–12.5 mm, which allows it to fit perfectly into the capsular bag (which measures about 10.5 mm in diameter). The diameter of the

Fig. 5-2-9 Surgeon’s view of an experimentally performed can-opener capsulectomy, with typical radial tears to the equator of the anterior capsule. The cornea and iris are removed from a human eye, obtained postmortem. Following clinical can-opener anterior capsulectomy, one to five radial tears invariably occur. (Reproduced with permission from Assia EI, Apple DJ, Tsai JC, Lim ES. The elastic properties of the lens capsule in capsulorrhexis. Am J Ophthalmol. 1991;111:628−32.)

Evolution of Intraocular Lens Implantation

Fig. 5-2-7 Surgeon’s view (cornea and iris removed) of a porcine eye showing the capsulorrhexis procedure. Notice the smooth edges of the anterior capsular tear, which is the key feature of this procedure.

Fig. 5-2-10 A modern, one-piece, all-PMMA, capsular IOL implanted experimentally in a human eye: posterior view (Miyake technique) of the eye (obtained postmortem). Note the excellent centration and a perfect fit within the capsular bag.

c iliary sulcus is only slightly larger (approximately 11.0 mm)53 and actually decreases with age. These rigid PMMA IOL designs have been found to be very satisfactory in pediatric IOL implantation.54, 55 As 90% of the growth of the infantile globe occurs during the first 18 months to 2 years (Fig 5-2-12), it is fair to assume that “adult” 12 mm lenses can be safely implanted in children this age and older, with the achievement of good results (Figs 5-2-12 and 5-2-13). The problem in the past with IOL implantation has been that of PCO. With present techniques, this is best prevented using primary posterior capsulectomy. Improved small-incision surgical techniques and IOL designs have resulted in a natural evolution toward foldable lenses.56–67 Most foldable lenses today are manufactured from silicone, hydrogel, or acrylic material (Figs 5-2-14 to 5-2-16). The earliest designs for which clinical usage was widespread were the plate lenses known as the “Mazzocco taco.” In early years these were manufactured poorly and often not implanted properly into the capsular bag, so many complications ensued. In recent years manufacturing quality has become much better, and these lenses are now satisfactory for clinical usage (Figs 5-2-17 and 5-2-18). The best plate lenses are those with large positioning holes that allow in-the-bag synechia formation, which enhances fixation and stability.64

399

5 THE LENS Fig. 5-2-11 Scanning electron micrograph of a well-designed, tumblepolished, modified C-loop, one-piece, all-PMMA posterior chamber IOL. The total length of this capsular IOL design is 12.0 mm. Note the excellent, smooth finish of this well-polished IOL. (Original magnification ×10.)

Fig. 5-2-13 Posterior view (Miyake technique) of an eye of a 2-year-old child (obtained postmortem). This was implanted experimentally with a 12-mm, one-piece, all-PMMA IOL in the capsular bag. Note the excellent fit in the capsular bag. (Reproduced with permission from Wilson ME, Apple DJ, Bluestein EC, Wang XH. Intraocular lenses for pediatric implantation: biomaterials, designs, and sizing. J Cataract Refract Surg. 1994;20:584−91.)

GROWTH OF GLOBE AND LENS CAPSULAR BAG

evacuated 11 capsular bag diameter (mm) 10 9 8 7 6

0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 age (years) 16–19 22 23 anterior–posterior axial length of globe (mm)

Fig. 5-2-12 Growth of the globe and lens capsular bag. These results are based on a study of 50 eyes obtained postmortem and demonstrate that the growth of the globe and lens capsular bag occurs relatively rapidly during the first 18 months to 2 years. (Reproduced with permission from Wilson ME, Apple DJ, Bluestein EC, Wang XH. Intraocular lenses for pediatric implantation: biomaterials, designs, and sizing. J Cataract Refract Surg. 1994;20:584−91.)

400

The most commonly implanted designs at present are three-piece lenses that consist of silicone, acrylic, or hydrogel optics. Plate lenses continue to provide excellent results. These lenses can be implanted through incisions smaller than 5 mm in length, and visual rehabilitation is now incredibly fast with various further modifications, such as clear corneal incisions and topical anesthesia. Such surgery is virtually analogous to arthroscopy of the eye. Lens design and manufacture have improved to such an extent that perhaps the most important factor in the achievement of a successful result is not the IOL itself but the quality of surgery. These factors are very important now that there are high standards for results following IOL implantation, especially in this era when IOL implantation is considered not only a means of optical rehabilitation after cataract removal but also a bona fide refractive procedure. The development of bi- and multifocal IOL designs is one example of this evolutionary process. An increased interest in clear lens extraction for myopia and the use of phakic IOLs also exemplifies the evolution toward refractive IOLs. It is of utmost importance to achieve symmetrical capsular-bag fixation and good cortical cleanup to minimize the chance for complications, such as lens decentration and formation of a Soemmerring ring.

Fig. 5-2-14 Posterior view (Miyake technique) of a well-implanted Advanced Medical Optics three-piece, silicone IOL. The lens is implanted following excellent cortical cleanup in a human eye obtained postmortem.

Fig. 5-2-15 Posterior view (Miyake technique) of a well-implanted Alcon AcrySof acrylic IOL. The lens is well centered in the capsular bag after thorough cortical removal.

5.2

Fig. 5-2-17 Scanning electron micrograph that shows the marked improvement in plate lens manufacture by the 1990s. Note the excellent overall design and manufacture finish. (Original magnification ×10.)

The development of foldable lenses is one of fine tuning. For example, much effort is now being expended to develop ever more tissue-friendly optic biomaterials. Figure 5-2-19 reveals a complication that may occur occasionally in patients who have silicone lenses and who require subsequent vitreoretinal surgery using silicone oil.68 Work is under way to address this complication by modifications of the biomaterial to change factors such as its surface characteristics.69 Work is also in progress on the attachment of different styles of haptic materials to the optic to achieve better and more stable fixation of the haptics in the capsular bag. Note that the various ultramodern designs of anterior chamber lenses developed for both aphakic and phakic implantations are considered to belong to generation VI. These include the various Kelman-Choyce designs and modifications by Baikoff and Clemente (see Fig. 5-2-4). These are categorized here to separate them from the myriad of generally inferior anterior chamber IOLs that were available in the earlier intermediate period between 1963 and 1990 (generation IV). The ultramodern designs are suitable for specific clinical indications and clearly should not be included in the generic concept that “all anterior chamber IOLs are bad.”

Recent Advances Our line of research at the Center for Research on Ocular Therapeutics and Biodevices, now transferred to the Moran Eye Center in Salt Lake City, Utah and renamed as the David J Apple MD Laboratories for Ophthalmic Devices Research, allows us to be in close contact not only

Fig. 5-2-18 A well-implanted STAAR-Chiron style silicone plate IOL, with excellent cortical removal and centration. Posterior view (Miyake technique) of the eye (obtained postmortem).

Evolution of Intraocular Lens Implantation

Fig. 5-2-16 A STAAR Surgical Corporation three-piece IOL with polyimide haptics: posterior view (Miyake technique) of an eye (obtained postmortem). The lens is well centered and positioned in a clean capsular bag.

Fig. 5-2-19 View of a patient who has silicone IOL and who later required vitreoretinal surgery with silicone oil. Note the dense bubbles that cover the optic surface, which impair both vision and the surgeon’s view into the eye.

with surgeons worldwide but also with virtually all companies manufacturing IOLs and related devices. One of the best means of discerning manufacturers’ trends is to determine where they are investing energy and funds for the future. On the basis of our contacts and relationships with industry and after a close review of the available scientific literature, we have noted some general principles and tendencies with regard to the development of new foldable IOLs. Focusing on IOLs manufactured in the United States, we have identified seven selected innovative directions. Listed in appropriate chronological order of their introduction, they are as follows: 1. Large fixation holes or foramina have been incorporated in the haptic components of one-piece plate designs (Fig. 5-2-20A). Fibrous adhesions often occur between the anterior and posterior capsules following ingrowth of fibrocellular tissue through the holes (see Fig. 5-2-20B,C). This helps enhance the fixation and stability of these designs within the capsular bag.70–72 It is important to note that this fibrous growth requires at least 2 weeks and often much more to establish itself and help anchor the IOL. This design feature has been incorporated into lenses manufactured from silicone (including the Staar toric IOL), hydrogel (hydrophilic acrylic IOLs, and Collamer (Staar CC4203VF) materials. 2. For three-piece foldable designs, the preferred haptic materials are the relatively rigid materials with good material memory, such as PMMA, polyimide (Elastimide), or polyvinylidene fluoride (PVDF)73, 74 (Fig. 5-2-21A−D). Examples of major designs of such lenses on the American market include the Advanced Medical Optics (AMO) SI40 NB with PMMA haptics, the Bausch & Lomb SoFlex C31UB and the Staar AQ-1016 with polyimide haptics, and the AMO CeeOn

401

5 THE LENS A

Fig. 5-2-20 Gross and light microscopic photographs of a pseudophakic human eye obtained postmortem, implanted with a silicone plate lens, with large fenestrations. (A) Miyake-Apple posterior photographic technique. The arrow indicates the fibrotic tissue growing through one of the large fenestrations. (B, C) Fusion between anterior and posterior capsules promoted by the fibrocellular tissue growing through the fenestration (Masson’s trichrome; original magnification ×100 and ×400, respectively). PC, Posterior capsule. (Reproduced from Apple DJ, Auffarth GU, Peng Q, Visessook N. Foldable intraocular lenses: evolution, clinicopatholgic correlations, complications. Thorofare, NJ: Slack; 2000.)

402

Edge 911 with PVDF haptics (previously Pharmacia). These haptics have appropriate memory characteristics that help enhance lens centration and stability and provide better resistance to postoperative contraction forces within the capsular bag. 3. One of the most important features that have been incorporated in new foldable lenses in terms of decreasing the incidence of PCO

Fig. 5-2-21 Gross photographs of four modern three-piece silicone lenses with different haptic materials. (A) From left to right: PMMA (CeeOn 912, Pharmacia Inc., Peapack, NJ), Elastimide (AQ-2003, Staar Surgical, Inc., Monrovia, CA), polyvinylidene fluoride (PVDF) (CeeOn Edge 911, Pharmacia Inc.), and Prolene (SI-30 NB, AMO, Irvine, CA). (B−D) Details of the optic-haptic junctions of the lenses having loops manufactured from relatively rigid materials (PMMA, Elastimide, and PVDF, respectively). (Reproduced from Izak AM, Werner L, Apple DJ, et al. Loop memory of different haptic materials used in the manufacture of posterior chamber intraocular lenses. J Cataract Refract Surg. 2002;28:1229−35.)

is the square, truncated optic edge. Various experimental animal s tudies by Nishi in Japan, analyses of human autopsy globes in our laboratory, as well as several clinical studies with the three-piece AcrySof lens (MA30BA and MA60BM), the first design identified with this geometric characteristic, demonstrated an enhanced barrier effect against cell migration/proliferation on the posterior capsule

5.2

Evolution of Intraocular Lens Implantation

Fig. 5-2-22 Light photomicrographs and schematic illustrations showing the subtle differences regarding the barrier effect of an IOL optic with a rounded edge versus a square truncated edge. (A) Photomicrograph of the site of implantation of an IOL optic with a rounded edge. Note the large Soemmering ring on the left (red stain). Note also the migration of cortical material (red material) onto the posterior peripheral surface of the lens optic, a phenomenon that sometimes occurs with a rounded edge. Rarely does such growth extend onto the central visual axis (Masson’s trichrome; original magnification ×100). (B) Round edge: some cells may squeeze behind the posterior peripheral aspect of the optic, creating a paracentral rim of opacification (arrows) but usually sparing the visual axis. (C) Photomicrograph of a case in which the Soemmering ring (red) remains totally confined to the right of the square optic edge, leaving the posterior capsule (lower left) cell-free (Masson’s trichrome; original magnification ×50). (D) Square truncated optic edge seems to provide an abrupt barrier (arrows), leaving the entire optical zone free of cells. AC, Anterior capsule; PC, posterior capsule. (A, B, and D, Reproduced from Peng Q, Visessook N, Apple DJ, et al. Surgical prevention of posterior capsule opacification. Part III. Intraocular lens optic barrier effect as a second line of defense. J Cataract Refract Surg. 2000;26:198−213. C, Reproduced from Werner L, Apple DJ, Pandey SK. Postoperative proliferation on anterior and equatorial lens epithelial cells. In: Buratto L, Werner L, Zanini M, Apple DJ, eds. Phacoemulsification: principles and techniques. Thorofare, NJ: Slack; 2002:603−23.)

Fig. 5-2-23 Gross and light microscopy photographs of the first human eye obtained postmortem with a single-piece AcrySof lens (Alcon Laboratories, Forth Worth, TX) accessioned in our center. (A) The lens is well centered and the capsular bag is clear. (B) Light photomicrograph of a histological section from the same eye. The arrow indicates the imprint of the square edge of the lens optic on the capsular bag, causing a barrier effect that prevented retained/regenerative cortical material from the Soemmering ring to migrate onto the posterior capsule, opacifying the visual axis (Masson’s trichrome; original magnification ×400). (Reproduced from Escobar-Gomez M, Apple DJ, Vargas LG, et al. Scanning electron microscopic and histologic evaluation of the AcrySof SA30AL acrylic intraocular lens. J Cataract Refract Surg. 2003;29(1):164−69.)

403

5 THE LENS

toward the visual axis.75–87 This IOL design feature has also been incorporated in other lenses such as the AMO Sensar IOL with the new OptiEdge optic configuration, a square posterior optic edge and a rounded anterior optic edge. Lenses manufactured from other materials, such as silicone (Pharmacia CeeOn Edge 911) and hydrophilic materials (Rayner Centerflex and the Ciba Vision MemoryLens), now present this design feature. The Bausch & Lomb Hydroview foldable hydrogel IOL does not yet have the truncated square optic edge technology, but the manufacturer is working to introduce it on updated models (Fig. 5-2-22). 4. Manufacturers have invested heavily and with great success in single-piece designs, all fabricated from the same material as the optic component. The Alcon (SA30AL and SA60AT) AcrySof IOL is a hydrophobic single-piece acrylic design that has provided excellent results (Fig. 5-2-23). 5. Manufacturers are also investing in the development of injector systems to be used with the new lens designs. 6. Perhaps the most energy and funding are being spent on new and complex IOLs that not only restore the refractive power of the eye after cataract surgery but also provide special features, including multifocality, toric corrections (Fig. 5-2-24A), pseudoaccommodation (Fig. 5-2-24B,C), postoperative adjustment of the IOL refractive power,

and image magnification (telescopic lenses) (Fig. 5-2-24D).88–91 Itemization of these IOL designs is not yet useful because proof of safety and efficacy is still in great flux. With any IOL, the issue of “biocompatibility” must be assessed. Not only do surgeons today seem to be seeking IOLs that are easy to insert/inject through small incisions − perhaps the main factor influencing manufacturers’ IOL development − but also more attention is being paid to the interaction of each IOL design within the surrounding capsular bag. Issues such as postoperative cell proliferation within the capsular bag, including PCO (Fig. 5-2-25), anterior capsule opacification (ACO) (Fig. 5-2-26), and interlenticular opacification (ILO) (Fig. 5-2-27) with piggyback IOLs, are used as one indication of lens biocompatibility.92–99 This goes far beyond the normal postoperative inflammatory reaction observed after cataract surgery with IOL implantation. Different studies from our laboratory demonstrated that the choice of IOL design and material can largely influence the outcome of these complications, but the role of surgical techniques should not be underestimated. Last but not least, a “perfect” IOL would not be effective in preventing excess cell proliferation within the capsular bag after bad surgery. 7. The renewed interest in phakic IOLs, which we now realize can potentially correct any refractive error, is also progressing rapidly, and itemization of special IOL models as being those of choice is

D C

404

Fig. 5-2-24 Special intraocular lenses. (A) Gross photograph of a toric lens (AA-4203TF or AA-4203TL Staar Surgical, Inc.). This lens has basically the same design as single-piece, plate silicone posterior chamber lenses with large fenestrations but with an incorporated cylindrical correction. (B,C) Schematic drawings representing two accommodative lenses, the AT-45 lens, manufactured by C&C Vision (Irvine, CA), and the AKKOMMODATIVE 1 CU, manufactured by HumanOptics (Erlangen, Germany), respectively. The first is essentially a plate haptic lens with Elastimide haptics. It is stated that redistribution of the ciliary body mass during effort for accommodation will result in increased vitreous pressure, which will move the optic of this lens anteriorly within the visual axis, creating a more plus powered lens. The second is a one-piece lens, manufactured from a hydrophilic acrylic material. It is stated that the special mechanical properties of this lens also enable it to change power during the contraction of the ciliary muscle. (D) Schematic drawing representing the implantable miniaturized telescope (IMT) (VisionCare Ophthalmic Technologies Inc., Yehud, Israel). This is the only intraocular device available that is designed specifically to improve vision of patients suffering from age-related macular degeneration. The IMT is composed of two parts, an optical cylinder and a carrying device. The optic cylinder is made of pure glass. The carrying device is made of black PMMA. The latter has a general configuration of a posterior chamber intraocular lens, with two modified C-loops or haptics that hold the device in the capsular bag. Once in place, the anterior part of the optic extends anteriorly for approximately 1 mm through the pupil. It is designed to be stabilized approximately 2 mm posterior to the corneal endothelium. (A-D, Reproduced from Werner L, Apple DJ, Schmidbauer JM. Ideal IOL (PMMA and Foldable) for year 2002. In: Buratto L, Werner L, Zanini M, Apple DJ, eds. Phacoemulsification: principles and techniques. Thorofare, NJ: Slack; 2002:435−52.)

these phakic lenses, designed to be inserted through small incisions (Figs 5-2-28 and 5-2-29). Although a large spectrum of lenses is available today, the IOL of choice still depends on a surgeon’s personal preference based on multiple factors personalized to each individual, largely influenced by different features unique to each patient, such as the patient’s history and clinical status, but also by the occurrence of intraoperative complications.

5.2 Evolution of Intraocular Lens Implantation

not yet possible. In our opinion, it is somewhat ironic that anterior chamber IOLs, previously relegated by many surgeons to a wastebasket of discarded devices, are now being resurrected and researched by both major and start-up manufacturers as a possible lens of choice for refractive correction.100–102 Lenses designed for iris fixation and placement in the posterior chamber are also being studied, with good results to date. There is a trend for the use of foldable materials for

Fig. 5-2-25 Gross photographs from pseudophakic human eyes obtained postmortem showing different examples of posterior capsule opacification. (A) The eye was implanted with a rigid three-piece PMMA lens, which presents asymmetric fixation (bag-sulcus). Massive opacification of the capsular bag can be observed. (B) Eye implanted with a one-piece PMMA lens, presenting an important Soemmering ring formation and posterior capsule opacification, which required Nd:YAG laser posterior capsulotomy. Note the proliferation of Elschnig pearls around the orifice of the posterior capsulotomy. (C) Eye implanted with a three-piece AcrySof lens. Although there is a significant Soemmering ring formation, the square edge of the lens prevented the retained/regenerative material from opacifying the visual axis. (A, Reproduced from Apple DJ, Solomon KD, Tetz MR, et al. Posterior capsule opacification. Surv Ophthalmol. 1992;37:73−116. B, Reproduced from Apple DJ. Influence of intraocular lens material and design on postoperative intracapsular cellular reactivity. Trans Am Ophthalmol Soc. 2000;98:257−83.)

Fig. 5-2-26 Gross and light microscopic photographs of a pseudophakic human eye obtained postmortem implanted with a three-piece silicone lens (SI-30 NB; AMO). (A,B) Opacification of the anterior capsule covering the lens optic from a posterior or Miyake-Apple view and from an anterior or surgeon’s view, respectively.

405

5 THE LENS C

Fig. 5-2-26, cont’d (C,D) Histological sections from the same eye showing the fibrocellular tissue attached to the inner surface of the anterior capsule at the capsulorrhexis edge (Masson’s trichrome and PAS stains, respectively; original magnification ×400). (A, Reproduced from Werner L, Apple DJ, Pandey SK. Postoperative proliferation of anterior and equatorial lens epithelial cells. In: Buratto L, Werner L, Zanini M, Apple DJ, eds. Phacoemulsification: principles and techniques. Thorofare, NJ: Slack; 2002:603−23.)

Fig. 5-2-27 Clinical, gross, and light microscopic photographs from a case of interlenticular opacification between two acrylic piggyback lenses implanted in a patient with high hyperopia (case of Dr Johnny L. Gayton, Warner Robins, GA). The opacity observed (A) was caused by a membrane-like material sandwiched between the two lenses, which are practically fused together in the center (B,C). Histological examination demonstrated the presence of retained/regenerative cortical material and pearls (D), similar to what is observed in cases of posterior capsule opacification (hematoxylin-eosin stain; original magnification ×400). (A−D, Reproduced from Gayton JL, Apple DJ, Peng Q, et al. Interlenticular opacification: clinicopathological correlation of a complication of posterior chamber piggyback intraocular lenses. J Cataract Refract Surg. 2000;26:330−36.)

406

5.2

Evolution of Intraocular Lens Implantation

Fig. 5-2-28 Clinical photographs of eyes implanted with different anterior chamber phakic intraocular lenses. (A) ZSAL-4 (Morcher, Stuttgart, Germany). This is a one-piece PMMA angle-fixated lens, which has features similar to those of the ZB 5M model (Baïkoff’s) concerning the haptic design and the angulation. Its optic is flat at the anterior surface and concave at the posterior surface. This allows more distance between the iris plane and the optic of the lens, also reducing the height of the optical edge, which leaves more space between it and the corneal endothelium. The lens is supplied in powers ranging from −10 to −23 diopters. It became available in Europe in January 1995. (B) Vivarte lens, manufactured by IOLTECH (La Rochelle, France). A manufacturing process termed selective polymerization allows the obtention of a one-piece IOL with flexible and rigid areas anywhere needed to optimize the mechanical properties of the lens. This angle-fixated lens thus has soft hydrophilic acrylic optic and footplates, while the haptics have rigidity similar to that of PMMA lenses. (C) Kelman Duet lens, manufactured by TEKIA, Inc. (Irvine, CA). This angle-fixated lens has two parts: an independent Kelman tripod PMMA haptic, with an overall diameter of 12.0, 12.5, or 13.0 mm, and a 5.5 mm monofocal silicone optic. The latter is injected into the anterior chamber and then fixated to the haptic by means of the optic eyelets and haptic tabs using a Sinskeytype hook. (D) Artisan lens (Ophtec, Groningen, Netherlands). This is a one-piece, iris-fixated lens manufactured from PMMA. Artisan haptics (fixation arms) attach to the midperipheral, virtually immobile iris stroma, thus allowing relatively unrestricted dilation and constriction of the pupil. Lenses with incorporated cylindrical correction are also available. (A−D, Reproduced from Werner L, Apple DJ, Izak AM. Phakic intraocular lenses: current trends and complications. In: Buratto L, Werner L, Zanini M, Apple DJ, eds. Phacoemulsification: principles and techniques. Thorofare, NJ: Slack; 2002:330−36.)

407

5 THE LENS A

Fig. 5-2-29 Gross and clinical photographs showing the two currently available posterior chamber phakic lenses. (A,B) Implantable contact lens (ICL) (Staar Surgical). This is a one-piece plate lens manufactured from a proprietary hydrophilic collagen polymer know as Collamer. It can be inserted or injected into the anterior chamber, and then the haptics are placed behind the iris with the help of a spatula. (C,D) Phakic refractive lens (PRL), manufactured by Medennium Inc. (Irvine, CA). This is also a one-piece plate lens, manufactured from silicone. (A–D, Reproduced from Werner L, Apple DJ, Izak AM. Phakic intraocular lenses: current trends and complications. In: Buratto L, Werner L, Zanini M, Apple DJ, eds. Phacoemulsification: principles and techniques. Thorofare, NJ: Slack; 2002:759−77.)

References

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1. Apple DJ, Ram J, Wang XH, Brown S. Cataract surgery in the developing world. Saudi J Ophthalmol. 1995;9(1):2–15. 2. Isaacs R, Ram J, Apple DJ. Cataract blindness in the developing world: is there a solution? J Agromed. 1996;3(4):7–21. 3. Kador PF. Overview of the current attempts toward the medical treatment of cataract. Ophthalmology. 1983;90:352–64. 4. Ridley H. Intra-ocular acrylic lenses. Trans Ophthalmol Soc UK. 1951;71:617–21. 5. Ridley H. Artificial intra-ocular lenses after cataract extraction. St Thomas Hosp Rep. 1952;7(2):12–4. 6. Apple DJ, Sims J. Harold Ridley and the invention of the intraocular lens. Surv Ophthalmol. 1995;40:279–92. 7. Apple DJ, Mamalis N, Loftfield K, et al. Complications of intraocular lenses: a historical and histopathological review. Surv Ophthalmol. 1984;29:1–54. 8. Apple DJ, Mamalis N, Brady SE, et al. Biocompatibility of implant materials: a review and scanning electron microscopic study. J Am Intraocul Implant Soc. 1984;10:53–66. 9. Apple DJ, Rabb MF. Ocular pathology: clinical applications and self-assessment, 5th ed. St Louis: CV Mosby; 1998. 10. Apple DJ, Kincaid MC, Mamalis N, Olson RJ. Intraocular lenses: evolution, designs, complications, and pathology. Baltimore: Williams & Wilkins; 1989. 11. Binkhorst CD. Lens implants (pseudophakoi) classified according to method of fixation. Br J Ophthalmol. 1967;51:772–4. 12. Binkhorst CD. About lens implantation. 2. Lens design and classification of lenses. Implant. 1985;3:11–4. 13. Ellingson FT. The uveitis-glaucoma-hyphema syndrome associated with the Mark VIII anterior chamber lens implant. J Am Intraocul Implant Soc. 1978;4:50–3. 14. Drews RC. The Barraquer experience with intraocular lenses: 20 years later. Ophthalmology. 1982;89:386–93. 15. Drews RC. Intracapsular versus extracapsular cataract extraction. In: Wilensky JT, ed. Intraocular lenses. Transactions of the University of Illinois Symposium on Intraocular Lenses. New York: Appleton-Century-Crofts; 1977. 16. Obstbaum SA, Galin MA. Cystoid macular edema and ocular inflammation: the corneo-retinal inflammatory syndrome. Trans Ophthalmol Soc UK. 1979;99:187–91. 17. Binkhorst CD. The iridocapsular (two-loop) lens and the iris-clip (four-loop) lens in pseudophakia. Trans Am Acad Ophthalmol Otolaryngol. 1973;77:589–617.

18. Choyce DP. The Mark VI, Mark VII and Mark VIII Choyce anterior chamber implants. Proc R Soc Med. 1965;58:729–31. 19. Kelman CD. Anterior chamber lens design concepts. In: Rosen ES, Haining WM, Arnott EJ, eds. Intraocular lens implantation. St Louis: CV Mosby; 1984. 20. Duffin RM, Olson RJ. Vaulting characteristics of flexible loop anterior chamber intraocular lenses. Arch Ophthalmol. 1983;101:1429–33. 21. Mamalis N, Apple DJ, Brady SE, et al. Pathological and scanning electron microscopic evaluation of the 91Z intra ocular lens. J Am Intraocul Implant Soc. 1984;10:191–9. 22. Reidy JJ, Apple DJ, Googe JM, et al. An analysis of semiflexible, closed-loop anterior chamber intraocular lenses. J Am Intraocul Implant Soc. 1985;11:344–52. 23. Waring GO III. The 50-year epidemic of pseudophakic corneal edema. Arch Ophthalmol. 1989;107:657–9. 24. Apple DJ, Brems RN, Park RB, et al. Anterior chamber lenses. I. Complications and pathology and a review of designs. J Cataract Refract Surg. 1987;13:157–74. 25. Apple DJ, Hansen SO, Richards SC, et al. Anterior chamber lenses. II. A laboratory study. J Cataract Refract Surg. 1987;13:175–89. 26. Auffarth GU, Wesendahl TA, Apple DJ. Are there acceptable anterior chamber intraocular lenses for clinical use in the 1990s? An analysis of 4104 explanted anterior chamber intraocular lenses. Ophthalmology. 1994;101:1913–22. 27. Auffarth GU, Wesendahl TA, Brown SJ, Apple DJ. Update on complications of anterior chamber intraocular lenses. J Cataract Refract Surg, Special Issue: Best Papers of 1994 ASCRS Meeting. 1994:70–6. 28. Auffarth GU, Wesendahl TA, Brown SJ, Apple DJ. Update on complications of anterior chamber intraocular lenses. J Cataract Refract Surg. 1995;22:1–7. 29. Apple DJ, Price FW, Gwin T, et al. Sutured retropupillary posterior chamber intraocular lenses for exchange or secondary implantation (The Twelfth Annual Binkhorst Lecture, 1988). Ophthalmology. 1989;96:1241–7. 30. Duffey RJ, Holland EJ, Agapitos PJ, et al. Anatomic study of transsclerally sutured intraocular lens implantation. Am J Ophthalmol. 1989;108:300–9. 31. Pearce JL. Experience with 194 posterior chamber lenses in 20 months. Trans Ophthalmol Soc UK. 1977;97:258–64. 32. Drews RC. The Pearce tripod posterior chamber intraocular lens: an independent analysis of Pearce’s results. J Am Intraocul Implant Soc. 1980;6:259–62.

33. Shearing SP. Evolution of the posterior chamber intraocular lenses. J Am Intraocul Implant Soc. 1984;10:343–6. 34. Apple DJ, Reidy JJ, Googe JM, et al. A comparison of ciliary sulcus and capsular bag fixation of posterior chamber intraocular lenses. J Am Intraocul Implant Soc. 1985;11:44–63. 35. Miyake K, Asakura M, Kobayashi H. Effect of intraocular lens fixation on the blood-aqueous barrier. Am J Ophthalmol. 1984;98:451–5. 36. Apple DJ, Lim ES, Morgan RC, et al. Preparation and study of human eyes obtained postmortem with the Miyake posterior photographic technique. Ophthalmology. 1990;97:810–6. 37. Assia EI, Castaneda VE, Legler UFC, et al. Studies on cataract surgery and intraocular lenses at the center for intraocular lens research. Ophthalmol Clin N Am. 1991;4:251–66. 38. Assia EI, Legler UFC, Apple DJ. The capsular bag after short- and long-term fixation of intraocular lenses. Ophthalmology. 1995;102:1151–7. 39. Apple DJ, Auffarth GU, Wesendahl TA. Pathophysiology of modern capsular surgery. In: Steinert RF, ed. Textbook of modern cataract surgery: technique, complication, and management. Philadelphia: WB Saunders; 1995. 40. Assia EI, Apple DJ, Lim ES, et al. Removal of viscoelastic materials after experimental cataract surgery in vitro. J Cataract Refract Surg. 1992;18:3–6. 41. Auffarth GU, Wesendahl TA, Solomon KD, et al. Evaluation of different removal techniques of a high viscosity viscoelastic (Healon GV). J Cataract Refractive Surg. Special Issue: Best Papers of 1994 ASCRS Meeting. 1994:30–2. 42. Glasser DB, Katz HR, Boyd JE, et al. Protective effects of viscous solutions in phakoemulsification and traumatic lens implantation. Arch Ophthalmol. 1989;107:1047–51. 43. Madsen K, Stenevi U, Apple DJ, Harfstrand A. Histochemical and receptor binding studies of hyaluronic acid and hyaluronic acid binding sites on corneal endothelium. Ophthalmic Pract. 1989;7(3):1–8. 44. Neuhann T. Theorie und operationstechnik des kapsulorhexis. Klin Monatsbl Augenheilkd. 1987;190:542–5. 45. Gimbel H, Neuhann T. Development, advantages and methods of continuous circular capsulorrhexis techniques. J Cataract Refract Surg. 1990;16:31–7. 46. Assia EI, Apple DJ, Tsai JC, Lim ES. The elastic properties of the lens capsule in capsulorrhexis. Am J Ophthalmol. 1991;111:628–32.

67. Apple DJ, Park SB, Merkley KH, et al. Posterior chamber intraocular lenses in a series of 75 autopsy eyes. I. Loop location. J Cataract Refract Surg. 1986;12:358–62. 68. Apple DJ, Tetz M, Hunold W. Lokalisierte Endophthalmitis: Eine bisher nicht beschriebene Komplikation der extrakapsulären Kataraktextraktion. In: Jacobic KW, Schott K, Gloor B, eds. I. Kongress der Deutschen Gesellschaft für Intraokularlinsen Implantation (DGII), I New York: Springer-Verlag; 1988. 69. Piest KL, Kincaid MC, Tetz MR, et al. Localized endophthalmitis: a newly described cause of the socalled toxic lens syndrome. J Cataract Refract Surg. 1987;13:498–510. 70. Kent DG, Peng Q, Isaacs RT, et al. Security of capsular fixation: small- versus large-hole plate-haptic lenses. J Cataract Refract Surg. 1997;23:1371–5. 71. Whiteside SB, Apple DJ, Peng Q, et al. Fixation elements on plate intraocular lens: large positioning holes to improve security of capsular fixation. Ophthalmology. 1998;105:837–42. 72. Kent DG, Peng Q, Isaacs RT, et al. Mini-haptics to improve capsular fixation of plate-haptic silicone intraocular lenses. J Cataract Refract Surg. 1998;24:666–71. 73. Assia EI, Legler UF, Castaneda VE, Apple DJ. Loop memory of posterior chamber intraocular lenses of various sizes, designs, and loop materials. J Cataract Refract Surg. 1992;18:541–6. 74. Izak AM, Werner L, Apple DJ, et al. Loop memory of different haptic materials used in the manufacture of posterior chamber intraocular lenses. J Cataract Refract Surg. 2002;28:1229–35. 75. Nishi O, Nishi K, Wickstrom K. Preventing lens epithelial cell migration using intraocular lenses with sharp rectangular edges. J Cataract Refract Surg. 2000;26:1543–9. 76. Apple DJ, Peng Q, Visessook N, et al. Surgical prevention of posterior capsule opacification. Part I. Progress in eliminating this complication of cataract surgery. J Cataract Refract Surg. 2000;26:180–7. 77. Peng Q, Apple DJ, Visessook N, et al. Surgical prevention of posterior capsule opacification. Part II. Enhancement of cortical clean up by focusing on hydrodissection. J Cataract Refract Surg. 2000;26:188–97. 78. Peng Q, Visessook N, Apple DJ, et al. Surgical prevention of posterior capsule opacification. Part III. Intraocular lens optic barrier effect as a second line of defense. J Cataract Refract Surg. 2000;26:198–213. 79. Werner L, Apple DJ, Pandey SK. Postoperative proliferation of anterior and equatorial lens epithelial cells. In: Buratto L, Osher RH, Masket S, eds. Cataract surgery in complicated cases. Thorofare, NJ: Slack; 2000:399–417. 80. Linnola RJ, Werner L, Pandey SK, et al. Adhesion of fibronectin, vitronectin, laminin and collagen type IV to intraocular lens materials in human autopsy eyes. Part I: histological sections. J Cataract Refract Surg. 2000;26:1792–806. 81. Linnola RJ, Werner L, Pandey SK, et al. Adhesion of fibronectin, vitronectin, laminin and collagen type IV to intraocular lens materials in human autopsy eyes. Part II: explanted IOLs. J Cataract Refract Surg. 2000;26: 1807–18. 82. Ram J, Pandey SK, Apple DJ, et al. Effect of in-thebag intraocular lens fixation on the prevention of posterior capsule opacification. J Cataract Refract Surg. 2001;27:1039–46. 83. Apple DJ, Peng Q, Visessook N, et al. Eradication of posterior capsule opacification. Documentation of a marked decrease in Nd:YAG laser posterior capsulotomy rates noted in an analysis of 5416 pseudophakic human eyes obtained postmortem. Ophthalmology. 2001;108:505–18.

84. Schmidbauer JM, Vargas LG, Peng Q, et al. Posterior capsule opacification. Int Ophthalmol Clin. 2001;41:109–31. 85. Pandey SK, Wilson ME, Trivedi RH, et al. Pediatric cataract surgery and intraocular lens implantation: current techniques, complications and management. Int Ophthalmol Clin. 2001;41:175–96. 86. Pandey SK, Cochener B, Apple DJ, et al. Intracapsular ring sustained 5-fluorouracil delivery system for prevention of posterior capsule opacification in rabbits: a histological study. J Cataract Refract Surg. 2002;28:139–48. 87. Vargas L, Peng Q, Apple DJ, et al. An evaluation of three modern single-piece foldable intraocular lenses: a clinicopathological study in a rabbit model with special reference to posterior capsule opacification. J Cataract Refract Surg. 2002;28:1241–50. 88. Fine IH, Hoffman RS, Packer M. Clear-lens extraction with multifocal lens implantation. Int Ophthalmol Clin. 2001;41:113–21. 89. Avitablie T, Marano F. Multifocal intraocular lenses. Curr Opin Ophthalmol. 2001;12:12–6. 90. Kaskaloglu M, Uretmen O, Yagci A. Medium-term results of implantable miniaturized telescopes in eyes with agerelated macular degeneration. J Cataract Refract Surg. 2001;27:1751–5. 91. Werner L, Kaskaloglu MM, Apple DJ, et al. Aqueous infiltration into an implantable miniaturized telescope. Ophthalmic Surg Lasers. 2002;33:343–8. 92. Werner L, Pandey SK, Escobar-Gomez M, et al. Anterior capsule opacification: a histopathological study comparing different IOL styles. Ophthalmology. 2000;107:463–71. 93. Werner L, Pandey SK, Apple DJ, et al. Anterior capsule opacification: correlation of pathologic findings with clinical sequelae. Ophthalmology. 2001;108:1675–81. 94. Apple DJ, Werner L. Complications of cataract and refractive surgery: a clinicopathological documentation. Trans Am Ophthalmol Soc. 2001;99:95–107; discussion 107–9. 95. Macky TA, Pandey SK, Werner L, et al. Anterior capsule opacification. Int Ophthalmol Clin. 2001;41:17–31. 96. Gayton JL, Apple DJ, Peng Q, et al. Interlenticular opacification: a clinicopathological correlation of a new complication of piggyback posterior chamber intra ocular lenses. J Cataract Refract Surg. 2000;26:330–6. 97. Werner L, Shugar JK, Apple DJ, et al. Opacification of piggyback IOLs associated to an amorphous material attached to interlenticular surfaces. J Cataract Refract Surg. 2000;26:1612–9. 98. Trivedi RH, Izak A, Werner L, et al. Interlenticular opacification of piggyback intraocular lenses. Int Ophthalmol Clin. 2001;41:47–62. 99. Werner L, Apple DJ, Pandey SK, et al. Analysis of elements of interlenticular opacification. Am J Ophthalmol. 2002;133:320–6. 100. Visessook N, Peng Q, Apple DJ, et al. Pathological examination of an explanted phakic posterior chamber intraocular lens. J Cataract Refract Surg. 1999;25:216–22. 101. Werner L, Apple DJ, Izak A, et al. Phakic anterior chamber intraocular lenses. Int Ophthalmol Clin. 2001;41:133–52. 102. Werner L, Apple DJ, Pandey SK, et al. Phakic posterior chamber intraocular lenses. Int Ophthalmol Clin. 2001;41:153–74.

5.2 Evolution of Intraocular Lens Implantation

47. Assia EI, Apple DJ, Tsai JC, et al. An experimental study comparing various anterior capsulectomy techniques. Arch Ophthalmol. 1991;109:642–7. 48. Assia EI, Apple DJ, Tsai JC, Morgan RC. Mechanism of radial tear formation and extension after anterior capsulectomy. Ophthalmology. 1991;98:432–7. 49. Wasserman D, Apple DJ, Castaneda VE, et al. Anterior capsular tears and loop fixation of posterior chamber intraocular lenses. Ophthalmology. 1991;98:425–31. 50. Assia EI, Legler UFC, Castaneda VE, et al. Clinicopathologic study of the effect of radial tears and loop fixation on intraocular lens decentration. Ophthalmology. 1993;100:153–8. 51. Auffarth GU, Wesendahl TA, Newland TJ, Apple DJ. Capsulorrhexis in the rabbit eye as a model for pediatric capsulectomy. J Cataract Refract Surg. 1994;20:188–91. 52. Faust KJ. Hydrodissection of soft nuclei. J Am Intraocul Implant Soc. 1984;10(1):75–7. 53. Ohmi S, Uenoyama K, Apple DJ. Implantation of IOLs with different diameters. Acta Soc Ophthalmol Jpn. 1992;96:1093–8. 54. Wilson ME, Apple DJ, Bluestein EC, Wang XH. Intraocular lenses for pediatric implantation: biomaterials, designs, and sizing. J Cataract Refract Surg. 1994;20:584–91. 55. Wilson ME, Wang XH, Bluestein EC, Apple DJ. Comparison of mechanized anterior capsulectomy and manual continuous capsulorrhexis in pediatric eyes. J Cataract Refract Surg. 1994;20:602–6. 56. Auffarth GU, Wilcox M, Sims JCR, et al. Analysis of 100 explanted one-piece and three-piece silicone intraocular lenses. Ophthalmology. 1995;102:1144–50. 57. Auffarth GU, Wilcox M, Sims JCR, et al. Complications of silicone intraocular lenses. J Cataract Refract Surg, Special Issue: Best Papers of 1995 ASCRS Meeting. 1995;38–41. 58. Auffarth GU, McCabe C, Wilcox M, et al. Centration and fixation of silicone intraocular lenses: an analysis of clinicopathological findings in human autopsy eyes. J Cataract Refract Surg. 1996;22:1281–5. 59. Buchen SY, Richards SC, Solomon KD, et al. Evaluation of the biocompatibility and fixation of a new silicone intraocular lens in the feline model. J Cataract Refract Surg. 1989;15:545–53. 60. Menapace R. Evaluation of 35 consecutive SI-30 phacoflex lenses with high-refractive silicone optic implanted in the capsulorrhexis bag. J Cataract Refract Surg. 1995;21:339–47. 61. Menapace R. English title: Current state of implantation of flexible intraocular lenses [in German]. Fortschr Ophthalmol. 1991;88:421–28. 62. Menapace R, Radax U, Amon M, Papapanos P. No-stitch, small incision cataract surgery with flexible intraocular lens implantation. J Cataract Refract Surg. 1994;20: 534–42. 63. Tsai JC, Castaneda VE, Apple DJ, et al. Scanning electron microscopic study of modern silicone intraocular lenses. J Cataract Refract Surg. 1992;18:232–5. 64. Apple DJ, Kent DG, Peng Q, et al. Verbesserung der befestigung von silikonschiffchenlinsen durch den gebrauch von positionierungslochern in der linsenhaptik, Proceedings of the 10th Annual Deutsche Gesellschaft fuer Intraokularlinsen Implantation Meeting, Budapest, Hungary, March 1996. 65. Percival SP, Pai V. Heparin-modified lenses for eyes at risk for breakdown of the blood-aqueous barrier during cataract surgery. J Cataract Refract Surg. 1993;19:760–5. 66. Apple DJ, Federman JL, Krolicki TJ, et al. Irreversible silicone oil adhesion to silicone intraocular lenses. A clinicopathologic analysis. Ophthalmology. 1996;103:1555–62.

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5.3

Patient Work-up for Cataract Surgery Frank W. Howes

Key features n

iscussion on patient work-up including ophthalmic and D medical considerations in the preoperative evaluation of lens surgery, including: n the morphology of lens opacities, the effects and diagnosis thereof n the optics of the eye including refractive correction modalities n the biometric measurements in standard and postrefractive eyes. The social and legal considerations in final aspects of the work-up are also discussed.

INTRODUCTION Any patient who needs to undergo cataract surgery, whether local or general anesthesia is used, requires an accurate ophthalmological workup and careful anamnesis. Even if a topical anesthetic is used, surgery is stressful for a patient, especially if there is a coexistent medical disorder. Therefore, the patient’s overall welfare is entrusted to a skilled physician, usually the anesthesiologist. The cataract surgeon concentrates on the eye and should not be distracted by the patient’s systemic needs during surgery, even if the surgeon possesses the requisite skills. Although most cataract procedures are uneventful with regard to the patient’s medical condition, any problem or crisis is potentially ruinous, especially if surgery becomes complicated or prolonged. It is therefore incumbent upon the surgical and anesthetic team to be aware of every patient’s medical status. Cataract management is a team affair. The family doctor provides the medical history and current therapeutic information. Nursing members of the team have more contact with the patient than does the surgeon, and they can address the patient’s immediate needs as well as provide a confidence-boosting ambience. Technical and administrative personnel complete the team, along with the anesthesiologist and ophthalmic surgeon.

MEDICAL HISTORY AND CURRENT THERAPEUTIC REGIMEN

410

A history of cardiac, bronchopulmonary, or cerebrovascular incidents, especially if recent, influences the timing and management of surgery. Diabetes mellitus and systemic hypertension are common in the population predisposed to operable cataract formation, and these conditions may adversely influence both the surgery and the postoperative course of events.1 Ram et al.,2 in a study of more than 6000 patients who underwent cataract surgery, discovered multiple morbidities that arose from a variety of conditions. The major causes included pulmonary disease, cardiovascular and hypertensive disorders, diabetes mellitus, and significant orodental problems that required intervention. Ram et al.2 also noted significant postoperative problems in 1.27% of their patients, nearly half of whom required hospitalization. Thus, they concluded that all patients for whom cataract surgery is planned should undergo evaluation for systemic disease to prevent morbidity, or even mortality, in the preoperative, intraoperative, and postoperative periods. It is not uncommon for thyroid disorders to be associated with

Table 5-3-1 MORBIDITY IN CATARACT SURGERY PATIENTS Condition

Percentage

Significant medical history

Diabetes mellitus

Systemic hypertension

Ischemic heart disease

Hypothyroidism

Undiagnosed tumors

cataract surgery; they may even be precipitated by the surgical intervention.3 Fisher and Cunningham4 noted an even higher morbidity in their cohort of patients who had cataract surgery (Table 5-3-1). The presence of disorders that might make cooperation difficult during surgery must be determined so that the operating environment can be optimized. These include Parkinson’s disease and other involuntary movement disorders involving the head, face, and lids; communication difficulty; and excessive fear or anxiety. These factors influence both the surgeon’s and the anesthesiologist’s decision about the form of anesthetic to use and the sedation required (see Chapter 5.6). The patient’s social history may provide useful information, especially with reference to smoking, because breathing difficulties during surgery and coughing after surgery could compromise the surgical outcome. Similarly, substance abuse may be linked to poor patient compliance during surgery, as well as having implications for postoperative medication and management. Good preoperative assessment and management can minimize the risks associated with operating on these patients. Systemic disorders may provide clues to the existence of an association between the morphology and the corresponding lens opacities (Table 5-3-2). When a systemic disorder is present, ensuring a good understanding of the pharmacological and other therapeutic measures used in its management is an essential component of the preoperative work-up.

GENERAL OPHTHALMIC HISTORY AND EXAMINATION It is important to establish whether there are coexistent ophthalmic conditions that may influence the cataract surgery, postoperative recovery, or outcome. Both eyes are assessed fully by routine ophthalmological work-up, which includes tonometry, slit-lamp biomicroscope examination, and posterior segment observations under mydriasis to estimate the visual outcome and risk category of surgery for the patient. Intercurrent ophthalmic disorders may prejudice the visual outcome; for example, uveitis may be exacerbated,5 herpes zoster may have left an anesthetic cornea,6 atopic disease may predispose the eye to infection,7 Fuchs’ endothelial dystrophy may predispose the eye to corneal edema, and diabetes mellitus increases the prospects of postoperative macular edema.1 Patient counseling on the procedure and postoperative expectations is a vital part of the preoperative work-up. A written explanation of the background and process of cataract surgery is invaluable.

Table 5-3-2 SYSTEMIC DISORDERS AND LENS OPACITIES Appearance in the Eye

Myotonic dystrophy

Blue dot cortical cataract and posterior subcapsular cataract

Wilson’s disease

Green sunflower cataract (copper) anterior or posterior subcapsular

Atopic dermatitis

Blue dot cortical cataract and posterior subcapsular cataract

Hypocalcemia

Discrete white cortical opacities

Diabetes mellitus

Snowflake opacities located in anterior and posterior subcapsular cortex

Acute onset diabetes

Cortical wedges caused by lens fiber swelling

Down’s syndrome

Snowflake opacities located in anterior and posterior subcapsular cortex

5.3

Fig. 5-3-1 Nuclear cataract. With continual generation of lens fibers in the equatorial periphery of the lens, the older material is continually compressed and eventually forms a nuclear cataract with changed optical density and altered transparency

Patient Work-up for Cataract Surgery

Systemic Disorder

SPECIFIC OPHTHALMIC EXAMINATION In addition to the above, the assessment of the patient having lens surgery requires an assessment of the lens itself, whether clear (in refractive lens exchange) or cataractous (for cataract surgery), and an assessment of the optics of the eye in order to provide the patient with a refractive outcome as close as possible to their desire.

ASSESSMENT OF LENS OPACITIES8 INTRODUCTION Age-related changes in the crystalline lens induce changes in visual function. The lens functions as an optical element and provides one third of the refractive power of the human eye. The eye’s optical properties depend on the power of the lens, which in turn is determined by its physical dimensions (curvatures and thickness) and its refractive index as well as its transmissibility and the organization of its internal components. The progressive insolubilization of lens protein with age is believed to cause density fluctuations, which scatter light and impair vision. The impact of a patient’s cataract on the retinal image may be appreciated on funduscopic examination, which shows the blur of fine retinal vessels. The clinician is unable to resolve the retinal capillaries directly because of the scattering of light by opacities in the patient’s lens. Light scattering also blurs the images of fine objects viewed by individuals with cataract.

DIAGNOSIS OF LENS OPACITIES Slit-lamp biomicroscopy is the major method used to observe and assess cataracts. However, the image seen often fails to correlate with the patient’s visual acuity or function. The relationship between alterations in the structural proteins, the increase in light scatter associated with conventional biomicroscopy, and the capacity of visual function is not a simple one. For all lens examinations, the pupil is dilated maximally.

Fig. 5-3-2 Cortical cataract.

In certain instances, crystals appear in the adult nucleus (or in the cortex) that, on slit-lamp examination, appear to be of different colors (polychromatic luster).

Cortical Opacities

The changes in transparency involve most of the cortex of the lens (Fig. 5-3-2). The changes evolve as follows: l Hydration of the cortex with development of subcapsular vacuoles; l Formation of ray-like spaces filled with liquid, which is at first transparent and later becomes opaque; l Lamellar separation of the cortex with development of parallel linear opacities; and l Formation of cuneiform opacities that originate at the periphery of the lens and spread toward the center.

Posterior Subcapsular Opacities

Posterior subcapsular opacities may develop as isolated entities or may be associated with other lens opacities. The opacity begins at the posterior polar region and then spreads toward the periphery. Often, granules and vacuoles are detectable in front of the posterior capsule.

Advanced Cataracts

The crystalline lens may swell and increase in volume because of cortical processes (intumescent cataract; Fig. 5-3-3). Complete opacification of the lens is called a mature or morgagnian cataract. If the liquefied cortical material is not, or is only partially, reabsorbed, the solid nucleus may “sink” to the bottom (Fig. 5-3-4). Reabsorption of the milky cortex causes a reduction in the lens volume, resulting in capsular folding (hypermature cataract).

CLASSIFICATION OF LENS OPACITIES

GRADING OF LENS OPACITIES

With age, the transparency of the lens decreases progressively and a wide variety of opacities may occur.9 The morphological types of senile cataract fall into four basic categories: nuclear, cortical, posterior subcapsular cataracts, and advanced. These cataract types can be graded clinically and can be measured photographically.

Gradations and classifications of cataracts are useful in determining the potential difficulty of cataract surgery, in cataract research, in studies to explore causation, and in trials of putative anticataract drugs. Devices designed to quantify lens opacification have been developed10 − these instruments (such as the Kowa Early Cataract Detector and the Scheimpflug Photo slit lamp) appear to be more accurate when used to assess the formation of nuclear cataracts than that of cortical cataracts. A rapid method for the gradation of cataract in epidemiological studies has been reported by Mehra and Minassian11 − the area of lenticular opacity is assessed by direct ophthalmoscopy and graded on a scale from 0 to 5. Highly reproducible, validated systems (Lens

Nuclear Opacities

Initially, an increase in optical density of the nucleus occurs (nuclear sclerosis). The fetal nucleus is first involved and then the whole adult nucleus. The increase in density is followed by an opacification (Fig. 5-3-1), which implies a change in color, namely from an initial clear, to yellow, to a subsequent brown (brownish cataract).

411

performed. The Preferred Practice Pattern of the American Academy of Ophthalmology recommends Snellen acuity as the best general guide to the appropriateness of surgery but recognizes the need for flexibility with due regard to a patient’s particular functional and visual needs, environment, and risks, which may vary widely.15 When the cataract is very dense and opaque, visual acuity may be reduced to light perception only (cataract is still the major cause of blindness throughout the world).

5 THE LENS

Contrast Sensitivity Reduction

Fig. 5-3-3 Intumescent cataract. The crystalline lens increases in volume because of swelling processes that involve the cortex.

Patients with cataracts commonly complain of loss of the ability to see objects outdoors in bright sunlight and of being blinded easily by oncoming headlamps in night-time driving.16 Typically, loss of contrast sensitivity in patients who have cataracts has been reported to be greater at higher spatial frequencies. All cataracts lower contrast sensitivity − the posterior subcapsular opacities have been reported to be the most destructive.

Myopic Shift

The natural aging of the human lens produces a progressive hyperopic shift. Nuclear changes induce a modification of the refractive index of the lens and produce a myopic shift that may be of several diopters or greater. It is possible to predict that an aging person who had emmetropia previously, but who can now read with no correction (“second sight”), is developing nuclear cataract. If the lens structure becomes heterogeneous, with cortical spoke cataract for example, the change in refractive index may be uneven and may produce some degree of internal astigmatism.

Monocular Diplopia Fig. 5-3-4 Morgagnian cataract. The nucleus is seen as a “suntan” or a dark shadow in the inferior third of the pupil.

Opacities Classification System III; see below) for cataract classification have been developed by Chylack et al.12 to define the effects of specific cataract type and extent very accurately; these enable the effects of specific cataract types on specific visual functions to be quantified.

Lens Opacities Classification System III

For nuclear opalescence (NO), a slit beam is focused on the lens nucleus and the density of the lens is compared with a set of standard photographs (opalescence and color). If the density is equal to or less than that corresponding to the first photograph, NO nuclear cataract (NC) is zero; NO NC is 1 if the density is equal to or less than that for the second photograph, and so on. The photographs represent lens nuclei of increasing density, and the patient’s cataract is graded accordingly. For cortical cataracts, a retroillumination view through the pupil is used to view the lens, focused first at the anterior capsule and then at the posterior capsule. The photographs are compared with standard photographs − each succeeding photograph shows the pupillary area covered by more cortical cataract. For posterior subcapsular cataract, a retroillumination view of the lens is used, focused at the posterior capsule. Again, the patient’s cataract is graded according to standard photographs (Fig. 5-3-5)

EFFECTS OF OPACITIES ON VISION The nature of the effect of opacity on vision varies according to the degree of the cataract and the cataract morphology. No single test adequately describes the effects of cataract on a patient’s visual status or functional ability.13

Visual Acuity Reduction

412

Measurement of visual acuity has been the standard tool by which to estimate the visual disability of patients and by which to detect changes in visual function induced by cataract over time.14 However, it has been found clinically that visual acuity can remain high despite age-related lens opacities: the severity of the visual disability measured using highcontrast Snellen acuity charts is not sensitive to visual disability characterized by loss of contrast sensitivity. Usually, visual acuity testing is conducted under ideal circumstances, which are not normally met in the real world, and so the results may not reflect visual disabilities that occur in less ideal conditions. Although not a definitive measurement of visual dysfunction, simple Snellen acuity is the most used index to determine whether cataract surgery should be

Monocular diplopia is common in patients who have lens opacities, particularly cortical spoke cataract and in conjunction with water clefts that form radial wedge shapes and contain a fluid of lower refractive index than the surrounding lens. The patients, in some cases, may complain of polyopia.

Glare

Even minor degrees of lens opacity cause glare because of the forward scatter of light.17 All forms of cataract can cause glare, especially cortical and posterior subcapsular. Such patients often see more poorly in daylight conditions and in the context of night driving. Unlike contrast sensitivity reduction, some glare may be produced by opacities that do not lie within the pupil diameter. The differences between measured visual acuity in a darkened room (and with a high-contrast chart) and acuity in ambient light that produces glare are interesting as subjective criteria for the justification of surgery.

Color Shift

The cataractous lens becomes more absorbent at the blue end of the spectrum, especially with nuclear opacities. Usually patients are not aware of this color visual defect, but it becomes obvious retrospectively after cataract surgery and visual rehabilitation.

Visual Field Loss

According to the morphology, the density, and the location of the opacities, the field of vision may be affected.

ASSESSMENT OF OPTICS AND BIOMETRY 18 Introduction The most common and successful method to replace crystalline lens power is to use an intraocular lens (IOL). The earliest documented IOL implant was performed by Harold Ridley in 1949.19 Ridley’s original IOL was made of polymethyl methacrylate (PMMA) and placed in the posterior chamber, in a manner very similar to that of the present method. Over the past 50 years, improvements in the purity of the PMMA, in the quality of lens manufacturing, and in the surgical techniques used have transformed this technique into one of the most successful surgical procedures performed today.

OPTICS Once surgery is performed, the eye is rendered aphakic. The optics of the aphakic eye is different from the phakic eye, and an aged phakic eye is different from a young phakic eye. The “normal” optics changes with

5.3

Lens Opacities Classification System 111 (LOCS 111)

Nuclear

Colour/ Opalescence

Patient Work-up for Cataract Surgery

N02 NC2

N03 NC3

N04 NC4

N05 NC5

N06 NC6

Cortical

N01 NC1

Posterior

Subcapsular

Fig. 5-3-5 Lens Opacities Classification System III simulation chart.

STANDARDIZED APHAKIC EYE

STANDARDIZED 72-YEAR-OLD PHAKIC EYE ultrasonic axial length (23.45 mm)

corneal vertex plane

optical axial length (23.65 mm)

optical axial length (23.65 mm) spectacle lens (–0.50 D)

2 principal plane of cornea (50 �m)

anterior chamber depth (3.74 mm)

retinal thickness (250 �m)

spectacle lens (+12.50 D)

2 principal plane of cornea (50 �m)

anterior chamber depth (3.74 mm)

retinal thickness (250 �m)

anterior iris plane

neye = 1.336

neye = 1.336 vertex distance (14 mm)

ultrasonic axial length (23.45 mm)

lens (4.70 mm)

cornea

iris

vertex distance (14 mm)

optical axis

cornea

retina

rant = 7.704 mm Kker = 43.81D, n = 1.3375 Kref = 43.27D, n = 4/3

nair = 1.000

Fig. 5-3-6 Standardized 72-year-old phakic eye. The values shown are the mean values for a phakic eye: keratometric power of the cornea (kker), net refractive power of the cornea (kref ), and anterior radius of the cornea (rant). Indices of refraction (n) are 1.336 for the aqueous and vitreous (neye) and 1.000 for air (nair).

age. With the advent of the IOL (pseudophakic eye) and its subsequent further development having reached a high level of sophistication, the optics of a pseudophakic eye can now mimic the optics of younger eyes. The normal 72-year-old human eye has a total dioptric power of approximately 58 D, with nearly 75% of the power from the cornea and 25% of the power from the crystalline lens (Fig. 5-3-6).20 Removal of the crystalline lens leaves the eye extremely deficient in dioptric power, which must be replaced to restore vision. The replacement of the dioptric power can be in the form of spectacles, contact lenses, corneal onlays, corneal implants, or IOLs. Although each modality can restore the patient’s vision, the optical consequences are dramatically different and must be understood by the clinician to avoid unnecessary complications.

optical axis iris

retina

Fig. 5-3-7 Standardized 72-year-old aphakic eye. The values shown are the mean values for an aphakic eye: keratometric power of the cornea (kker), net refractive power of the cornea (kref ), and anterior radius of the cornea (rant). Indices of refraction (n) are 1.336 for the aqueous and vitreous (neye) and 1.000 for air (nair).

APHAKIA Figure 5-3-7 shows the aphakic eye with a spectacle lens at a vertex of 14 mm to correct the patient’s vision. Replacement of the crystalline lens power with a spectacle lens causes the image that is formed on the patient’s retina to be roughly 25% larger than the image formed with the crystalline lens. The actual magnification is determined by the exact power of the aphakic spectacles. There is approximately 2% of magnification for each diopter of power in the spectacles. The average aphakic spectacle is therefore 12.5 D. The magnification from aphakic spectacles causes other optical aberrations, such as a ring scotoma (Fig. 5-3-8), jack-in-the-box phenomenon (Fig. 5-3-9), and a pincushion distortion (Fig. 5-3-10). Because the image through the spectacles is magnified by 25%, the actual field of view through

413

JACK-IN-THE BOX PHENOMENON

RING SCOTOMA

THE LENS

c b

x 3

2 1

entrance pupil a

b c

c d

d Fig. 5-3-8 Ring scotoma. Area X on the diagram. This angle increases proportionally with the power of the aphakic correction. A +10.00DS aphakic correction subtends an angle of approximately 9˚ depending on the back vertex distance. The reason for the scotoma, as can be seen in the diagram, is the disparity in refraction between the first ray out of the aphakic lens correction (b) and the first ray to pass through the aphakic correction (c). The prismatic effect ray c causes all the imagery at x (ext b-c) to be lost as can be seen by the zero b-c disparity on the retina. This occurs in a ring all the way around the lens rim and retina, hence the term ring scotoma.

Fig. 5-3-9 Jack-in-the-box phenomenon. This is caused by an eye moving peripherally across an aphakic correction as seen in the diagram. The ring scotoma as seen in Fig 5-3-8 moves centrally. As the eye moves fixation from d to the peripheral image a, the lost image x (c-b) disappears hence image 2 disappears and on the retina moves directly from 1 to 3 giving the impression of disappearance then sudden reappearance – jack-in-the-box! If contact lenses are worn, they move with the eye and hence jack-in-the-box does not occur.

DISTORTION FROM SPECTACLE LENSES WITH OBLIQUE ANGLES OF GAZE Pincushion distortion from plus lenses to correct hypermetropia

Barrel distortion from minus lenses to correct myopia

Normal

Fig. 5-3-10 Distortion from spectacle lenses with oblique angles of gaze.

414

the spectacles is reduced by 25%, which makes it impossible to see the 25% of the peripheral field that would be seen normally through spectacles with no power. The result is an annulus of no vision, or ring scotoma. When the image of an object moves from the extreme visual field toward the center of fixation, as it passes through the ring scotoma it disappears until it moves into the central island of vision. This jumping into and out of the patient’s vision has been referred to as the jack-inthe-box phenomenon.21–23 Driving a motor vehicle thus becomes very

difficult to perform, as does any activity in which objects move rapidly across the visual field. Pincushion distortion is a property of all plus lenses and is proportional to their dioptric power. This distortion makes a square look like a pincushion − the corners of the square have a stretched-out appearance, and the sides are pushed in, as shown in Fig. 5-3-10. Every object viewed through aphakic spectacles is distorted in this way, which makes rectangular objects, such as doors and boxes,

STANDARDIZED PSEUDOPHAKIC SCHEMATIC EYE ultrasonic axial lengh (23.45 mm) optical axial lengh (23.65 mm) spectacle lens (–0.50 D)

2 principal plane of cornea (50 �m) effective lens position (5.25 mm)

anterior chamber depth (3.74 mm)

retinal thickness (250 �m)

anterior iris plane neye = 1.336 vertex distance (14 mm) cornea

optical axis thin intraocular lens (21.19 D) iris

retina

rant = 7.704 mm Kker = 43.81D, n = 1.3375 Kref = 43.27D, n = 4/3 nair = 1.000

Fig. 5-3-11 Standardized 72-year-old pseudophakic eye (thin IOL). The values shown are the mean values for a pseudophakic eye: keratometric power of the cornea (kker), net refractive power of the cornea (kref ), and anterior radius of the cornea (rant). Indices of refraction (n) are 1.336 for the aqueous and vitreous (neye) and 1.000 for air (nair). Using these values, the required thin IOL power is 21.19 D at an effective lens position (ELP) of 5.25 mm.

appear like a pincushion. For an architect or draftsman, these distortions make the job extremely difficult or impossible to perform. The distortions created by aphakic spectacles necessitated the development of other modalities, such as IOL and corneal onlays or inlays.

Corneal Contact Lenses, Onlays, and Inlays

To correct aphakia at the corneal plane involves the use of contact lenses or surgery that adds dioptric power to the cornea. As the position at which the optical correction is made moves closer to the retina, the necessary dioptric power increases but the subsequent magnification decreases. The power at the corneal plane that is equivalent to 12.5 D at a vertex of 12 mm is 14.7 D; a patient who needs 12.5 D in aphakic spectacles would need 14.7 D in a soft or rigid contact lens. At the corneal plane the magnification is 6−8%. This value is near the limit of aniseikonia (image size disparity between the two eyes),24, 25 so most unilaterally aphakic patients can have binocular vision, with the aphakic eye corrected using a contact lens and the other eye phakic. Binocular vision is not possible with one aphakic spectacle and a normal phakic lens. Corneal onlays, such as epikeratophakia, and inlays are not used commonly in clinical settings. The optical effects are no different from those of a contact lens, but onlays and inlays have the advantage that the patient need provide no maintenance. However, the excellent success of contact lenses and IOLs means that surgical techniques to correct aphakia at the cornea are not reasonable clinical alternatives at this time.

Pseudophakia

Figure 5-3-11 shows a posterior chamber lens in-the-bag following cataract extraction. Just as the average spectacle power for aphakia is 12.5 D, the average power of an equiconvex IOL in-the-bag is approximately 21 D. The average magnification of an IOL in this position is 1.5%, compared with the original crystalline lens. For an anterior chamber IOL the average power would be less, approximately 18 D, and the magnification would be approximately 2.0%. Although some discerning patients can detect this disparity by alternately covering each eye, almost everyone can achieve binocular vision with one eye pseudophakic and the other phakic.26

pseudophakic lens design

The IOLs currently available are either biconvex, convexoplano, or meniscus. As a result of clinical performance and optical analysis, the majority of lenses implanted today are biconvex.27, 28 The reasons for

5.3 Patient Work-up for Cataract Surgery

corneal vertex plane

the emergence of this design as the most superior are both optical and mechanical. The quality of the optical design of an IOL is measured on the basis of its performance with respect to tilting, decentration, and spherical aberration. In terms of each of these, the positive meniscus lens performs miserably and rarely is used today. The original design concept was to create a “laser space,” so that the posterior surface of the lens would not be in contact with the posterior capsule; this avoids pitting of the lens with neodymium:yttrium−aluminum−garnet (Nd:YAG) capsulotomy. When a meniscus lens is tilted or decentered, the induced astigmatism and power change are dramatic. A 10°−15° tilt can induce enough regular and irregular astigmatism to make the spectacle correction intolerable and results in a best corrected vision of less than 20/20 (6/6), simply because of the poor optics. Convexoplano IOLs (convex on the front surface and flat on the posterior surface) were the first to be designed. They are the simplest to manufacture, because one surface is flat and all the optical power lies in the other surface. These lenses have performed well over the years, but degradation of the retinal image with lens tilt or decentration is still greater than it is with biconvex lenses. Optical studies to determine the optimal lens design have shown that a biconvex design with a front surface much steeper than the back appears to minimize this aberration for most humans.29 No clinical studies have demonstrated a difference in the spherical aberration of a convexoplano lens with respect to that of a biconvex lens that is steeper on the front surface. The optimal optical and mechanical performance of an IOL in the human eye is that of biconvex lenses. In addition to minimizing the effects of tilt, decentration, and spherical aberrations, a convex posterior surface may reduce the migration of lens epithelial cells, a migration that may lead to opacification of the capsule; this may be an additional�� mechanical �� advantage of biconvex over convexoplano lenses. The biconvex IOL has become the predominant lens style used today because of its superior optical and mechanical clinical performance.27

Edge design (see Chapter 5.2)

Reflections, shimmering peripheral lights, and flashes usually are related to the edge design of a lens. Flat edges from truncation (oval optics) or flat edges in round optics create unwanted external and internal reflections that the patient may see in low light levels.30 Therefore, in the past most lenses had rounded edges to avoid coherent reflected images. Square edge design more recently has been noted to reduce posterior capsular opacification, hence modifications to optimize the properties of both.

Optical transmission

The optical transmission through the human eye to the retina usually is considered to be in the range 400−700 nm in wavelength. The cornea filters any wavelength shorter than 300 nm, and the crystalline lens filters out any wavelength shorter than 400 nm. When the crystalline lens is removed, wavelengths of 300−400 nm reach the retina. In the late 1970s much discussion ensued as to whether the short unfiltered wavelengths that could reach the retina could cause syneresis of the vitreous, macular degeneration, cystoid macular edema, and erythropsia. The results of research into these questions have led to the development of ultraviolet light filtration in almost all IOLs as well as yellow filters in some lenses to reduce the blue light hazard. Some questions have been raised regarding potential sleep disturbance with these filters as the diurnal rhythm regulating rods in the peripheral retina respond to blue light.31

Material

Commercially available IOLs mainly are made of PMMA, silicone, or acrylic. Silicone and acrylic lenses are foldable, so they can be implanted through small incisions (2.2−3.5 mm in length). The index of refraction for PMMA is 1.491, that for silicone is in the range 1.41−1.46, depending on the model and manufacturer, and for acrylic it is 1.55. The higher the index of refraction, the flatter the curvatures of the lens needs to be to achieve the same refractive power. For a 20 D biconvex IOL with 10 D on each surface, the acrylic lens has the flattest curvatures and the silicone the steepest. As a consequence of the flatter curvatures, the acrylic lens is thinner than the PMMA lens, which, in turn, is thinner than the silicone lens, provided all else is equal. The velocity of ultrasound for these materials at eye temperature (35°C) is 2658 m/second for PMMA, 980−1090 m/second for silicone,

415

and 2180 m/second for acrylic.32 All three lens materials have performed well clinically.

THE LENS

Three other special types of IOLs are manufactured currently − multifocal, toric and aspheric. Multifocal IOLs have enjoyed a success similar to that of multifocal contact lenses. Multifocal IOLs produce two or more focal points, which create a focused and defocused image on the retina. The result is an image that is approximately 30% reduced in contrast with respect to monofocal lenses and unwanted optical images can be seen at night, such as halos or rings around headlights.33 The reduced image quality must be weighed against the patient’s desire to be less spectacle dependent. With (multifocal) contact lens failure, the problem is solved by returning to spectacles. A patient who is dissatisfied with a multifocal IOL is more difficult to deal with, and lens exchange occasionally is required. The success of these lenses is based almost entirely on appropriate patient selection. Toric IOLs are simply spherocylindric lenses, just like spectacles. If the toric lens is aligned properly with the patient’s corneal astigmatism and the magnitude is correct, the patient’s corneal astigmatism can be neutralized. The magnitude of the cylinder in the IOL must be approximately 1.4 times the astigmatism in the cornea to neutralize completely the corneal astigmatism; for corneal astigmatism of 1.0 D, the cylinder in the IOL must be 1.4 D. Manufacturers usually provide two nominal toricities and recommend using the one that best fits the particular patient on the basis of a nomogram. As long as the lens is within 30° of the intended axis, the patient has less astigmatism in the spectacles than in the cornea. If the lens is misaligned by more than 30°, the patient has greater astigmatism in the spectacles than in the cornea. It is obvious that the lens must fixate well and not rotate from the axis of the original correct placement, otherwise the patient’s refraction fluctuates and the benefit of a toric lens diminishes. Aspheric lenses are designed to minimize spherical aberration and mimic more closely the optics of younger eyes to produce better optics. The aging crystalline lens causes loss of total eye asphericity (the prolate cornea contributes significantly to aspheric optimization) and the aspheric lenses are designed to restore the asphericity of younger optics. The major contribution that needs to be made by the IOL, before the niceties of the speciality lenses, is pure dioptric accuracy. Ophthalmic research has led to the development of a number of different formulas for the calculation of the appropriate dioptric power for any given eye. The essence of the measurements for the formulas and methods of calculation is given in the following paragraphs.

Specialty IOLs

MEASUREMENTS34 INTRODUCTION Fyoderov et al.35 first estimated the optical power of an IOL using vergence formulas in 1967. Between 1972 and 1975, when accurate ultrasonic “A” scan units became available commercially, several investigators derived and published theoretical vergence formulas.36–41 All of these formulas were identical, except for the form in which they were written and the choice of various constants, such as retinal thickness, optical plane of the cornea, and optical plane of the IOL.42 The slightly different constants accounted for less than 0.50 D in the predicted refraction. The use of different constants arose as a result of differences in lens styles, “A” scan units, keratometers, and surgical techniques used by the investigators.

IOL CALCULATIONS THAT REQUIRE AXIAL LENGTH Theoretical Formulas

416

The theoretical formula for IOL power calculations has not changed since the original description by Fyoderov et al.35 in 1967. Although several investigators presented the theoretical formulas in different forms, the only differences were slight variations in the values of retinal thickness and corneal index of refraction. Six variables in the formula exist: l Net corneal power (K) l Axial length (AL) l IOL power (IOLP)

ffective lens position (ELP) E Desired refraction (DPostRx) l Vertex distance (V) Normally, IOL power is chosen as the dependent variable and found by using the other five variables, where distances are given in millimeters and refractive powers are given in diopters, as in equation 5-3-1. l l

Equation 5-3-1 IOLP = (1336 /[ AL − ELP ]) − (1336 /[1336 /{1000 /([1000 / DpostRx] − V ) + K } − ELP ]) The only variable that cannot be chosen or measured preoperatively is ELP. The improvements in IOL power calculations over the past 30 years are a result of improvements in the predictability of the variable ELP (see Fig. 5-3-11 for the physical locations of the variables). The term effective lens position (ELP) was adopted by the United States Food and Drug Administration in 1995 to describe the position of the lens in the eye, because the often-used term anterior chamber depth (ACD) is not anatomically accurate for lenses in the posterior chamber and can lead to confusion for the clinician. The ELP used for IOLs before 1980 was a constant of 4 mm for every lens in every patient (first-generation theoretical formula). This value actually worked well in most patients, because the majority of lenses implanted were of iris clip fixation type, in which the principal plane averages approximately 4 mm posterior to the corneal vertex. In 1981, Binkhorst improved the prediction of ELP by using a single variable predictor, the axial length, as a scaling factor for ELP (second-generation theoretical formula).43 If the patient’s axial length was 10% greater than normal (normal being 23.45 mm), the ELP used was increased by 10%. The average value of ELP used was increased to 4.5 mm, because the preferred location of an implant was in the ciliary sulcus, approximately 0.5 mm deeper than the iris plane. Also, most lenses were convexoplano, similar to the shape of the iris-supported lenses. By 1997 the average ELP used had increased to 5.25 mm. This increased distance has occurred primarily for two reasons: 1. The majority of implanted IOLs are biconvex, which moves the principal plane of the lens even deeper into the eye. 2. The desired location for the lens is in the capsular bag, which is 0.25 mm deeper than the ciliary sulcus. In 1988, it was proved2 that the use of a two-variable predictor (axial length and keratometry) could significantly improve the prediction of ELP, particularly in unusual eyes (third-generation theoretical formula). The original Holladay 1 formula was based on the geometric relationships of the anterior segment. Although several investigators have modified the original Holladay 1 formula, no comprehensive studies have shown any significant improvement using only these two variables. In 1995, Olsen et al.44 published a four-variable predictor that used keratometry and axial length, preoperative anterior chamber depth, and lens thickness. Their results showed an improvement over the two-variable prediction formulas, because the more information that is used to define the anterior segment value, the better the ELP can be predicted. (It is well known from prediction theory that the more variables that can be measured to describe an event, the more accurately the outcome can be predicted.) Holladay et al.45 discovered that the anterior segment and posterior segment of the human eye often are not proportional in size, which causes significant error in the prediction of the ELP in extremely short eyes (axial length < 20 mm). The authors found that even in eyes less than 20 mm in axial length, the anterior segment was completely normal in the majority of cases. Because the axial lengths were so short, the two-variable prediction formulas severely underestimated ELP, which explains part of the large hyperopic prediction errors with the two-variable prediction formulas. Once this problem was recognized, the authors began to take additional measurements on eyes that had extremely small or extremely large axial lengths, to determine whether the prediction of ELP could be improved by being able to describe the anterior segment more accurately. Table 5-3-3 shows the clinical conditions that illustrate the independence of the anterior segment size and the axial length. For a year, data cohorts were gathered from 35 investigators around the world. Several additional measurements of the eye were taken, but only seven preoperative variables (axial length, corneal power, horizontal corneal diameter, anterior chamber depth, lens thickness, preoperative refraction, and age) were found to improve significantly the prediction of ELP in eyes of axial length in the range 15−35 mm.

TABLE 5-3-3 CLINICAL CONDITIONS THAT DEMONSTRATE THE INDEPENDENCE OF THE ANTERIOR SEGMENT SIZE AND AXIAL LENGTH Axial Length Short

Normal

Long

Small

Small eye nanophthalmos

Microcornea

Normal

Axial hyperopia

Normal

Axial myopia

Large

Megalocornea

Large eye

Axial hyperopia

Buphthalmos Axial myopia

The improved accuracy of the prediction of ELP is not totally because of changes in the formula; it also is a function of the technical skills of surgeons who implant lenses in the capsular bag consistently. A 20 D IOL that is displaced 0.5 mm axially from the predicted ELP results in an error of approximately 1.00 D in the stabilized postoperative refraction. However, when using piggy-back lenses that total 60 D, the same axial displacement of 0.5 mm causes a 3 D refractive error; the error is directly proportional to the power of the implanted lens. This direct relationship is why the problem is much less evident in extremely long eyes, because the implanted IOL is either low plus or minus to achieve emmetropia following cataract extraction. Predictions for patients who have eyes with axial lengths in the range 22−25 mm and corneal powers in the range 42−46 D will be accurate using current third-generation formulas (Holladay 1,46 SRK/T,47 and Hoffer Q48). In cases outside this range, the Holladay 2 formula should be used to ensure accuracy.

Normal Cornea with No Previous Keratorefractive Surgery Refractive lens exchange (RLE) for high myopia and hyperopia

The intraocular power calculations for RLE are the same as those for when a cataract is present. The patients usually are much younger, however, so the loss of accommodation should be discussed thoroughly. The actual desired postoperative refraction should be discussed, also, because a small degree of myopia (−0.50 D) may be desirable to someone who has no accommodation so that the dependence on spectacles can be reduced. This procedure usually is reserved for patients who are outside the range of other forms of refractive surgery. Consequently, the values of axial length, keratometry, and other factors usually are quite different from those of the typical cataract patient because of the degree of refractive error. In most cases of high myopia, the axial lengths are extremely long (> 26 mm). In cases of high hyperopia, the axial lengths are very short (< 21 mm).

Myopia

In patients who have myopia that exceeds 20 D, removal of the lens often results in postoperative refractions near emmetropia with no implant. The exact result depends on the power of the cornea and the axial length. The recommended lens powers usually range from −10 D to +10 D, but the correct axial length measurement is very difficult to obtain in these cases because of the abnormal anatomy of the posterior pole. Staphylomas often are present in these eyes and the macula often is not at the location in the posterior pole where the “A” scan measures the axial length. In such cases, a “B” scan is recommended to locate the macula (fovea) and recheck the value determined using the “A” scan. Variations of 3−4 D may occur because the macula is on the edge of the staphyloma, but the “A” scan measures to the deepest part of the staphyloma. Such a variation results in a hyperopic error, because the distance to the macula is much shorter than the distance to the center of the staphyloma. The third-generation theoretical formulas give excellent predictions if the axial length is stable and its measurements are accurate.

Hyperopia

For patients who have axial lengths shorter than 21 mm, the Holladay 2 formula should be used. In such cases, the size of the anterior segment has been shown to be unrelated to axial length.45 In many of

these patients, the anterior segments are normal, only the posterior segment is abnormally short. In a few cases, however, the anterior segment is proportionately small with respect to the axial length (nanophthalmos). The differences in the size of the anterior segment in these cases can cause an average of 5 D hyperopic error when third-generation formulas are used, because they predict the depth of the anterior chamber to be very shallow. Use of the newer formula can reduce the prediction error in these eyes to less than 1 D. Accurate measurements of axial length and corneal power are especially important in these cases, because any error is magnified by the extreme dioptric powers of the IOLs. It is important to note, however, that if piggy-back lenses are used to achieve a high power then the variation in ELP between bag-bag lenses and sulcus-bag lenses can cause a refractive surprise of up to 4 D.

Patient Work-up for Cataract Surgery

Anterior Segment Size

5.3

METHODS TO DETERMINE AXIAL LENGTH Axial length can be determined by optical methods and ultrasonic methods. A comparison of optical, ultrasonic, and immersion biometry methods will reduce the likelihood of outliers. The IOL Master provides accurate axial lengths in clear lenses but cannot provide accurate information with more advanced lens opacities. Ultrasonic measurement, on the other hand, is less dependent on the density of the cataract. Immersion biometry reduces the likelihood of corneal compression but has slightly less control over alignment. An examination of all methods where possible will enhance accuracy.

Patients with Previous Keratorefractive Surgery Background

The number of patients who have had keratorefractive surgery (radial keratotomy (RK), photorefractive keratectomy (PRK), or laser-assisted in situ keratomileusis (LASIK)) has increased steadily over the past 20 years. With the advent of the excimer laser, the number is predicted to increase dramatically. To determine corneal power accurately in such cases is difficult; usually it is the determining factor in the accuracy of the predicted refraction following cataract surgery. Fortunately, the presence of previous corneal refractive surgery makes no significant difference to the accuracy of axial length measurement, or any of the other parameters required for IOL power calculation. Nevertheless, to provide this group of patients with the same accuracy of IOL power calculations as provided for standard cataract patients presents an especially difficult challenge to the clinician.

Methods to determine corneal power

To determine accurately the central corneal refractive power is the most important and difficult part of the entire IOL calculation process. The explanation is quite simple − instruments used to measure corneal power make too many incorrect assumptions for corneas that have irregular astigmatism; the cornea can no longer be compared to a sphere centrally, the posterior radius of the cornea is no longer 1.2 mm steeper than the anterior corneal radius, and so on. As a result of these limitations, the calculation method and the trial hard contact lens method are the most accurate, followed by corneal topography, automated keratometry and, finally, manual keratometry.

Calculation method

For the calculation method, three parameters must be known − the k readings and refraction before the keratorefractive procedure, and the stabilized refraction after the keratorefractive procedure. It is important

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that the stabilized postoperative refraction be measured before any myopic shifts from nuclear sclerotic cataracts occur. Also, it is possible for posterior subcapsular cataracts to cause an apparent myopic shift, similar to capsular opacification, in which the patient wants more minus in the refraction to make the letters appear smaller and darker. The concept, described in 1989,49 subtracts the change in refraction caused by the keratorefractive procedure at the corneal plane from the original k readings before the procedure, to arrive at a calculated postoperative k reading. This method usually is the most accurate because the preoperative k values and refraction usually are accurate to ±0.25 D. An example calculation is given in Box 5-3-1.

Trial hard contact lens method

The trial hard contact lens method requires a plano hard contact lens with a known base curve and a patient whose cataract does not prevent refraction to approximately ±0.50 D. This tolerance usually requires a visual acuity of better than 20/80. The patient’s spheroequivalent refraction is determined by normal refraction. The refraction then is repeated with the hard contact lens in place. If the spheroequivalent refraction does not change with the contact lens, then the power value for the patient’s cornea must be the same as that for the base curve of the plano contact lens. If the patient has a myopic shift in the refraction with the contact lens, then the power value for the base curve of the contact lens is greater than that of the cornea by the amount of the shift. If there is a hyperopic shift in the refraction with the contact lens, then the power value for the base curve of the contact lens is less than that for the cornea by the amount of the shift. For example, take a patient who has a current spheroequivalent refraction of +0.25 D. With a plano hard contact lens of base curve 35.00 D placed on the cornea, the spherical refraction changes to −2.00 D. Because the patient experiences a myopic shift with the contact lens, the power value for the cornea must be lower than that for the base curve of the contact lens by 2.25 D. Therefore, the cornea must be 32.75 D (35.00−2.25 D), which is slightly different from the value obtained by the calculation method (see Box 5-3-1). This method is compromised by the possible lack of accuracy of the refractions, which may be limited by the cataract.

Corneal topography

418

Current corneal topography units measure more than 5000 points over the entire cornea and more than 1000 points within the central 3 mm. This additional information provides greater accuracy in determining the power of corneas with irregular astigmatism compared with the data yielded by keratometry. The computer in topography units allows the measurement to account for the Stiles-Crawford effect, actual pupil size, and so on. These algorithms allow a very accurate determination of the anterior surface of the cornea. They provide no information, however, about the posterior surface of the cornea. In order to determine accurately the total power of the cornea, the power of both surfaces must be known. In normal corneas that have not been subjected to keratorefractive surgery, the posterior radius of curvature of the cornea averages 1.2 mm less than that of the anterior surface.50 For a person who has an eye with an anterior corneal radius of 7.5 mm and using the standardized keratometric index of refraction of 1.3375, the corneal power would be 45.00 D. Several studies have shown that this power overestimates the total power of the cornea by approximately 0.56 D. Hence, most IOL calculations today use a net index of refraction of 1.3333 (4/3) and the anterior radius of the cornea to calculate the net power of the cornea. Using this lower value, the total power of a cornea with an anterior radius of 7.5 mm would be 44.44 D. This index of refraction has provided excellent results in normal corneas for IOL calculations. Following keratorefractive surgery, the assumptions that the central cornea can be approximated by a sphere (no significant irregular astigmatism or asphericity) and that the radius of curvature of the posterior cornea is 1.2 mm less than that of the anterior cornea are no longer true. Corneal topography instruments can account for the changes in the anterior surface, but they are unable to account for any differences in the relationship to the posterior radius of curvature. In RK, the mechanism of having a peripheral bulge and central flattening apparently causes similar changes in both the anterior and posterior radii of curvature, with the result that using the net index of refraction for the cornea (4/3) usually gives fairly accurate results, particularly for optical zones larger than 4−5 mm. In RKs with optical zones of 3 mm or less,

the accuracy of the predicted corneal power diminishes. Whether this inaccuracy occurs as a result of the additional central irregularity with small optical zones or of the difference in the relationship between the front and back radii of the cornea is unknown at this time. Studies in which the posterior radius of the cornea is measured are necessary to answer this question. In PRK and LASIK, inaccuracies in the measurement of net corneal power are almost entirely due to the change in the relationship of the radii at the front and back of the cornea, because the irregular astigmatism in the central 3 mm zone usually is minimal. In these two procedures, the anterior surface of the cornea is flattened, with little or no effect on the posterior radius. Using a net index of refraction (4/3) overestimates the power of the cornea by 14% of the change induced by the PRK or LASIK; if the patient had a 7 D change in the refraction at the corneal plane from a PRK or LASIK with spherical preoperative k values of 44 D, the actual power of the cornea is 37 D, but the topography units give 38 D. If a 14 D change in the refraction occurs at the corneal plane, the topography units overestimate the power of the cornea by 2 D. In summary, corneal topography units do not provide accurate central corneal power following PRK, LASIK, or RKs with optical zones of 3 mm or less. In RKs with larger optical zones the topography units become more reliable. The calculation method and hard contact lens trial always are more reliable. Topography does, however, provide an excellent overview of central and peripheral corneal shape, the preoperative knowledge of which is valuable in the management of actual surgical intervention with respect to the management of the prevention and correction of corneal astigmatism (qv).

Automated keratometry

Automated keratometers usually are more accurate than manual keratometers for corneas of small optical zone (= 3 mm) RKs, because they sample a smaller central area of the cornea (nominally 2.6 mm). In addition, the automated instruments often have additional eccentric fixation targets that provide more information about the paracentral cornea. When a measurement error on an RK cornea occurs, the instrument almost always gives a central corneal power that is greater than the true refractive power of the cornea. This error occurs because the samples at 2.6 mm are very close to the paracentral knee of the RK. The smaller the optical zone and the greater the number of the RK incisions, the greater the probability and magnitude of the error. Most automated instruments have reliability factors given for each measurement to help the clinician decide on the reliability of the measurement. Automated keratometry measurements following LASIK or PRK yield accurate values of the front radius of the cornea, because the transition areas are far outside the 2.6 mm zone that is measured. The measurements still are not accurate, however, because the assumed net index of refraction (4/3) is no longer appropriate for the new relationship of the front and back radius of the cornea after PRK or LASIK, just as with the topographic instruments. The change in central corneal power as measured by the keratometer used in PRK or LASIK must be increased by 14% to determine the actual refractive change at the plane of the cornea. Hence, the automated keratometer overestimates the power of the cornea proportionately to the amount of PRK or LASIK performed.

Manual keratometry

Manual keratometers provide the least accurate measure of central corneal power following keratorefractive procedures, because the area that they measure usually is larger than 3.2 mm in diameter. Therefore, measurements in this area are extremely unreliable for RK corneas that have optical zones less than or equal to 4 mm. The one advantage of the manual keratometer is that the examiner actually is able to see the reflected mires and the amount of irregularity present. To see the mires does not help obtain a better measurement, but it does allow the observer to discount the measurement as unreliable. The manual keratometer has the same problem with PRK and LASIK as topographers and automated keratometers and, therefore, is no less accurate. The manual keratometer overestimates the change in the central refractive power of the cornea by 14% following PRK and LASIK.

Choosing the desired postoperative refraction target

The procedure to determine the desired postoperative refractive target is no different from that used for other patients who have cataracts, in whom the refractive status and the presence of a cataract in the other

BOX 5-3-1 THE CALCULATION METHOD

Step 1 To calculate the spheroequivalent refraction for refractions at the corneal plane (SEQC) using the spheroequivalent refraction at the spectacle plane (SEQS) at a given vertex (V), use equations 5-3-5 and 5-3-6: Equation 5-3-5

SEQS = sphere + 0.5(cylinder)

Equation 5-3-6

SEQC = 1000 /[(1000 / SEQS ) − V ]

Using equations 5-3-5 and 5-3-6, we find the preoperative SEQS and SEQC are: Preop SEQS = − 10.00 + 0.5(1.00) = − 9.50D Preop SEQC = 1000 [(1000 − 9.50 ) − 14.00] = − 8.38 The postoperative spheroequivalent refraction at the corneal plane would be: Postop SEQS = − 0.25 + 0.5 (1.00 ) = + 0.25 Postop SEQC = 1000 1000 0.25 = + 0.25 Step 2 To calculate the change in refraction at the corneal plane, use equation 5-3-7 Equation 5-3-7 Change in refraction = preoperative SEQC − postoperative SEQC = −8..38 − ( + 0.25) = − 8.63 D Step 3 To calculate the postoperative corneal refractive power, use equation 5-3-8 Equation 5-3-8

mean mean         Mean postoperative k =  preoperative  −  refraction at     corneal plane  k     = 42.00 − 8.63 = 33.37 D This value is the calculated central power of the cornea following the keratorefractive procedure. For IOL programs that require two k readings, this value is entered twice.

eye are the major determining factors. A complete discussion as to how to avoid refractive problems with cataract surgery is beyond the scope of this text (for a thorough discussion see Holladay and Rubin51). A short discussion of the major factors follows. If the patient has binocular cataracts, the decision is much easier because the refractive status of both eyes can be changed. The most important decision is whether the patient prefers to be myopic and read without glasses, or near emmetropic and drive without glasses. In some cases the surgeon and patient may choose the intermediate distance (−1.00 D) for the best compromise. To target for monovision is certainly acceptable, provided the patient has used monovision successfully in the past. Monovision in a patient who has never experienced this condition may cause intolerable anisometropia and require further surgery. Monocular cataracts restrict the choice of postoperative refraction, because the refractive status of the other eye is fixed. The general rule is that the operative eye must be within 2 D of the nonoperative eye in order to avoid intolerable anisometropia. In most cases this means the other eye is matched or a target of up to 2 D nearer emmetropia is set; if the nonoperative eye is −5.00 D, then the target is −3.00 D for the operative eye. If the patient successfully wears a contact in the unoperative eye or has demonstrated already the ability to accept monovision, an exception can be made to the general rule. It must be stressed, however, that should the patient not be able to continue wearing a contact lens, the necessary glasses for binocular correction may be intolerable and additional refractive surgery may be required.

Special limitations of iol power calculation formulas

As discussed previously, the third-generation formulas (Holladay 1, Hoffer Q, and the SRK/T) and the newer Holladay 2 are much more accurate than previous formulas the more unusual the eye. Older

IOL CALCULATIONS USING k VALUES AND PREOPERATIVE REFRACTION Formula and Rationale for Using Preoperative Refraction Versus Axial Length

5.3 Patient Work-up for Cataract Surgery

Mean preoperative k = 42.50 × 90° 41.50 × 18 0° = 42.00 Preoperativerefraction = − 10.00 / + 1.00 × 90 ( vertex = 14.00mm) Postoperativerefraction = − 0.25 + 1.00 × 90 ( vertex = 14.00mm)

formulas, such as the SRK1, SRK2, and Binkhorst 1, should not be used in these cases. None of these formulas gives the desired result if the central corneal power is measured incorrectly. The resulting errors almost always are in the hyperopic direction following keratorefractive surgery, because the measured corneal powers usually are greater than the true refractive power of the cornea. To further complicate matters, the newer formulas often use keratometry as one of the predictors to estimate ELP of the IOL. In patients who have had keratorefractive surgery, the corneal power is usually much flatter than normal and certainly flatter than before the keratorefractive procedure. In short, the ELP of a patient who has a 38 D cornea with no keratorefractive surgery would not be expected to be similar to that of a patient who has a 38 D cornea with keratorefractive surgery. New IOL calculation programs are being developed now to handle these situations and will improve predictions for these cases.

In a standard cataract removal with IOL implantation, the preoperative refraction is not very helpful for the calculation of the power of the implant, because as the crystalline lens is removed, so the dioptric power is being removed and then replaced. In cases in which power is not being reduced in the eye, such as secondary implant in aphakia, piggyback IOL in pseudophakia, or a minus IOL in the anterior chamber of a phakic patient, the necessary IOL power for a desired postoperative refraction can be calculated from the corneal power and preoperative refraction-knowledge of the axial length is not necessary. The formula used to calculate the necessary IOL power is given in equation 5-3-2,52 where ELP is the expected lens position in millimeters (distance from corneal vertex to principal plane of IOL), IOLP is the IOL power in diopters, k is the net corneal power in diopters, PreRx is the preoperative refraction in diopters, DPostRx is the desired postoperative refraction in diopters, and V is the vertex distance in millimeters of refractions. Equation 5-3-2 IOLP = 1336 /[1336 /{(1000 /[{1000 / Pr eRx} − V ]) + k} − ELP] −

1336[1336 /{(1000 / [{1000 / DPostRx} − V ]) + k} − ELP ]

Cases in Which to Use the Calculation from Preoperative Refraction

As mentioned above, the appropriate cases for which preoperative refraction and corneal power are used include the following: l Secondary implant in aphakia l Secondary piggy-back IOL in pseudophakia l A minus anterior chamber IOL in a high myopic phakic patient In each of these cases dioptric power is not being diminished in the eye, so the problem is simply to find the IOLP at a given distance behind the cornea ELP that is equivalent to the spectacle lens at a given vertex distance in front of the cornea. If emmetropia is not desired, then an additional term, the desired postoperative refraction (DPostRx), must be included. The formulas for calculating the predicted refraction and the back calculation of the ELP are given in Holladay.20 Use of the formula for particular cases is outlined below.

Secondary Implant for Aphakia

The patient discussed here is 72 years old and is aphakic in the right eye and pseudophakic in the left eye. The right eye can no longer tolerate an aphakic contact lens. The capsule in the right eye is intact and a posterior chamber IOL is desired. The patient is −0.50 D in the left eye and would like to be the same in the right eye. The mean keratometric k is 45.00 D, aphakic refraction is +12.00 sphere at vertex of 14 mm, manufacturer’s anterior chamber depth (ACD) lens constant is 5.25 mm, and the desired postoperative refraction is −0.50 D. Each of the values above can be substituted into equation 5-3-2 except for the manufacturer’s ACD and the measured k reading. The labeled values on IOL boxes are primarily for lenses implanted in the bag. Because this lens is intended for the sulcus, 0.25 mm should be

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subtracted from 5.25 mm to give the equivalent constant for the sulcus. The ELP, therefore, is 5.00 mm. The k reading must be converted from the measured keratometric value (n = 1.3375) to the net k reading (n = 4/3), for the reasons described previously under corneal topography. The conversion is performed by multiplying the measured k reading by the fraction obtained in equation 5-3-3 and inserting this into equation 5-3-4. Equation 5-3-3

INVESTIGATIONS FOR FURTHER SURGICAL REFINEMENT CORNEAL TOPOGRAPHY53

Conversion fraction = ([ 4 / 3] − 1) / (1.3375 − 1)

Using the mean refractive K, aphakic refraction, vertex distance, ELP for the sulcus, and the desired postoperative refraction in equation 5-3-2, the patient needs a 22.90 D IOL. A 23.00 D IOL would yield a predicted refraction of −0.57 D.20

Over the years many different techniques for the construction and closure of incisions for cataract surgery have been proposed, each with its own claimed advantages. More recently, corneal topography has provided an objective means by which to compare the effects of various surgical parameters on optical outcome. Nowadays, the aim of cataract surgery is to return patients to good uncorrected vision. This requires that their final refraction be within 1 D of emmetropia or a predetermined ametropic result, and that preexisting and surgically induced astigmatism be minimized.54 To achieve this, the refractive element of each stage of surgery has to be optimized, which, particularly in difficult cases, is facilitated by the use of corneal topography.

Secondary Piggy-Back IOL for Pseudophakia

PREOPERATIVE TOPOGRAPHY

= (1 / 3) / 0.3375 = 0.98765

Equation 5-3-4 Mean refractive k = Mean keratometric K × conversion fraction = 45.00 × 0.98765 = 44.44D

In patients who have a significant residual refractive error following the primary IOL implant, it often is easier surgically and more predictable optically to leave the primary implant in place and calculate the secondary piggy-back IOL power to achieve the desired refraction. This method does not require knowledge of the power of the primary implant or of the axial length; it is particularly important in cases in which the primary implant is thought to be mislabeled. The formula works for plus or minus lenses; however, negative lenses only now are becoming available. The patient discussed here is a 55-year-old man who had a refractive surprise after the primary cataract surgery and was left with a +5.00 D spherical refraction in the right eye. No cataract is present in the left eye, and the lens is plano. The surgeon and the patient both desire postoperative refraction of −0.50 D, which was the target for the primary implant. The refractive surprise is felt to be caused by a mislabeled IOL, which is centered in the bag and very difficult to remove. The secondary piggy-back IOL will be placed in the sulcus. This is very important, because trying to place the second lens in the bag several weeks after primary surgery is very difficult. More importantly, it could displace the primary lens posteriorly, thus reducing its effective power and leaving the patient with a hyperopic error. To place the lens in the sulcus minimizes this posterior displacement. The mean keratometric k is 45.00 D, pseudophakic refraction is +5.00 sphere at vertex of 14 mm, manufacturer’s ACD lens constant is 5.25 mm, and the desired postoperative refraction is −0.50 D. Use of the same style lens and constant as in the case above and modifying the k reading to net power, equation 5-3-2 yields a +8.64 D IOL for a 0.50 D target. The nearest available lens is +9.0 D, which would result in −0.76 D. In these cases extreme care should be taken to ensure that the two lenses are well centered with respect to one another. Decentration of either lens can result in poor image quality and can be the limiting factor in the patient’s vision.

Primary Minus Anterior Chamber IOL in a High Myopic Phakic Patient

420

3.50 and modifying the k reading to net corneal power yields −18.49 D for a desired refraction of −0.50 D. If a −19.00 D lens is used, the patient would have a predicted postoperative refraction of −0.10 D.

The calculation for a minus IOL in the anterior chamber is the same as for the aphakic calculation of an anterior chamber lens, with the exception that the power of the lens is negative. In the past, these lenses were reserved for high myopia that could not be corrected by radial keratotomy or photorefractive keratectomy. Because most of these lenses fixate in the anterior chamber angle, concerns of iritis and glaucoma have been raised. Nevertheless, several cases have been performed with good refractive results. Because successful laser-assisted in situ keratomileusis procedures have been performed in myopias up to −20.00 D, these lenses may be reserved for myopia that exceeds this power. Interestingly, the power of the negative anterior chamber implant is very close to the spectacle refraction for normal vertex distances. Consider a case in which the mean keratometric k is 45.00 D, phakic refraction is −20.00 sphere at vertex of 14 mm, manufacturer’s ACD lens constant is 3.50 mm, and the desired postoperative refraction is −0.50 D. Using an ELP of

The preoperative assessment of corneal topography has two roles in cataract surgery. First, as an alternative to keratometry, it can provide a representative measure of the corneal curvature or power necessary to calculate IOL power. Second, knowledge of the magnitude and location of pre-existing astigmatism is important if it is to be reversed by appropriate placement and construction of the wound during surgery.

CALCULATION OF IOL POWER Prior to cataract surgery, the power of the IOL required to give the desired postoperative refraction is determined using measurements of corneal curvature and axial length in a mathematical formula. The final refractive result is dependent upon the accuracy of the biometric data and its appropriate use in the relevant calculations. For these calculations, the corneal curvature commonly is measured by keratometry, and the mean of the two readings is used in the formula. For the majority of normal corneas, the small variability of the keratometry readings gives an accuracy of IOL power to within the 0.5 D step interval of manufactured lenses. In this group, variability in the measurement of the axial length tends to be the main source of discrepancy in the IOL power prediction. In contrast, this is not necessarily the case for patients who have corneal pathology or who have undergone previous corneal or refractive procedures.55 When the cornea is irregular, a better prediction of the required IOL power can be obtained using corneal topography rather than keratometry to measure the corneal curvature.56, 57 As a result of the generation of many more data points, corneal topography has the advantage that it represents these corneas more accurately; but with it comes the difficulty of knowing which data points to use in the IOL power calculations. Moreover, different sets of data points may be more accurate with different formulas.55 Examples of the data points that may be used include:57 l�� Keratometric equivalent at the 3 mm zone (average of the steepest and flattest meridians) l Average curvature of the 3 mm ring l Average curvature of the 4 mm ring l Mean central corneal power l Centrally weighted mean corneal power On the whole, measurements that use a greater number of data points that are nearer the central cornea are the most useful.

Planning the Incision Corneal topography may be used to assess the magnitude, location, and regularity of pre-existing corneal astigmatism. Vector analysis may be used to calculate the induced astigmatism that needs to be added to the existing astigmatism to produce the desired spherical end result. This may be achieved either by astigmatically neutral cataract surgery combined with a refractive corneal procedure, or by the appropriate modifi-

Incision Location

BOX 5-3-2 ISSUES TO DISCUSS WITH A PATIENT PRIOR TO CATARACT SURGERY l l l

Surgically induced change in corneal contour is less for the more peripheral incisions in the sclera or limbus55 than for those that involve the cornea. Incisions on the periphery of the steep axis create a central flattening effect and an associated amelioration of the astigmatism.

Incision Length and Proximity to Visual Axis

A huge quantity of literature now exists to support the theory that smaller incisions are associated with less surgically induced change in corneal contour, a more stable refraction, earlier visual recovery, and a better uncorrected visual acuity, particularly early after surgery.59–61 Since the introduction of IOLs that have flexible optics and injection apparatus, smaller incisions have been possible. Some IOLs have been shown to pass through an astigmatically neutral 2.2 mm incision. Incisions from 3 mm to 4.1 mm in width can be used for both execution of the surgery and titration of astigmatic correction by flattening the steep axis. In addition, as mentioned above, titration of proximity to the visual axis will vary the power of the astigmatic correction (see Chapter 5.4)

STANDARD KERATOMETRY Keratometry is a widely available alternative to videokeratoscopy for the measurement of corneal curvature or power. However, as discussed above, it makes measurements over a very small area of cornea,62 which is acceptable in most regular corneas, the central portions of which are broadly either spherical or spherocylindrical. However, for more irregular corneas, the additional data provided by videokeratoscopy are preferred.

INDICATIONS FOR SURGERY AND INFORMED CONSENT The indications for surgery vary from patient to patient, especially with the current minimally invasive nature of cataract and lens implant surgery (compared with such surgery performed only a few years ago). The visual needs of patients vary according to their ages, occupations, and leisure interests. A cataract may not be symptomatic. Visual symptoms and outcome expectation affect the benefit−risk ratio. Although the risks of technically well-performed small incision surgery are few in a healthy eye, patients require enough information on which to base the decision to proceed. Most patients are inclined to accept the professional judgment of the ophthalmic surgeon, but it is implicit that an adult of sound mind has the right to determine whether surgery should proceed. Therefore, in the context of cataract surgery, how much information is it necessary for an ophthalmologist to disclose to a patient? To what extent should an ophthalmologist shield a patient from the anxieties that can accompany a full explanation of diagnosis and treatment? An ophthalmologist must strike a balance between providing enough information to enable the patient to give informed consent with respect to treatment and engendering the confidence and trust that encompasses a joint decision to proceed. The surgeon shoulders the major responsibility for this, which should be accepted as a consequence of medical and specialist training. In the application of professional judgment, the consideration of alternative management strategies, risks, and benefits allows a patient to make some sort of informed evaluation of the options. Statistical information based on published data may be confusing: Where does the patient fit into the statistics? What are the personal outcome statistics for the surgeon who offers advice? What guarantees are there that a particular surgeon will perform the surgery? A problem arises if potential material risks and dangers are not disclosed to a patient before surgery and a complication occurs. The patient may claim that, with prior knowledge of such a risk, he or she would not have consented to the surgery. A risk is material when a rational patient considers the risk of undergoing a certain type of treatment to be significant.

T he purpose of the surgery The surgical procedure The anesthetic requirements Commonly experienced visual conditions after the surgery, even if temporary That temporary postsurgical visual conditions may become permanent under certain conditions The serious complications that may follow surgery Potential pain or ocular discomfort The refractive requirements after the surgery (the need to wear and the provision of spectacles and/or contact lenses) The potential need for additional procedures (planned staged procedures) Alternative management of the condition

Problems that arise from consent to perform surgical procedures can be minimized but not completely avoided, because every contingency cannot be reviewed completely. Taking the following steps will ensure that a thorough approach has been used. Appropriate patient education is required − the procedure is described in a manner that allows the patient to appreciate what will be done to treat the eye. Although the decision to proceed has to be the patient’s, the surgeon must not pass all the responsibility on to the patient; rather, the surgeon should communicate the appropriate degree of confidence in the procedure’s outcome. The surgeon has to assume much of the responsibility for treatment advice, because the patient cannot appreciate the intricacies of every surgical situation. Ultimately, the patient has to have faith in the ability of the surgeon not only to carry out the procedure but also to make the judgment that the benefits far outweigh the risks. An analogous situation might be that of a passenger contemplating a journey on a commercial airliner. If the passenger inquires of the pilot what the potential risks are, common sense suggests that the answer would be that they are high in number but low in expectation. A passenger who decides to make the trip has confidence in the airline and the aircrew to complete a successful journey. So it is with surgery: the patient must have confidence in the ability of the surgeon and the surgical team to carry out a successful procedure without knowing each and every pitfall that exists. Alternative stratagems for the management of an ophthalmic condition are explained to the patient to enable patient participation in the final direction of treatment. When uncertainties exist, the patient is advised of the predictability of the planned procedure, its stability, and its safety. Statistical information on outcome is of limited value when given in a general sense. Few surgeons are in a position to give specific statistical information about the outcome of their own practices or of certain procedures. The patient must be given adequate time to decide. At the end of the consultation, a patient must have an opportunity to consider the treatment that has been advised or to reverse a decision to proceed. It is inappropriate to obtain a patient’s signed consent for a procedure and then proceed on very short notice (the same day) with that treatment. The delay between consent and treatment must be sufficient to allow the patient to consider the matter fully. To ensure that a patient is fully informed with regard to consent for a surgical procedure, the issues listed in Box 5-3-2 should be covered. The patient should sign a consent form that states that the procedure has been explained fully in language that is comprehensible and that there has been sufficient opportunity to ask questions and reconsider consent prior to surgery. A written guide helps patients comprehend the nature of the planned surgery. Any surgical intervention is essentially a matter of trust and confidence − the trust of the patient in the surgeon’s ability and integrity, and the trust of the surgeon in the patient’s ability to comprehend and follow the process and to comply with prescriptions for managing the condition before, during, and after surgery.

5.3 Patient Work-up for Cataract Surgery

cation of the cataract incision.54, 58 In the latter, the incision is centered on the steep meridian, and the wound construction−placement−closu re combination that will produce the required astigmatic correction is carried out. The effect can be further titrated against the topography by selective suture removal under certain circumstances.

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REFERENCES 1. W agner T, Knaflic D, Rauber M, Mester U. Influence of cataract surgery on the diabetic eye: a prospective study. Ger J Ophthalmol. 1996;5:79–83. 2. Ram J, Pandav SS, Ram B, Arora FC. Systemic disorders in age related cataract patients. Int Ophthalmol. 1994;18:121–5. 3. Hamed LM, Lingua DN. Thyroid disease presenting after cataract surgery. J Pediatr Ophthalmol Strabismus. 1990;27:10–5. 4. Fisher SJ, Cunningham RD. The medical profile of cataract patients. Geriatr Clin. 1985;1:339–44. 5. Jacquerie F, Comhaire-Poutchinian Y, Galand A. Cataract extraction in uveitis. Bull Soc Belge Ophthalmol. 1995;259:9–17. 6. Lightman S, Marsh RJ, Powell D. Herpes zoster ophthalmicus; a medical review. Br J Ophthalmol. 1981;65:539. 7. Hara T, Hoshi N, Hara T. Changes in bacterial strains before and after cataract surgery. Ophthalmology. 1996;103:1876–9. 8. Chitkara DK, Colin J. Morphology and visual effects of lens opacities of cataract. In: Yanoff M, Duker JS, eds. Ophthalmology, 2nd ed. St Louis: Mosby; 2004:280–2. 9. Cardillo Piccolino F, Altieri G. Classification of cataract: In: Concepta�� Angellini�� , ed. Cataract. Roma: M Zingirian; �� 1985 . 10. Harding JJ. Cataract epidemiology. Curr Opin Ophthalmol. 1990;1:10–15. 11. Mehra V, Minassian DC. A rapid method of grading cataract in epidemiological studies and eye surveys. Br J Ophthalmol. 1988;72:801–3. 12. Chylack �� Jr�� LT�� , Wolfe JK, Singer DM, et al. The Lens Opacities Classification System III. Arch Ophthalmol. 1993;111:831–6. 13. Phelps Brown NA. The morphology of cataract and visual performance. Eye. 1993;7:63–7. 14. Lasa MS, Datiles MB, Freidlin V. Potential vision tests in patients with cataracts. Ophthalmology. 1995;102: 1007–11. 15. American Academy of Ophthalmology. Preferred Practice Pattern: Cataract in the otherwise healthy adult eye. San Francisco: American Academy of Ophthalmology; 1989. 16. Regan D, Giaschi DE, Fresco BB. Measurement of glare sensitivity in cataract patients using low-contrast letter chart. Ophthalmic Physiol Opt. 1993;13:115–23. 17. Lasa MS, Podgor MJ, Datiles MB, et al. Glare sensitivity in early cataracts. Br J Ophthalmol. 1993;77:489–91. 18. Holladay JT. Optics of aphakia and pseudophakia. In: Yanoff M, Duker JS, eds. Ophthalmology, 2nd ed. St Louis: Mosby; 2004:283–6. 19. Ridley H. Intraocular acrylic lenses. A recent development in the surgery of cataract. Br J Ophthalmol. 1952;36:113–22. 20. Campbell CJ, Koester CJ, Rittler MC, Tackaberry RB. The optics of the eye. In: Physiological optics. Hagerstown: Harper & Row; 1974:99–110. 21. Michaels DD. Aphakia and pseudophakia. In: Michaels DD, ed. Visual optics and refraction. St Louis: Mosby; 1985:506–27.

22. R ubin ML. Optics for clinicians. 2nd ed. Gainesville: Triad; 1974:�� 249–54.� 23. Milder B, Rubin ML. Aphakia. In: Milder B, Rubin ML. The fine art of prescribing glasses, 2nd ed. Gainesville: Triad; 1991:283–309. 24. Milder B, Rubin ML. Anisometropia. In: Milder B, Rubin ML, eds. The fine art of prescribing glasses, 2nd ed. Gainesville: Triad; 1991:217–53. 25. Burian HM, von Noorden GK. Visual acuity and aniseikonia. In: Binocular vision and ocular motility. St Louis: Mosby; 1974:130–41. 26. Holladay JT, Rubin ML. Avoiding refractive problems in cataract surgery. Surv Ophthalmol. 1988;32:357–60. 27. Holladay JT, Prager TC, Bishop JE, Blaker JW. The ideal intraocular lens. CLAO J. 1983;9:15–9. 28. Holladay JT. Evaluating the intraocular lens optic. Surv Ophthalmol. 1986;30:385–90. 29. Atchison DA. Optical design of intraocular lenses. I. On-axis performance. Optom Vision Sci. 1989;66: 492–506. 30. Masket S, Geraghty E, Crandall AS, et al. Undesired light images associated with ovoid intraocular lenses. J Cataract Refract Surg. 1993;19:690–4. 31. Mainster M. Violet and blue light blocking intraocular lenses: Photoreceptors versus photoreception. Br J Ophthalmol. 2006;90:784–92. 32. Yang S, Lang A, Makker H, Azleski E. Effect of silicone sound speed and intraocular lens thickness on pseudophakic axial length corrections. J Cataract Refract Surg. 1995;21:442–6. 33. Holladay JT, Van Dijk H, Lang A, et al. Optical performance of multifocal intraocular lenses. J Cataract Refract Surg. 1990;16:413–22. 34. Holladay JT. Measurements. In: Yanoff M, Duker JS, eds. Ophthalmology, 2nd ed. St Louis: Mosby; 2004:287–92. 35. Fedorov SN, Kolinko AI, Kolinko AI. Estimation of optical power of the intraocular lens. Vestn Oftalmol. 1967;80:27–31. 36. Fedorov SN, Galin MA, Linksz A. A calculation of the optical power of intraocular lenses. Invest Ophthalmol. 1975;14:625–8. 37. Binkhorst CD. Power of the prepupillary pseudophakos. Br J Ophthalmol. 1972;56:332–7. 38. Colenbrander MC. Calculation of the power of an iris clip lens for distant vision. Br J Ophthalmol. 1973;57:735–40. 39. Binkhorst RD. The optical design of intraocular lens implants. Ophthalmic Surg. 1975;6:17–31. 40. van der Heijde GL. The optical correction of unilateral aphakia. Trans Am Acad Ophthalmol Otolaryngol. 1976;81:80–8. 41. Thijssen JM. The emmetropic and the iseikonic implant lens: computer calculation of the refractive power and its accuracy. Ophthalmologica. 1975;171:467–86. 42. Fritz KJ. Intraocular lens power formulas. Am J Ophthalmol. 1981;91:414–5. 43. Binkhorst RD. Intraocular lens power calculation manual. A guide to the author’s TI 58/59 IOL power module. 2nd ed. New York: Richard D Binkhorst; 1981.

44. O lsen T, Corydon L, Gimbel H. Intraocular lens power calculation with an improved anterior chamber depth prediction algorithm. J Cataract Refract Surg. 1995;21:313–9. 45. Holladay JT, Gills JP, Leidlein J, Cherchio M. Achieving emmetropia in extremely short eyes with two piggyback posterior chamber intraocular lenses. Ophthalmology. 1996;103:1118–23. 46. Holladay JT, Prager TC, Chandler TY, et al. A three-part system for refining intraocular lens power calculations. J Cataract Refract Surg. 1988;13:17–24. 47. Retzlaff JA, Sanders DR, Kraff MC. Development of the SRK/T intraocular lens implant power calculation formula. J Cataract Refract Surg. 1990;16:333–40. 48. Hoffer KJ. The Hoffer Q formula: a comparison of theoretic and regression formulas. J Cataract Refract Surg. 1993;19:700–12. 49. Holladay JT. IOL calculations following RK. J Refract Corneal Surg. 1989;5:203. 50. Lowe RF, Clark BA. Posterior corneal curvature. Br J Ophthalmol. 1973;57:464–70. 51. Holladay JT, Rubin ML. Avoiding refractive problems in cataract surgery. Surv Ophthalmol. 1988;32:357–60. 52. Holladay JT. Refractive power calculations for intraocular lenses in the phakic eye. Am J Ophthalmol. 1993;116: 63–6. 53. Corbett MC, Rosen ES. Corneal topography in cataract surgery. In: Yanoff M, Duker JS, eds. Ophthalmology, 2nd ed.. St Louis: Mosby; 2004:309–14. 54. Nordan LT, Lusby FW. Refractive aspects of cataract surgery. Curr Opin Ophthalmol. 1995;6:36–40. 55. Koch DD, Haft EA, Gay C. Computerized video keratographic analysis of corneal topographic changes induced by sutured and unsutured 4 mm scleral pocket incisions. J Cataract Refract Surg. 1993;19(Suppl):166–9. 56. Sanders RD, Gills JP, Martin RG. When keratometric measurements do not accurately reflect corneal topography. J Cataract Refract Surg. 1993;19(Suppl):131–5. 57. Cuaycong MJ, Gay CA, Emery J, et al. Comparison of the accuracy of computerized videokeratoscopy and keratometry for use in intraocular lens calculations. J Cataract Refract Surg. 1993;19(Suppl):178–81. 58. Nielsen PJ. Prospective evaluation of surgically induced astigmatism and astigmatic keratotomy effects of various self-sealing small incisions. J Cataract Refract Surg. 1995;21:43–8. 59. Hayashi K, Hayashi H, Nakao F, Hayashi F. The correlation between incision size and corneal shape changes in sutureless cataract surgery. Ophthalmology. 1995;102:550–6. 60. Martin RG, Sanders DR, Miller JD, et al. Effect of cataract wound incision size on acute changes in corneal topography. J Cataract Refract Surg. 1993;19(Suppl):170–7. 61. Kohnen T, Dick B, Jacobi KW. Comparison of the induced astigmatism after temporal clear corneal incisions of different sizes. J Cataract Refract Surg. 1995;21:417–24. 62. Wilson SE, Klyce SD. Advances in the analysis of corneal topography. Surv Ophthalmol. 1991;35:269–77.

PART 5 THE LENS

Indications for Lens Surgery/ Indications for Application of Different Lens Surgery Techniques

5.4

Frank W. Howes

Key features n n n n n

L ens surgery is the most common eye operation. Technical indications for lens surgery are divided into two main categories: medical and optical. Socioeconomic conditions of a country is another indication for lens surgery. All lens surgery for whatever indication is properly considered refractive surgery. Lens surgery may be divided into four major categories by technique: lens repositioning (couching), lens removal, lens replacement, and lens enhancement.

INTRODUCTION The indications for lens surgery today may be classified into two main categories: 1. Medical, which might more properly be called surgical or pathological indication, and 2. Optical, currently referred to as refractive indication. Medical indications arise from pathological states of the lens of varying causes, usually related to lens clarity, lens position, or other lensrelated conditions, such as inflammation or glaucoma. Non-lens-related conditions may also be an indication for lens surgery, such as aniridia. Surgical or pathological indications have existed for centuries, if not millennia, and are generally indisputable. Refractive indications for lens surgery, in contrast, include clear-lens ametropic refractive states. These are relatively new indications, only decades old, and they may or may not be considered pathological conditions; in some academic settings, in past decades, surgery for such conditions was considered controversial, if not contraindicated. However, the ophthalmic subspecialty of refractive surgery gained a secure and permanent foothold in the late 1990s. Now, refractive lens surgery is rapidly becoming a common tool in the armamentarium of both cataract and refractive surgeons. The lens plays such a significant role in the visual refractive system of the eye that many, if not all, of the medical conditions of the lens also interfere with its optics. Similarly, surgical removal of the lens immediately and permanently alters the refractive state of the eye. Today, therefore, all lens surgery, for whatever indication, has properly come to be considered refractive surgery.

MEDICAL INDICATIONS FOR LENS SURGERY Lenticular Opacification (Cataract)

The medical indications for lens surgery (Box 5-4-1) are true pathological states, some of which may threaten the integrity of the whole organ (the eye). They also interfere with a major ocular function, focused vision. Lenticular opacification obstructs the pathway of light; reduces the available quantity of light; scatters light off axis; reduces contrast sensitivity; diminishes color intensity; reduces resolution acuity; may alter lens texture in such a way to contribute to a decrease in

Box 5-4-1 Medical Indications for Lens Surgery I. Lenticular opacification (cataract) II. Lenticular malposition A. Subluxation B. Dislocation III. Lenticular malformation A. Coloboma B. Lenticonus C. Lentiglobus D. Spherophakia IV. Lens-induced inflammation A. Phacotoxic uveitis (phacoanaphylaxis) B. Phacolytic glaucoma C. Phacomorphic glaucoma V. Lenticular tumor A. Epithelioma B. Epitheliocarcinoma VI. Facilitatory (surgical access) A. Vitreous base B. Ciliary body C. Ora serrata

a ccommodation amplitude, particularly in the case of presenile nuclear sclerosis; and, in the case of progressive nuclear sclerosis, often results in a myopic alteration of a previously stable lifelong refractive state. Cataract, depending on severity, is a condition of the eye that, by interfering with vision, can simultaneously interfere with certain activities in life. It is generally agreed that surgical intervention is indicated when there is “functional” visual impairment. In highly structured societies, governments or third-party health insurance carriers pay for such surgical procedures, and these same institutions often set standards for lens surgery indications. Visual acuity of 20/50 or worse as measured on a Snellen chart in dim ambient (mesopic) illumination with maximal refractive correction is an acceptable level of cataract to indicate surgery, according to the American Academy of Ophthalmology. Visual acuity of 20/50 or worse when tested with bright light imposition on the pupil, or glare testing, is considered a surgical level of cataract dysfunction in many states in the United States. Reduction of contrast sensitivity can be demonstrated and quantified, and the type and degree of lens opacification may be subjectively quantified by slit-lamp examination and categorized according to the Lens Opacification System III (LOCS-III) devised by Chylack et al.1 The degree to which the opacification obstructs light can, additionally, be measured by laser interferometry.2 Progressive changes in cataract density over time can be documented by Scheimpflug photography of nuclear cataracts3 and by Neitz-Kawara retroillumination photography of posterior subcapsular cataracts.4 In developed societies where surgical technology is advanced, perceived economic conditions may be the factors that determine the prevalence and definition of “cataract blindness” for a population, and this changes as conditions change. In many underdeveloped nations, the prevalence of cataract blindness is determined by the availability of care. In structured economic societies, third-party

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payers and governmental regulatory agencies are not very interested in the results of these sophisticated methods of analyzing loss of lens function; they are more interested in how the loss of lens function interferes with life functions. Loss of functional impairment due to visual impairment may range from minor impairment in luxury lifestyles, such as inability to follow a golf ball; to moderate impairment, such as inability to see well enough to drive an automobile; to severe impairment of life support functions, such as inability to see the units on an insulin syringe or the instructions on a bottle of cardiac medication − or even food on the table. Examples of such tests are the Visual Function Index (VF-14)5–8 and the Activities of Daily Vision Scale (ADVS).9, 10

Cataract in the presence of other ocular disorders

The decision whether and when to remove a cataract in an otherwise healthy eye usually depends on the cataract’s impact on the visual function of the eye and the impact of that level of visual impairment on the person’s life. In healthy eyes whose only disorder is cataract, the presumed outcome after uncomplicated surgery is better vision than before surgery. Indeed, in the most technologically advanced societies, patients are requesting emmetropia, restoration of accommodation, and have even engaged in lawsuits when the desired refractive outcome was not achieved. In these “healthy” eyes, however, high-volume cataract surgeons experience a rate of intraoperative and postoperative complications of less than 2% or, conversely, an uncomplicated rate of 98%. Thus, when one applies a risk-benefit ratio with such a high degree of success, surgery is usually the mutually agreed on course. However, such may not be the case when the cataract is associated with other disorders, especially if they are contributing factors to the loss of vision of an eye. Therefore, such conditions as amblyopia, corneal opacification, vitreous opacification, maculopathy, retinopathy, glaucoma, and optic neuropathy may alter or delay the decision to operate, based not so much on the expected risks but rather on the limited benefits. In some cases, lens surgery is indicated to preserve peripheral vision only for functional ambulation. In other cases, a progressive condition of the posterior segment is an indication for lens surgery, even when the expectation for visual improvement may be minimal.11 Systemic conditions may also play a role in deciding whether and when to remove a cataract. Is the patient’s diabetes under control? Has there been a stroke with hemianopia? Is the patient on systemic anticoagulants? Is the patient terminally ill or immunologically suppressed? Does the patient have Alzheimer’s disease or severe mental retardation? Thus, the decision to remove a cataract may become a collaborative endeavor with participation by the patient, the patient’s family, the patient’s primary physician, the surgeon, a governmental agency, and a third-party payer. The decision, thus, is determined not only by technological findings and expectations but also by a “holistic” evaluation of the impact of such a decision on that person’s life, as defined by that society.

424

Lenticular Malposition

Subluxation, i.e., displacement of the lens within the posterior chamber, and dislocation, i.e., displacement of the lens out of the posterior chamber into the anterior chamber or vitreous, of the lens are different degrees of the same phenomenon and result from dysfunction of the zonule. The zonule may be defective as a result of congenital malformation, total or partial agenesis, or a hereditary metabolic disorder, such as Marfan’s syndrome. Chronic inflammation and pseudoexfoliation have been shown to be associated with a weakness in the zonular fibers or their attachments. Ocular trauma is an obvious cause. Subluxation, in the absence of associated sequelae, may not be visually significant and may not be an indication for lensectomy. Similarly, complete dislocation of an intact lens into the inferior vitreous may be a quiescent event in the absence of inflammation and may simply produce a state of refractive aphakia, correctable nonsurgically with a spectacle or contact lens or surgically with intraocular lens (IOL) implantation. Subluxation to the extent that the equator of the lens is visible in the midsized pupil is usually visually significant, causing glare, fluctuating vision, and monocular diplopia. This symptom complex would qualify for lens surgery.

Lenticular Malformation

These conditions of abnormal lens development are congenital. They may be genetic, hereditary, or the result of intrauterine infection or trauma. These conditions include lens coloboma, lenticonus, lentiglobus, and spherophakia, as well as varieties of congenital cataract. Partial iris coloboma or total aniridia, whether congenital, traumatic, or surgical, may be an indication for lens surgery to improve visual function or for cosmesis. The availability of aniridia IOLs (Fig. 5-4-1A) and opaque endocapsular rings (see Fig. 5-4-1B,C) offers great improvements for such patients. The indications for surgery depend on the degree to which the specific malformation interferes with vision or the integrity of the involved eye. Such abnormalities may be associated with amblyopia. Early detection and surgical intervention should be incorporated with a plan for amblyopia therapy.

Lens-Induced Ocular Inflammation

Phacoanaphylactic endophthalmitis (phacotoxic uveitis) occurs in an immunologically mature and competent host and is related to physical or chemical disruption of the lens capsule. Surgery may be the appropriate treatment for this form of ocular inflammation.

Lens-Induced Glaucoma

Inflammatory glaucoma (phacolytic glaucoma)

Phacolytic glaucoma occurs in an eye with a mature lens in which the lens capsule is intact. Denatured, nonantigenic liquefied lens material leaks out through the intact lens capsule and elicits a macrophagic, inflammatory reaction. The macrophages, engorged with lens material,

Fig. 5-4-1 Iris defect prostheses. (A) Aniridia intraocular lens with opaque peripheral “pseudoiris.” (B) Aniridia endocapsular ring. (C) Iris coloboma endocapsular ring (diaphragm type 96G). (Courtesy of Morcher, GMBh, Germany.)

clog the open angle, leading to a secondary open-angle glaucoma. Removal of the lens is usually curative, obviating the need for other forms of medical or surgical pressure management. Similarly, removal of the lens in this instance is also curative. The growth of the lens with age progressively engulfs anterior segment space, and may ultimately lead to acute angle-closure glaucoma through the mechanism of pupil block. This is more likely in hyperopic eyes due to the short axial length and already crowded anterior segments. Lens removal and replacement with an intraocular lens greatly increases anterior segment space and, in most instances, resolves the glaucoma.

REFRACTIVE INDICATIONS FOR LENS SURGERY The refractive indications for lens surgery include all the classic well-known refractive states of the “healthy” eye, which is why these new indications for lens surgery have been somewhat controversial. There may be no true histopathology to most of these eyes; however, some, such as those with extreme axial myopia, may be at risk for true pathology following surgical intervention. In addition, the historical development of spectacles and contact lenses, having long antedated the development of modern lens surgery, created a mind-set among academics that “inborn errors of refraction” are not diseases and are therefore not conditions to be treated with medicine or surgery, especially if such treatment might unnecessarily endanger an eye or expose an otherwise “healthy” eye to undue risk. Although there may be merit to that argument, it is a concept that is rapidly losing popularity. In fact, the voice of tradition seems to have become almost silent on this issue. Whether prudent or not, the global anterior segment ophthalmic surgical community has embarked on a new and enticing endeavor − rendering the human population emmetropic. The process began as an idea before its time in the 1950s, with the failed attempts of Sato at endothelial radial keratotomy and Barraquer and others at phakic anterior chamber IOL implantation. The ophthalmic surgical “technical revolution” that ensued over the following decades led to renewed interest in the surgical correction of refractive errors 30 years later in the 1980s, this time as an idea whose time had come. Refinements in ocular anesthesia, incision technology, lensectomy techniques, ophthalmic visco-surgical device (OVD) tissue protection, and IOL manufacturing and implantation allowed the successful return of the concept of intraocular correction of refractive errors, including both clear lensectomy and phakic implantation. All this, combined with the multitude of new keratorefractive procedures, has actually led to the development of

INDICATIONS FOR DIFFERENT LENS SURGERY TECHNIQUES Surgery affecting the human lens can be organized historically by chronology of development (Table 5-4-1) or divided into four major categories by technique (Box 5-4-2): lens repositioning, lens removal, lens replacement, and lens enhancement. Lens repositioning, traditionally known as “couching,” is perhaps the oldest form of lens surgery and is still in use in some developing countries today. In stark contrast, at the other end of the historical spectrum is the most recent category of lens surgery, that of lens functional enhancement. These new investigational techniques involve surgical procedures designed to enhance accommodation in the presbyopic eye.

5.4 Indications for Lens Surgery/Indications for Application of Different Lens Surgery Techniques

Pupil block and angle closure (phacomorphic glaucoma)

a new, bona fide ophthalmic surgical subspecialty, that of refractive surgery. Almost all the operable tissues and spaces of the eye have, over decades, come under investigation as locations for refractive surgical modulation: corneal epithelial surface, corneal stroma, corneal endothelial surface, anterior chamber, iris, pupil, posterior chamber, lens, and sclera. The lens, therefore, assumes its role among the others as a popular location for surgical refractive modulation for those who prefer a familiar procedure that spares the cornea and saves the economic expense of an excimer laser. Those who decry the lenticular approach emphasize all the potential intraoperative and postoperative complications attendant with invasive intraocular procedures. Despite the controversy, clear lens replacement stands as a viable procedure today for both myopia and hyperopia, and now that it is possible to ameliorate astigmatism (Fig. 5-4-2A), modulate higher order aberration, and reduce presbyopic symptoms (see Fig. 5-4-2B,E), patient demand for these services have increased dramatically in recent times. Aspheric lenses (see Fig. 5-4-2C) have recently been introduced with the expanding knowledge of higher order aberration control. These IOLs can be used to correct, modify, or maintain naturally occurring wave-front detected aberrations. Multifocal IOLs (see Fig. 5-4-2B) represent some of the first attempts at the intraocular correction of presbyopia. Other attempts at the development of a truly accommodative pseudophakos have included the intracapsular injection of liquid silicone12–14 and the intracapsular placement of high-water-content poly-HEMA lenses, a liquid siliconefilled intracapsular balloon,15, 16 multiple IOLs (polypseudophakia)17, 18 (see Fig. 5-4-2D), and more recently the flexing haptic accommodative IOLs (see Fig. 5-4-2E).

Fig. 5-4-2 Older and modern intraocular lens modifications providing functions additional to pure spherical dioptric correction. (A) Alcon toric IOL with blue light filter (Acryosof IOL). (B) Alcon multifocal IOL with apodized rings also with blue light filter (Acryosof IOL). (C) Bausch and Lomb (B&L) Akreos aspheric IOL. (Courtesy of B&L Australia.)

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Fig. 5-4-2, cont’d (D) Older style accommodative PMMA polypseudophakic intraocular lens. (Courtesy of T. Hara.) (E) The C&C Vision CrystaLens model AT-45 silicone multipiece intraocular lens. (Courtesy of C&C Inc.)

Table 5-4-1 HISTORY OF CATARACT SURGERY TECHNIQUES Year

Technique

Place

Surgeon

800

Couching

India

Unknown

1015

Needle aspiration

Iraq

Unknown

1100

Needle aspiration

Syria

Unknown

1500

Couching

Europe

Unknown

1745

ECCE inferior incision

France

Daviel

1753

ICCE by thumb expression

England

Sharp

1860

ECCE superior incision

Germany

von Graefe

1880

ICCE by muscle-hook zonulysis and lens tumble

India

Smith

1900

ICCE by capsule forceps

Germany

Verhoeff Kalt

1940

ICCE capsule suction erysiphake

Europe

Stoewer I. Barraquer

1949

ECCE posterior chamber IOL and operating microscope

England

Ridley

1951

Anterior chamber IOLs

Italy Germany

Strampelli Dannheim

1957

ICCE by enzyme zonulysis

Spain

J. Barraquer

1961

ICCE by capsule cryoadhesion

Poland

Krawicz

1967

ECCE by phacoemulsification

United States

Kelman J. Shock

1975

Iris-pupil supported IOLs

Netherlands

Binkhorst Worst

1984

Foldable IOLs

United States South Africa

Mazzocco Epstein

ECCE, Extracapsular cataract extraction; ICCE, intracapsular cataract extraction; IOL, intraocular lens.

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The indications for a particular lens surgery technique may be determined by several factors (Box 5-4-3). Different medical conditions or pathological states of the eye and the lens may favor one technique over another. In some countries, the availability of equipment, as well as the level of training of the surgeon, may be factors that dictate technique. Certain countries have governmental agencies, professional organizations, academic institutions, insurance payers, or surgical facilities that regulate and control the types of surgical techniques surgeons may perform. For the purpose of this text, however, only specific medical or pathological conditions of the eye are discussed as factors determining the choice of surgical technique.

Couching

This is the oldest technique of lens surgery; it has been performed for more than 1000 years and is still in use today in some developing countries. The original method was an extracapsular technique that involved the placement of a sharp needle through the sclera at the pars plana, behind the iris, until the tip of the needle was visible in the pupil in front of the lens. The anterior capsule was then scratched open with the needle tip, and the nucleus was pushed inferiorly until the pupillary space appeared clear. This early extracapsular technique, which was being performed long before the development of topical anti-inflammatory medications, was associated with inflammation, secondary glaucoma, posterior

Box 5-4-2 Lens Surgery Techniques

Box 5-4-3 Lens Removal Techniques: Ocular Indications I. Intracapsular extraction A. Zonular absence/dialysis B. Lens subluxation C. Lens dislocation II. Nuclear delivery A. Status of cornea 1. Low endothelial cell count 2. Guttate dystrophy B. Status of cataract 1. Brunescent nuclear sclerosis 2. Cataracta nigra C. Torn posterior capsule during phacoemulsification D. Zonulodialysis III. Phacosection A. Same corneal, cataract, and capsular indications as nuclear delivery B. Astigmatism management IV. Phacoemulsification A. Status of cornea 1. Normal endothelial cell count 2. No guttate dystrophy B. Status of cataract 1. Immature nuclear sclerosis 2. Cortical or subcapsular cataract C. Astigmatism management

synechiae, pupillary block, Soemmerring’s rings, and capsular opacification, not to mention endophthalmitis. Considering current technology, there may be no indications for extracapsular couching today. Intracapsular couching, however, is another matter. This procedure was (and still is) performed without anesthesia with the patient in the sitting position, sometimes outdoors. However, couching can also be performed safely under an operating microscope in a matter of minutes following enzymatic zonulysis with α-chymotrypsin. Unlike the exposed nucleus and cortex in the extracapsular method, the intact, encapsulated, dislocated crystalline lens in the intracapsular method is immunologically inert. The low skill level required and the low cost of this simple, safe, fast, and effective procedure make it an attractive alternative for economically disadvantaged developing countries, which harbor a large majority of the world’s estimated 18 million cataract blind.

5.4 Indications for Lens Surgery/Indications for Application of Different Lens Surgery Techniques

I. Lens repositioning (“couching”) A. Extracapsular B. Intracapsular 1. Physical (instrumental) zonulysis 2. Pharmacological (enzymatic) zonulysis II. Lens removal A. Total (intracapsular) 1. Capsule forceps 2. Suction erysiphake 3. Cryoextraction B. Partial (extracapsular) 1. Anterior capsulotomy/capsulectomy a. Discontinuous b. Continuous (capsulorrhexis) c. Linear 2. Nucleus removal a. Assembled delivery (large incision) (1) Expression (“push”) (2) Extraction (“pull”) b. Disassembled extraction (1) Phacosection (2) Phacoemulsification-aspiration (a) Ultrasound (i) linear (ii) torsional (b) Laser (c) Water jet (d) Impeller 3. Cortex removal a. Irrigation b. Aspiration III. Lens replacement (intraocular lens implantation) A. Locations 1. Anterior chamber a. Angle fixation b. Iris fixation 2. Pupil 3. Posterior chamber a. Iris fixation (sutured or enclavated) b. Ciliary sulcus (sutured or unsutured) 4. Lens capsule a. Anterior capsule (1) Haptic sulcus/optic bag (2) Optic posterior chamber/haptic bag b. Intracapsular (“in the bag placement”) c. Posterior capsule (haptic bag/optic Berger’s space) 5. Pars plana (sutured) B. Optic materials 1. Hydrophobic a. PMMA b. Silicone c. Acrylic 2. Hydrophilic a. Poly-HEMA b. Acrylic c. Collagen-copolymer C. Optic types 1. Monofocal a. Spherical (1) Plus (2) Minus b. Toric c. Telescopic d. Prismatic 2. Multifocal 3. Accommodative IV. Lens enhancement: reversal of presbyopia by scleral expansion A. Ciliary cerclage B. Radial anterior ciliary sclerotomy

Intracapsular Extraction

The intracapsular method of lens removal has not been the procedure of choice in industrialized nations since the development of modern extracapsular techniques in the late 1970s, primarily because of lower rates of postoperative posterior segment complications such as hemorrhage, vitreous loss, retinal detachment, and cystoid macular edema. Current indications for planned intracapsular extraction, therefore, are related to intraocular conditions that preclude safe and successful extracapsular surgery. The absence or lysis of a significant number of zonular fibers, which may occur as an isolated congenital anomaly or as a result of Marfan’s syndrome, pseudoexfoliation, trauma, or following pars plana surgery, may be an indication for intracapsular extraction. Significant subluxation or dislocation of the lens may leave no other option except for removal of the lens in its capsule (see Chapter 5.10). Traditionally, intracapsular extraction involved removal of the complete intact lens through a large incision measuring 11−16 mm. In earlier years these eyes were left aphakic with aphakic spectacle correction offered where available. Bilateral surgery was invariably necessary to minimize aniseikonic problems, although contact lens correction was also satisfactory. Many of these eyes have subsequently had secondary IOLs implanted, with the choice of IOL being angle based, iris fixed (anterior or posterior), or sutured to the ciliary sulcus Modern sulcus fixation IOLs now have design features that enable them to fibrose into the ciliary processes and sulcus (Fig. 5-4-3), minimizing the chances of posterior dislocation common in previous sulcus fixation IOLs. In addition these lenses are foldable allowing small-incision surgery and adherence to the principles of astigmatism avoidance and correction. In the majority of primary situations

427

THE LENS

Fig. 5-4-3 Examples of newer intraocular lens designs for use in eyes without capsular support. (A) Artisan IOL for iris fixation, either anterior or posterior. (B) FH1000 (Lenstec) hydrophilic acrylic foldable IOL for sulcus fixation by suture with long-term stability by fibrosis through peripheral haptic fibrosis holes shown. The radius of the haptics matches a 13-mm-wide sulcus (3) and the optic is reinforced to counteract any torsional forces. Length of IOL: 13.25 mm (1); optic width: 6.0 mm (2).

for intracapsular surgery, the wound needs to be large and hence constructed appropriately for minimization of astigmatism induction (see Chapter 5.10).

Large-Incision Nuclear Expression Cataract Surgery (Extracapsular Extraction)

This technique became popular in the 1980s as surgeons, who had been performing large-incision intracapsular extraction and anterior chamber implantation, desired the benefits derived from an intact posterior capsule and posterior chamber implantation. The technique persists today and is performed in great numbers, particularly in Asian countries, where the more advanced small-incision techniques of phacoemulsification and foldable lens implantation are not yet available for the masses. In those countries where phacoemulsification and foldable lens implantation are rapidly becoming standard, the only ocular indication for planned nuclear delivery may be an advanced nucleus that is too hard to be emulsified safely. Corneas at risk for developing irreversible edema, such as those with low endothelial cell counts or guttate dystrophy, may be relative indications for nuclear delivery. However, small-incision lens surgery in the presence of highrisk corneas remains a viable option, particularly when highly retentive dispersive OVDs are used in combination with endolenticular or intercapsular phacoemulsification. Another indication for nuclear delivery is the occurrence of a tear in the posterior capsule during phacoemulsification. Although it may be possible to continue to emulsify the nucleus over OVD or over a lens glide (Michelson technique), a large capsular tear with presentation of vitreous may preclude safe emulsification, necessitating incision enlargement and nuclear delivery.

Small-Incision Nuclear Expression Cataract Surgery (“Mini-nuc” and Other Techniques)

428

These techniques involve delivering the nucleus not as a single intact unit in one step through a large incision, but in parts through a small incision. The nucleus may be separated concentrically, delivering the smallest endonucleus separately from outer layers of epinucleus. This technique may be performed through a 7−8 mm sutureless scleral incision using side-port irrigation through a chamber maintainer to hydroexpress the nuclear components, which delaminate as they pass through the incision. This has been called the “mini-nuc” technique.19 By bisecting or trisecting the nucleus further by instrumentation, achieving geometrical nuclear division in the anterior chamber and removing the small sections linearly with forceps or by hydrostatic pressure, incisions as small as 3−4 mm may be achieved.20 The indications for these techniques are the same as those for intact nuclear delivery, as a manual extracapsular technique, with the addition

of astigmatism management. Unlike long-incision, single-stage nuclear delivery, small-incision phacosection may induce no change in astigmatism, particularly if a foldable lens is used and all is accomplished through a 3 mm scleral incision. The choice for this type of surgery relates to the surgeon’s experience, socioeconomic factors, and instrumentation availability.

Phacoemulsification

This technique of nucleus removal has been performed through incisions ranging from 3.2 mm down to less than 1.0 mm. Combined with foldable lens implantation, the major advantage of phacoemulsification is the small incision. Current techniques use self-sealing, sutureless scleral and clear corneal incisions measuring 2.3−3.2 mm. These incisions are astigmatically neutral. Corneal incisions can be moved centrally from the limbus and can be grooved as two-plane, two-stage incisions, allowing the reduction of pre-existing astigmatism, especially when used in combination with astigmatic keratotomy.28 Therefore, the presence of corneal cylinder is an indication for phacoemulsification and foldable lens implantation, just as is the absence of corneal cylinder. The status of both the nucleus and the cornea factors into the decision whether to perform phacoemulsification. It has been observed that with certain phacoemulsification techniques there is a greater loss of endothelial cells. This relates to the duration of the ultrasound, the intensity of the ultrasound, and the proximity to the corneal endothelium. The more compromised the endothelium, the more care required, particularly in eyes with denser nuclei requiring increased energy for removal. OVDs do protect the corneal endothelium and techniques such as the “soft shell” technique,21 which retains good endothelial coverage during the procedure, should be used in these eyes. When phacoemulsification was originally performed in the anterior chamber and in the iris plane, high-risk corneas and dense nuclei were considered contraindications, and nuclear delivery was recommended. However, long ultrasound times have been shown to be well tolerated when the ultrasonic energy is confined to the capsular bag. Newer emulsification techniques,22 together with high vacuum, have also been shown to reduce ultrasound times, providing further protection to the cornea (Box 5-4-4). Newer modalities of nuclear emulsification have evolved including torsional phacotip movement combined with the usual axial ultrasound induced movement, as well as the nonultrasound modalities such as neodymium:YAG laser;23–27 erbium:YAG laser;28–30 pulsed water jet; “plasma blade” molecular bond disruption; impeller aspiration-emulsification; and others.

Lens Capsule Surgery

When capsulectomy was first conceived, it was performed in discontinuous fashion, either as multiple punctures (“can-opener”) with a bent needle or cystotome or as triangular (Kelman) or square (Gills) capsulectomies facilitated with scissors (Fig. 5-4-4). Discontinuous openings, being weak, allow easy dislocation of the nucleus anteriorly for either delivery

Box 5-4-4 Phacoemulsification Techniques

5.4

Fig. 5-4-4 Anterior capsulectomy shapes used for extracapsular cataract surgery. (Courtesy of Advanced Medical Optics Inc.)

or emulsification. However, they are also prone to developing multiple radial anterior tears out to the equator, with possible extension around to the posterior capsule.31 Postoperatively, they have a high rate of posterior synechia formation and anterior IOL loop dislocation.32 Plate-haptic lenses are contraindicated in the presence of a discontinuous anterior capsular opening, as they have also been shown to dislocate anteriorly postoperatively. There is, therefore, rarely a current indication for a discontinuous capsulectomy, except possibly in the case of advanced nuclear sclerosis with absence of a red reflex and nonavailability of a biological capsule stain, such as trypan blue or indocyanine green. Continuous curvilinear capsulectomy (CCC), also known as capsulorrhexis,33 is much more desirable than previous discontinuous methods. The continuous anterior capsular opening is stronger and more resistant to radial tearing than are discontinuous openings.34 The continuous anterior capsulectomy of the appropriate size and shape has also been shown to retain IOL haptics of all designs and materials within the capsular bag postoperatively virtually 100% of the time. A circular opening of 4−5 mm also readily retains the nucleus for in situ or endolenticular emulsification techniques. Larger openings of 6−7 mm allow nuclear prolapse for intact delivery, phacosection, or anterior chamber emulsification. Continuous openings that are too small may contract postoperatively due to fibrous metaplasia of lens epithelial cells obstructing not only the patient’s vision but also the doctor’s view, precluding examination and treatment of fundus disorders. YAG laser anterior capsulectomy would then be indicated, just as posterior capsulectomy is indicated for posterior capsular opacification. The ideal continuous anterior capsular opening is 1.0 mm smaller than the diameter of the lens optic to be implanted. The capsular contents may also be removed through a linear capsulectomy (see Fig. 5-4-4) rather than a full capsulectomy. Both discontinuous and continuous linear capsulectomy techniques have been employed for nuclear delivery35 and emulsification.36 The advantage of these intercapsular techniques, if the anterior capsule is left intact during surgery, is protection of the cornea. Leaving the anterior capsule in place also offers the postoperative possibility of total encapsulation of an accommodative pseudophakos. The implantation of a pliable refractive material into a complete, intact lens capsule may establish the potential for pseudophakic accommodation. Animal experimental trials were begun in the early 1980s, first by Schanzlin’s group, who evacuated the capsular contents through a 3 mm linear capsulectomy and injected liquid silicone in rabbit eyes.37 These procedures worked surgically; however, the resultant optical power of the liquid injectable material could not be controlled, the anterior capsules became opacified by white fibrosis in a few weeks, and accommodative function was not determined. In the late 1980s, Nishi et al.16 developed a liquid silicone-filled intracapsular balloon and placed it in monkey eyes. The power of the IOL was now controllable, and Scheimpflug photography demonstrated 6 D of apparent accommodation. Also in the late 1980s, the first potentially accommodating IOLs were placed in human eyes; they were 66% water, poly-HEMA “full-size” expandable IOLs.38 Unfortunately, none of these first human subjects, approximately 46 in number, demonstrated accommodation. More recent designs are those of flexible hinged haptic silicone and acrylic IOLs (see example Fig. 5-4-2E) that provide some accommodation; unfortunately, this effect is generally

lost with bag fibrosis. Intraocular IOL power adjustment systems are undergoing research at the time of writing (Calhoun Vision)39 giving surgeons the opportunity to modify postsurgical refraction. This will assist with the management of biometric error, monovision induction, reduction, and enhancement. Residual lens epithelial cell activity and visual axis obstruction following cataract surgery continues to be a major concern. The posterior capsule can opacify as a result of lens epithelial cell migration and hyperplasia (Fig. 5-4-5), and the anterior capsule can opacify as a result of lens epithelial cell (LEC) fibrous metaplasia (Fig. 5-4-6). In addition, excessive fibrosis can result in contraction of the entire capsule with deformation of the IOL haptics, decentration of the IOL optic, and zonular dialysis with capsular bag subluxation or dislocation. Efforts to prevent unwanted postoperative LEC activity have included primary posterior capsulotomy40 and methods of mechanically cleaning the capsule, including vacuuming, vacuuming with ultrasound, curettage, and cryosurgery (Box 5-4-5).41 Attempts at pharmacologically disabling the LEC have included hypotonic hydrolavage, antiprostaglandins,42, 43 anti metabolites,44 and immunosuppressors.45 These techniques are currently under investigation. In addition, newer IOL materials that are hydrophilic, such as polyHEMA, acrylic, and collagen-copolymer, appear to stimulate very low levels of lens epithelial hyperplasia and almost no fibrous metaplasia. The possibility of using hydrophilic IOLs as drug delivery systems is also very attractive. However, the most recent clinical advancement that has been demonstrated to reduce the incidence of posterior capsular opacification is the use of IOL optics with “square edge design.” These are manufactured in both acrylic and silicone. The square edge has been shown to be a physical barrier to the central posterior migration of LECs.32

Indications for Lens Surgery/Indications for Application of Different Lens Surgery Techniques

I. Location A. Anterior chamber (Kelman, Brown) B. Iris plane (Kratz) C. Posterior chamber (supracapsular) (Maloney) D. Capsule (endolenticular, in situ) 1. Anterior capsulectomy (Sinskey) 2. Anterior capsulotomy (intercapsular) (Hara) II. Techniques A. Carousel B. Chip-and-flip (Fine) C. Phacofracture 1. Divide-and-conquer (Gimbel) 2. Four-quadrant pregrooved (Shepherd) 3. Nonstop chop (Nagahara) 4. Stop-and-chop (Koch) 5. Double chop (Kammann)

Zonular Surgery

The preceding discussion of the surgical management of the lens capsule concentrated on endocapsular techniques and management of the viable lens epithelial cells on the interior surface of the lens capsule. The discussion would be incomplete if it did not address a significant, difficult, new area of capsular surgery that deals with an abnormality of the exterior capsule − management of the weak or partially absent zonule. In most cases, the goal of this type of lens surgery is the same as that for eyes without a compromised zonule: to remove the contents of the capsular bag though a CCC and replace the contents with a foldable IOL. However, in these cases, the goal is extended to include performing the surgery without further compromising the zonule, without disrupting the vitreous, without jeopardizing the long-term integrity of the capsulozonular apparatus, and, if possible, to recircularize and recenter a subluxed capsule. To accomplish these surgical goals and avoid a long incision, intra capsular extraction, vitrectomy, and anterior chamber IOL, several modifications to the standard procedure are planned for eyes with compromised zonules. In these eyes, there is some zonular support to the capsule (partial zonular absence), enough of a circumference of attached fibers to support CCC and implantation of an endocapsular ring. If only a small percentage of the zonule is attached, or if the zonule is completely absent, intracapsular extraction with anterior chamber IOL or sutured posterior chamber IOL may be the only technique available.

429

5 THE LENS Fig. 5-4-5 Posterior capsular opacification by lens epithelial cell hyperplasia.

Box 5-4-5 Lens Epithelial Cell Surgery I. Primary procedures A. Mechanical 1. Capsular polishing 2. Capsular vacuuming 3. Capsular vacuuming with ultrasound 4. Capsular curettage 5. Capsular cryotherapy B. Pharmacological 1. Hypotonic hydrolavage 2. Antimetabolites 3. Antiprostaglandins C. Immunological 1. Monoclonal antibodies D. Prophylactic posterior capsulotomy/capsulectomy (CCC) II. Secondary procedures A. Invasive 1. Capsulotomy/capsulectomy (CCC) 2. Curettage 3. Vacuuming B. Noninvasive 1. Nd:YAG laser capsulotomy/capsulectomy

430

Endocapsular rings were originally conceived in Japan, not for the purpose of supporting the zonule, but for the purpose of placing pressure on the equatorial lens epithelial cells to prevent posterior capsular opacification. Two models were manufactured in the early 1990s. A completely closed circular model, made of silicone for foldability and implantability through a 3 mm incision, was designed by Hara (Fig. 5-4-7A), and an open polymethyl methacrylate (PMMA) model was designed by Nagamoto. It was subsequently demonstrated in clinical trials and by phase-contrast videography of living LECs (Nagamoto and Bissen-Miyajima) that the presence of a ring in the capsular equator had no effect on the viability and migratory activity of LECs. Witchell et al. in Germany also designed an open PMMA ring for the purpose of supporting capsules with compromised zonules (see Fig. 5-4-7B), and Cionni (Cincinnati, Ohio) designed modifications to the PMMA capsule tension rings (CTRs) to allow them to be sutured to the eye wall,46 thus creating a synthetic “pseudozonule” attached to an intracapsular skeletal supporting apparatus (see Fig. 54-7C). When surgery on such eyes is planned, if OVD is to be used for the CCC, care must be taken not to overinflate the eye, especially with a dispersive OVD, as this may stress or further tear zonular fibers. A CCC can usually be performed and should be large. This facilitates hydrodissection and allows for the possibility of nuclear hydroexpression or viscoexpression. Complete hydrodissection is essential so that nuclear manipulations place no stress on the remaining zonular fibers. Similarly, expressing the nucleus through the large CCC into the supracapsular space, the pupillary plane, or the anterior chamber allows for nuclear emulsification safely away from the zonulocapsular apparatus.

Fig. 5-4-6 Anterior capsular fibrosis. (A) Asymmetric and (B) symmetric anterior capsule fibrosis leading to varying degrees of capsular phimosis. (Courtesy of John Shephard MD, Las Vegas, Nevada.)

If the zonule is weak or absent in only a limited meridional arc such that there is no decentration or subluxation of the capsule, a simple CTR can be implanted. These simple rings can be implanted with forceps or by injection with a special instrument (Geuder) and can be implanted at any stage in the surgical procedure: l After hydrodissection, before phacoemulsification l During phacoemulsification l After phacoemulsification, before cortical aspiration l During cortical aspiration l After cortical aspiration, before IOL implantation Additionally to minimize zonular stress for any of the manipulations after the creation of a CCC, iris hooks may be used but fixed to the CCC instead of the iris, thus stabilizing the capsular bag/zonular complex. If there is capsular subluxation, a Cionni CTR may be implanted; ideally, the ring is sutured to the sclera in the meridian that is the center of the arc of zonular absence. The ring will recentralize the capsule, and the suture will recentralize the capsule and will re-elevate a posteriorly tilted capsule to the zonular plane. Another modification to the routine technique is that of lowering the infusion bottle to a level that provides the slowest stream of irrigation beyond a drip, such that the phacotip is cooled and the chamber is maintained, but excessive volume with posterior displacement of the lens is avoided. The Cionni ring type of sutured skeletal support of the capsule is often strong enough to support careful endocapsular phacoemulsification techniques. Chopping performed with equicentripetal forces places no lateral stress on the zonule. When choosing an IOL, it would be ideal to implant a material that induces no fibrous metaplasia of the lens epithelial cells and a design that blocks the formation of central posterior capsular opacification. Therefore, PMMA and silicone are not ideal materials for these eyes. Among those currently available, the IOL of choice is one with an acrylic optic

5.4

Fig. 5-4-7 Solutions past and present for zonular deficiency. (A) Complete closed circular, foldable silicone endocapsular ring. (Courtesy of T. Hara.) (B) Open PMMA endocapsular ring. (Courtesy of Morcher, GMBh, Germany.) (C) Cionni-modified endocapsular ring for suturing to sclera to create a pseudozonule. (Courtesy of Morcher, GMBh, Germany.)

and a square posterior edge. There are now a number of models from various companies that are available (see Fig. 5-4-2A–C, Fig. 5-4-8). Additionally, these hydrophobic acrylics unfold in a very slow, controlled fashion that produces zero stress on the capsule or zonule.

Surgery for Presbyopia

These new and experimental procedures are designed to enhance lens function; that is, they are performed to improve the amplitude of accommodation in a presbyopic eye. These procedures are intended for purely presbyopic noncataractous eyes with no lenticular pathology other than the normal physiological middle-aged loss of accommodative function. Although one could theoretically make a case for clear lens replacement with an accommodative pseudophakos, it has never been conclusively demonstrated that loss of elasticity of the lens is the sole or even the major cause of presbyopia − in fact, more to the contrary. Changes have been shown to occur in the area of insertion of the zonular fibers, as well as in the configuration of the ciliary muscle. With only this limited knowledge, the present procedures represent the first attempts at the surgical correction of presbyopia by altering the ciliary architecture. Scleral expansion over the ciliary muscle by implantation of four circumferential PMMA rods or by radial sclerotomy, restoring tension to the flaccid zonular fibers, has been shown in early clinical studies to have poor success at restoring some accommodative power to the ciliary-zonule-lens mechanism. Surgery is still therefore limited, in the majority, to the induction of monovision (usually corneal but in many instances by lensectomy, modifiable by piggy-back sulcus-placed lenses, single vision, or multifocal).

Monovision

Monovision is the state of anisometropia geared towards emmetropia in one eye (usually the dominant eye) and near weighted ametropia (myopia) usually in the nondominant eye. Strictly optically speaking, a myopic outcome of −3.00 D would provide a near focal point at 33 cm. This amount of anisometropia would in many instances produce asthenopic symptoms. In practice, patients need only small amounts of residual myopia to be able to read and perform near visual tasks. The target refraction, which, in the nondominant monovision reading eye, provides the best reading acuity with the least distance acuity loss with and with least anisometropic asthenopia is between −0.75 DS and −1.50 DS. This amount of ametropia provides the easiest rehabilitation for the monovision patient. In spite of these guidelines, patients should still undergo, at the very least, a loose lens (trial frame) demonstration of the monovision and, at best, a prolonged contact lens simulation of the suggested surgical treatment. This route maximizes significantly the number of satisfied patients after the surgery.

Astigmatism

As discussed above, the surgeon attending to the needs of the lensectomy patient, whether of medical or refractive indication, needs to maintain a holistic approach to the correction of their patient’s problem. In order

Fig. 5-4-8 Many intraocular lenses are now produced with squared posterior edges to minimize lens epithelial cell migration towards the visual axis. This example shows the AMO Sensar AR40e, with rounded anterior edge and squared posterior edge. (Courtesy of Advanced Medical Optics Inc.)

to optimize the outcome of the patient, the following items need to be considered: 1. The removal of the opacity or error in the optical system (the cataract or lensectomy); 2. The accurate correction of the optical state of the eye (biometry techniques and formulas, astigmatism induction avoidance, and pre-existing astigmatism correction); and 3. The execution of the surgery in the safest possible way in the prevailing circumstances to minimize complication (sterility, incision creation and location, wound closure, peroperative antibiotics, surgical technique, etc.) and while assessing and attending to these items, ensuring that the best combination of techniques provides the optimal solution for the patient and that includes maintaining the ability to readdress nonoptimal outcomes. The management of the astigmatism in lens surgery (or any anterior segment surgery) has become an essential and integral part of the execution of the operation. A number of techniques have been described to control astigmatism, both in minimizing induction and treating pre-existent cylindrical error. The most useful technique that covers the most common astigmatic errors is “on axis” incision for small-incision surgery (i.e., operative incision placement on the periphery of steep axis of the astigmatism). Other schools of thought suggest that the surgery be performed with the smallest incision possible (astigmatically neutral), then placing the on axis incisions in the appropriate meridian, either partial thickness (limbal relaxing incision − LRI, vertical partial thickness corneal incisions)47 or penetrating (penetrating astigmatic keratotomy − PAK, self-sealing, full-thickness, penetrating incisions, obliquely orientated through the cornea). PAK is the most effective means of controlling astigmatism but does implicate corneal penetration, the mechanism of the power of the procedure. Keeping the incisions single pass and thus reducing instrument passage, enhances the watertight closure, minimizes wound leak, and potentially minimizes infective risk. The power of correction in PAK can be enhanced further by creating a second

Indications for Lens Surgery/Indications for Application of Different Lens Surgery Techniques

431

Table 5-4-2 PENETRATING ASTIGMATIC SURGERY (PAK) NOMOGRAM

THE LENS

Cyl to Correct

Incision Size (mm)

Distance from Visual Axis (mm)

Opposite Incision Size (mm)

Distance from Visual Axis (mm)

1.00–1.50

3.2

6.0

nil

1.50–2.00

3.5

6.0

nil

2.00–2.50

3.8 mm

Limbal arcades

nil

2.50–3.00

4.1 mm

5.5

nil

2.50–3.00

3.5

5.5

3.5

5.5

3.00–3.50

3.5

5.0

3.5

5.0

3.50–4.00

3.5

4.5

4.1

5.0

4.00–5.00

4.1

4.5

4.1

4.5

5.00–6.00

4.1

4.5

4.1

4.0

6.00–7.00

4.1

4.0

4.1

4.0

> 7.00*

4.1

4.0

4.1

4.0

Initial overcorrection

Incisions may be sutured in first month

Initial undercorrection

Widen pre-exisiting incisions (possible AC cohesive OVD required)

>7.00 (plus regression or undercorrection)*

Secondary peripheral incisions at 3 months (nomogram)

> 4.00 in penetrating keratoplasty

Primary incisions in H/D junction/secondary incisions peripheral (except when combined with lens surgery) Peripheral incisions on merits of residual astigmatic error as per nomogram

*AC, anterior chamber; cyl, cylinder (astigmatism); H/D, host/donor; OVD, ophthalmic viscosurgical device.

keratotomy on the opposite side of the first incision (180° opposed). The effect is greatest with penetration, reaching corrections as high as 6−7 D of astigmatism with a single pair of incisions. The PAK nomogram listed in Table 5-4-2 demonstrates the titration of the astigmatic corrective effect by variation of incision width against the optical zone radius (OZR − the proximity of the incision to the pupil/astigmatic centrum).48 When this surgery is doubled by further peripheral incision pairs, astigmatic ameliorative effects of up to 10−12 D are noted, which is particularly useful in the correction of corneal graft ametropia,49 either stand alone or in conjunction with lensectomy (or any anterior segment procedure). In the execution of high cylinder correction, patients’ axes must be marked prior to lying down for anesthesia, local, topical, or general, to avoid cyclotorsional error.

Being on the cornea, this form of astigmatic correction is very stable, but astigmatic correction can also be executed by correctly orientated toric IOL insertion. A number of these lenses are now available on the market. High toric corrections require custom manufacture (> 3.00 DC).

ACKNOWLEDGMENT This chapter is based on Chapter 42 from the last edition of this book (Grabow HB. Indications for lens surgery and different techniques. In: Yanoff M, Duker JS, eds. Ophthalmology, 2nd ed. St Louis: Mosby; 2004:315−25)

REFERENCES

432

1. C hylack LT Jr, Wolfe JK, Singer DM, et al. The lens opacities classification system. Version III (LOCS-III). Arch Ophthalmol. 1993;111:831. 2. Lasa MSM, Datiles MB III, Freidlin V. Potential vision tests in patients with cataracts. Ophthalmology. 1995;102:1007–11. 3. Datiles MB III, Magno BV, Freidlin V. Study of nuclear cataract progression using the National Eye Institute Scheimpflug system. Br J Ophthalmol. 1995;79:527–34. 4. Lopez JLL, Freidlin V. Datiles MB III. Longitudinal study of posterior subcapsular opacities using the National Eye Institute computer planimetry system. Br J Ophthalmol. 1995;79:535–40. 5. Steinberg EP, Tielsch JM, Schein OD, et al. The VF-14: an index of functional impairment in patients with cataract. Arch Ophthalmol. 1994;112:630–8. 6. Steinberg EP, Tielsch JM, Schein OD, et al. National study of cataract surgery outcomes: variation in 4-month postoperative outcomes as reflected in multiple outcome measures. Ophthalmology. 1994;101:1131–41. 7. Schein OD, Steinberg EP, Cassard SD, et al. Predictors of outcome in patients who underwent cataract surgery. Ophthalmology. 1995;102:817–23. 8. Cassard SD, Patrick DL, Damiano AM, et al. Reproducibility and responsiveness of the VF-14: an index of functional impairment in patients with cataracts. Arch Ophthalmol. 1995;113:1508–13. 9. Mangione CM, Phillips RS, Lawrence MG, et al. Improved visual function and attenuation of declines in healthrelated quality of life after cataract extraction. Arch Ophthalmol. 1994;112:1419–25.

10. M angione CM, Orav EJ, Lawrence MG, et al. Prediction of visual function after cataract surgery: a prospectively validated model. Arch Ophthalmol. 1995;113: 1305–11. 11. Edwards MG, Schachat AP, Bressler SB, Bressler NM. Outcome of cataract operations performed to permit diagnosis, to determine eligibility for laser therapy, or to perform laser therapy of retinal disorders. Am J Ophthalmol. 1994;118:440–4. 12. Gindi JJ, Wan WL, Schanzlin DJ. Endocapsular cataract surgery. I. Surgical technique. Cataract. 1985;2(5):6–10. 13. Haefliger E, Parel J-M, Fantes F, et al. Accommodation of an endocapsular silicone lens (Phaco-ersatz) in the nonhuman primate. Ophthalmology. 1987;94:471–7. 14. Haefliger E, Parel J-M. Accommodation of an endocapsular silicone lens (Phaco-ersatz) in the aging rhesus money. J Refract Corneal Surg. 1994;10:550. 15. Nishi O. Refilling the lens of the rabbit eye after endocapsular cataract surgery. Folia Ophthalmol Jpn. 1987;38:1615–8. 16. Nishi O, Hara T, Hayashi F, et al. Further development of experimental techniques for refilling the lens of animal eyes with a balloon. J Cataract Refract Surg. 1989;15:584–8. 17. Hara T, Hara T, Yasuda A, Yamada Y. Accommodative intraocular lens with spring action. Part 1. Design and placement in an excised animal eye. Ophthalmic Surg. 1990;21:128–33. 18. Hara T, Hara T, Yasuda A, et al. Accommodative intraocular lens with spring action. Part 2. Fixation in the living rabbit. Ophthalmic Surg. 1992;23:632–5.

19. B lumenthal M, Assia EI. Extracapsular cataract extraction. In: Nordan LT, Maxwell WA, Davison JA, eds. The surgical rehabilitation of vision. New York: Gower; 1992: ch 10. 20. McIntyre DJ. Cataract surgery: techniques, complications and management. In: Steinert RF, ed. Phacosection cataract surgery. Philadelphia: WB Saunders; 1995. :119–22. 21. Arsinhoff SA. The viscoelastic soft shell technique. In: Kohnen T, Koch D, eds. Essentials in ophthalmology, Ch 3.10. Berlin, Heidelberg: Springer-Verlag; 2005: 50–6. 22. Fine IH, Packer M, Hoffman RS. Nucleofractis techniques. In: Kohnen T, Koch D, eds. Essentials in ophthalmology Ch 2.5. Berlin, Heidelberg: Springer-Verlag; 2005 :25–32. 23. Dodick JM, Christiansen J. Experimental studies on the development and propagation of shock waves created by the interaction of short Nd:YAG laser pulses with a titanium target. J Cataract Refract Surg. 1991;17:794–7. 24. Grabner G, Alzner E. Dodick laser phacolysis: thermal effects. J Cataract Refract Surg. 1999;25:800–3. 25. Kanellopoulos AJ, Dodick JM, Brauweiler P, Alzner E. Dodick photolysis for cataract surgery. Ophthalmology. 1999;106:2197–202. 26. Huetz WW, Eckhardt B. Photolysis using the Dodick-ARC laser system for cataract surgery. J Cataract Refract Surg. 2001;27:208–12. 27. Kanellopoulos AJ. Laser cataract surgery: a prospective clinical evaluation of 1000 consecutive laser cataract procedures using the Dodick photolysis Nd:YAG system. Ophthalmology. 2001;108:649–55.

36. H ara T, Hara T. Intraocular implantation in an almost completely retained capsular bag with a 4.5 to 5.0 millimeter linear dumbbell opening in the human eye. Ophthalmic Surg. 1992;23:545–50. 37. Gindi JJ, Wan WL, Schanzlin DJ. Endocapsular cataract surgery. I. Surgical technique. Cataract. 1985;2(5):6–10. 38. Blumenthal M., Clinical evaluation of full-size hydrogel lens − concept and reality. Six years experience. Presented at Symposium on Cataract, IOL, and Refractive Surgery, Boston, April 9, 1991. 39. Werner L, Mamalis N. Adjustable power intraocular lenses. In: Kohnen T, Koch D, eds. Essentials in ophthalmology, Ch 4.4.7, Berlin, Heidelberg: Springer-Verlag; 2005. :80–1. 40. Galand A, Galand A, van Cauenberge F, Moosavi J. Posterior capsulorrhexis in adult eyes with intact and clear capsules. J Cataract Refract Surg. 1996;22:458–61. 41. Hara T, Hara T. Observations on lens epithelial cells and their removal in anterior capsule specimens. Arch Ophthalmol. 1988;106:1683–7. 42. Nishi O, Nishi K, Yamada Y, Mizumoto Y. Effect of indomethacin-coated posterior chamber intraocular lenses on post-operative inflammation and posterior capsular opacification. J Cataract Refract Surg. 1995;21:574–8.

43. T etz M, Ries M, Lucas C, et al. Inhibition of posterior capsule opacification by an intraocular-lens-bound sustained drug delivery system: an experimental animal study and literature review. J Cataract Refract Surg. 1996;22:1070–8. 44. Power WJ, Neylav D, Collum LMT. Daunomycin as an inhibitor of human lens epithelial cell proliferation in culture. J Cataract Refract Surg. 1994;20:287–90. 45. Goins KM, Optiz JR, Fulcher SFA, et al. Inhibition of proliferating lens epithelium with antitransferrin receptor immunotoxin. J Cataract Refract Surg. 1994;20:513–5. 46. Ahmed II, Crandall AS. Ab externo scleral fixation of the Cionni modified capsular tension ring. J Cataract Refract Surg. 2001;207:977–81. 47. Khng C, Fine IH, Packer M, Hoffman RS. Improved precision with the millimeter caliper for limbal relaxing incisions. J Cataract Refract Surg. 2005;31:1671–2. 48. Howes F. Penetrating astigmatic keratotomy. Presentation ESCRS, Paris, France, 2004. 49. Howes F. Penetrating astigmatic keratotomy, nomogram II. Presentation AUSCRS, Hayman Island, Australia, 2006.

5.4 Indications for Lens Surgery/Indications for Application of Different Lens Surgery Techniques

28. N eubaur CC, Stevens S. Erbium:YAG laser cataract removal: role of fiber-optic delivery system. J Cataract Refract Surg. 1999;25:514–20. 29. Hoh H, Fischer E. Pilot study on erbium laser phaco emulsification. Ophthalmology. 2001;107:1053–62. 30. Duran SD, Zato M. Erbium:YAG laser emulsification of the cataractous lens. J Cataract Refract Surg. 2001;27:1025–32. 31. Assia E, Apple D, Barden O, et al. An experimental study comparing various anterior capsulectomy techniques. Arch Ophthalmol. 1991;109:642–7. 32. Apple D, Park S, Merkley K, et al. Posterior chamber intraocular lenses in a series of 75 autopsy eyes. Part I. Loop location. J Cataract Refract Surg. 1986;12:358–62. 33. Gimbel HV, Neuhann T. Development, advantages, and methods of the continuous circular capsulorrhexis technique. J Cataract Refract Surg. 1990;16:31–7. 34. Assia E, Apple D, Tsai J, Lim E. The elastic properties of the lens capsule in capsulorrhexis. Am J Ophthalmol. 1991;111:628–32. 35. Galand A. A simple method of implantation within the capsular bag. Am Intra-ocular Implant Soc J. 1983;9: 330–2.

433

PART 5 THE LENS

The Pharmacotherapy of Cataract Surgery

5.5

Steve A. Arshinoff and Yvonne A.V. Opalinski

Key features n�� n�� n��

n��

harmacotherapeutic agents are used in preoperative, P intraoperative, and postoperative periods of cataract surgery. Preoperative medications are used to dilate the pupils, as prophylactic antibiotics, and as anesthetics. Intraoperative pharmacotherapeutic agents include irrigating solutions and additives to irrigating solutions, as well as ophthalmic viscosurgical devices and intracameral antibiotics. Postoperative medications include antibiotics, corticosteroids, and nonsteroidal anti-inflammatory drugs.

INTRODUCTION With current ongoing rapid evolution of cataract surgical techniques, corresponding change in the pharmacotherapeutic management of cataract patients is inevitable. In this chapter, current pharmacotherapeutic practices in the pre-, intra-, and postoperative periods are reviewed.

PREOPERATIVE MEDICATIONS Table 5-5-1 provides a summary of commonly used preoperative pharmacotherapeutic routines for cataract surgery.

Pupil Dilatation

434

Sympathomimetic mydriatic agents (such as phenylephrine 2.5%) and parasympatholytic cycloplegics (such as tropicamide or cyclopentolate 1.0%) usually are used together before extracapsular nuclear expression or phacoemulsification. If used in excess, sympathomimetics increase the risk of a severe systemic hypertensive response and the associated systemic risks in the elderly.1 For this reason, phenylephrine 10% is not recommended for routine use. To assist in adequate pupil dilatation, pilocarpine and other cholinergic miotics should be discontinued 12–24 hours before surgery (approximately twice the expected duration of action of the specific agent). Topical nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used in cataract surgery to prevent pupillary miosis, reduce surgically induced inflammation, and prevent postoperative cystoid macular edema.2 Administration of NSAIDs decreases prostaglandin synthesis by the inhibition of cyclooxygenase, thus preventing the transformation of arachidonic acid into prostaglandins.2, 3 Prostaglandin E2 (PGE2) enhances the constrictor action of the iris sphincter through a mechanism that is not dependent on cholinergic receptors.4, 5 Topical flurbiprofen 0.03%, the first agent to be used for this indication, was demonstrated to be clinically superior to topical indomethacin 1%.5 Currently, diclofenac 0.1% and ketorolac 0.5% are used for the same indication.6 Although diclofenac and flurbi profen adequately maintain mydriasis during surgery,7 ketorolac appears to inhibit miosis more effectively than either.8 In order to simplify preoperative drop regimens, it is becoming more common practice for centers to mix all preoperative dilating drops together and administer them as a plegett approximately half an hour preoperatively. The specific agents and doses vary among centers. Intracameral mydriatic solutions using cyclopentolate 0.1%, phenylephrine 1.5%, and Xylocaine 1% or tropicamide 0.5%, phenylephrine 5%, and diclofenac 0.1%, in preservative-free solutions, have proven safe

to the corneal endothelium and effective in producing and maintaining pupillary dilatation.9–11 Effective redilatation has also occurred using these mydriatics intracamerally during surgery on contracted pupils.12

Anti-Infective Prophylaxis

Prophylactic antibiotic use in cataract surgery has been an accepted practice for decades. Preoperatively, the most important source of potential infectious organisms is the patient’s own natural conjunctival and skin flora. Intraoperative cultures indicate that 5% of intraocular surgeries result in measurable anterior chamber contamination from indigenous flora, but the vast majority of these patients develop no clinical adverse sequelae.13 Cultures taken from the conjunctiva and anterior chamber of patients who subsequently developed endophthalmitis usually yielded the same bacterial strains. Staphylococci (Staphylococcus epidermidis and S. aureus), diphtheroids (Corynebacterium), streptococci (Streptococcus viridans), and gram-negative bacilli (anaerobic Propionibacterium acnes and others) are the most common infecting agents in decreasing order of occurrence.14 Administered medications should adequately cover the bacteria most likely to cause potential endophthalmitis during the operative and perioperative period, during which bacteria can gain entrance into the anterior chamber. Before cataract surgery, topical anti-infective regimens have included gramicidin−neomycin−polymyxin B sulfate, aminoglycosides such as gentamicin or tobramycin (which provide gram-negative and Pseudomonas coverage), and the fluoroquinolones − ciprofloxacin, norfloxacin, ofloxacin 0.3%,7, 15, 16 or levofloxacin 0.5%. Of these, levofloxacin provided superior coverage and anterior chamber penetration, before fourth generation fluoroquinolone became available.17–20 The fourth generation fluoroquinolones, gatifloxacin 0.3% and moxifloxacin 0.5%, are currently the preferred agents, offering better penetration than previous generations (moxifloxacin appears to be better than gatifloxacin),21 broader spectrum coverage, and lower incidence of bacterial resistance, and are equally safety.22–24 Antibacterial prophylaxis for cataract surgery is an issue that has recently risen to prominence with the confirmation of an increasing incidence of postoperative endophthalmitis since the advent of clear corneal incisions.25 Some authors have suggested that beginning antibacterial antibiotic prophylaxis 3 days preoperatively may yield superior intraocular drug levels at surgery.26–28 There has been considerable concern that the prophylactic use of potent antibiotics in large numbers of healthy cataract patients contributes to the development of resistant bacterial strains; however, recently even the conservative and rather authoritarian voice of the Medical Letter stated that “Medical letter consultants believe that ophthalmic use of antibacterials is much less likely than systemic use to select for resistant organisms.”29 Nevertheless, complete conjunctival sterility, through the elimination of such flora, is not usually possible with the use of preoperative antibiotics alone.7 The topical antiseptic povidone-iodine 5% instilled as a single drop 10–30 minutes before surgery is one of the most effective measures to decrease this bacterial flora30 and appears equal in efficacy to preoperative topical antibiotics.31

Anesthetics

Anesthetics are covered fully in Chapter 5.6. Local injection anesthesia, both retrobulbar and peribulbar, is declining in popularity, while the use of intracameral nonpreserved lidocaine has gained popularity over the last few years, as has topical lidocaine gel. Lidocaine gel is claimed to provide increased corneal hydration and anesthesia equal to that of injections and drops32, 33 while minimizing patient discomfort, but its popularity seems to be decreasing, possibly due to unwanted epithelial side effects, such as decreased clarity and erosions.

TABLE 5-5-1 COMMONLY USED AGENTS IN THE ROUTINE PREOPERATIVE PHARMACOTHERAPY OF CATARACT SURGERY Concentration

Dosage

Nonsteroidal anti-inflammatory drugs to prevent miosis

Diclofenac Ketorolac Flurbiprofen Indomethacin

0.10% 0.50% 0.03% 1%

1 drop 4 times over 1 h preceding surgery

Cycloplegics

Tropicamide Cyclopentolace

1% 1%

1 drop 4 times over 1 h preceding surgery

Mydriatics

Phenylephrine

2.50%

1 drop twice over 0.5 h preoperatively

Antibiotic prophylaxis

Gramicidin– neomycin– polymyxin B Gentamicin Tobramycin Ciprofloxacin Ofloxacin Gatifloxacin Moxifloxacin Trimethoprim–polymyxin B

0.025 mg/ml 2.5 mg/ml 10.000 IU/ml 0.30% 0.30% 0.30% 0.30% 0.30% 0.50% 1 mg/ml (10.000 IU/ml)

1 drop 4 times over 1 h preceding surgery

Anesthetic: retrobulbar or parabulbar

Lidocaine Mepivacaine Bupivacaine

1–2% 1–2% 0.25–0.75%

3–9 ml

Anesthetic: intracameral

Isotonic, nonpreserved lidocaine

1–2%

0.1–0.6 ml

Anesthetic: topical

Proparacaine Tetracaine Benoxinate (oxybuprocaine) Lidocaine Bupivacaine

1–2% 0.50% 0.40% 4% 0.75%

1–2 drops prior to surgery, and then every 10 minutes or as needed during surgery

INTRAOPERATIVE MEDICATIONS Additives to Irrigating Solutions, Intracameral Antibiotics, and Other Intraocular Drugs Used During the Surgical Procedure

Table 5-5-2 gives a summary of commonly used intraoperative pharmacotherapeutic routines. In general, the addition of antibiotics, mydriatics, epinephrine (adrenaline), or lidocaine (lignocaine) is not recommended by the companies that produce irrigating solutions for cataract surgery, because any effect on stabilizers and preservatives in the solutions could alter their pH, chemical balance, or osmolarity and influence the potential toxicities of both irrigating solution and additive alike. Caution is therefore advised if any alteration to commercial irrigating solutions is considered. To prevent intraoperative miosis, nonpreserved epinephrine (1:1000) 0.5 mL/500 mL of irrigating solution is added frequently. This concentration appears not to be toxic to the corneal endothelium and allows normal endothelial function.34 The intraoperative use of antibiotics in irrigating solutions is a controversial issue in cataract surgery. It appears that surgical technique may play the most critical role in anterior chamber contamination, and the antibiotics administered in irrigating solutions may contribute minimally to reduce the risk of endophthalmitis.13, 35, A case of coagulase-negative staphylococcal endophthalmitis has been reported despite intraoperative vancomycin (1 mg/0.1 mL) injected intravitreally.36 Nevertheless, vancomycin (20 μg/mL (0.02 mg/mL)) in combination with gentamicin (8 μg/mL (0.008 mg/mL)), added to the irrigating solution, has been reported to eradicate gram-positive, coagulase-negative micrococci,37 with minimal associated complications.38 Gentamicin alone has been used intraoperatively in the dosage range of 8−80 μg/mL added to the irrigating solution, which appears sufficient to avoid retinal toxicity and at the same time decrease the intracameral bacterial load.39 Surgeons recognize that the postsurgical capsular bag is a sequestered avascular site that harbors a foreign body (the intraocular lens) and may act as the nidus for most cases of endophthalmitis. Vancomycin (1 mg in 0.1 mL balanced salt solution (BSS)) was the first agent to be used by injection directly into the capsular bag as the final step in the surgical procedure, and was introduced by James Gills in the early 1990s. This mode of delivery is considered superior to adding antibiotics to the irrigating solution because the concentration achieved in the anterior

5.5 The Pharmacotherapy of Cataract Surgery

Class and Agent

chamber is much higher; furthermore, it is done at the very end of surgery, leaving a high dose in the anterior chamber for the early postoperative period.40 There was considerable discussion among clinicians and researchers about the safety and efficacy of intracameral injections until a large, multicenter, prospective, randomized, controlled European Society of Cataract and Refractive Surgeons (ESCRS) study showed intracameral cefuroxime (first proposed by Montan et al.) to be effective in producing an 80% reduction in endophthalmitis rates, thus settling the argument.41–43 Other intracameral antibiotics (cefazolin,44, 45 gatifloxacin,46 and moxifloxacin47) have been used and have yielded similar, or better, endophthalmitis reduction rates than those achieved by Montan et al. or the ESCRS study. There is general consensus that intracameral antibiotics are effective in dramatically reducing postoperative endophthalmitis, but also a widespread belief that cefuroxime, found to be so effective in the ESCRS study, may not be the best choice of agent.48 This area is, at the time of writing, one of the most actively debated issues in the field of ophthalmology. Rapid miosis can be produced at the end of the surgical procedure using one of two available intraocular parasympathomimetics − acetylcholine chloride 1% or carbachol 0.01%.49 Current preparations have shown no evidence of endothelial toxicity, and the choice of agent depends on the desired clinical features. Acetylcholine 1% has an onset time of less than 1 minute, has a relatively brief duration of action, and results in miosis for 10 minutes, whereas carbachol 0.01% takes 2 minutes to act and its effect has a duration of 2−24 hours. Both agents lower postoperative intraocular pressure spikes.50 Low-molecular-weight heparin, enoxaparin (10 IU/mL added to standard irrigating solution), produces a decreased inflammatory response immediately after cataract surgery with minimal side effects (e.g., hemorrhage).51, 52 Enoxaparin’s potential in cataract surgery requires further evaluation. A preliminary study using ozonated water (4 ppm concentration) in anterior chamber irrigation confirmed its bactericidal effects and may potentially present another tool against endophthalmitis.53

Irrigating Solutions

In the early days of phacoemulsification, the only irrigating solutions available were normal saline, Plasma-Lyte, and lactated Ringer’s solution. The main difficulty with these solutions was endothelial cell toxicity, which resulted in dysfunction and destruction. Irrigating solutions with calcium, glutathione, and bicarbonate form more physiologically

435

TABLE 5-5-2 COMMONLY USED AGENTS IN THE ROUTINE PREOPERATIVE PHARMACOTHERAPY OF CATARACT SURGERY Class and Agent

THE LENS

Agents added to irrigating solutions

Concentration

Antibiotics Vancomycin plus Gentamicin Gentamicin Sympathomimetics to prevent miosis Nonpreserved epinephrine

Agents used at the end of the procedure

Antibiotics Vancomycin Cefuroxime Cefazolin Gatifoxacin Moxifloxacin Parasympathomimetrics Acetylcholine Carbachol

Dosage

20 μg/ml 8 μg/ml 8–80 μg/ml

0.3–0.5 ml of 1:1000 nonpreserved epinephrine 500 ml irrigating solution 0.1 ml intracapsularly via sideport at end of procedure

1 mg/0.1 ml 1 mg/0.1 ml 1 –2.5 mg/0.1 ml 100 μg/0.1 ml 100 μg/0.1 ml

0.5 ml injected into anterior chamber via sideport to cause miosis

1% 0.01%

TABLE 5-5-3 CHEMICAL COMPOSITION OF HUMAN AQUEOUS HUMOR, VITREOUS HUMOR, BSS PLUS, AND BSS Ingredient

Human Aqueous Humor

Human Vitreous Humor

BSS Plus

BSS

Sodium

162.9

144

160

155.7

Potassium

2.2–3.9

5.5

10.1

Calcium

1.8

1.6

3.3

Magnesium

1.1

1.3

1.5

Chloride

131.6

177

130

128.9

Bicarbonate

20.15

–

Phosphate

0.62

0.4

–

Lactate

2.5

7.8

–

Glucose

2.7–3.7

3.4

–

Ascorbate

1.06

–

Glutathione

0.0019

–

0.3

–

Citrate

–

5.8

Acetate

–

28.6

7.38

–

7.4

7.6

Osmolality (mOsm)

304

–

305

298

(Adapted from Edelhauser HF. Intraocular irrigating solutions. In: Lamberts DW, Potter DE, Potter DE, eds. Clinical Ophthalmic Pharmacology. Boston: Little, Brown and Company; 1987, pp. 431–44.)

436

balanced solutions (Table 5-5-3).54 Several comparative studies have found BSS Plus to be superior to BSS and other irrigating solutions and protective of the corneal endothelium. Unlike BSS, BSS Plus is physiologically similar to human aqueous and vitreous, especially with regard to calcium concentration and the addition of glucose, glutathione, and bicarbonate. BSS Plus maintains endothelial cell function over periods ranging from 15 minutes to in excess of a few hours.41 The buffer in BSS Plus is bicarbonate, which is an improvement over the sodium acetate and citrate buffers in BSS. Nevertheless, BSS Plus is used much less frequently than BSS, due to the high price of BSS Plus, and the progressive reduction in irrigating fluid volume used in surgery, as techniques improve over time. Corneal surface irrigation to maintain hydration and surgical clarity has traditionally been performed throughout intraocular procedures with BSS. The development of an elastoviscous hylan surgical shield (HSS) 0.45%, which decreases the surgeon’s dependence on manual corneal irrigation, has proved to be an improvement over BSS in maintaining corneal hydration and clarity intraoperatively.55 Some surgeons use a drop of ophthalmic viscosurgical device (OVD) on the cornea at the beginning of surgery to produce this effect; OVD may not be as effective as HSS but it is more readily available.

OPHTHALMIC VISCOSURGICAL DEVICES The introduction of Healon in 1980 for use in ocular surgery ushered in the era of viscosurgery. Because OVDs tend to consist of solutions of long-chain biopolymers (almost always hyaluronic acid or hydroxypropyl methylcellulose) in low concentration, they are all pseudoplastic in their rheological behavior. Their physical properties tend to correlate (i.e., the most viscous solution is also the most elastic and the most cohesive) and are a function of the chain length distribution of the rheologically important constituent polymer and its concentration. Recently, the advent of DisCoVisc, a viscous dispersive OVD, demonstrated that we can escape the strict correlation between viscosity and cohesion in OVDs, resulting in a new classification, based upon zero-shear viscosity and cohesive−dispersive properties (measured as the cohesion−dispersion index, CDI) (Table 5-5-4). It is apparent that OVDs cannot be referred to generically, as each one has different rheologic properties, and are not interchangeable, in that many surgical maneuvers can be achieved more easily with one type of OVD than another. Before the advent of viscoadaptive OVDs, superviscous-cohesive and viscous-cohesive OVDs were recognized as the best for creating, stabilizing, and maintaining spaces (to deepen the anterior chamber in the presence of positive vitreous pressure, to stabilize the anterior chamber to facilitate capsulorrhexis,

TABLE 5-5-4 NEW CLASSIFICATION OF COMMON OVDs INCLUDING DisCoVisc Cohesive OVDs CDI ≥ 30 (%asp/mmHg)

7 – 8 × 106 (ten millions)

I. Viscoadaptives* – Healon5 – iVisc (MicroVisc) Phaco – BD MultiVisc

Dispersive OVDs CDI < 30 (%asp/mmHg)

II. Higher viscosity cohesives

II. Higher viscosity dispersives

1 – 5 × 106 (millions)

A. Superviscous cohesives – Healon GV – iVisc (MicroVisc, HyVisc) Plus – BD Visc

A. Superviscous dispersives – none

105 – 106 (hundred thousands)

B. Viscous cohesives – Healon – iVisc (MicroVisc, HyVisc) – Viscorneal Plus – Provisc – Opegan Hi – Viscorneal – Biolon Prime – Biolon – Amvisc Plus – Amvisc – Coese – Biocorneal

B. Viscous dispersives – DisCoVisc

III. Lower viscosity cohesives

5.5 The Pharmacotherapy of Cataract Surgery

Zero-Shear Viscosity Range (mPa.s)

III. Lower viscosity dispersives

104 – 105 (ten thousands)

A. Medium viscosity cohesives – none

A. Medium viscosity dispersives – Viscoat – Biovisc – Rayvisc – Opelead – Vitrax – Cellugel

103 – 104 (thousands)

B. Very low viscosity cohesives – none

B. Very low viscosity dispersives – Opegan – OccuCoat, ICell, Ocuvis, Visilon, Hymecel, Adatocel, Celoftal (HPMCs)

mPa.s, miliPascal seconds; CDI, c�� o�� hesion–dispersion index �� (% �� aspirated/mmHg); OVD, ophthalmic viscosurgical device. *Viscoadaptives, because of their peculiar “adaptive” behavior when exposed to different degrees of turbulence, may behave either as extremely cohesive or pseudo-dispersive OVDs. Similarly, CDI measurements may differ under different conditions of testing.

and to keep the capsular bag open and taut to facilitate foldable intra ocular lens implantation). Conversely, medium and lower viscositydispersive OVDs are excellent for the selective isolation of areas of the intraocular surgical field and for enabling fluid partition of the anterior chamber (to protect marginal corneas from the turbulence of phacoemulsification, or to keep a frayed piece of iris or bulging vitreous away from the phacoemulsifying or irrigation-aspiration tip).56 Superviscous-cohesive and viscous-cohesive OVDs cannot be used to partition fluid-filled spaces. To achieve the benefits of both types of older OVDs and avoid having to deal with their disadvantages, the “soft shell technique” can be utilized.57–59 Healon5 and MicroVisc Phaco (iVisc Phaco, Hyvisc Phaco, BD MultiVisc) are viscoadaptive OVDs that exhibit either highly viscous cohesive or pseudodispersive properties, depending on fluid turbulence in the anterior chamber. 60 Dispersive behavior of lower viscosity OVDs and pseudodispersive behavior of viscoadaptives are very different.60, 61 These characteristics allow their use for chamber partitioning and yield enhanced versatility over earlier OVDs during phacoemulsification.62–66 The “ultimate soft shell technique” further enhances the scope of utility of viscoadaptive OVDs,67, 68 and enables the benefits of the soft shell technique to be attained using a single viscoadaptive OVD. DisCoVisc is a new viscous dispersive OVD with zero-shear velocity similar to Healon, but resembles Viscoat’s dispersive properties, thus permitting the chamber maintenance properties of Healon and the dispersive endothelial protection of Viscoat using a single OVD syringe.61

POSTOPERATIVE MEDICATIONS Postoperative drugs are listed in Table 5-5-5.

Antibiotics

Postoperative regimens of topical antibiotics vary but generally consist of one drop to the operated eye 4−6 times daily for 1−2 weeks. The duration of treatment varies from 5 days in uncomplicated surgery to weeks if prolonged inflammation occurs. Topical treatment is so efficacious that the use of injections and collagen shields is increasingly falling out of favor. Increasing resistance to antibiotics that have been used for decades and the lack of resistance to newer drugs (e.g., gentamicin versus moxifloxacin or gatifloxacin) also influence the selection of postoperative anti-infective prophylaxis. Subconjunctival injections of antibiotics deliver high levels to the aqueous humor but have a greater risk associated with their administration, notably perforation of the eye, macular infarction, and retinal toxicity. Oral or parenteral antibiotics, such as the fluoroquinolones, may reach substantial levels in the anterior chamber but do not provide any advantages over topical routes of administration and are associated with increased side effects.69, 70 Collagen shields, with a dissolution time of 12 hours, have been introduced to decrease the frequency of drop application and to increase the drug concentration, and its duration, in the cornea and anterior chamber. The shields, presoaked in an antibiotic and corticosteroid solution such as tobramycin and dexamethasone, or netilmicin and betamethasone, are placed on the eye immediately after surgery, and have been associated with minimal adverse effects.71 A preoperative 60-minute application of a singleuse collagen shield delivery system, presoaked in ofloxacin for 10 minutes, has also been proposed to achieve superior aqueous drug levels at the onset of surgery.72 Postoperative application of collagen shields appears to be superior to subconjunctival injections of the same antibiotic−corticosteroid mix in terms of efficacy, toxicity, safety, and reduction of patient discomfort. It has been advised to use caution with collagen shields in the absence

437

Table 5-5-5 COMMONLY USED AGENTS IN THE ROUTINE POSTOPERATIVE PHARMACOTHERAPY OF CATARACT SURGERY

THE LENS

Class and Agent

Concentration

Dosage

Corticosteroids

Dexamethasone Prednisolone Betamethasone

0.10% 1% 0.10%

1 drop 4 times daily for 3–4 weeks postoperatively

Nonsteroidal anti-inflammatory drugs

Diclofenac Ketorolac

0.10% 0.50%

1 drop 4 times daily for 4 weeks postoperatively

Antibiotics

Gramicidin–neomycin–polymyxin B Gentamicin Tobramycin Ciprofloxacin Ofloxacin Gatifloxacin Moxifloxacin Trimethoprim–polymyxin B

0.025 mg/ml 2.5 mg/ml 10, 000 1U/ml 0.30% 0.30% 0.30% 0.30% 0.30% 0.50% 1 mg/ml (10, 000 1U/ml)

1 drop 4 times daily for 3–4 weeks postoperatively

of a well-sealed wound, because concentrations of some antibiotics in the shield may become toxic if they leach into the anterior chamber.13 Furthermore, some combinations of antibiotic and corticosteroid have produced toxic precipitates.50 The use of postoperative collagen shields has not been widely adopted. They have become much less of an issue recently, as the intraocular concentrations of fourth generation fluoroquinolones, the antibiotics currently most commonly recommended perioperatively for cataract patients, achieve sufficient intraocular levels with topical drops alone.

Corticosteroids and Nonsteroidal Anti-Inflammatory Drugs

438

Topical corticosteroids and NSAIDs are used after cataract surgery to reduce postoperative noninfectious inflammation. Corticosteroids and NSAIDs appear to be equally efficacious in decreasing inflam mation,6, 73, 74 and there is no difference between them in terms of astigmatic decay. The development of an intraocular biodegradable drug delivery system containing dexamethasone appears to be an effective alternative to topical drops,75 and because a variety of drugs may be bound to the polymer matrix, it may play a role in the long-term prevention or treatment of cystoid macular edema. Topical NSAIDs have a specific advantage over corticosteroids if there are contraindications to corticosteroid use in a particular patient, such as corticosteroid-responsive elevations of intraocular pressure, recurrent herpes simplex infection,76 or concern about delayed wound healing.77 Ketorolac 0.5% has been shown to be equally effective as a single agent in antimiotic and antiinflammatory activity when compared with an NSAID−prednisolone 1% combination.78 There is, however, an increased risk of corneal or scleral perforation in the presence of an epithelial defect when NSAIDs are used alone, without concomitant administration of topical steroids.79, 80 Pretreatment with an NSAID decreases the postoperative level of inflammation, provided the medication is administered over a period of 3 days.81, 82 Both corticosteroids and NSAIDs are used postoperatively, either interchangeably or together, although not as a single solution. The addition of an NSAID to an antibiotic−steroid postoperative regimen has been reported to decrease the incidence of noninfectious postoperative inflammatory conditions.83 The corticosteroids dexamethasone 0.1%, prednisolone 1%, and betamethasone 0.1% are used most commonly. A new steroid, rimexolone 1%, seems equal in efficacy with less potential intraocular pressure increase than either dexamethasone or prednisolone because its lipophilic nature reduces intraocular penetration.84 In a recent study, a single intraoperative sub-Tenon’s injection of triamcinolone (30−40 mg)85, 86 or intracameral triamcinolone (1.8− 2.8 mg)87 seemed to reduce the inflammatory response postoperatively. The most frequently used topical NSAIDs are diclofenac 0.1% and ketorolac 0.5%.88, 89 Corticosteroid and NSAID regimens are the same and consist of one drop to the affected eye four times daily for up to 4 weeks, usually in conjunction with a topical antibiotic. Combination NSAID−antibiotic drops have been formulated to minimize the number of different bottles a patient must use postoperatively, without altering either the drug’s efficacy or penetration.90

LATE POSTOPERATIVE MEDICATIONS Treatment of Endophthalmitis

Endophthalmitis has been treated with antibiotics systemically, intravitreally, and topically. See Chapter 7.9 for details.

Treatment of Cystoid Macular Edema

Cystoid macular edema (CME) usually manifests 1−3 months postoperatively as either decreased visual acuity or changes on fluorescein angiography that result from serous exudate leaking from incompetent intraretinal capillaries into the outer plexiform layer of Henle.91 Most patients spontaneously recover, with full restoration of visual acuity within 6 months; however, it may require 1−2 years for full spontaneous resolution to occur.2 In approximately one third of severe clinically significant macular edema patients, macular edema may persist, accompanied by decreased visual acuity. Prophylaxis and treatment have been suggested in the form of systemic and topical NSAIDs. Oral NSAIDs, with regimens of indomethacin 25 mg three times daily 1 week before surgery and 3 weeks postoperatively,2 or ibuprofen 200 mg preoperatively and postoperatively, have received mixed reviews.92 Literature supports the efficacy of topical NSAIDs,93–95 such as flurbiprofen 0.03%, diclofenac 0.1%, and ketorolac 0.5%, used prophylactically and after surgery to reduce inflammation.96 Piroxicam 0.5% solution used postoperatively appears to be as effective as diclofenac, but causes less ocular irritation.97 Usually, preoperatively and postoperatively, one drop is administered four times daily for up to 3 weeks to prevent CME. Frequently, in the acute postoperative period topical corticosteroids are used in conjunction with NSAIDs in the treatment of CME,98 although their combined effect has once again been questioned.99 In chronic cases, management continues until resolution.2 It has been suggested that indefinite NSAID treatment may be required to maintain CME regression,100 which increases interest in the utility of a long-term, intraocular drug delivery system.67 Once established, CME has been treated with oral acetazolamide, topical corticosteroids with NSAIDs, or posterior sub-Tenon’s injection of long-acting corticosteroids (see Chapter 6.33). Single-dose intracameral, intraoperative, and multiple intravitreal postoperative injections of triamcinolone have also safely prompted regression of chronic CME with minimal changes in intraocular pressure.73, 101–103 Recently, oral cyclooxygenase-2-inhibitors (10 mg daily) were found to successfully resolve CME that was unresponsive to oral or topical NSAIDS in a small number of patients, with improvement in visual acuity,104 as has high-dose methylprednisolone (1000 mg for 3 days)105 in the past. Antiglaucomatous prostaglandin analogs such as latanoprost may enhance disruption of the blood−aqueous barrier, increasing the incidence of CME after cataract surgery, but this appears to be a response to the drug’s preservative, and not the drug itself. The concurrent application of NSAIDs decreases the incidence of CME secondary to these medications and does not adversely influence the antiglaucoma drug’s effect on intraocular pressure.106, 107

REFERENCES 27. M ather R, Karenchak LM, Romanowski EG, et al. Fourth generation fluoroquinolones: new weapons in the arsenal of ophthalmic antibiotics. Am J Ophthalmol. 2002;133:463–6. 28. Kim DH, Stark WJ, O’Brien TP, Dick JD. Aqueous penetration and biological activity of moxifloxacin 0.5% ophthalmic solution and gatifloxacin 0.3% solution in cataract surgery patients. Ophthalmology. 2005;112:1992–6. 29. Ophthalmic moxifloxicin (Vigamox), gatifloxacin (Zymar). The Medical Letter. 2004;46(issue 1179):25. 30. Dereklis DL, Bufidis TA, Tsiakiri EP, Palassopoulos SI. Preoperative ocular disinfection by the use of povidoneiodine 5%. Acta Ophthalmol. 1994;72(5):627–30. 31. Chaudhary U, Nagpal RC, Malik AK, Kumar A. Comparative evaluation of antimicrobial activity of polyvinylpyrrolidone (PVP)-iodine versus topical antibiotics in cataract surgery. J Indian Med Assoc. 1998;96(7):202–4. 32. Koch PS. Efficacy of lidocaine 2% jelly as a topical agent in cataract surgery. J Cataract Refract Surg. 1999;25:632–4. 33. Assia EI, Pras E, Yehezkel M, et al. Topical anesthesia using lidocaine gel for cataract surgery. J Cataract Refract Surg. 1999;25:635–9. 34. Glasser DB, Edelhauser HF. Toxicity of surgical solutions. Int Ophthalmol Clin. 1989;29:179–87. 35. Parkkari M, Paivarinta H, Salminen L. The treatment of endophthalmitis after cataract surgery. J Ocular Pharmacol Ther. 1995;11:349–59. 36. Townsend-Pico WA, Meyers SM, Langston RH, Costin JA. Coagulase-negative staphylococcus endophthalmitis after cataract surgery with intraocular vancomycin. Am J Ophthalmol. 1996;121:318–9. 37. Han DP, Wisniewski SR, Wilson LA, et al. Spectrum and susceptibilities of microbiologic isolates in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol. 1996;122:1–7. 38. Sobaci G, Tuncer K. Effect of intraoperative antibiotics in irrigating solution on aqueous humor contamination. Eur J Ophthalmol. 2003;13:773–8. 39. Dickey JB, Thompson KD, Jay WM. Intraocular gentamicin sulfate and post cataract anterior chamber aspirate cultures. J Cataract Refract Surg. 1994;20:373–7. 40. Han DP, Wisniewski SR, Wilson LA, et al. Spectrum and susceptibilities of microbiologic isolates in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol. 1996;122:1–17. 41. Montan PG, Wejde G, Koranyi G, Rylander M. Prophylactic intracameral cefuroxime. JCRS. 2002;28:977–81. 982–7. 42. Seal DV, Barry P, Gettinby G, et al. ESCRS study of prophylaxis of endophthalmitis after cataract surgery: Case for a European multicentre study. J Cataract Refract Surg. 2006;32:396–406. 43. Barry P, Seal DV, Gettinby G for the ESCRS Endophthalmitis Study Group, et al. ESCRS study of prophylaxis of postoperative endophthalmitis after cataract surgery: Preliminary report of principal results from a European multicenter study. J Cataract Refract Surg. 2006;32:407–10. 44. Garat M, Moser CL, Alonso-Tarres C, Martin-Baranera M, Alberdi A. Intracameral cefazolin to prevent endophthalmitis in cataract surgery: A 3 year retrospective study. JCRS. 2005;31:2230–4. 45. Romero P, Mendez I, Salvat M, et al. Intracameral cefazolin as prophylaxis against endophthalmitis in cataract surgery. J Cataract Refract Surg. 2006;32:438–41. 46. Donnenfeld E, Snyder R, Kannellopoulos J, et al Presented at the annual meeting of the American Society of Cataract & Refractive Surgery, April 2004. 47. Arshinoff SA. Intracameral Vigamox for antibacterial prophylaxis in cataract surgery. A review of my experiences. Cataract Refract Surg Today. 2007;4:1–3. 48. O’Brien TP, Arshinoff SA, Mah FS. Perspectives on antibiotics for postoperative endophthalmitis prophylaxis: potential role of moxifloxacin. J Cataract Refract Surg.2007;33:1790–1800. 49. �� Roberts CW. Intraocular miotics and postoperative inflammation. J Cataract Refract Surg. 1993;19:731–4. 50. Arshinoff SA, Calogero DX, Bilotta R, et al. The problems associated with OVD use in cataract surgery. Presented by S Senft at the annual meeting of the American Society of Cataract and Refractive Surgery, San Diego, CA, April 16–22, 1998. 51. Rumelt S, Stolovich C. Intraoperative enoxaparin minimizes inflammatory reaction after pediatric cataract surgery. Am J Ophthalmol. 2006;141:433–7. 52. Kruger A, Amon M. Effect of heparin in the irrigation solution on post-operative inflammation and cellular reaction on the intraocular lens surface. J Cataract Refract Surg. 2002;28:87–92.

53. T akahashi H, Fujimoto C. Anterior chamber irrigation with an ozonated solution as prophylaxis against infectious endophthalmitis. J Cataract Refract Surg. 2004;30:1773–80. 54. McDermott ML, Edelhauser HF, Hack HM, Langston RH. Ophthalmic irrigants: a current review and update. Ophthalmic Surg. 1988;19:724–33. (review). 55. Arshinoff SA, Khoury E. HsS versus a balanced salt solution as a corneal wetting agent during routine cataract extraction and lens implantation. J Cataract Refract Surg. 1997;23:1211–25. 56. Arshinoff SA. Dispersive and cohesive viscoelastics in phacoemulsification. Ophthalmic Pract. 1995;13:98–104. 57. Arshinoff SA. The viscoelastic soft shell technique for compromised corneas and anterior chamber compartmentalization. Presented at the American Society of Cataract and Refractive Surgery Symposium on Cataract, IOL, and Refractive Surgery, Seattle, Washington DC, 1996. 58. Arshinoff SA. “Soft shell” technique uses two types of viscoelastics. Reported by Harvey Black. Ocular Surg News, Int. Ed. 1996;7(10):20. 59. Kim H, Joo CK. Efficacy of the soft-shell technique using Viscoat and Hyal-2000. J Cataract Refract Surg. 2004;30:2366–70. 60. Arshinoff SA, Wong E. Understanding, retaining, and removing dispersive and pseudodispersive ophthalmic viscosurgical devices. J Cataract Refract Surg. 2003;29:2318–23. 61. Arshinoff Steve A, Jafari Masoud. A New Classification of Ophthalmic Viscosurgical Devices (OVDs) − 2005. J Cataract Refract Surg. 2005;31:2167–71. 62. Arshinoff SA, Hofman I. Prospective, randomized trial comparing MicroVisc Plus and Healon GV in routine phacoemulsification. J Cataract Refract Surg. 1998;24:814–20. 63. Miller KM, Colvard M. Randomized clinical comparison of Healon GV and Viscoat. J Cataract Refract Surg. 1999;25:1630–6. 64. Rainer G, Menapace R, Findl O, et al. Intraocular pressure after small incision cataract surgery with Healon5 and Viscoat. J Cataract Refract Surg. 2000;26:271–6. 65. Arshinoff SA. Why Healon5. The meaning of viscoadaptive. Ophthalmic Pract. 1999;17:332–4. 66. Arshinoff SA. Healon5. In: Buratto L, Giardini P, Bellucci R, eds. Viscoelastics in ophthalmic surgery. Thorofare, NJ: Slack Inc.; 2000. :393–9. 67. Arshinoff S. The ultimate soft-shell technique. Ophthalmic Pract. 2000;18:289–90. 68. Arshinoff SA. Using BSS with viscoadaptives in “the ultimate soft shell technique“. J Cataract Refract Surg. 2002;28:1509–14. 69. Bron AM, Pechinot AP, Garcher CP, et al. The ocular penetration of oral sparfloxacin in humans. Am J Ophthalmol. 1994;117:322–7. 70. Mounier M, Ploy MC, Chauvin M. Study of intraocular diffusion of ofloxacin in humans and rabbits. Pathol Biol. 1992;40:529–33. 71. Haaskjold E, Ohrstrom A, Uusitalo RJ, et al. Use of collagen shields in cataract surgery. J Cataract Refract Surg. 1994;20:150–3. 72. Taravella MJ, Balentine J, Young DA, et al. Collagen shield delivery of ofloxacin to the human eye. J Cataract Refract Surg. 1999;25:562–5. 73. Simone JN, Pendelton RA, Jenkins JE. Comparison of the efficacy and safety of ketorolac tromethamine 0.5% and prednisolone acetate 1% after cataract surgery. J Cataract Refract Surg. 1999;25:699–704. 74. Hirneiss C, Neubaur AS. Comparison of prednisolone 1%, rimexolone 1% and ketorolac tromethamine 0.5% after cataract extraction. Graefes Arch Clin Exp Ophthalmol. 2005;243:768–73. 75. Chang DF, Garcia IH, Hunkeler JD, et al. Phase II results of an intraocular steroid delivery system for cataract surgery. Ophthalmology. 1999;106:1172–7. 76. Masket M. Comparison of the effect of topical corticosteroids and nonsteroidals on postoperative corneal astigmatism. J Cataract Refract Surg. 1990;16:715–8. 77. Barba KR, Samy A, Lai C, et al. Effect of topical anti- inflammatory drugs on corneal and limbal wound healing. J Cataract Refract Surg. 2000;26:893–7. 78. Snyder RW, Siekert RW, Schwiegerling J, et al. Acular as a single agent for use as an antimiotic and anti- inflammatory in cataract surgery. J Cataract Refract Surg. 2000;26:1225–7. 79. Arshinoff SA, Mills MD, Haber S. The pharmacotherapy of photorefractive keratectomy. J Cataract Refract Surg. 1996;22:1037–44. 80. Arshinoff SA, Opalinski Y. The pharmacotherapy of photorefractive keratectomy (PRK). Comp Ophthalmol Update. 2003;4:225–33. Editorial follows on pp 235–236.

5.5 The Pharmacotherapy of Cataract Surgery

1. H offman BB, Lefkowitz RJ. Catecholamines and sympathomimetic drugs. In: Hardman JG, Limberg LE, Goodman Gilman A, et al, eds. The pharmacological basis of therapeutics. Toronto: Pergamon Press; 1990:187–220. 2. Flach AJ. Cyclo-oxygenase inhibitors in ophthalmology. Surv Ophthalmol. 1992;36:259–84. 3. Arshinoff SA, Mills M, Haber S. Pharmacotherapy of photorefractive keratectomy. J Cataract Refract Surg. 1996;22:1037–44. 4. Keates R, McGowan K. Clinical trial of flurbiprofen to maintain pupillary dilation during cataract surgery. Ann Ophthalmol. 1984;16:919–21. 5. Miyake K. The significance of inflammatory reactions following cataract extraction and intraocular lens implantation. J Cataract Refract Surg. 1996;22(Suppl):759–63. 6. Flach AJ, Kraff MC, Sanders DR, Tanenbaum L. The quantitative effect of 0.5% ketorolac tromethamine solution and 0.1% dexamethasone sodium phosphate solution on postsurgical blood-aqueous barrier. Arch Ophthalmol. 1988;106:480–3. 7. Roberts C. Comparison of diclofenac sodium and flurbiprofen for inhibition of surgically induced miosis. J Cataract Refract Surg. 1996;22(Suppl):780–6. 8. Srinivasan R. Topical ketorolac tromethamine 0.5% versus diclofenac sodium 0.1% to inhibit miosis during surgery. J Cataract Refract Surg. 2002;28:517–20. 9. Lundberg B, Behndig A. Intracameral mydriatics in phacoemulsification cataract surgery. J Cataract Refract and Surg. 2003;29:2366–71. 10. Bendig A, Eriksson A. Evaluation of surgical performance with intracameral mydriatics in phacoemulsification surgery. Acta Ophthalmol Scand. 2004;82:144–7. 11. Hirowatari T, Kazuhiro T. Evaluation of a new pre operative ophthalmic solution. Can J Ophthalmol. 2005;40:58–62. 12. Backstrom G, Behndig A. Redilatation with intracameral mydriatics in phacoemulsification surgery. Acta Ophthalmol Scand. 2006;84:100–4. 13. Samad A, Solomon LD, Miller MA, Mendelson J. Anterior chamber contamination after uncomplicated phacoemulsification and intraocular lens implantation. Am J Ophthalmol. 1995;120:143–50. 14. Starr MB, Lally JM. Antimicrobial prophylaxis for ophthalmic surgery. Surv Ophthalmol. 1995;39:485–501. 15. Donnenfeld ED, Schrier A, Perry HD. Penetration of topically applied ciprofloxacin, norfloxacin and ofloxacin into the aqueous humor. Ophthalmology. 1994; 101:902–5. 16. Leeming JP, Diamond JP, Trigg R. Ocular penetration of topical ciprofloxacin and norfloxacin drops and their effect upon eyelid flora. Br J Ophthalmol. 1994;78:546–8. 17. Koch HR, Kulus SC. Corneal penetration of fluoroquinolones: aqueous humor concentrations after topical application of levofloxacin 0.5% and ofloxacin 0.3% eyedrops. J Cataract Refract Surg. 2005;31:1377–85. 18. Yamada M, Ishikawa K. Corneal penetration of simultaneously applied levofloxacin, norfloxacin and lomefloxacin in human eyes. Acta Ophthalmol Scand. 2006;84:192–6. 19. Healy DP, Holland EJ. Concentrations of levofloxacin, ofloxacin and ciprofloxacin in human corneal stromal tissue and aqueous humor after topical administration. Cornea. 2004;23:255–63. 20. Yamada M, Mochizuki H. Aqueous humor levels of topically applied levofloxacin, norfloxacin and lomefloxacin in the same human eyes. J Cataract Refract Surg. 2003;29:1771–5. 21. Kim DH, Stark WJ. Aqueous penetration and biological activity of Moxifloxacin 0.5% ophthalmic solution and gatifloxacin 0.3% solution in cataract surgery patients. Ophthalmology. 2005;112:1992–6. 22. Price M, Quillin C. Effect of gatifloxicin ophthalmic solution 0.3% on human corneal endothelial cell density and aqueous humor gatifloxicin concentrations. Curr Eye Res.. 2005;30:563–7. 23. Solomon R, Donnenfeld ED. Penetration of topically applied gatifloxacin 0.35, moxifloxacin 0.5% and ciprofloxacin 0.3% into the aqueous humor. Ophthalmology. 2005;112:466–9. 24. McCulley JP, Caudle D. Fourth generation fluoroquinolone penetration into the aqueous humor of humans. Ophthalmology. 2006;113:955–9. 25. Taban M, Behrens A, Newcomb RL, et al. Acute endophthalmitis following cataract surgery. Arch Ophthalmol. 2005;123:613–20. 26. Solomon R, Donnenfeld E, Perry H, et al Aqueous humor concentrations from topically applied ocular fluoroquinolones. Poster presented at Annual Meeting of the Association for Research in Vision and Ophthalmology, Fort Lauderdale, FL, April, 2004.

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5 THE LENS

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81. R oberts CW. Pretreatment with topical diclofenac sodium to decrease postoperative inflammation. Ophthalmology. 1996;103:636–9. 82. El-Harazi SM, Ruiz RS, Feldman RM, et al. Efficacy of preoperative versus postoperative ketorolac tromethamine 0.5% in reducing inflammation after cataract surgery. J Cataract Refract Surg. 2000;26: 1626–30. 83. Arshinoff SA, Strube YNJ, Ning J, Yagev R. Simultaneous bilateral cataract surgery. J Cataract Refract Surg. 2003;29:1281–91. 84. Yaylali V, Ozbay D. Efficacy and safety of rimexolone 1% versus prednisolone acetate 1% in the control of post-operative inflammation following phacoemulsification cataract surgery. Int Ophthalmol. 2004; 25:65–8. 85. Paganell F, Cardillo JA. A single intraoperative sub- Tenon’s triamcinolone acetonide injection for the treatment of post-cataract surgery inflammation. Ophthalmology. 2005;112:1481. 86. Negi AK, Browing AC. Single perioperative triamcinolone injection versus standard post-operative steroid drops. J Cataract Refract Surg. 2006;32:468–74. 87. Gills JP, Gills P. Effect of intracameral triamcinolone to control inflammation following cataract surgery. J Cataract Refract Surg. 2005;31:1670–1. 88. Flach AJ, Lavelle CJ, Olander KW, et al. The effect of ketorolac tromethamine solution 0.5% in reducing postoperative inflammation after cataract extraction and intraocular lens implantation. Ophthalmology. 1988;95:1279–84. 89. Solomon KD, Cheetham JK, DeGryse R, et al. Topical ketorolac tromethamine 0.5% ophthalmic solution in ocular inflammation after cataract surgery. Ophthalmology. 2001;108:331–7.

90. K iller HE, Borruat FX, Blumer BK, et al. Corneal penetration of diclofenac from a fixed combination of diclofenac-gentamicin eye drops. J Cataract Refract Surg. 1998;24:1365–70. 91. Jaffe NS. Cystoid macular edema (Irvine-Gass syndrome). In: Klein E, ed. Cataract surgery and its complications, 4th ed.. Toronto: Mosby; 1984. :426–41. 92. Yanuzzi LA, Klein RM, Wallyn RH, et al. Ineffectiveness of indomethacin in the treatment of chronic cystoid macular edema. Am J Ophthalmol. 1977;84:517–9. 93. Rossetti L, Bujtar E, Castoldi D, et al. Effectiveness of diclofenac eye drops in reducing inflammation and the incidence of cystoid macular edema after cataract surgery. J Cataract Refract Surg. 1996;22(Suppl):794–9. 94. Miyake K, Masuda K, Shirato S, et al. Comparison of diclofenac and fluorometholone in preventing cystoid macular edema after small incision cataract surgery: a multicentred prospective trial. Jpn J Ophthalmol. 2000;44:58–67. 95. Holzer MP, Solomon KD. Comparison of ketorolac and loteprednol 0.5% for inflammation after phacoemulsification. J Cataract Refract Surg. 2002;28:93–9. 96. Rho D. Treatment of acute pseudophakic cystoid macular edema: Diclofenac versus ketorolac. J Cataract Refract Surg. 2003;29:2378–84. 97. Scuderi B, Driussi GB. Effectiveness and tolerance of piroxicam 0.5% and diclofenac sodium 0.1% in controlling inflammation after cataract surgery. Eur J Ophthalmol. 2003;13:536–40. 98. Heier JS, Topping TM, Baumann W, et al. Ketorolac versus prednisolone versus combination therapy in the treatment of acute pseudophakic cystoid macular edema. Ophthalmology. 2000;107:2034–9. 99. Singal N, Hopkins J. Pseudophakic cystoid macular edema: ketorolac alone versus ketorolac and prednisolone. Can J Ophthalmol. 2004;39:245–50.

100. Weisz JM, Bressler NM, Bressler SB, et al. Ketorolac treatment of pseudophakic cystoid macular edema identified more than 24 months after cataract extraction. Ophthalmology. 1999;106:1656–9. 101. Conway MD, Canakis C. Intravitreal triamcinolone acetonide for refractory chronic pseudophakic cystoid macular edema. J Cataract Refract Surg. 2003;29:27–33. 102. Jonas JB. Kreissig. Intravitreal triamcinolone for pseudophakic cystoid macular edema. Am J Ophthalmol. 2003;136:384–6. 103. Ozkiris A, Erkilic K. Complications of intravitreal injection of triamcinolone acetonide. Can J Ophthalmol. 2005;40:63–8. 104. Reis A, Birnbaum F. Cyclooxygenase-2-inhibitors: a new therapeutic option in the treatment of macular edema after cataract surgery. J Cataract Refract Surg. 2005;31:1337–40. 105. Abe T, Hayasaka S, Nagaki Y, et al. Pseudophakic cystoid macular edema treated with high-dose intravenous methylprednisolone. J Cataract Refract Surg. 1999;25:1286–8. 106. Miyake K, Ota I, Mackubo K, et al. Latanoprost accelerates disruption of the blood-aqueous barrier and the incidence of angiographic cystoid macular edema in early postoperative pseudophakias. Arch Ophthalmol. 1999;117:34–40. 107. Miyake K, Ota I, Ibaraki N, et al. Enhanced disruption of the blood-aqueous barrier and the incidence of angiographic cystoid macular edema by topical timolol and its preservative in early postoperative pseudophakia. Arch Ophthalmol. 2001;119:387–94.

PART 5 THE LENS

Anesthesia for Cataract Surgery Donna L. Greenhalgh

Key features n n n

onsideration of patient characteristics. C Local anesthesia: considerations, sedatives used, local anesthetics used. Local techniques: topical, intraocular, deep topical fornix nerve block, retrobulbar, peribulbar, and sub-Tenon’s; advantages, disadvantages, and complications. General anesthesia: techniques, advantages, disadvantages, and complications.

5.6

Anticoagulants

Patients on oral anticoagulants and antiplatelet therapy, including aspirin and clopidogrel, should continue with these throughout surgery.5–7 The risks of cardiovascular complications outweigh the risk of hemorrhage, especially if the patient has had a drug-eluting stent inserted. General anesthesia, sub-Tenon’s, or topical local anesthesia is recommended.

Diabetes mellitus

Local anesthesia causes least disruption to diabetic management but with new anesthetic agents recovery is rapid. General anesthesia is well tolerated.

Local anesthesia

INTRODUCTION The advent of small, self-sealing incisions for phakoemulsification has led to a change in anesthetic practice. Akinesis and very low intraocular pressures are not essential, allowing the use of topical and local techniques like peribulbar and sub-Tenon’s blocks. A team approach is necessary, with the surgeon concentrating on the operation and the anesthetist looking after the patient under general or local anesthesia.

MEDICAL ASPECTS OF ANESTHESIA FOR CATARACT SURGERY Cataract Type and Associated Medical Conditions

Cataracts can be either congenital or acquired. They may be an ocular manifestation of a systemic disease. There is a relatively high incidence of uncommon medical conditions in younger cataract patients. Patients with acquired cataracts are usually elderly; the average age is 75 and has associated comorbidities such as ischemic heart disease and chronic obstructive airway disease. One study showed that 84% of patients had at least one concomitant serious medical disease.1 In an audit of 1000 cases in Auckland 43% were ASA3-4.2 There is a significant increase in overall mortality in those with concurrent hypertension (48%), ischemic heart disease (38%), a history of hypothyroidism (18%), diabetes (16%), and a history of a new malignancy (3%).3 The Royal Colleges of Anaesthetists and Ophthalmologists recommend a full history and appropriate investigations on appropriate patients. However, apart from an ECG, unless specifically indicated, preoperative investigations have not been shown to influence the outcome in patients having local anesthesia for cataract surgery.4

Specific conditions

Ischemic heart disease

441

Ischemia can be provoked by stress at the prospect of local or general anesthesia. Neither should be given within 6 months of a myocardial infarction or 3 months following angioplasty or coronary revascularization. Phenylephrine drops can result in a significant rise in blood pressure and should be administered cautiously. The oxidative damage resulting in cataract formation is linked to free radical formation and atherosclerosis, which explains the high proportion of patients with ischemic heart disease.3

Local anesthesia can be classified into topical, retrobulbar block, peri bulbar block, and sub-Tenon’s block.

General Considerations

The main advantage of local anesthesia is a conscious and alert patient. Sedation can result in a confused uncooperative patient in the middle of an operation. However, certain patients can become stressed at the thought of being awake, especially during insertion of the block, and short-term sedation with either midazolam (1–3 mg) or propofol (10–30 mg) can be useful.8 To undergo local anesthesia, a patient must be medically fit. Many comorbidities render a local anesthetic unsuitable, especially if the patient is unable to lie flat. Recommendations are that patients having local anesthesia without sedation or low-dosage sedation need not be starved, while standard fasting times should be followed for deeper sedation or general anesthesia.9 It is now accepted that small amounts of clear fluids can be permitted 2 hours prior to surgery. Minimal monitoring should include ECG and pulse oximetry as many elderly patients become hypoxic lying flat, even without sedation. Intravenous access should be secured. The elderly and those with systemic illnesses should be anesthetized in an appropriate environment with back up facilities if inpatient or critical care is required.9 Supplemental oxygen is given to avoid hypoxia and minimize claustrophobia. Rebreathing can occur under the drapes even at 6 L/minute of oxygen. Nonmedical personnel often carry out preoperative assessment prior to surgery. Accurate listing for local or general anesthesia can be a problem as many patients have concomitant disease. A questionnaire filled in by patients has been shown to be a good initial screening tool with supplemental medical input as required.8 Many patients have visual experiences under local anesthesia; in one survey 16% found this distressing.10 Counseling preoperatively has been shown to be beneficial in reducing the distress.11, 12 All operating room personnel must be trained in basic life support and at least one member should have advanced training. The Joint Royal Colleges in the United Kingdom recommend that an anesthetist be present throughout, whether general or local anesthesia is used, and is essential if sharp needle technique or sedation is used. For patients undergoing topical anesthesia or sub-Tenon’s block, an anesthetist does not need to be available in the theatre block,9 unless the site is isolated.13 In various studies intervention by an anesthetist was necessary: in 37%,14 8.1%,15 and 4.0%16 of cases. In another study 50% required intervention for drugs, 41% for antihypertensive therapy, 17% other interventions, and 2.5% for severe cardiovascular complications. The Joint Royal Colleges advise that due to a high intervention rate an anesthetist be present.17, 18

l l

THE LENS

l l l l l l l

l l l l l

Patients for whom local anesthesia is contraindicated are those: Who are unable to cooperate (e.g., with mental impairment) In whom communication is difficult (e.g., inability to speak the language or deafness) Who have involuntary movements (e.g., those with Parkinson’s disease) Who are unable to lie flat or still Who have uncontrolled coughing or sneezing Who are severely anxious or claustrophobic Undergoing bilateral surgery For whom prolonged or difficult surgery is likely For whom general anesthesia is preferred, whether by the patient, the surgeon, or the anesthetist The objectives of local anesthesia are as follows:12 Ensure that the block procedure is painless Provide globe and conjunctival anesthesia Obtain maximal akinesia of the globe and orbicularis oculi Obtain a low pressure within the orbit and globe Avoid local and systemic complications

Sedative Agents Commonly Used in Local Anesthesia

Midazolam, a short-acting, water-soluble benzodiazepine with a halflife of 2 hours, has both amnesic and anxiolytic properties, lacks venous sequelae, and allows rapid patient recovery. It is given slowly intravenously in 1 mg increments. Adequate time must be given for it to work in the elderly otherwise oversedation can easily result. Overdoses can be reversed with flumazenil, a benzodiazepine antagonist, but its half-life is 1 hour, so re-sedation can be a problem. Propofol, a short-acting phenol, is an intravenous induction agent suitable for infusion and sedation. It is characterized by a rapid and clear-headed recovery, with a low incidence of nausea and vomiting. It causes respiratory depression and a fall in blood pressure. Propofol and midazolam have been used for patient-controlled sedation. This has been shown to significantly reduce patients’ level of anxiety, and they remain cooperative enough to press the button, eliminating the unpredictability of elderly patients’ reaction to sedation. Midazolam has a greater risk than propofol of stacking doses, resulting in oversedation.19 Dexmedetomidine, an α2 agonist, has been used as a sedative agent with good effect.20 Fentanyl is a potent, short-acting narcotic analgesic with duration of action of about 30 minutes. Given in doses of 25–50 μg, it provides analgesia with minimal sedation. However, it has the side effects of all narcotic analgesics, including respiratory depression, nausea, and vomiting. Remifentanil is an ultra-short-acting analgesic metabolized by esterases, resulting in an elimination half-life of 3–10 minutes and administered by infusion. It produces intense analgesia, but it needs to be supplemented because it also wears off within 3–10 minutes of the infusion being stopped.21 It can cause a marked fall in heart rate and blood pressure, so should be used with caution in elderly, frail patients. It is not recommended for use as a sole agent.

Topical Anesthesia

Sixty per cent of all cataracts are performed under topical anesthesia in the United States. Benoxinate 0.4%, an ester anesthetic, is one of the most frequently used because of its high degree of safety. Other commonly used agents are tetracaine 0.5% or 1% amethocaine and proparacaine (proxymetacaine) 0.5%; both are short acting (20 minutes) and are the least toxic to the corneal epithelium. Lidocaine 4% and bupivacaine 0.5% and 0.75% have a longer duration of action but an increased associated corneal toxicity. Absolute contraindications are true allergy to local anesthetics and nystagmus. The advantages and disadvantages of topical anesthesia are given in Box 5-6-1.22 Topical anesthesia may be combined with subconjunctival anesthesia. This allows subconjunctival and scleral manipulations to be carried out, with good toleration by patients.

Technique

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The aim is to block the nerves that supply the superficial cornea and conjunctiva; namely, the long and short ciliary, nasociliary, and lacrimal nerves. The patient should be warned that application of the drops on

Box 5-6-1 Advantages and Disadvantages of Topical Anesthesia ADVANTAGES l No risk associated at needle insertion l No risk of periocular hemorrhage or hyphema with clear corneal incisions; systemic anticoagulation can be continued without any worry l Functional vision is maintained; advantageous for uniocular patients l No postoperative diplopia or ptosis l Patients are fully alert DISADVANTAGES l An awake and talkative patient can be distracting for the surgeon l No akinesia of the eye l If difficulties or problems occur the anesthesia may not be adequate ADVERSE EFFECTS OF TOPICAL OCULAR ANESTHETICS l Direct corneal effects – alteration of lacrimation and tear film stability l Epithelial toxicity – healing has been shown to be delayed when an epithelial defect occurs (lidocaine does not appear to affect healing) l Endothelial toxicity – this occurs when penetrating trauma is present and appears to be related to the preservative benzalkonium l Systemic effects – lethal toxicity (this is only a problem with cocaine) l Allergy and idiosyncratic reactions – contact dermatitis is the most common and occurs with proparacaine most frequently SECONDARY ADVERSE EFFECTS l Surface keratopathy

the surface of the cornea stings (except for proxymetacaine). Drops are administered before the placement of the drapes. As visual perception is not lost, the patient is asked to focus on the light, the intensity of which is reduced. The subconjunctival injection of antibiotics can be painful, but this can be avoided by including these in the infusion bottle. Use of this technique is increasing throughout both the United States and Europe (up to 60% of surgeons in the United States choose this method),22 although several studies show inferior analgesia compared to peribulbar and sub-Tenon’s blocks.23, 24 There is no akinesia of the eye with the following techniques, so they are suitable only for experienced surgeons.25

Intraocular lidocaine

Intraocular lidocaine has been used to provide analgesia during surgery. The solution used is 1% isotonic, nonpreserved lidocaine 0.3 mL administered intramurally. At present, no side effects have been reported, except for possible transient retinal toxicity if lidocaine is injected posteriorly in the absence of a posterior capsule. Its use obviates the need for intravenous and regional anesthetic supplementation in most patients. Adequate anesthesia is obtained in about 10 seconds.25 Intrameral bupivacaine has also been used without problems.26

Deep topical fornix nerve block/limbal

This technique has been superceded by topical and sub-Tenon’s block. It does not confer any advantage over these techniques and can be painful to administer, and will not be discussed further.

Retrobulbar Block

With this technique the aim is to block the oculomotor nerves before they enter the four rectus muscles in the posterior intraconal space. This block has been superseded by peribulbar block as the risk of serious complications is greatly reduced with peribulbar block and so only a limited description is given.27 The eye is kept in the neutral position and a sharp 25- or 27-gauge needle less than 31 mm in length is inserted at the lower temporal orbital margin (Fig. 5-6-1). It is directed posteriorly at an angle of 10 degrees to the horizontal until the equator of the globe is passed and then directed slightly upward and medially (Fig. �� 5-6-2)�� . Local anesthetic (2–4 mL) is injected slowly after aspiration to check intravascular or subdural placement. Any global movement is noted, as this is indicative of sclera puncture. The eye is not moved as this may increase the risk of optic nerve injury. The advantages and disadvantages of retrobulbar block are given in Box 5-6-2.

Box 5-6-2 Advantages and Disadvantage of Retrobulbar Block

INJECTION SITE FOR RETROBULBAR BLOCK

DISADVANTAGE l The main disadvantage of retrobulbar blocks is that the complication rate is higher than for peribulbar blocks – the reason for the development of the peribulbar block

Overall, there is a 1–3% chance that complications will occur with retrobulbar block. These include: l Retrobulbar hemorrhage l Ocular perforation (< 0.1% incidence, but 1 in 140 injections in myopic eyes)28 l Subarachnoid or intradural injection, leading to brainstem anesthesia in 1 in 350–500 patients l Respiratory depression or arrest (0.29% incidence) l Optic nerve contusion and atrophy l Retinal vascular occlusion l Grand mal seizure l Decreased visual acuity l Hypotony (< 8 mmHg) l Contralateral amaurosis l Muscle complications: ptosis from levator aponeurosis dehiscence, entropion and diplopia following extraocular muscle injection l Pulmonary edema l Oculocardiac reflex, usually produced by pressure on the globe (vasovagal bradycardias are more common)

Anesthesia for Cataract Surgery

ADVANTAGES l A retrobulbar block is reliable for producing excellent anesthesia and akinesia l The onset of the block is quicker than with peribulbar; it usually occurs within 5 minutes l Low volumes of anesthetic result in a lower intraorbital tension and less chemosis than with peribulbar blocks l Loss of visual acuity occurs in a greater number of patients compared to peribulbar blocks, though this can be volume dependent; some patients may be distressed by being able to see throughout the procedure

5.6

site of injection

Fig. 5-6-1 Injection site for retrobulbar block. The injection site through the lower lid lies halfway between the lateral canthus and the lateral limbus. (Adapted from Sanderson Grizzard W. Ophthalmic anaesthesia. Ann Ophthalmol. 1989;21:265–94.)

ADVANCEMENT OF NEEDLE IN RETROBULBAR BLOCK

Peribulbar Block

The principle of this technique is to instill the local anesthetic outside the muscle cone and avoid proximity to the optic nerve. This utilizes high volumes of anesthetic and the application of a pressure device. The local anesthetic agents do not differ from those used in retrobulbar block, but typically shorter needles are used.

Technique

The volume varies from 3 to 10 mL; the average is 5–7 mL. Again, the eye is in primary gaze. Local anesthetic drops are applied for the initial injection. This is at the inferotemporal lower orbital margin, midway between the lateral canthus and the lateral limbus. The 27- or 25-gauge needle is advanced parallel to the plane of the orbital floor. Local anesthetic is injected at a depth of about 2.5 cm from the inferior orbital rim (in an eye of normal axial length). As with retrobulbar blocks, no resistance to injection should be felt, and aspiration should be performed27 (Fig. 5-6-3). After 5 minutes, the amount of akinesia is assessed. Often, a second injection is required to block the superior oblique. A 25-gauge, 2.5 cm needle is inserted between the medial canthus and the caruncle, which is another relatively avascular area; then the needle is directed immediately backward. The medial check ligament often is penetrated, and the medial rectus can be injected at this point. At a depth of 1.5 cm, another 5 mL of solution is injected to produce a more complete block, with akinesia of the orbicularis oculi and levator palpebrae superioris. This avoids the alternative option of injecting the superotemporal region and causing ecchymosis of the eyelid. A Honan balloon or pressure-lowering device is applied for 20–30 minutes. Four milliliters of local anesthetic can increase the intraocular pressure by over 6.2 mmHg; ocular compression can decrease the intraocular pressure by 8.8 mmHg after 5 minutes and by 14.3 mmHg after 40 minutes. A single medial canthus injection has been described at the junction of the caruncle and medial canthus, which is usually at the junction of the

Fig. 5-6-2 Advancement of needle in retrobulbar block. The needle is advanced beyond the equator of the globe and then directed toward an imaginary point behind the macula, with care taken not to cross the midsagittal plane of the eye. (Adapted from Sanderson Grizzard W. Ophthalmic anaesthesia. Ann Ophthalmol. 1989;21:265–94.)

medial two thirds and lateral two thirds of the lower orbital rim. This is easily learned, and fewer injections decrease the complication rate. Both during insertion of the block and the procedure itself, peribulbar block has been reported to be more painful than using topical anesthesia.29, 30 It is important that adequate training is given to decrease complications for all these blocks.31 The advantages and disadvantages of peribulbar block are given in Box 5-6-3.

Local anesthetic agent

The most common mixture used is bupivacaine 0.5% plus lidocaine 2% plus hyaluronidase 150 international units. The mixture (5–8 mL) is injected slowly to avoid patient discomfort. Aspiration prior to injection minimizes the risk of intravascular or subdural injection. Other agents used are mepivacaine 1–2%, lidocaine 1–2% alone, bupivacaine 0.25–0.75% alone or with lignocaine and prilocaine 3%.30 Levobupivacaine 5 mg/mL is better than ropivacaine 0.75%.31, 32 Levobupivacaine is the L-isomer of bupivacaine with a higher safety index, especially in terms of cardiac side effects. A single medial canthus injection of 7–9 mL of 2% articaine has also been used to good effect.33 Articaine is an amide local anesthetic of low toxicity, which has rapid onset and disperses quickly.34, 35

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PERIBULBAR/INFEROTEMPORAL PERICONAL INJECTION

THE LENS site of injection A

Fig. 5-6-3 Inferotemporal periconal injection. (A) The needle enters the orbit at the junction of its floor with the lateral wall, very close to the bony rim. (B) The needle passes backward in a sagittal plane parallel to the orbit floor. (C) It passes the globe equator when the needle-hub junction reaches the plane of the iris. (D) After test aspiration, up to 10 mL anesthetic solution is injected. (Adapted from Hamilton RC. Techniques of orbital regional anaesthesia. Br J Anaesth. 2001;86:473–6.)

Epinephrine 5 μg/mL may be added to improve the onset time, quality, and duration of the block. However, it should be avoided in patients who have ischemic heart disease, tachycardia, and hypertension. Also, epinephrine has been implicated in optic artery thrombosis secondary to vasoconstriction. A 50% decrease in pressure in the ophthalmic artery has been noted, so it should be avoided in patients with generalized atherosclerosis. Hyaluronidase breaks down C1–C4 bonds between glucosamine and glucuronic acid in connective tissue, which enables the local anesthetic to permeate the tissues more effectively. The required quantity of local anesthetic is therefore reduced, and the time to onset is decreased. Hyaluronidase may help prevent damage to extraocular muscles, especially the inferior rectus muscle preventing diploplia.36, However, this anesthetic is an expensive choice. A “painless” local anesthetic to initially anesthetize the skin and subcutaneous tissues can be helpful. The solution is made by adding 1.5 mL of lidocaine 2% to 15 mL of balanced salt solution, altering the pH and pKa of the solution. Amethocaine or Emla cream applied to the skin at least 1 hour preoperatively removes the pain of injection if the needle passes through the skin.

Complications

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Globe perforation is more commonly associated with retrobulbar and peribulbar local anesthesia. However, there has been a case report following sub-Tenon’s anesthesia in a patient who had had previous retinal surgery. Caution is advised in patients who have had prior surgery, thinned sclera, or excess scar tissue.37 Globe perforation has also been reported following injection of local anesthetic into the lid for removal of a hordeolum.38 Risk factors for globe perforation are: l�� High myopia, axial length greater than 26 mm39, 40 l�� Atkinson gaze l�� Sharp injection needle;10, 40 however, blunt needles do not prevent perforation41 l�� Previous scleral buckling procedure l�� Inexperience in performing local blocks l�� Poor patient compliance. Signs of globe perforation are: l�� Vitreous hemorrhage (100%), usually on the first postoperative day40, 42 l�� Subretinal hemorrhage (76%) l�� Retinal breaks along the inferior vascular arcade (76%) l�� Retinal detachment (14%) Retinal detachment is often associated with poor visual outcome, but it is improved with prompt recognition and referral to specialized centers.43, 44 Treatment with scleral buckling, pars plana vitrectomy, and silicone oil tamponade has been recommended.45

Box 5-6-3 Advantages and Disadvantages of Peribulbar Block ADVANTAGES l The risk of complications associated with peribulbar block is low l Peribulbar block has all the advantages of retrobulbar block DISADVANTAGES l Peribulbar blocks have all the disadvantages of retrobulbar blocks, but they occur less frequently l The quality of akinesia and anesthesia may not be as good as with retrobulbar block l Often more than one injection is required l The block takes much longer to work—it can take up to 30 minutes l The Honan balloon may be uncomfortable for the patient l Chemosis occurs in 80% of cases, which makes operating conditions difficult l In 5.8% of both retrobulbar and peribulbar blocks, ptosis can remain for up to 90 days l One perforation for every 140 peribulbar blocks in eyes > 26 mm axial length

Sub-Tenon’s Block

This involves surface anesthesia and access to the sub-Tenon’s capsule to administer the local anesthetic. In the United Kingdom this is now the commonest technique, comprising 43% of cases.46

Anatomy

This is described fully elsewhere in the book. Briefly, Tenon’s capsule is a facial sheath, a thin membrane enveloping the eyeball and separating it from orbital fat. The inner surface is smooth and shiny, separated from the outer surface of the sclera by a potential space, the episcleral space or sub-Tenon’s. Anteriorly, the sheath is fastened to the sclera approximately 1.5 cm to the corneal scleral junction. Posteriorly, it is fused with the meninges around the optic nerve. It has been suggested that it is a lymph space. There are numerous delicate bands crossing the space.

Technique

The conjunctiva is anesthetized first with drops of the local anesthetic of choice. The commonest approach is by the infranasal quadrant as this allows good distribution of the anesthetic while

Box 5-6-4 ADVANTAGES AND DISADVANTAGES OF SUB-TENON’S BLOCK

Fig. 5-6-4 Incision for sub-Tenon’s block. Arrows point to conjunctiva, Tenon’s capsule, and shining sclera under the Tenon’s capsule. (Reprinted with kind permission from Kumar CM, Williamson S, Manickham B. A review of subTenon’s block: current practice and recent development. Eur J Anaesthesiol. 2005;22:567–7, figure 2c, European Academy of Anaesthesiology, published by Cambridge University Press.)

decreasing the risk of damage to the vortex veins. The eye is cleaned and the patient asked to look upwards and outwards. Aseptically, the conjunctiva and Tenon’s capsule are picked up 3–5 mm away from the limbus using nontoothed forceps (Moorfields forceps)47 (Fig. 5-6-4). A small incision is made through these layers using scissors (Wescott scissors) exposing the sclera. A sub-Tenon’s cannula is inserted: either a 25 mm long cannula, curved posteriorly with a flat profile and a blunt end hole or an anterior sub-Tenon’s cannula (Greenbaum), a 15 G, 1.2 cm long, blunt, flat-bottomed and D-shaped cannula, designed so the opening on the flat bottom faces the sclera after insertion. The cannula is advanced posteriorly halfway between the horizontal and vertical equators of the globe. Some resistance is met at this point as the scleral Tenon bridging fibers are entered. Slow injection allows advancement of the needle and pushes the tissues away. Three to five milliliters of local anesthetic are injected; the greater the volume, the greater the akinesis. Lignocaine 2% is the gold standard; bupivacaine 0.5% and articaine 2% have also been used. Hyaluronidase can be added. Adrenaline is not advised, as discussed previously. A Honan’s balloon can be used to increase dispersal. There is only a small rise in the intraocular pressure, which is insignificant with this type of block.48 Comparison with peribulbar anesthesia shows that sub-Tenon’s block is a suitable alternative with better akinesia, improved consistency, and a quicker onset.27, 49 When compared with topical anesthesia, subTenon’s provides superior pain relief and patient satisfaction.23, 50 The advantages and disadvantages of sub-Tenon’s block are given in Box 5-6-4. Complications are mainly minor, though orbital inflammation, scleral perforation, sight threatening, cardiovascular collapse, and lifethreatening complications have been reported.13, 48, 51

GENERAL ANESTHESIA General anesthesia is performed on those patients who are unsuitable candidates for local anesthesia; it is the method of choice for babies, children, and some young adults. Previously it was necessary to intubate, paralyze, and ventilate the patient. However, with the advent of phacoemulsification and small incision surgery, plus the use of propofol with a laryngeal mask, it is now feasible to have the patient breathing spontaneously. Intubation was needed before because of the competition for space around the operative site. To enable the endotracheal tube to be tolerated, the patient had to be anesthetized deeply with volatile agents of high concentration, or paralyzed. Not intubating the patient allows a lighter anesthetic to be given, decreasing cardiovascular depression and improving recovery. In patients of 80 years or more, psychomotor testing showed that

Disadvantages The local anesthetic agent must be injected into the capsule – double perforation of the capsule results in anesthetic leaking out, which decreases the effectiveness of the block Although it is an advantage that the globe can be moved under instruction, it is important the eye is not moved at other times – the use of stabilizing sutures is advised Dissection of the capsule must be carried out under sterile conditions

Anesthesia for Cataract Surgery

Advantages Less painful than peribulbar block Better analgesia than topical anesthesia Complications rarely serious No increase in intraocular pressure occurs with the administration of local anesthetic Surgery can begin almost immediately Lasts for 60 minutes and supplemental anesthetic agent can be given The globe can be voluntarily moved at the surgeon’s instruction Low dose and low volume of anesthetic agent are used

5.6

Box 5-6-5 Advantages and Disadvantages of General Anesthesia ADVANTAGES l Patient comfort l Ideal operating conditions – a quiet, immobile patient and soft eye l Allows for rapid alterations in intraocular pressure if required l The method of choice for difficult cases l Effective for more patients l No risk of any of the complications associated with local anesthetic blocks l No residual paralysis of the eye when the patient is awake l Bilateral surgery can be performed, which is advantageous in the frail, elderly, and medically “unfit“ l Better conditions for teaching DISADVANTAGES l Slightly slower turnaround times, if only one anesthetist is available l More expensive

total intravenous anesthesia with propofol and remifentanil resulted in significantly faster recovery of cognitive function compared with etomidate-fentanyl-isoflurane.52 A recent study that compared balanced anesthesia with total intravenous anesthesia (TIVA) showed similar cardiovascular effects but decreased nausea and vomiting, faster recovery, better patient satisfaction, and lower costs with TIVA.53, 54

Technique

Spontaneous respiration

A laryngeal mask is inserted and anesthesia is maintained with either a continuous propofol infusion or a volatile agent of choice. Targetcontrolled infusion regimes are commonly employed. Propofol 4.5 μg/mL bolus for induction followed by 3.26 μg/mL maintenance target infusion levels can be combined with either an alfentanil (target blood concentration 25 ng/mL) or remifentanil (1–1.5 ng/mL) infusion, although propofol plus topical anesthesia is sufficient. The use of a laryngeal mask enables faster turnaround times and reduces the cough associated with extubation. It provides a stable, easily controlled anesthetic with rapid recovery and a low incidence of nausea and vomiting.

Ventilation

The traditional method involves endotracheal intubation, although controlled ventilation is possible with laryngeal masks, combining the benefits of not intubating with a paralyzed patient. Suxamethonium is avoided, if possible, as a transient rise in intraocular pressure occurs

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5 THE LENS

with its use. Short-acting nondepolarizers are used in preference along with an induction agent. Maintenance consists of using a volatile agent of choice or a propofol infusion. Although changeovers may be slower, especially if single handed, this technique also provides a stable, easily controlled anesthetic and is the method of choice for certain patients for whom spontaneous respiration is inappropriate (e.g., the obese and patients who cough despite adequate anesthetic).

Conclusion

Both spontaneous respiration and ventilation methods are suitable for day-case anesthesia. They are both widely used in all other specialties. Both propofol and the new volatile agents sevoflurane and desflurane provide a rapid and clear-headed recovery. Hypotension needs to be aggressively treated with vasoconstrictors such as ephedrine or metaraminol, to minimize morbidity. The advantages and disadvantages of general anesthesia are given in Box 5-6-5.

POSTOPERATIVE CARE FOR BOTH LOCAL AND GENERAL ANESTHESIA Cataract extraction by phakoemulsifcation is relatively pain free. In the majority of cases, simple analgesics are sufficient. Non-steroidal anti-inflammatory drugs can be used with caution in the elderly. These can be given orally, intravenously, or rectally and topically. Topical nonsteroidal analgesics can decrease pain and inflammation55 and have been shown to be equally effective in reducing the inflammatory response when compared with corticosteroids, with fewer side effects. Corticosteroids can be reserved for cases with more severe inflammation.56 Topical local anesthesia can be used as an adjunct as well, as it reduces systemic anesthetic requirements. This may help reduce postoperative nausea and vomiting by avoiding the use of opiates, although opiates are rarely needed for pain relief with this type of surgery. Propofol also has antiemetic properties.

REFERENCES

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1. Fisher SJ, Cunningham RD. The medical profile of cataract patients. Geriatr Clin North Am. 1985;1:339–44. 2. Guise P. Aeroplanes rarely crash nowadays, therefore they don’t need pilots: anaesthesia, anaesthetics and cataract surgery. Clin Exp Ophthalmol. 2005;33:451–2. 3. Hu FB, Hankinson SE, Stampfer MJ, et al. Prospective study of cataract extraction and the risk of coronary heart disease in women. Am J Epidemiol. 2001;153:875–81. 4. The Royal College of Anaesthetists & The Royal College of Ophthalmologists. Local anesthesia for intraocular surgery. London: Royal College of Anaesthetists & The Royal College of Ophthalmologists; July, 2001. 5. Jonas JB, Pakdaman B, Saunder G. Cataract surgery under systemic anticoagulant therapy with coumarin. Eur J Opthalmol. 2006;16:30–2. 6. Hirschman DR, Morby LJ. A study of the safety of continued anticoagulation for cataract surgery patients. Nurs Forum. 2006;41:30–7. 7. Ong-Tone L, Paluck EC, Hart-Mitchell RD. Perioperative use of warfarin and aspirin in cataract surgery by Canadian Society of Cataract and Refractive Surgery members: survey. J Cataract Refract Surg. 2005;31:991–6. 8. MacPherson R. Structured assessment tool to evaluate patient suitability for cataract surgery under local anaesthesia. Br J Anaesth. 2004;93:521–4. 9. The Royal College of Anaesthetists. Guidance on the Provision of Ophthalmic Anaesthesia Services, Ch 10. London: The Royal College of Anaesthetists; 2004:49–52. 10. Tan CS, Eng KG, Kumar CM. Visual experiences during cataract surgery: what anaesthesia providers should know. Eur J Anaesthesiol. 2005;22:413–9. 11. Voon LW, Au Eong KG, Saw SM, et al. Effect of preoperative counseling on patient fear from the visual experience during phakoemulsification under topical anesthesia: Multicenter randomized clinical trial. J Cataract Refract Surg. 2005;31:1966–9. 12. Leo SW, Lee LK, Au Eong KG. Visual experience during phacoemulsification under topical anaesthesia: a nationwide survey of Singapore ophthalmologists. Clin Exp Ophthalmol. 2005;33:578–81. 13. Ruschen H, Bremner F, Carr C. Complications after subTenon’s eye block. Anesth Analg. 2003;96:273–7. 14. Rosenfield S, Litinski S, Snyder D, et al. Effectiveness of monitored anaesthesia care in cataract surgery. Ophthalmology. 1999;108:1256–61. 15. Brymerski J. Loco standby anaesthesia during ophthalmological surgery in local anaesthesia. Klin Oczna. 2004;106:609–11. 16. Zakrzewski PA, Friel T, Fox G, Braga-Mele R. Monitored anesthesia care provided by registered respiratory care practitioners during cataract surgery: a report of 1957 cases. Ophthalmology. 2005;112:272–7. 17. Heindl B. Frequency of intervention and risk factors in monitored anesthesia care in ophthalmic surgery – a retrospective analysis. Anasthesiol Intensivmed Notfallmed Schmerzther. 2005;40:340–4. 18. Eichel R, Goldbery I. Anaesthesia techniques for cataract surgery: a survey of delegates to the Congress of the International Council of Ophthalmology, �� 2002. Clin Exp Ophthalmol. 2005; 33:469–72. 19. Pac-Soo CK, Deacock S, Lockwood G, et al. Patientcontrolled; sedation for cataract surgery using peribulbar block. Br J Anaesth. 1996;77:370–4.

20. Abdalla MI, Al Mansouri F, Bener A. Dexmedetomidine during local anesthesia. J Anesth. 2006;20:54–6. 21. Dal D, Demirtas M, Sabin A, et al. Remifentanil versus propofol sedation for peribulbar anesthesia. Middle East J Anesthesiol. 2005;18:583–93. 22. Irle S, Luckefahr MH, Tomalla M. Topical anesthesia as routine procedure in cataract surgery – evaluation of pain and complications in 1010 cases. Klin Monatsbl Augenheilkd. 2005;222:36–40. 23. Srinivasan S, Fern AI, Selvaraj S, Hasan S. Randomised double-blind clinical trail comparing topical and subTenon’s anaesthesia in routine cataract surgery. Br J Anaesth. 2004;93:683–6. 24. Ruschen H, Celaschi D, Bunce C, Carr C. Randomised control trial of sub-Tenon’s block versus topical anaesthesia for cataract surgery: a comparison of patient satisfaction. Br J Ophthalmol. 2005;89:291–3. 25. Nicholson G, Mantovani C, Hall GM. Topical anaesthesia for cataract surgery. Br J Anaesth. 2001;86:900. 26. Anderson NJ, Nath R, Anderson CJ, Edelhauser HF. Comparison of preservative free bupivacaine vs. lidocaine for intrameral anesthesia: a randomized clinical trial and in vitro analysis. Am J Ophthalmol. 1999;127:393–402. 27. Hamilton RC. Techniques of orbital regional anesthesia. Br J Anaesth. 1995;75:88–92. 28. Edge R, Navon S. Scleral perforation during retrobulbar and peribulbar anesthesia: risk factors and outcome in 50 000 consecutive injections. J Cataract Refract Surg. 1999;25:1237–44. 29. Coelho RP, Weissheimer J, Romao E, Velasco e Cruz AA. Pain induced by phacoemulsion without sedation using topical or peribulbar anesthesia. J Cataract Refract Surg. 2005;31:385–8. 30. Deruddre S, Benhamou D. Medial canthus single-injection peribulbar anesthesia: a prospective randomized comparison with classic double-injection peribulbar anesthesia. Reg Anesth Pain Med. 2005;30:255–9. 31. Kleinman B, Perlman J, Anderson C, et al. A collaborative regional ocular anesthesia training program: successes and failures. J Clin Anesth. 1999;11:301–4. 32. Bedi A, Carabine U. Peribulbar anaesthesia: a doubleblind comparison of three local anaesthetic solutions. Anaesthesia. 1999;54:67–71. 33. Di Donato A, Fontana C, Lancia F, Celleno D. Efficacy and comparison of 0.5% levobupivacaine with 0.75% ropivacaine for peribulbar anaesthesia in cataract surgery. Eur J Anaesthesiol. 2006;Mar 1:1–4. 34. Allman KG, McFaden JG, Armstrong J, et al. Comparison of articaine and bupivacaine/lidocaine for single medial canthus peribulbar anaesthesia. Br J Anaesth. 2001;87:584–7. 35. Ozdemir M, Ozdemir G, Zencirci B, Oksuz H. Articaine versus lidocaine plus bupivacaine for peribulbar anaesthesia in cataract surgery. Br J Anaesth. 2004;92:231–4. 36. Hameda S, Devys JM, Xuan TH, et al. Role of hyaluronidase in diploplia after peribulbar anaesthesia for cataract surgery. Ophthalmology. 2005;112:879–82. 37. Frieman BJ, Friedberg MA. Globe perforation associated with subtenon’s anesthesia. Am J Ophthalmol. 2001;131:520–1. 38. Kim JH, Yang SM, Kim HW, Oh J. Inadvertent ocular perforation during lid anesthesia for hordeolum removal. Korean J Ophthalmol. 2006;20:199–200.

39. Modarres M, Parvaresh MM, Hashemi M, Peyman GA. Inadvertent globe perforation during retrobulbar injection in high myopes. Int Ophthalmol. 1997–1998; 21:17–85. 40. Berglin L, Stenkula S Algvere PV. Ocular perforation during retrobulbar and peribulbar injections. Ophthalmic Surg Lasers. 1995;26:429–34. 41. Grizzard WS, Kirk NW, Pavan PR, et al. Perforating ocular injuries caused by anesthesia personnel. Ophthalmology. 1991;98:1011–6. 42. Wearne MJ, Flaxel CJ, Gray P, et al. Vitreoretinal surgery after inadvertent globe penetration during local ocular anesthesia. Ophthalmology. 1998;105:371–6. 43. Duker JS, Belmont JB, Benson WE, et al. Inadvertent globe perforation during retrobulbar and peribulbar anesthesia. Patient characteristics, surgical management and visual outcome. Ophthalmology. 1991;98:519–26. 44. Gillow JT, Aggarwal RK, Kirby GR. Ocular perforation during peribulbal anaesthesia. Eye. 1996;10:533–6. 45. Rosenthal G, Bartz-Schmidt KU, Engels B, et al. Primary use of silicone oil tamponade in the management of perforating globe injury secondary to inadvertent local anaesthesia injection for ophthalmic surgery. Int Ophthalmol. 1997–1998;21:349–52. 46. Eke T, Thompson J. Severe adverse events associated with local anaesthesia for cataract surgery in the UK and Ireland. Abstract presented at the World Congress of Ophthalmic Anaesthesia, 15 April 2004, London. 47. Kumar CM, Williamson S, Manickham B. A review of subTenon’s block; current practice and recent development. Eur J Anaesthesiol. 2005;22:567–77. 48. Alwitty A, Koshy Z, Browning AC, et al. The effect of sub-Tenon’s anaesthesia on intraocular pressure. Eye. 2001;27:1221–6. 49. Ripart J, Lefrant J-Y, Vivien B, et al. Ophthalmic regional anesthesia medial canthus episcleral (sub-Tenon) anesthesia is more efficient than peribulbar anesthesia. Anesthesiology. 2000;92:1278–85. 50. Parkar T, Gogate P, Deshpane M, et al. Comparison of sub-Tenon anaesthesia with peribulbar anaesthesia for manual small incision cataract surgery. Indian J Ophthalmol. 2005;53:255–9. 51. Mukherji S, Esakowitz L. Orbital inflammation after sub-Tenon’s anesthesia. J Cataract Refract Surg. 2005;31:2221–3. 52. Kubitz J, Epple J, Bach A, et al. Psychomotor recovery in very old patients after total intravenous anaesthesia for cataract surgery. Br J Anaesth. 2001;86:203–8. 53. Weilbach C, Scheinichen D, Thissen U, et al. Anaesthesia in cataract surgery for elderly people. Anasthesiol Instensivmed Notfallmed Schmerzther. 2004;39:276–80. 54. Weibach C, Scheinichen D, Raymondos K, et al. Assessment of anesthesia methods in ophthalmologic surgery by patients, surgeons and anesthesiologists. Ophthalmologe. 2005;102:783–6. 55. Goguen ER, Roberts CW. Topical NSAIDS to control pain in clear corneal cataract extraction. Insight. 2004;29(3):10–1. 56. Simone J, Whitacre M. Effects of anti-inflammatory drugs following cataract extraction. Curr Opin Ophthalmol. 2001;12:1263–7.

PART 5 THE LENS

5.7

Phacoemulsification David Allen

Key features n n n n

n n

TORSIONAL PHACOEMULSIFICATION USING THE KELMAN TIP

hanging phaco “power” is achieved by changing the stroke length C of needle vibration, not by changing the frequency. It is not possible to directly compare phaco “power” used between different manufacturers’ machines. While still controversial, evidence is accumulating that direct mechanical action is the most important factor in phacoemulsification. Power modulation significantly increases the efficiency of longitudinal phaco as well as improving the thermal safety. It is less important with the new torsional phaco. Modern pump systems are very efficient and high vacuums can be achieved very quickly with modern flow-based (peristaltic) systems. In a flow-based machine the aspiration flow rate can be adjusted completely independently of the preset vacuum limit. In a vacuum-based (venturi) machine the aspiration flow rate is generated by the pressure difference between the vacuum chamber and the eye. Therefore, the two cannot be completely dissociated and a high vacuum will always result in higher flow rates than a lower vacuum. Modern machines use a variety of strategies to minimize post occlusion surge. Postocclusion surge potential is directly related to the maximum set vacuum for any given needle/sleeve/tubing complex.

INTRODUCTION As surgical techniques for the removal of cataract and drug modulation of the consequent biological responses have become more refined, the problems of postoperative infection and inflammation are less prominent in the thinking of lens surgeons. As a consequence, it has become possible to concentrate on the further refinement of the actual process of lens removal. Phacoemulsification (phaco) offers the surgeon the possibility to break the nucleus into smaller pieces and even into a fine emulsion of material, all of which can be removed through the probe used to achieve the break-up. As a result, it is now possible to minimize trauma to the structures of the eye and to have minimal impact on its shape as a consequence of modern cataract surgery. Achieving this, however, requires the use of very powerful tools. Unfortunately, many surgeons fail to understand the principles that underlie the machines they use. As a consequence of this relative ignorance, the surgery is sometimes performed less efficiently and possibly more dangerously than necessary.

Historical Review

In February 1965 Charles Kelman propounded the view that the ultrasonic tool used at that time by some dentists to help descale teeth could also be used to fragment the nucleus of the crystalline lens and allow its removal without the need for a large incision. This liberated a powerful force, previously untried within the eye, but the equipment involved was large, inefficient, and extremely heavy. Nevertheless, he and others persevered.1–4 Kelman’s first operation using phaco on a human eye took 3 hours. At that time the patients were either left aphakic or the incision needed considerable enlargement to allow insertion of the then relatively new, rigid intraocular lenses (IOLs). Three developments − the technological progress of

axis of rotation

incision

cutting edge

Fig. 5-7-1 Torsional phacoemulsification using the Kelman tip. Diagram to show how torsion around the center of the shaft is translated into a sweeping motion at the tip of the Kelman phaco needle. (Drawing courtesy of Alcon Surgical.)

the 1970s and 1980s (particularly in solid-state electronic control mechanisms), new surgical techniques (particularly continuous curvilinear capsulorrhexis5), and the development of high-quality, foldable IOLs6 − acted synergistically to enable the development of modern phaco surgery despite the considerable early resistance to this new technique.7 Surgeons are now presented with increasingly sophisticated equipment that allows much more control of the surgical process. Understanding the basic principles of the equipment allows the surgeon to maximize this potential.

HANDPIECES AND TIPS The phaco handpiece houses an ultrasonic transducer − a device that converts electrical energy into mechanical vibratory energy. Some crystals exhibit a relationship between mechanical stress and electricity − they are piezoelectric. If an electric charge is applied to opposite faces of these crystals, a strain appears in the structure, which results in deformation. Standard handpieces couple the crystal to the phaco-tip in such a way that the tip moves backwards and forwards when the crystals deform. Recently, Alcon Surgical (Fort Worth, TX, USA) have introduced a handpiece (OZil) that can cause the tip to tort or twist when the crystals deform. It is constructed in such a way that when oscillating at 36 kHz the crystals produce torsion and when stimulated at 43 kHz they produce traditional linear movement. If a tip with a bend in the shaft (e.g., Kelman tip) is attached to such a handpiece, then the twisting of the shaft is converted into a sweeping side-to-side motion at the end of the tip (Fig. 5-7-1).

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The frequency at which a handpiece is set to work depends on the design and materials used. For each combination of mass and material a particular frequency exists at which the transducer works most efficiently. Adjustment of the power setting on the machine affects the stroke length (the distance traveled by the tip during one cycle) but not the frequency. Power is expressed as a percentage of the maximum travel the crystal-tip complex can produce. It is clear that if the frequency remains constant but the distance traveled in each stroke increases, the acceleration of the tip and the maximum speed it reaches must be greater. It is now possible to have the control unit continually “autotune” the handpiece: small adjustments can be made to compensate for the effects of changes in temperature, in the mass in contact with the tip, etc. Machines that use this principle vary the electrical power delivered to the crystals so that for a given commanded power the stroke length remains constant regardless of whether the tip is in a fluid medium or in contact with a very hard nucleus. It is important to recognize that the power settings on the machine console are indicative only. Some systems have a nonlinear relation between commanded power and stroke length. The smallest stroke (at minimum power setting) also varies among systems. In one commercially available system, 20% power produces tip travel of 50 μm, whereas this travel is reached only at 60% power in another machine. As a consequence, any comparisons between the ‘efficiency’ of different phaco machines based on comparisons of ‘power used’ are spurious. The physical mechanisms that break up nuclear material when a phaco tip is used have been difficult to elucidate, and until recently the relative importance of the various factors has been unclear.8, 9 We now know that the direct mechanical hammer-like effect of the extremely hard titanium tip coming into contact with the lens material is probably the most important. A phaco tip operated at a frequency of 44 kHz has a maximum speed of 66 ft/second (20 m/second) when operated at full power, and the acceleration of the tip is > 168 300 ft/second2 (> 51 000 m/second2). Under these conditions, direct impact of the tip breaks frictional forces within the nuclear material. This direct effect is reduced, however, by the forward-propagating acoustic waves or fluid and particle waves generated by the tip, which tend to push away any piece of nucleus in contact with the tip. However, it is possible that the acoustic shock waves themselves tend to weaken or break some of the bonds that hold nuclear material together. The role of cavitation in breaking down lens material has recently been shown to be insignificant. In a laboratory study of phacoemulsification performed in a hyperbaric chamber, the effectiveness of phaco was seen to be undiminished in conditions were cavitation was suppressed.10 Various tip designs are available for the surgeon, but there are three key design variations. The Kelman tip has a 22° angle in the tip shaft 3.5 mm from the tip. This design is thought to enhance the emulsification action of the tip, as well as allowing the surgeon to use it as a manipulator. Some tips have a flared termination of the tip (i.e., the outer diameter at the end of the tip is greater than that 1–2 mm behind). This again is thought to enhance the emulsification, but also the inner lumen has a restriction behind the flare that helps to suppress postocclusion surge. Some tips have fluting along the outside of the shaft that allows some fluid to continue to inflow, even if the silicone irrigation sleeve is compressed onto the shaft. This reduces the possibility of thermal damage in the incision.

POWER MODULATION

448

While some form of simple power modulation (pulsed phaco) has been available for a long time, the introduction in 2001 of the Whitestar software for the AMO Sovereign phaco machine (Advanced Medical Optics, Santa Ana, CA, USA) marked a paradigm shift in the way surgeons controlled the application of phaco power. Break-up of phaco into pulses or bursts has two advantages. First, the pauses (off period) allow the machine fluidics to pull material back into contact with the tip following repulsion caused by the jack-hammer effect in traditional longitudinal phaco. Second, the pauses prevent significant build-up of heat due to frictional movement within the incision, making thermal damage to the cornea less likely. Several machines now allow almost infinite variation of both duty cycle (the ratio of on-time to off-time) and the length of the on period. It has been shown that such power modulation significantly improves the ‘efficiency’ of phacoemulsification (i.e., quicker surgery and reduced amount of phaco energy used).11 The Whitestar software already mentioned has a specific occlusion mode whereby, if it is selected, the machine can make adjustments to the power modulations when occlusion is detected.

VACUUM RISE-TIME

vacuum 800 (mmHG) 700 600 500 400 300 200 100 0

0.5

ASP rate 20 mL/minute ASP rate 40 mL/minute ASP rate 60 mL/minute

1.5

2.5

time (seconds)

Fig. 5-7-2 Vacuum rise-time as a function of aspiration rate. Graph showing the effect of increasing aspiration rate (pump speed) on the time to reach certain vacuum levels.

When first introduced, pulses had a fixed duty cycle of 50% (i.e., the period with power on and with power off were equal) but power was variable, while bursts were of fixed width, usually with fixed power also. Now, with the enhanced modulations possible on several platforms, this distinction has become blurred and it is probably no longer helpful to try to distinguish between them in advanced machines.

PUMPS AND FLUIDICS The function of the phaco pump is twofold: to hold the nucleus onto the tip and to remove debris created by the tip. With modern techniques the pump is also increasingly used to aspirate directly the softer parts of the nucleus. There are two pump principles in general use − flow-driven and vacuum-driven. A hybrid type of pump was briefly available in the Concentrix module of the Bausch & Lomb Surgical (Rochester, NY, USA) Millennium phaco machine. At least one manufacturer is developing a vacuum pump that can be used as a flow-driven pump if required.

Flow Based (Peristaltic)

Roller pumps that rotate against compressible tubing or membrane generate flow; this “milks” fluid along the lumen and creates a pressure gradient between pump and anterior chamber. Recent design changes in the pumps and sophisticated microprocessor controls have resulted in powerful and well-controlled pump systems. Although the earlier peristaltic systems had a reputation for being unresponsive, modern systems are capable of producing a 500 mmHg (66.5 kPa) vacuum in under 1 second. The rate at which fluid is aspirated through the unoccluded phaco tip is set at the machine console in milliliters per minute. A low value allows events within the anterior chamber to happen slowly; a high value speeds up events and generates more “pulling power.” Fine adjustments of flow, by changing the speed at which the pump turns, allow for personal surgical style or different operating conditions. Recent advanced systems sense when the tip is occluded partially and then make adjustments to the pump to compensate for reduced aspiration. The second pump parameter that can be adjusted is the vacuum level at which, once achieved, the pump stops. When the tip becomes occluded, the pump continues to turn and move fluid into the cassette, lowering the pressure in the tubing between tip and cassette. Once the preset vacuum has been reached, the pump effectively stops for as long as that vacuum level holds. The rate at which the maximum set vacuum level is reached is directly proportional to the flow rate, so that for a particular machine a level of 460 mmHg is reached in 1.0 second when the flow rate is set at 20 mL/min but reaches 470 mmHg in 0.5 seconds when it is set at 40 mL/min (Fig. 5-7-2).

Vacuum Based

Anterior Chamber hydrodynamics

It is important to understand the correct meaning of various terms used to describe the fluid dynamics of phaco. Normally, “flow” is used to mean evacuation flow out of the eye. Fluid also flows out of the eye at a variable rate through the incisions. To avoid confusion, if flow into the eye is being described, it is necessary to use the term “inflow.” The rate of fluid inflow is determined by the height difference between the drip chamber of the fluid reservoir and the eye. Inflow is almost always passive; it is modulated by the resistance of the tubing and by any compression of the inflow sleeve around the phaco tip. It is essential that the inflow potential (the maximum possible under free-flow conditions) at least equals, and if possible exceeds, the maximum transient outflow (combined incisional flow and machine-generated flow), otherwise anterior chamber collapse occurs. “Vacuum” is taken to mean the preset maximum vacuum level indicated on the console. In neither peristaltic nor vacuum-based systems is the vacuum present in the anterior chamber. In traditional longitudinal phaco, an active phaco tip (power applied) produces forces that push material away from it. This is countered by the vacuum that holds the material to the tip. The new torsional phaco mode (Alcon) generates a sweeping horizontal movement without repulsion, and lower vacuums can be used. When a surgeon uses a technique that involves sculpting (e.g., “divide and conquer”12 or “stop and chop”13), a relatively low flow (≤ 20 mL/min), with no tip occlusion, is required. The low flow allows sculpting near or even onto the capsule,

5.7 Phacoemulsification

These systems generate an adjustable level of vacuum in a chamber in the machine: usually a Venturi pump is used. It is the pressure difference between this chamber and the tip that generates flow. Once the tip is occluded, fluid continues to be removed from the tubing until the pressure within it equals that in the vacuum chamber. It is possible, however, to introduce a damping effect into the system so that the equilibration of pressures does not take place instantaneously. In a standard vacuum system, because the flow rate is generated by the pressure gradient, increasing the vacuum increases the flow and vice versa. These two parameters cannot normally be modulated independently, although this will be possible with a new vacuum pump in development.

without the risk of drawing the capsule into the port, and a tip slope of 30° or 45° allows the surgeon both to see the tip and to minimize occlusion potential. For subsequent nucleus fragment consumption (or initially in chop techniques), a high flow (20–40 mL/min) is required to pull the nucleus toward the tip, along with high vacuum (200–600 mmHg) to hold it in contact for emulsification. Occlusion in these circumstances is enhanced by rotation of the tip so that the opening is aligned with the edge of nucleus being grasped, or by using a 0° tip. Many phaco systems now offer the surgeon the opportunity to adjust the fluidics performance, particularly vacuum rise-time, once occlusion has been achieved. Some surgeons, for example, continue to prefer relatively low aspiration flow rates during the acquisition of nucleus fragments, but set the machine to significantly increase the flow rate (and hence speed of achieving the preset vacuum) once the tip is occluded. Another example would be the reduction in flow rate on occlusion that some surgeons use when dealing with very soft cataracts or epinucleus. Since 2001 many surgeons have become interested in the concept of micro-incisional phaco. This was first performed in a biaxial mode; the infusion was dissociated from what became a ‘bare’ aspiration tip by use of a separate cannula inserted through a separate incision. Each incision is only 1−1.5 mm wide, and there are a number of IOLs that can be inserted through sub 2 mm incisions. The reduced maximum incision size results in smaller changes to corneal curvature induced by the surgery. Another theoretical advantage is that in coaxial phaco, the infusion ports in the infusion sleeve around the phaco tip are positioned close to the aspiration port and therefore can create turbulent flow that can disrupt the attractive force generated by aspiration. Until recently these forces, which can be disruptive to the attractive aspiration force, have been unavoidable and therefore ignored. However, the main advantage of biaxial phaco is that these forces are now separated. Critics of biaxial surgery point to the degraded fluidics that may be produced by a nonconforming bare solid cannula passing through a corneal incision; either incisional leakage must be significant, or the incision is so tight as to risk significant tearing of corneal stroma and Descemet’s membrane. New sleeves for coaxial microincision phaco have now been developed that allow coaxial phaco to be performed through 2 mm incisions or smaller. This has been achieved by a combination

IOP DURING POSTOCCLUSION CYCLE

lOP

occlusion breaks high outflow reduces lOP

unobstructed flow

partial occlusion

full occlusion

infusion recovers lOP

AC recovery

unobstructed flow

Fig. 5-7-3 Intraocular pressure (IOP) during postocclusion surge. IOP initially maintained by bottle height. Slight rise when tip occluded. When occlusion breaks, large pressure difference between tubing and anterior chamber (AC) results in rapid outflow of fluid causing IOP to drop rapidly until infusion restores “normal” IOP.

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5 THE LENS

of modifications: reduced internal diameter, thinner walls, and an ultra smooth external surface reducing resistance to insertion into a small incision. Whether using biaxial or coaxial microincision techniques, it is important that surgeons understand the importance of fluidics, and ensure that the inflow potential through the reduced sleeve or the separate infusion instrument is greater than the maximum outflow during postocclusion surge with their particular combination of machine, needle, and vacuum settings.

POSTOCCLUSION SURGE With any pump design, in the occluded state, vacuum is generated in the lumen of the tubing. In an unmodulated system, when the occlusion breaks, fluid rushes into the tubing to equilibrate the pressure difference between the anterior chamber and the lumen − “postocclusion surge” (Fig. 5-7-3). During the period of occlusion, the walls of the tubing tend to collapse in proportion to the increase in vacuum. On

r elease of the occlusion the tubing re-expands and often rebounds, which results in a larger postocclusion surge. In addition, if the foot pedal is still in position two (i.e., irrigation and aspiration), the pump may immediately begin to turn. The difference between the outflow surge and the compensating inflow from the irrigation bottle determines the stability of the anterior chamber. Modern phaco systems use a variety of strategies to reduce the problems associated with postocclusion surge. The internal diameter of both the phaco needle (and any restrictions such as seen in the flared needle) and outflow tubing modulate the outflow surge. More rigid outflow tubing reduces the rebound effect. The effective inflow diameter (the gap between the outer wall of the tip and the inner wall of the sleeve in coaxial phaco, or the internal diameter and outflow port diameters of the irrigation instrument in biaxial phaco), along with the bottle height, determines the amount of inflow and how well it compensates for surge. Finally, frequent sampling of the pressure in the inflow and outflow lines can be used to predict or immediately detect outflow surge, and pump behavior can be modified.

REFERENCES 1. K elman C. Phaco-emulsification and aspiration. A new technique of cataract removal. A preliminary report. Am J Ophthalmol. 1967;64:23–35. 2. Kelman C. Cataract emulsification and aspiration. Trans Ophthalmol Soc UK. 1970;90:13–22. 3. Kraff MC, Sanders DR, Lieberman HL. Total cataract extraction through a 3-mm incision: a report of 650 cases. Ophthalmic Surg. 1979;10:46–54. 4. Cohen SW, Kara G, Rizzuti AB, et al. Automated phakotomy and aspiration of soft congenital and traumatic cataracts. Ophthalmic Surg. 1979;10:38–45. 5. Gimbel HV, Neuhann T. Development, advantages, and methods of the continuous circular capsulorrhexis technique. J Cataract Refract Surg. 1990;16:31–7.

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6. A llarakia L, Knoll RL, Lindstrom RL. Soft intraocular lenses. J Cataract Refract Surg. 1987;13:607–20. 7. Illiff CE. Phacoemulsification − why? Trans Am Acad Ophthalmol Otolaryngol. 1977;83:213–15. 8. Pacifico RL. Ultrasonic energy in phacoemulsification: mechanical cutting and cavitation. J Cataract Refract Surg. 1994;20:338–41. 9. Davis PL. Mechanism of phacoemulsification. Letter to the editor. J Cataract Refract Surg. 1994;20:672–3. 10. Zacharias J. Role of jackhammer effect and cavitation in phacoemulsification. Presented at ASCRS Annual Meeting, San Francisco, USA, March 18–22, 2006.

11. A llen D. Power modulation with the Alcon Infiniti lens system. Presented at ASCRS Annual Meeting, San Diego, USA, May 1–5, 2004. 12. Gimbel HV. Divide and conquer nucleofractis phacoemulsification: development and variations. J Cataract Refract Surg. 1991;17:281–91. 13. Koch PS, Katzen LE. Stop and chop phacoemulsification. J Cataract Refract Surg. 1994;20:566–70.

PART 5 THE LENS

Refractive Aspects of Cataract Surgery

5.8

Emanuel S. Rosen

Key features n n n n n n

nderstand corneal shape pre operation. U Value of corneal topography in lens surgery. Prevent induced corneal astigmatism. Treat astigmatism post operation. By incisions. By corneal laser surgery.

INTRODUCTION When Sir Harold Ridley implanted a human eye with a replacement lens (intraocular lens, IOL) in 1949 he initiated the changing role of cataract surgery.1 As IOL implantation technology matured over the following years, cataract surgery became more than just removing a clouding crystalline lens; it allowed the replacement IOL to be varied to adjust the intrinsic refractive error or ametropia. In other words, there are two strategies for surgical intervention: first removing the impediment of a cataractous lens and then simultaneously incorporating an IOL of measured dioptric power to neutralize existing ametropia. Of course, there are many other aspects to the refractive aspects of cataract surgery. Accurate biometry is vital and readers are referred to that aspect of cataract management in general in Chapter 10-12 in this volume. Cataract surgery in eyes that have previously undergone corneal refractive surgery require special formulae to calculate the correct IOL power after keratometric values have been changed by that surgery. Astigmatism management is a fundamental refractive need in cataract surgery and will be considered here. Latterly, with the advent of clinical aberrometers and their application in refractive surgery, cataract replacement is now taking advantage of the deeper understanding of the relationship, in a refractive sense, between the cornea and the lens. Near, intermediate and distance vision needs have to be satisfied by lens replacement, a task fulfilled by emergent multifocal IOL technology, pseudo-accommodative IOLs, and the future fulfillment of true accommodating IOLs. The bases for refractive correction as an aspect of cataract surgery are accurate biometry on the one hand and corneal topography on the other.

CORNEAL INCISIONS Tejedor and Murube2 investigated the best location of clear cornea incision in phacoemulsification, depending on pre-existing corneal astigmatism in a randomized clinical trial and noncomparative interventional case series. Five hundred and seventy-four patients in five stages were assigned to the following types of incision: superior or temporal (n = 89), superior (n = 141), superior or superior plus relaxing (n = 102), nasal or temporal (n = 156), and incisions based on applying the conclusions of preceding and current studies (n = 86). Visual acuity, refraction, biomicroscopy, keratometry, and videokeratography (Fourier analysis) were performed before and after phacoemulsification and intraocular lens implantation through a 3.5 mm incision. In patients without corneal astigmatism, corneal changes induced were greater in superior than in temporal incisions. After a superior incision (preoperative steep

eridian at 90°), a shift of 90° away was less likely with at least 1.5 D m of astigmatism. A perpendicular, relaxing, limbal incision decreased corneal changes. Nasal incisions induced greater corneal change than temporal incisions (preoperative steep meridian at 180°). A shift of this meridian 90° away was more likely with astigmatism < 0.75 D with temporal incisions and < 1.25 D with nasal incisions. In summary, for cataract clear corneal incisions: l A superior incision is recommended for at least 1.5 D of astigmatism with a steep meridian at 90° l A temporal incision is recommended for astigmatism less than 0.75 D and steep meridian at 180° l A nasal incision is recommended for at least 0.75 D of astigmatism with a steep meridian at 180° Beltrame et al.3 compared astigmatic and topographic changes induced by different oblique cataract incisions in 168 eyes having phacoemulsification, which were randomly assigned to one of three groups: 3.5 mm clear corneal incision (CCI), 60 eyes (see Figs 5-8-1 to 5-8-7 for similar examples); 5.5 mm sutured CCI, 54 eyes; 5.5 mm scleral tunnel, 54 eyes. Incisions lay on the 120° semi-meridian. Corneal topography was performed preoperatively and 1 week and 1 and 3 months postoperatively. Simulated keratometric readings were used to calculate astigmatism amplitude and surgically induced astigmatism (SIA). Postoperative topographic changes were determined by subtracting the preoperative from the postoperative numeric map readings. At 3 months postoperatively, the mean SIA in the right and left eyes, respectively, was 0.68 D ± 1.14 (SD) and 0.66 ± 0.52 D in the 3.5 mm CCI group, 1.74 D ± 1.4 D and 1.64 ± 1.27 D in the 5.5 mm CCI group, and 0.46 ± 0.56 D and 0.10 ± 1.08 D in the scleral tunnel group. Right and left eyes showed similar SIA amplitude but different SIA axis orientation. The SIA was significantly higher in the 5.5 mm CCI group than in the other two groups 1 and 3 months postoperatively (p < 0.01). All groups showed significant wound-related flattening and nonorthogonal steepening at two opposite radial sectors. Topographic changes were significantly higher in the 5.5 mm CCI group and significantly lower in the scleral tunnel group. Right and left eyes showed similar SIA amplitude but different SIA axis orientation and topographic modifications, probably because of the different superotemporal and superonasal corneal anatomic structure. The 5.5 mm CCI induced significantly higher postoperative astigmatism, SIA, and topographic changes.

ASTIGMATIC INCISIONS Limbal Relaxing Incisions

Kaufmann et al.4 compared limbal relaxing incisions (LRIs) with placement of the corneal cataract incision on the steepest keratometric meridian for the reduction of pre-existing corneal astigmatism at the time of cataract surgery. In a prospective single-center study, patients having 1.5 D or more of keratometric astigmatism were randomly assigned to two surgical techniques: on-steep meridian incisions (SMIs) consisting of a single clear corneal cataract incision centered on the steepest corneal meridian; or LRIs consisting of two arcuate incisions straddling the steepest corneal meridian and a temporal clear corneal incision. Vector analysis of the target axis flattening effect was used to assess the efficacy of treatment. The eyes of 71 patients were evaluated, 33 in the SMI group and 38 in the LRI group. Six weeks postoperatively, the flattening effect was 0.41 D (median and interquartile range 0.15−0.78 D) in the

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5 THE LENS

SMI group and 1.21 D (range 0.43−2.25 D) in the LRI group (p = 0.002). After 6 months, the flattening effect was 0.35 D (range 0−0.96 D) and 1.10 D (range 0.25−1.79 D), respectively (p = 0.004), thus confirming that the amount of astigmatism reduction achieved at the intended meridian was significantly more favorable with the LRI technique, which remained consistent throughout the follow-up period.

LARGE CLEAR CORNEAL INCISION

Opposite Clear Corneal Incisions (OCCIs)

Lever and Dahan5 were the first surgeons to demonstrate that in cataract surgery, the clear corneal incision (CCI) has a small flattening effect on corneal curvature, which can be used to reduce pre-existing astigmatism (PEA). Adding an identical, penetrating CCI opposite the first one enhances the flattening effect. The extent of flattening affecting the optical zone of the cornea is dependent on the width of the clear corneal tunnel incision and the way it is constructed. Whilst an algorithm can be devised, in general it is incumbent upon each surgeon to devise his or her own algorithm as the location of the incision, the knife used, and the length of the tunnel are difficult to standardize. Suffice to say, the wider the incision and the more centrally it is placed the greater the effect it will have. The local flattening of the incision only has a central effect if it is wide enough. Figures 5-8-1 to 5-8-19 fully illustrate incisions, their effect, and the healing process as depicted by corneal topography and aberrometry. It is recommended that surgeons wishing to utilize the technique study the effects of their own clear corneal incisions through the medium of corneal topography and thereby derive a personal nomogram. Paired opposite CCIs (OCCIs) are placed on the steepest meridian in order to achieve a reduction in the dioptric power of the central cornea. One CCI is used to perform cataract surgery, and the opposite CCI is made to ensure symmetry of the flattening effect and therefore to modulate PEA. Lever & Dahan5 used 2.8−3.5 mm OCCIs in 33 eyes

O.Z

Fig. 5-8-3 Large clear corneal incision − more effect. O.Z, optical zone.

Fig. 5-8-4 3.7 mm clear corneal incision videokeratograph. Note localized flattening of cornea close to incision but affecting optical zone also. Fig. 5-8-1 Clear corneal incision (2.5 mm).

SMALL CLEAR CORNEAL INCISION

O.Z

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Fig. 5-8-2 Small clear corneal incision – no central effect. O.Z, optical zone.

Fig. 5-8-5 Topography map of 3.7 mm clear corneal incision. See videokeratograph Fig. 5-8-4. Map illustrates central effect of larger peripheral clear corneal incision with resulting nonorthogonal astigmatic hemimeridia.

5.8 Refractive Aspects of Cataract Surgery

Fig. 5-8-6 Topography map of 3 mm clear corneal incision. Peripheral flattening of cornea but no central effect. Fig. 5-8-9 Superior opposite clear corneal incision to correct 5 D astigmatism 50 degree arc length.

Fig. 5-8-7 Topography map of 2.5 mm clear corneal incision. No peripheral flattening of the cornea or central effect.

Fig. 5-8-10 Inferior opposite clear corneal incision to correct 5 D astigmatism 50 degree arc length.

OPPOSITE CLEAR CORNEAL INCISION

O.Z

Fig. 5-8-8 Opposite clear corneal incision to correct preoperative astigmatism. Diagram to illustrate symmetry of incisions designed to correct each half of the steep meridian bow tie.

Fig. 5-8-11 Postoperative topography map following opposite clear corneal incision for 5 D astigmatism. Note 4 hemimeridia but no manifest or topographic astigmatism

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5 THE LENS Fig. 5-8-12 Topographic map illustrating preoperative astigmatism OD (right eye) −15.5/+3.0 x 90. Fig. 5-8-13 Preoperative, postoperative, and difference topography maps to illustrate opposite clear corneal incision (OCCI) effect. OCCI OD −15.5/+3.0 x 90 Plano post-op (4.5 mm OCCI); effect of each OCCI illustrated by dotted lines.

Fig. 5-8-14 Preoperative, postoperative, and difference topography maps to illustrate opposite clear corneal incision effect. OCCI OD −15.5/+3.0 x 90 Plano postop (4.5 mm OCCI).

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with PEA greater than 2.00 D undergoing cataract surgery. The mean astigmatism correction achieved with this technique was 2.06 D. This technique is simple and effective and yields stable results that rival those of arcuate keratotomy. The OCCI technique has a potential application for the correction of astigmatism in general refractive surgery. Qam-mar and Mullaney6 evaluated the astigmatic correcting effect of OCCIs on the steep corneal meridian axis in 14 patients with cataracts. Fifteen eyes of 14 cataract patients with a mean age of 78.4 years ± 6.38 (SD) (range 69−90 years) were studied. The inclusion criterion was a topographic astigmatism of more than 2 D. Paired 3-step self-sealing opposite clear corneal incisions were made 1 mm anterior to the limbus on the steep meridian with a 3.2 mm keratome. One incision was used for standard phacoemulsification, and the other was left for astigmatic correction. The mean preoperative and postoperative topographic corneal astigmatism was 3.26 ± 1.03 D (range 2.30−5.80 D) and 2.02 ± 1.04 D (range 0.20−4.00 D), respectively. They achieved a mean astigmatic correction of 1.23 ± 0.49 D (range 0.30−2.20 D). The mean surgically corrected astigmatism by vector analysis was 2.10 ± 0.79 D (range 0.80−3.36 D).

As others have shown,5, 6 paired, opposite clear corneal incisions on the steep corneal meridian corrects astigmatism in cataract surgical eyes utilizing routine surgical instruments. Tadros et al.7 evaluated the effect of on-axis, opposite clear corneal incisions (OCCIs) in phacoemulsification on reducing preoperative corneal astigmatism and to predict the astigmatic outcome of the incisions in a prospective study on 103 patients who had on-steep meridian OCCIs as a part of routine phacoemulsification with foldable intraocular lens (IOL) implantation performed by one surgeon. Keratometry was done 6−8 weeks postoperatively. The differences in the preoperative and postoperative corneal astigmatism and corneal spherical equivalent (SE) were recorded. SIA was calculated using vector analysis. Tadros et al. showed that the mean reduction in corneal astigmatism was 0.50 D (p < 0.001). The mean SIA was 1.57 D (95% confidence interval (CI): 1.42 to 1.71). There was a weak association between the SIA and the patient’s age and axis of preoperative astigmatism. The mean change in SE was +0.02 D (95% CI: −0.08 to +0.12) indicating that steep meridian OCCIs are a reliable and practical way of reducing pre-existing corneal astigmatism. The change in SE was negligible and thus can be ignored during biometry.

5.8 Refractive Aspects of Cataract Surgery

Fig. 5-8-15 OS (left eye) pre-op OS +10.25/−4.5×175 = 6/6 post-op 6/6- , +1.25/−0.75×155 = 6/5. Note flattening of preoperative cylinder in difference map and residual nonorthogonal astigmatic hemimeridia but not significantly reflected in manifest refraction.

Fig. 5-8-16 Corneal aberrations post-op illustrating trefoil and coma aberrations. See topography map in Fig. 5-8-15.

l l l l l l

The features of OCCIs may be summarized as follows: OCCIs cause negligible effect on spherical equivalent and therefore do not influence biometric calculations Paired incisions are used for symmetrical effect Asymmetric OCCIs are used for asymmetric (bow tie) astigmatism OCCIs are to be placed on a steep corneal meridian The bulk of the cornea is preserved in case of the need for minor astigmatic correction by arcuate keratotomies OCCIs may also be referred to as opposite penetrating astigmatic keratotomies (OPAK)

Arcuate Corneal Incisions

Baykara M et al.8 investigated the refractive outcomes after arcuate keratotomy for astigmatism in 16 eyes of 11 patients with astigmatism who had arcuate keratotomies using the Terry astigmatome. The mean age of the patients was 36 years ± 10 (SD). The mean corneal astigmatism was −4.0 ± 1.1 D (range −2.2 to −6.0 D) preoperatively and −1.8 ± 0.8 D (range −0.6 to −3.0 D) postoperatively. The mean surgically

reduced corneal astigmatism was 2.5 ± 0.6 D without intraoperative or postoperative complications. Titiyal et al.9 evaluated the efficacy of paired intraoperative arcuate transverse keratotomies at a 7 mm-diameter zone along with a 3.5 mm clear corneal phaco tunnel on the steeper axis to correct pre-existing astigmatism in a prospective randomized case-control study on 34 eyes of 28 patients with age-related cataract. The patients were divided into two groups: in one group (17 eyes) intraoperative arcuate keratotomy was coupled with phacoemulsification on the steeper meridian (arcuate keratotomy group; mean preoperative astigmatism 2.28 ± 0.89 D); in the other group (17 eyes) phacoemulsification was performed on the steeper meridian without arcuate keratotomy (control group; mean preoperative astigmatism 2.04 ± 0.50 D). There was a mean reduction in keratometric astigmatism in the keratotomy group of 1.26 ± 0.54 D (p = 0.0067) and in the control group of 0.48 ± 0.60 D (p = 0.0423). The difference in reduction of keratometric astigmatism between the two groups was statistically significant (p = 0.0296). Surgically induced refractive change at 8 weeks follow-up was 2.15 ± 1.13 D in the keratotomy group and 1.50 ± 1.32 D in the control group (p = 0.046). The coupling ratio was −1.10 D ± 0.43 D in the keratotomy group at 8 weeks after surgery while the control group was −0.82 D ± 0.38 D, demonstrating that a combination of intraoperative arcuate keratotomy with steep-axis phacoemulsification incision is more effective than steep-axis phacoemulsification incision alone in reducing pre-existing astigmatism.

POSTCATARACT CONDUCTIVE KERATOPLASTY Postcataract surgery hyperopic overshoot can be adjusted by conductive keratoplasty (CK) just as intrinsic low-to-moderate hyperopia can be corrected. McDonald et al.10 documented the 1-year safety, efficacy, and stability results of 355 eyes treated in a multicenter study of CK to correct low-to-moderate hyperopia in a nonrandomized comparative (self-controlled) trial. Twenty surgeons at 13 centers performed CK on the eyes of all patients enrolled in a multicenter, 2-year, United States Phase III clinical trial. Treated eyes had +0.75 to +3.00 D of hyperopia and ≤ 0.75 D of cylinder. Patients were 40 years of age or older in whom low-energy, high-frequency current was applied directly into the peripheral corneal stroma through a delivery tip inserted at 8 to 32 treatment spots. The number of treatment spots was increased for increasing levels of hyperopia, but the amount of radiofrequency energy

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5 THE LENS Fig. 5-8-17 OD (right eye) pre-op +10.25/−4.5×175 = 6/6-2 post-op +0.25 = 6/5 UCVA 6/5. Topography maps illustrating sequential healing responses of cornea to opposite clear corneal incision effect. Difference map illustrates flattening of original astigmatism. Manifest refraction virtually plano. Final map illustrates typical 4 hemimeridia with spherical optical zone.

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Fig. 5-8-18 Large map to illustrate 4 hemimeridia and essentially spherical optical zone with virtually plane manifest refraction seen in Fig. 5-8-17.

Fig. 5-8-19 Corneal aberrations post-op seen in Fig. 5-8-18 despite which the vision was excellent.

remained constant. Emmetropia was intended. All eyes were treated once (with no re-treatments). At 1 year, uncorrected visual acuity was ≤ 20/20 in 56%, ≤ 20/25 in 75%, and ≤ 20/40 in 92% of eyes. The manifest refractive spherical equivalent refraction was within 0.50 D in 63%, within ± 1.00 D in 89%, and within ± 2.00 D in 99%. Seven of 355 eyes lost 2 lines of best spectacle-corrected visual acuity at 1 year, but no eye lost > 2 lines. One eye of 355 had induced cylinder of > 2.00 D. The cycloplegic refractive spherical equivalent changed a mean of 0.25 ± 0.50 D between months 3 and 6, 0.11 ± 0.41 D between months 6 and 9, and 0.11 ± 0.35 D between months 9 and 12. Refractive stability seemed to be attained by 6 months and remained stable through 12 months. Histology and confocal microscopy showed deep penetration of the treatment into the stroma. Endothelial cell counts were not changed by the treatment suggesting that CK seems to be safe, effective, and stable for correcting low-to-moderate spherical hyperopia in patients 40 years old or older.

POSTCATARACT LASIK Kim et al.11 evaluated the safety and efficacy of laser-assisted in situ keratomileusis (LASIK) to correct refractive error following cataract surgery in a retrospective study reviewing 23 eyes of 19 patients treated with LASIK for refractive error following cataract surgery. The Summit Apex Plus and Ladarvision excimer laser and the SKBM microkeratome were used. The mean age was 63.5 years (range 50−88 years). The mean length of follow-up was 8.4 months (range 1−12 months) and mean interval between cataract surgery and LASIK was 12 months (range 2.5−46 months). The mean preoperative spherical equivalent refraction (SEQ) for myopic eyes was −3.08 ± 0.84 D (range −4.75 to −2.00 D) and for hyperopic eyes was +1.82 ± 1.03 D (range +0.75 to +3.00 D). The mean improvement following LASIK surgery was greater for myopic than hyperopic eyes (myopic, 2.54 ± 1.03 D versus hyperopic, 1.73 ± 0.62 D; p = 0.033). The percentage of patients within ± 0.5 D of

Fig. 5-8-20 Pellucid marginal corneal degeneration. An example where preoperative corneal topography would have revealed the defect that resulted in “unexplained” poor visual result post surgery.

intended refraction post-LASIK surgery was 83.3% for myopic eyes and 90.9% for hyperopic eyes and all eyes were within ± 1.0 D of intended (p < 0.001). The percentage of eyes with uncorrected visual acuity of 20/40 or better in the myopic group improved from none preoperatively to 91.7% postoperatively (p < 0.001) and in the hyperopic group improved from 27.3% preoperatively to 90.9% postoperatively (p = 0.008). No eyes lost 2 or more lines of best-corrected visual acuity. Kuo et al.12 reviewed cases of patients who had excimer laser refractive surgery to correct unintentional or undesired ametropia after cataract extraction with IOL implantation. In this retrospective noncomparative review of consecutive cases, the Wilmer Laser Vision Correction Center’s database was searched for patients who had had LASIK or photorefractive keratectomy to correct ametropia after cataract extraction with IOL implantation. Using the Visx Star excimer laser system (Visx, Inc.), 11 procedures were performed in 11 eyes of 10 patients a mean of 47 months (range 2−216 months) after cataract

5.8 Refractive Aspects of Cataract Surgery

e xtraction with IOL implantation. Except for one patient with a silicone plate lens, all patients received 3-piece PMMA IOLs. The mean age at time of excimer treatment was 75 years (range 70−81 years). Before laser surgery, the mean spherical equivalent of patient eyes was −3.76 D ± 2.50 (SD) (range −6.50 to +0.75 D), spherical refraction ranged from −9.00 D to plano, and the highest cylindrical refraction was +5.50 D. At last follow-up (mean 12.2 months; range 1−38 months), the mean manifest spherical equivalent was −0.88 ± 1.43 D (range −2.75 to +2.13 D). Changes in mean manifest spherical equivalent were highly significant (p = 0.03, Wilcoxon signed rank test for paired values). There was no difference between targeted and achieved postoperative refraction (p = 0.34, Wilcoxon test). Increasing age was correlated with a hyperopic shift (r = 0.525, p = 0.05). All patients were satisfied with their final uncorrected visual acuity (UCVA), which improved in every case. Except for one patient in whom an epiretinal membrane developed, best spectaclecorrected visual acuity remained unchanged or improved. This series of patients, who were a few decades older than the typical excimer laser candidate, illustrated the case that laser refractive surgery was a safe, effective, and predictable method in correcting ametropia after cataract extraction with IOL implantation. It demonstrated a viable, less invasive alternative to intraocular surgery.

POSTCATARACT PIGGY-BACK IOLS Hsuan et al.13 assessed the role of the Staar Surgical implantable contact lens (ICL) for the correction of pseudophakic anisometropia. Six patients with pseudophakic anisometropia ranging from 2.0 to 7.9 D (mean 4.4 D) were given implantable contact lenses as an alternative to IOL exchange or conventional piggy-back IOLs. All patients had a reduction in anisometropia to asymptomatic levels. The mean reduction was 3.15 D. No patient experienced adverse effects. The implantable contact lens offers an alternative approach to the management of pseudophakic anisometropia, thereby avoiding some of the risks associated with IOL exchange, corneal refractive surgery, and conventional piggy-back IOLs as the ICL is a very thin lens which is easily and safely placed in the ciliary sulcus in front of the pseudophakos.

VALUE OF CORNEAL TOPOGRAPHY Figure 5-8-20 illustrates the importance of preoperative corneal topography in ensuring that the eye to be operated upon is fully understood: “Understand before you treat.”

REFERENCES 1. R idley H. The cure of aphakia. In: Rosen ES, Haining WM, Arnott AJ, eds. IOL implantation, New York: Mosby: 1979:37–43. 2. Tejedor J, Murube J. Choosing the location of corneal incision based on preexisting astigmatism in phacoemulsification. Am J Ophthalmol. 2005;139:767–76. 3. Beltrame G, Salvetat ML, Chizzolini M, Driussi G. Corneal topographic changes induced by different oblique cataract incisions. J Cataract Refract Surg. 2001;27: 720–7. 4. Kaufmann C, Peter J, Ooi K, et al. The Queen Elizabeth Astigmatism Study Group. Limbal relaxing incisions versus on-axis incisions to reduce corneal astigmatism at the time of cataract surgery. J Cataract Refract Surg. 2005;31:2261.

5. L ever J, Dahan E. Opposite clear corneal incisions to correct pre-existing astigmatism in cataract surgery. J Cataract Refract Surg. 2000;26:803–5. 6. Qam-mar A, Mullaney P. Paired opposite clear corneal incisions to correct preexisting astigmatism in cataract patients. J Cataract Refract Surg. 2005;31:1167–70. 7. Tadros A, Habib M, Tejwani D, et al. Opposite clear corneal incisions on the steep meridian in phacoemulsification: early effects on the cornea. J Cataract Refract Surg. 2004;30:414–7. 8. Baykara M, Dogru M, Ozcetin H. Refractive outcomes after arcuate keratotomy using the Terry astigmatome. J Cataract Refract Surg. 2003;29:2397–400. 9. Titiyal JS, Baidya KP, Sinha R, et al. Intraoperative arcuate transverse keratotomy with phacoemulsification. J Refract Surg. 2002;18:725–30.

10. M cDonald MB, Hersh PS, Manche EE, et al. Conductive Keratoplasty United States Investigators Group. Conductive keratoplasty for the correction of low to moderate hyperopia: U.S. clinical trial 1-year results on 355 eyes. Ophthalmology. 2002;109:1978–89. discussion 1989–90. 11. Kim P, Briganti EM, Sutton GL, et al. Laser in situ keratomileusis for refractive error after cataract surgery. J Cataract Refract Surg. 2005;31:979–86. 12. Kuo IC, O’Brien TP, Broman AT, et al. Excimer laser surgery for correction of ametropia after cataract surgery. J Cataract Refract Surg. 2005;31:2104–10. 13. Hsuan JD, Caesar RH, Rosen PH, et al. Correction of pseudophakic anisometropia with the Staar Collamer implantable contact lens. J Cataract Refract Surg. 2002;28:44–9.

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PART 5 THE LENS

Small Incision Cataract Surgery Mark Packer, I. Howard Fine and Richard S. Hoffman

Key features n

I ncremental advances in technique and technology since the invention of phacoemulsification in the 1960s have paved the way to improved outcomes and enhanced expectations for cataract extraction. The refinement of incision placement and architecture, as well as the reduction of final incision size occasioned by the development of foldable, injectable intraocular lenses, has allowed reduction of postoperative astigmatism and enhancement of refractive cataract surgery. The continuous curvilinear capsulorrhexis has facilitated remarkable advances in phacoemulsification technique, beginning with sculpting techniques such as divide and conquer and trending to today's preferred horizontal and vertical chopping methods. The use of hydrodissection to lyse cortical-capsular connections and the use of hydrodelineation to permit phacoemulsification within the protective layer of the epinucleus has improved the efficiency of phacoemulsification. Power modulations such as pulse and burst mode, as well as millisecond level control of ultrasound power application, have allowed reduction of the energy required for cataract extraction, protection from thermal wound injury, and enhancement of the rapidity of postoperative visual rehabilitation. The separation of irrigation from aspiration made possible by bimanual microincision phacoemulsification represents an advance in the fluidic behavior of the intraocular environment, permitting greater control of every step of the cataract extraction procedure.

INTRODUCTION Phacoemulsification (phaco) means disassembly and removal of the crystalline lens, usually through a small incision. From its introduction in the late 1960s to the present, phaco has evolved into a highly effective method of cataract extraction. Incremental advances in surgical technique and the simultaneous redesign and modification of technology have permitted an increase in safety and efficiency. Among the advances that have shaped modern phaco are incision construction, continuous curvilinear capsulorrhexis, cortical cleaving hydrodissection, hydrodelineation, and nucleofractis techniques. The refinement of cataract removal through a small incision has improved phaco and permitted rapid visual rehabilitation and excellent ocular structural stability.

INCISION CONSTRUCTION AND ARCHITECTURE

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The availability of foldable intraocular lenses (IOLs) that can be inserted through small unsutured phacoemulsification incisions1 has created a trend away from scleral tunnel incisions to clear corneal incisions.2 Kratz is generally credited as the first surgeon to move from the limbus posteriorly to the sclera in order to increase appositional surfaces, thus enhancing wound healing and reducing surgically induced astigmatism.3, 4 Girard and Hoffman were the first to name the posterior incision a “scleral tunnel incision” and were, along with Kratz,

5.9

the first to make a point of entering the anterior chamber through the cornea, creating a corneal shelf.5 In 1989, McFarland used this incision architecture and recognized that these incisions allowed for the phacoemulsification and implantation of lenses without the need for suturing.6 Maloney, who was a fellow of Kratz, advocated a corneal shelf to his incisions, which he described as strong and waterproof.7 Ernest recognized that McFarland’s long scleral tunnel incision terminated in a decidedly corneal entrance. He hypothesized that the posterior “corneal lip” of the incision acted as a one-way valve, thus explaining the mechanism for self sealability (Presentation at the De- partment of Ophthalmology, Wayne State University School of Medi- cine, Detroit, MI, 28 February, 1990). In April of 1992, Fine presented his self-sealing temporal clear corneal incision at the annual meeting of the American Society of Cataract and Refractive Surgery.8 There have been surgeons who have favored corneal incisions for cataract surgery prior to their recent popularization. In 1968, Charles Kelman stated that the best approach for performing cataract surgery was with phacoemulsification through a clear corneal incision utilizing a triangular-tear capsulectomy and a grooving and cracking technique in the posterior chamber.9 Harms and Mackenson in Germany published an intracapsular technique using a corneal incision in 1967.10 Troutman was an early advocate of controlling surgically induced astigmatism at the time of cataract surgery by means of the corneal incision approach.11 Arnott in England utilized clear corneal incisions and a diamond keratome for phacoemulsification although he had to enlarge the incision for introducing an IOL.12 Galand in Belgium utilized clear corneal incisions for extracapsular cataract extraction in his envelope technique13 and Stegman of South Africa has a long history of having utilized the cornea as the site for incisions for extracapsular cataract extraction (Stegmann R, personal communication, 3 December, 1992). Finally, perhaps the leading proponent of clear corneal incisions for modern era phacoemulsification was Kimiya Shimizu of Japan.14 In 1992, Fine began routinely utilizing clear corneal cataract incisions with closure by a tangential suture modeled after Shepherd’s technique.15 Within a very short period, the suture was abandoned in favor of self-sealing corneal incisions.16 Through the demonstrated safety and increased utilization of these incisions by pioneers in the United States, including Williamson, Shepherd, Martin, and Grabow,17 these incisions became increasingly popular and utilized on an international basis. Rosen demonstrated by topographical analysis that clear corneal incisions 3 mm or less in width do not induce astigmatism.18 This find- ing led to increasing interest because of better predictability of T-cuts, arcuate cuts, and limbal relaxing incisions for managing pre-existing astigmatism at the time of cataract surgery. Surgeons recognized many other advantages of the temporal clear corneal incision, including better preservation of pre-existing filtering blebs19 and options for future filtering surgery, increased stability of refractive results because of decreased effects from lid blink and gravity, ease of approach, elimination of the bridle suture and iatrogenic ptosis, and improved drainage from the surgical field via the lateral canthal angle. Single plane incisions, as first described by Fine,20 utilized a 3.0 mm diamond knife. After pressurizing the eye with viscoelastic through a paracentesis, the surgeon placed the blade on the eye so that it completely applanated the eye with the point of the blade positioned at the leading edge of the anterior vascular arcade. The knife was advanced in the plane of the cornea until the shoulders, 2 mm posterior to the point of the knife, touched the external edge of the incision. Then the point of the blade was directed posteriorly to initiate the cut through

Descemet’s membrane in a maneuver known as the dimple-down technique. After the tip entered the anterior chamber, the initial plane of the incision was re-established to cut through Descemet’s in a straightline configuration. Williamson was the first to utilize a shallow 300−400 μm grooved clear corneal incision.21 Langerman later described the single hinge incision, in which the initial groove measured 90% of the depth of the cornea anterior to the edge of the conjunctiva.22 Surgeons employed adjunctive techniques to combine incisional keratorefractive surgery with clear corneal cataract incisions. Osher described the construction of arcuate keratotomy incisions at the time of cataract surgery for the correction of pre-existing corneal astigmatism. Kershner used the temporal incision by starting with a nearly full-thickness T-cut through which he then made his corneal tunnel incision. For large amounts of astigmatism he used a paired T-cut in the opposite side of the same meridian.23 Finally, the popularization of limbal relaxing incisions by Gills24 and Nichamin25 added an additional means of reducing pre-existing astigmatism. The 3-D Blade (Rhein Medical, Tampa, FL) improved incision construction with differentially sloped bevels on its anterior and posterior surfaces (Fig. 5-9-1). This design allowed the surgeon to touch the eye at the site of the external incision location and advance the blade in the plane of the cornea without dimpling down. The differential slopes allowed the forces of tissue resistance to create an incision characterized by a linear external incision, an arcuate tunnel with a 2 mm chord length, and a linear internal incision.26 Following phacoemulsification, lens implantation, and removal of residual viscoelastic, stromal hydration of the clear corneal incision can be performed in order to help seal the incision.16 Stromal hydration is performed by gently irrigating balanced salt solution into the stroma at both edges of the incision with a 26- or 27-gauge cannula. An intra operative Seidel test may be used to ensure sealing. Clear corneal incisions, by nature of their architecture and location, have some unique complications associated with them. If one incidentally incises the conjunctiva at the time of the clear corneal incision, chemotic ballooning of the conjunctiva can develop, which may compromise visualization of anterior structures. In this case, the conjunctiva may be snipped to permit decompression. Early entry into the anterior chamber may result in an incision of insufficient length to be self-sealing. In addition, incisions that are too short or improperly constructed can result in an increased tendency for iris prolapse. A single suture may be required in order to ensure a secure wound at the conclusion of the procedure. On the other hand, a late entry may result in a corneal tunnel so long that the phaco tip creates striae in the cornea and compromises the view of the anterior chamber.

5.9 Small Incision Cataract Surgery

Fig. 5-9-1 An anterior chamber optical computed tomography scan (Visante OCT, Carl Zeiss Meditec, Dublin, CA) taken on the first day postoperatively demonstrates that the clear corneal incision is actually curvilinear, not a straight line. It is an arcuate incision, which is considerably longer than the chord length originally estimated for the length of the incision. It is very important to note that the architecture of the incision allows for a fit not unlike tongue and groove paneling, which adds a measure of stability to these incisions and makes sliding of one surface over the other considerably less likely.

Manipulation of the phacoemulsification handpiece intraoperatively may result in tearing of the roof of the tunnel, especially at the edges, resulting in compromise of the incision’s self-sealability. Tearing of the internal lip can also occur, resulting in compromised self-sealability or, rarely, small detachments or scrolling of Descemet’s membrane in the anterior edge of the incision. Of greater concern has been the potential for incisional burns.27 When incisional burns develop in clear corneal incisions there may be a loss of self-sealability. Closure of the wound may induce excessive amounts of astigmatism. In addition, manipulation of the incision can result in an epithelial abrasion, which can compromise self-sealability because of the lack of a fluid barrier by an intact epithelium. Without an intact epithelial layer, the corneal endothelium does not have the ability to help appose the roof and floor of the incision through hydrostatic forces. In a large survey performed for the American Society of Cataract and Refractive Surgery by Masket,28 there was a slightly increased incidence of endophthalmitis in clear corneal cataract surgery compared to scleral tunnel surgery. Colleaux and Hamilton29 found no significant difference in the rate of endophthalmitis with respect to clear corneal versus scleral tunnel incisions in a retrospective review of 13 886 consecutive cataract operations. They reported a significant prophylactic effect of subconjunctival antibiotic injection, but found no benefit to preoperative antibiotic drops. In an evidence-based update, Ciulla, Starr and Masket found that current literature most strongly supports the use of preoperative povidone-iodine antisepsis.30 They found little change in the risk of endophthalmitis in the United States over time, from 0.12% in 1984 to 0.13% in 1994. A recent review of the literature on postoperative endophthalmitis concluded that: The reports of endophthalmitis analyzed from peer-reviewed ophthalmic journals suggest the incidence of endophthalmitis has increased, ranging from 0.1 to 0.18% in different countries. This may be related to factors related to the incision. Although some resistance has been detected, fourth generation fluoroquinolones appear to be an appropriate antibiotic for endophthalmitis prophylaxis to complement povidone use, due to spectrum, mode of action and penetration.31 Experimental studies in cadaver eyes have demonstrated reduced integrity of clear corneal incisions under certain conditions.32 A relationship between wound leakage, with resultant hypotony, and endophthalmitis has also been reported.33 One large study has shown an increase of endophthalmitis that coincides temporally with increasing use of clear corneal incisions.34 Other case series have shown an equal distribution of endophthalmitis between surgeries using different types of incision.35 Some studies point to the multifactorial nature of endophthalmitis and the importance of every step from antisepsis of the surgical field to postoperative topical antibiotic treatment.36 The authors of one recent review of the literature conclude that, “There is no conclusive evidence of the relationship between clear corneal incision and endophthalmitis. It seems, however, that in certain situations clear corneal incision may play a role in the occurrence of endophthalmitis.” 37 Clear corneal cataract incisions have become and are expected to remain the dominant option for cataract extraction and IOL implantation throughout the world. With clear corneal incisions we have achieved minimally invasive surgery with immediate visual rehabilitation.

CONTINUOUS CURVILINEAR CAPSULORRHEXIS Implantation of the IOL in an intact capsular bag facilitates the permanent rehabilitative benefit of cataract surgery. For many years, surgeons considered a “can-opener” capsulectomy satisfactory for both planned extracapsular cataract extraction and phaco. In 1991, Was- serman and associates38 performed a postmortem study that showed that the extension of one or more V-shaped tears toward the equator of the capsule produced instability of the IOL and resulted in IOL malposition. We are fortunate to have benefited from the work of Calvin Fer- cho, who developed continuous tear capsulectomy (Presentation at the Welsh Cataract Congress, 9 September, 1986) and Gimbel and Neuhann, who popularized continuous curvilinear capsulorrhexis (CCC).39–41 The technique of CCC is not difficult to learn if certain basic principles are observed: 1. The continuous capsular tear should be performed in a deep, stable anterior chamber. We advocate using a viscoelastic substance that

459

5 THE LENS A

Fig. 5-9-2 Backwards traction on the capsular flap forms the basis of a predictable technique for rescuing the capsulorrhexis from a radial tear-out. As shown here in the case of an opaque cataract with trypan blue capsule stain, the tear has extended too far to the periphery (A). Therefore the flap is unfolded and laid back in the plane of the capsulorrhexis from where it was torn (B). The flap is then pulled with reverse tangential force until the capsule tears back toward the center (C). Construction of the capsulorrhexis may then continue (D).

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deepens the anterior chamber and stretches the anterior capsule. The use of a viscoelastic material accomplishes two important goals: A. It creates space for safe instrumentation in the anterior chamber. B. By making the anterior capsule taut and pushing the lens posteriorly it resists the action of posterior pressure, which tends to cause the capsular tear to move peripherally. 2. The tear is started at the center of the capsule. This way the origin of the tear is included within the termination of the tear. 3. Once the initial flap is mobilized, it is inverted to permit a smooth tearing action, such as would be achieved in tearing a piece of pa- per. This principle is the same whether a cystotome, bent needle or forceps is used to create the capsulectomy. 4. The continuous tear proceeds either clockwise or counter-clockwise in a controlled and deliberate fashion, the surgeon regrasping with the forceps or repositioning the point of the cystotome/bent needle on the inverted flap to control the vector of the tear. As we have indicated, it is essential to control the course of the capsular tear. A tear that begins moving peripherally or in a radial fashion is a signal that a condition exists that requires immediate attention. Further progress of the tear should be stopped and the depth of the anterior chamber assessed. Frequently, the cause of the peripheral course of the tear is shallowing of the anterior chamber. Adding more viscoelastic to deepen the anterior chamber opposes the posterior pressure, makes the lens capsule taut, widens the pupil, and permits inspection of the capsule. One important technique for redirection of the capsulorrhexis has recently been described by Little.42 In order to rescue the capsulorrhexis, the force applied to the capsular flap is reversed but maintained in the plane of the anterior capsule. It is necessary to first unfold the capsular flap so that it lies flat against the lens cortex as it did prior to being torn. This unfolding is most safely and effectively accomplished using viscoelastic to manipulate the flap. Force can then be applied with the capsule forceps holding the capsular flap as near to the root of the tear as possible and pulling backwards, along

the circumferential path of the completed portion of the rhexis. Traction should be applied in the horizontal plane of the capsule and not upward. The initial pull should be circumferentially backward, and then, whilst holding the flap under tension, directed more centrally to initiate the tear. The tear will uniformly and predictably propagate toward the center of the capsule (Fig. 5-9-2). In the event that the capsule will not tear easily and the entire lens is being pulled centrally, this rescue maneuver should be abandoned to avoid a wrap-around capsular tear. Alternate rescue techniques such as completing the capsulectomy from the opposite direction or making a relieving cut in the flap edge and continuing in the same direction would be appropriate alternatives. If the tear has extended peripherally and cannot be safely redi- rected, one option is to create a small tangential incision at the origin of the CCC with Vannas scissors and to direct the tear in the opposite direction to include the peripheral extension. If this maneuver cannot be accomplished and the discontinuity in the CCC remains, it is probably wisest to make several other small incisions in the capsular rim so that the peripheral force is distributed evenly, reducing the likelihood that a tear will extend around the lens equator. A similar situation may occur upon completion of the CCC. Again, at this point it is essential that the origin of the peripheral portion of the CCC be included within the circumference of the tear. If this maneuver is performed correctly, it will result in a totally blended edge or it will form a small centripetally peaked area (cardioid). If the end of the CCC results in a V-shaped centrifugally oriented peak, however, this acts as a discontinuity in the anterior capsular opening and may extend peripherally, with the attendant consequences mentioned above. The use of a vital dye to stain the anterior capsule in the absence of a good red reflex constitutes an important adjunctive technique for capsulorrhexis construction. The surgeon makes the sideport incision and then fills the anterior chamber with air. The dye, either indocyanine green or trypan blue, is injected into the chamber. The air and residual dye are then exchanged for viscoelastic. Despite the absence of a red reflex the capsule is now easy to see.

of the grooves. The nucleus is then rotated 90°, and additional fractures are made until four separate quadrants are isolated. A short burst of phaco power is then used to embed the phaco tip into one quadrant, and it is pulled into the center for emulsification. The second instrument can help elevate the apex of the quadrant to facilitate its mobilization.

HYDRODISSECTION AND HYDRODELINEATION

Chip and Flip Technique

Hydrodissection has traditionally meant the injection of fluid into the cortical layer of the lens to separate the nucleus from the cortex and capsule.43 Following the adoption of capsulorrhexis, hydrodissection became a critical step to mobilize, disassemble and remove the nucleus.44–47 Fine first described cortical cleaving hydrodissection, which is designed to cleave the cortex from the capsule and leave the cortex attached to the epinucleus.48 Cortical cleaving hydrodissection usually eliminates the need for cortical cleanup as a separate step in cataract surgery.

Cortical Cleaving Hydrodissection

The anterior capsular flap is initially elevated with a 26-gauge blunt cannula. Firm and gentle continuous irrigation results in a fluid wave that cleaves the cortex from the posterior capsule. The lens bulges forward because fluid is trapped by equatorial cortical-capsular connections. Depressing the central portion of the lens with the side of the cannula forces fluid around the equator and lyses cortical-capsular connections. Adequate hydrodissection is demonstrated by rotation of the nuclear-cortical complex.

Hydrodelineation

Hydrodelineation describes separation of the epinuclear shell from the endonucleus by the irrigation.49 Circumferential division reduces the volume of the central portion of nucleus removed by phacoemulsification, allowing safer grooving and smaller, more easily mobilized quadrants after cracking or chopping. The epinucleus acts as a protective cushion within which phacoemulsification forces can be confined. Fur- ther, the epinucleus keeps the bag on stretch throughout the procedure, making capsule rupture unlikely. The 26-gauge cannula is placed in the nucleus, off center to either side, and directed at an angle downward and forward toward the central plane of the nucleus. When the nucleus starts to move, the endonucleus has been reached. At this point, the cannula is directed tangentially to the endonucleus, and a to-and-fro movement of the cannula is used to create a tunnel within the nucleus. The cannula is backed out of the tunnel approximately halfway, and gentle but steady pressure on the syringe allows fluid to enter the distal tunnel without resistance. A circumferential golden or dark ring will outline the endonucleus. Occasionally, an arc will result and surround approximately one quadrant of the endonucleus. In this instance, the procedure can be repeated in multiple quadrants until a golden or dark ring verifies complete circumferential division of the nucleus.

NUCLEOFRACTIS TECHNIQUES The recognition that the nuclear mass could be divided and removed from within the protective layer of the epinucleus and that the CCC could withstand the forces involved in nuclear cracking influenced the remarkable evolution of phaco from Kelman’s initial procedure9 to today’s techniques.

Divide and Conquer

In the divide and conquer technique described by Gimbel,50 a deep crater is sculpted into the center of the nucleus including the posterior plate. Sections are then fractured from the rim. Rather than emulsify the sections as they are broken away, they are left in place to maintain tension on the capsule and facilitate rotation. After the rim is completely fractured each segment is brought to the center for safe emulsification.

Phaco Fracture

In phaco fracture, a popular technique described by Shepherd,51 the surgeon sculpts a groove from the 12 to 6 o’clock position. The width of the groove should be one and a half to two times the diameter of the phaco tip. Using the phaco handpiece and a second instrument, the surgeon rotates the nucleus 90°. A second groove is sculpted perpendicular to the first, in the form of a cross. Sculpting continues until the red reflex is seen at the bottom of the grooves. A bimanual cracking technique is used to create a fracture through the nuclear rim in the plane of one

Introduced by Fine,52 and useful for softer grades of nuclei, this procedure relies on a nucleus that rotates freely within the capsular bag. Ini- tially, a central bowl is sculpted in the nucleus until a thin central plate remains. The second instrument engages the subincisional nuclear rim to move the inferior nuclear rim toward the center. Clock-hour pieces of rim are emulsified as the nucleus is rotated. Once the entire rim is removed, the second instrument is used to elevate the remaining central thinned nuclear plate (the chip), which is then emulsified. The epinucleus is engaged at the 6 o’clock position with aspiration alone. As the phaco tip is moved superiorly, the second instrument pushes the epinucleus toward the 6 o’clock position, thereby tumbling the epinuclear bowl and permitting it to be aspirated (the flip).

5.9 Small Incision Cataract Surgery

The technique of CCC has provided important advantages both for cataract surgery and IOL implantation. Because endolenticular or in situ phaco must be performed in the presence of an intact continuous capsulotomy opening, the capsulorrhexis has also served as a stimulus for modification of phaco techniques.

Crack and Flip Technique

Fine and colleagues modified Shepherd’s phaco fracture technique by adding hydrodelineation, resulting in the crack and flip technique.53 Sculpting two deep grooves at right angles to each other that extend to the golden ring permits bimanual nucleus cracking. Only the endonucleus cracks, since the epinucleus is separated from it by hydrodelineation. Each quadrant is then sequentially removed with the use of pulsed phaco and moderate aspiration. The second instrument elevates the apices of each quadrant so that the tip of the phaco needle can be totally occluded to aid in aspiration. Once the nucleus is removed, the epinucleus is aspirated as with the chip and flip technique.

Phaco Chop

Nagahara first introduced the phaco chop technique by using the natural fault lines in the lens nucleus to create cracks without creating prior grooves (Presentation at the American Society of Cataract and Refractive Surgery Film Festival, 1993). The phaco tip is embedded in the center of the nucleus after the superficial cortex is aspirated. A second instrument, the phaco chopper, is then passed to the equator of the nucleus, beneath the anterior capsule, and drawn to the phaco tip to fracture the nucleus. The two instruments are separated to widen the crack. This procedure is repeated until several small fragments are created, which are then emulsified. Because they encountered difficulty mobilizing the nuclear fragments, Koch and Katzen54 modified this procedure in their stop and chop technique. Before chopping they created a central groove or central crater, depending on the density of the nucleus.

Choo Choo Chop and Flip

Fine described the “choo-choo chop and flip” technique in 1998.55 Sub- sequently, we correlated the reduction of ultrasound energy with this technique to improvement in uncorrected postoperative day 1 visual acuity.56 A 30° standard tip is used bevel down. After aspirating epinucleus uncovered by the capsulorrhexis, a Fine/Nagahara chopper (Rhein Medical, Tampa, FL) is placed in the golden ring by touching the top center of the nucleus with the tip and pushing the tip peripherally so that it reflects the capsulorrhexis. The chopper is used to stabilize the nucleus by lifting and pulling toward the incision slightly, after which the phaco tip lollipops the nucleus in either pulse mode at 2 pulses/second or 80 millisecond burst mode. Burst mode utilizes fixed power and duration with variable interval. In pulse mode, there is variable power with fixed duration and interval. These power modulations reduce total ultrasound energy and increase hold. Once the tip is buried in the center of the nucleus vacuum is maintained in foot position 2. The Fine/Nagahara chopper is moved in the direction of the sharp edge as indicated by the groove on the instrument. The nucleus is scored by bringing the chopper to the side of the phaco needle. It is chopped in half by pulling the chopper to the left and slightly down while moving the phaco needle, still in foot position 2, to the right and slightly up (Fig. 5-9-3). Then the nuclear complex is rotated 90°. The chop instrument is again brought into the golden ring, the heminu- cleus is lollipopped, scored, and chopped with the resulting wedge now lollipopped on the phaco tip and evacuated. The nucleus is rotated so that wedges can be scored, chopped, and removed by high vacuum assisted by short bursts or pulses of phaco. The size of the wedges is varied according to the density of the nucleus.

461

CHOO CHOO CHOP AND FLIP Performing the initial chop

Flipping the epinuclear shell

Using ultrasound power

THE LENS A

Fig. 5-9-3 Choo choo chop and flip technique. The surgeon performs the initial chop of the nucleus by deeply embedding the phaco needle in the center of the nucleus using ultrasound power, and then maintaining a hold on the nucleus with high vacuum in foot pedal position 2 without ultrasound as the horizontal chopper is brought from the golden ring to the side of the phaco needle to score the nucleus. The surgeon then completes the chop by separating the instruments with a slight upward movement of the phaco tip and a slight downward movement of the chopper (A). Each quadrant of nuclear material is in turn impaled, chopped, mobilized, and consumed with high vacuum and low amounts of ultrasound power (B). Finally, the epinuclear shell is flipped with a helpful push from the chopper (C).

After evacuation of all endonuclear material, the epinuclear rim is trimmed in each of the three quadrants, mobilizing cortex. As each quadrant of the epinuclear rim is rotated to the distal position in the capsule and trimmed, the cortex in the adjacent capsular fornix flows over the floor of the epinucleus and into the phaco tip. The floor is pushed back to keep the bag on stretch until three of the four quadrants of the epinuclear rim and cortex have been evacuated. The epinuclear rim of the fourth quadrant is then used as a handle to flip the epinucleus. As the remaining portion of the epinuclear floor and rim is evacuated from the eye, most of the time the entire cortex is evacuated with it. If there is cortex remaining following removal of all the nucleus and epinucleus, there are three options. The phacoemulsification handpiece can be left high in the anterior chamber while the second handpiece strokes the cortex-filled capsular fornices. Frequently, this results in floating up of the cortical shell as a single piece and its exit through the phacoemulsification tip (in foot position 2) because cortical cleaving hydrodissection has cleaved most of the cortical capsular adhesions. Alternatively, if one wishes to complete cortical cleanup with the irrigation-aspiration handpiece prior to lens implantation, the residual cortex can almost always be mobilized as a separate and discrete shell and removed without turning the aspiration port down to face the posterior capsule. The third option is to viscodissect the residual cortex by injecting a dispersive viscoelastic through the posterior cortex onto the posterior capsule. The viscoelastic material spreads horizontally, elevating the posterior cortex and draping it over the anterior capsular flap. At the same time the peripheral cortex is forced into the capsular fornix. The posterior capsule is then deepened with a cohesive viscoelastic and the IOL is implanted, leaving anterior residual cortex anterior to the IOL. Removal of residual viscoelastic material accompanies mobilization and aspiration of the residual cortex. Chopping techniques replace ultrasound with mechanical forces for nuclear disassembly. High vacuum holds material at the tip and high flow allows efficient aspiration. These techniques maximize safety and control. Chopping achieves minimum morbidity and maximum visual rehabilitation.

Bimanual Microincision Phacoemulsification

462

Microincision cataract surgery (MICS) and companion IOL is today possible through new ultrasound power modulations and new instrumentation, including forceps for construction of the capsulorrhexis, irrigating choppers, and bimanual irrigation and aspiration sets. Pro- ponents of performing phaco through two paracentesis-type incisions claim reduction of surgically induced astigmatism, improved chamber stability in every step of the procedure, better followability due

to the physical separation of infusion from ultrasound and vacuum, and greater ease of irrigation and aspiration with the elimination of one unique subincisional region. In the 1970s, Girard attempted to separate infusion from ultrasound and aspiration, but abandoned the procedure because of thermal injury to the tissue.57, 58 Shearing et al. performed phaco through two 1.0 mm incisions using a modified anterior chamber maintainer and a phaco tip without the irrigation sleeve.59 They reported a series of 53 cases and found that phaco time, overall surgical time, total fluid use, and endothelial cell loss were comparable to those measured with their standard phaco techniques. Crozafon described the use of Teflon-coated phaco tips for bimanual high-frequency pulsed phaco, and suggested that these tips would reduce friction and therefore allow surgery with a sleeveless needle (Presentation at the 14th Meeting of the Japanese Society of Cataract and Refractive Surgery, Kyoto, Japan, July, 1999). Tsuneoka and colleagues determined the feasibility of using a 1.4 mm (19-gauge) incision and a 20-gauge sleeveless ultrasound tip to perform phaco.60 They found that outflow around the tip through the incision provided adequate cooling, and performed this procedure in 637 cases with no incidence of wound burn.61 Additionally, less surgically induced astigmatism developed in the eyes operated with the bimanual technique. Agarwal and colleagues developed a bimanual technique, “Phakonit,” using an irrigating chopper and a bare phaco needle passed through a 0.9 clear corneal incision.62 They achieved adequate temperature control through continuous infusion and use of “cooled balanced salt solution” poured over the phaco needle. Soscia et al. have shown in studies on cadaver eyes that phacoemulsification with the Sovereign WhiteStar system (AMO, Santa Ana, CA), using a bare 19-gauge aspiration needle, will not produce a wound burn at the highest energy settings unless all infusion and aspiration are occluded.63, 64 WhiteStar represents a power modulation of ultrasonic phacoemulsification that virtually eliminates the production of thermal energy. Referred to as “cold phaco,” WhiteStar allows reduction of the duration of energy pulses to the millisecond range. Alio has compared outcomes of MICS with coaxial phacoemulsification and demonstrated significantly lowered mean phacoemulsification time, mean total phacoemulsification percent, mean EPT, and surgically induced astigmatism.65 Fine has described the benefits of bimanual microincision phacoemulsification for refractive lens surgery. He notes that capsulorrhexis construction, cortical cleaving hydrodissection, lens extraction in the iris plane, and residual cortex removal are facilitated by microincision surgery. This technique offers improved surgeon control throughout the procedure and added safety by maintaining continuous pressuriza- tion of the eye while removing the lens far from the posterior capsule.66 Weikert has noted that bimanual microincisional cataract surgery has been performed successfully using all of the major phacoemulsification

5.9 Small Incision Cataract Surgery

Fig. 5-9-4 Basic steps of a vertical chop technique with bimanual microincision phaco include (A) deeply embedding the phaco tip in the center of the nucleus and maintaining high vacuum as the irrigating chopper blade is brought down just distal to the phaco needle; lollipopping (B), mobilizing, and consuming a nuclear quadrant; and (C) flipping the epinuclear shell using the stream of irrigation fluid as a pushing tool.

platforms.67 Technological advances in ultrasound power management, including millisecond length pulses and variable duty cycles, and enhanced fluidics, such as low compliance tubing and in-line filter elements, have improved the safety profile and efficiency of this technique. New intraocular lens designs and surgical instrumentation permit intraocular lens insertion through corneal incisions measuring 2 mm or less. Clinical results achieved with bimanual microincisional cataract surgery and new microincision lenses are comparable to those obtained with conventional coaxial phacoemulsification and established intraocular lenses. Bimanual microincision cataract surgery is a promising surgical technique that continues to grow as phacoemulsification technology and intraocular lens designs evolve (Fig. 5-9-4).

CONCLUSION Since the time of Charles Kelman’s inspiration in the dentist’s chair (while having his teeth ultrasonically cleaned), incremental advances in phacoemulsification technology have produced ever-increasing benefits for patients with cataract. The competitive business environment and the wellspring of surgeons’ ingenuity continue to demonstrate synergistic activity in the improvement of surgical technique and technology. Future advances in cataract surgery will continue to benefit our patients as we develop new phacoemulsification techniques and technology.

REFERENCES 1. F ine IH. Architecture and construction of a self-sealing incision for cataract surgery. J Cataract Refract Surg. 1991;17:672–76. 2. Leaming DV. Practice styles and preferences of ASCRS members − 2001 survey. J Cataract Refract Surg. 2002;28:1681. 3. Colvard DM, Kratz RP, Mazzocco TR, Davidson B. Clinical evaluation of the Terry surgical keratometer. Am Intraocular Implant Soc J. 1980;6:249–51. 4. Masket S. Origin of scleral tunnel methods. [Letter to the Editor] J Cataract Refract Surg. 1993;19:812–3. 5. Girard LJ, Hoffman RF. Scleral tunnel to prevent induced astigmatism. Am J Ophthalmol. 1984;97:450–6. 6. McFarland MS. Surgeon undertakes phaco, foldable IOL series sans sutures. Ocular Surgery News 1990;8. 7. Maloney WF, Grindle L. Textbook of phacoemulsification. Fallbrook, CA: Lasenda Publishers; 1988:31–39. 8. Brown DC, Fine IH, Gills JP, et al. The Future of foldables. Ocular Surgery News. 1992; August 15 (Suppl); Panel discussion held at the 1992 annual meeting of the American Society of Cataract and Refractive Surgery.

9. K elman CD. Phacoemulsification and aspiration: a new technique of cataract removal: a preliminary report. Am J Ophthalmol. 1967;64:23. 10. Harms H, Mackensen G. Intracapsular extraction with a corneal incision using the Graefe knife. In: Blodi FC, ed. Ocular surgery under the microscope. Stuttgart, Germany: Georg Thieme Verlag; 1967 :144–153. 11. Paton D, Troutman R, Ryan S. Present trends in incision and closure of the cataract wound. Highlights Ophthalmol. 1973;14:3,176. 12. Arnott EJ. Intraocular implants. Trans Ophthalmol Soc UK 1981;101:58–60. 13. Galand A. La technique de l’enveloppe. Pierre Mardaga: Liege, Belgium; 1988. 14. Shimizu K. Pure corneal incision. Phaco Foldables. 1992;5:6–8. 15. Shepherd JR. Induced astigmatism in small incision cataract surgery. J Cataract Refract Surg. 1989;15:85–8. 16. Fine IH. Corneal tunnel incision with a temporal approach. In: Fine IH, Fichman RA, Grabow HB, eds. Clear-corneal cataract surgery & topical anesthesia. Thorofare, NJ: Slack, Inc.; 1993:5–26.

17. F ine IH, Fichman RA, Grabow HB. Clear-corneal cataract surgery & topical anesthesia. Thorofare, NJ: Slack, Inc.; 1993. 18. Rosen ES. Clear corneal incisions: a good option for cataract patients. A Roundtable Discussion. Ocular Surgery News, 1 February, 1998. 19. Park HJ, Kwon YH, Weitzman M, Caprioli J. Temporal corneal phacoemulsification in patients with filtered glaucoma. Arch Ophthalmol. 1997;115:1375–80. 20. Fine IH. Self-sealing corneal tunnel incision for smallincision cataract surgery. Ocular Surgery News,1 May, 1992. 21. Williamson CH. Cataract keratotomy surgery. In: Fine IH, Fichman RA, Grabow HB, eds. Clear-corneal cataract surgery & topical anesthesia. Thorofare, NJ: Slack, Inc.; 1993:87–93. 22. Langerman DW. Architectural design of a self-sealing corneal tunnel, single-hinge incision. J Cataract Refract Surg. 1994;20:84–8. 23. Kershner RM. Clear corneal cataract surgery and the correction of myopia, hyperopia, and astigmatism. Ophthalmology. 1997;104:381–9.

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24. G ills JP, Gayton JL. Reducing pre-existing astigmatism. In: Gills JP, ed. Cataract surgery: The state of the art. Thorofare, NJ: Slack, Inc.; 1998:53–66. 25. Nichamin L. Refining astigmatic keratotomy during cataract surgery. Ocular Surgery News,15 April, 1993. 26. Fine IH. New blade enhances cataract surgery − Techniques Spotlight. Ophthalmology Times. 1 September, 1996. 27. Fine IH. Special Report to ASCRS Members: Phacoemulsification incision burns. Letter to American Society of Cataract and Refractive Surgery members, 1997. 28. Taher B. Endophthalmitis: State of the prophylactic art. Eyeworld News. 1997; August:42–43. 29. Colleaux KM, Hamilton WK. Effect of prophylactic antibiotics and incision type on the incidence of endophthalmitis after cataract surgery. Can J Ophthalmol. 2000;35:373–8. 30. Ciulla TA, Starr MB, Masket S. Bacterial endophthalmitis prophylaxis for cataract surgery. Ophthalmology. 2002;109:13–26. 31. Soriano ES, Nishi M. Endophthalmitis: incidence and prevention. Curr Opin Ophthalmol. 2005;16:65–70. 32. Taban M, Sarayba MA, Ignacio TS, et al. Ingress of India ink into the anterior chamber through sutureless clear corneal cataract wounds. Arch Ophthalmol. 2005;123:643–8. 33. Wallin T, Parker J, Jin Y, et al. Cohort study of 27 cases of endophthalmitis at a single institution. J Cataract Refract Surg. 2005;31:735–41. 34. West ES, Behrens A, McDonnell PJ, et al. The incidence of endophthalmitis after cataract surgery among the U.S. Medicare population increased between 1994 and 2001. Ophthalmology. 2005;112:1388–94. 35. Miller JJ, Scott IU, Flynn HW Jr, et al. Acute-onset endophthalmitis after cataract surgery (2000−2004): incidence, clinical settings, and visual acuity outcomes after treatment. Am J Ophthalmol. 2005;139:983–7. 36. Cole RE, Acord DR. Preoperative and intracameral antibiotic prophylaxis and intraocular contamination during cataract surgery. J Cataract Refract Surg. 2004;30:2239–40. 37. Lundström M. Endophthalmitis and incision construction. Curr Opin Ophthalmol. 2006;17:68–71.

38. W asserman D, Apple D, Castaneda V, et al. Anterior capsular tears and loop fixation of posterior chamber intraocular lenses. Ophthalmology. 1991;98:425. 39. Neuhann T. Theorie und operationstechnik der kapsulorhexis. Klin Monatsbl Augenheilkd. 1987;190:542. 40. Gimbel HV, Neuhann T. Development, advantages and methods of the continuous circular capsulorrhexis technique. J Cataract Refract Surg. 1990;16:31. 41. Gimbel HV, Neuhann T. Letter to the editor: Continuous curvilinear capsulorrhexis. J Cataract Refract Surg. 1991;17:110. 42. Little BC, Smith JH, Packer M. Little capsulorrhexis tearout rescue. J Cataract Refract Surg. 2006;32:1420–2. 43. Faust KJ. Hydrodissection of soft nuclei. Am Intraocular Implant Soc J. 1984;10:75–7. 44. Davison JA. Bimodal capsular bag phacoemulsification: A serial cutting and suction ultrasonic nuclear dissection technique. J Cataract Refract Surg. 1989;15:272–82. 45. Sheperd JR. In situ fracture. J Cataract Refract Surg. 1990;16:436–40. 46. Gimbel HV. Divide and conquer nucleofractis phacoemulsification: Development and variations. J Cataract Refract Surg. 1991;17:281–91. 47. Fine IH. The chip and flip phacoemulsification technique. J Cataract Refract Surg. 1991;17:366–71. 48. Fine IH. Cortical cleaving hydrodissection. J Cataract Refract Surg. 1992;18:508–12. 49. Anis A. Understanding hydrodelineation: The term and related procedures. Ocular Surg News. 1991;9:134–7. 50. Gimbel HV. Divide and conquer nucleofractis phacoemulsification. J Cataract Refract Surg. 1991;17:281. 51. Shepherd JR. In situ fracture. J Cataract Refract Surg. 1990;16:436. 52. Fine IH. The chip and flip phacoemulsification technique. J Cataract Refract Surg. 1991;17:306. 53. Fine IH, Maloney WF, Dillman DM. Crack and flip phacoemulsification technique. J Cataract Refract Surg. 1993;19:797. 54. Koch PS, Katzen LE. Stop and chop phacoemulsification. J Cataract Refract Surg. 1994;20:566.

55. F ine IH. The choo-choo chop and flip phacoemulsification technique. Operative Tech Cataract Refract Surg. 1998;1:61–5. 56. Fine IH, Packer M, Hoffman RS. Use of power modulations in phacoemulsification. J Cataract Refract Surg. 2001;27:188–97. 57. Girard LJ. Ultrasonic fragmentation for cataract extraction and cataract complications. Adv Ophthalmol. 1978;37:127–35. 58. Girard LJ. Pars plana lensectomy by ultrasonic fragmentation 1984, part II: operative and postoperative complications, avoidance or management. Ophthalmic Surg. 1984;15:217–20. 59. Shearing SP, Relyea RL, Loaiza A, Shearing RL. Routine phacoemulsification through a one-millimeter nonsutured incision. Cataract. 1985;2(2):6–10. 60. Tsuneoka H, Shiba T, Takahashi Y. Feasibility of ultrasound cataract surgery with a 1.4 mm incision. J Cataract Refract Surg. 2001;27:934–40. 61. Tsuneoka H, Shiba T, Takahashi Y. Ultrasonic phaco emulsification using a 1.4 mm incision: Clinical results. J Cataract Refract Surg. 2002;28:81–6. 62. Agarwal A, Agarwal A, Agarwal S, et al. Phakonit: phacoemulsification through a 0.9 mm corneal incision. J Cataract Refract Surg. 2001;27:1548–1552. 63. Soscia W, Howard JG, Olson RJ. Bimanual phacoemulsification through 2 stab incision. A wound-temperature study. J Cataract Refract Surg. 2002;28:1039–43. 64. Soscia W, Howard JG, Olson RJ. Microphacoemulsification with WhiteStar. A wound-temperature study. J Cataract Refract Surg. 2002;28:1044–6. 65. Alió J, Rodríguez-Prats JL, Galal A, Ramzy M. Outcomes of microincision cataract surgery versus coaxial phacoemulsification. Ophthalmology. 2005;112:1997–2003. 66. Fine IH, Hoffman RS, Packer M. Optimizing refractive lens exchange with bimanual microincision phacoemulsification. J Cataract Refract Surg. 2004;30:550–4. 67. Weikert MP. Update on bimanual microincisional cataract surgery. Curr Opin Ophthalmol. 2006;17:62–7.

PART 5 THE LENS

Manual Cataract Extraction Frank W. Howes

Definition: Removal of crystalline lens by nonautomated or manual techniques.

Key features n�� n�� n�� n�� n��

ajor developments in cataract surgery over the past 20 years. M Evolution of techniques with experience. Intracapsular cataract extraction or large incision full lens extraction. Extracapsular cataract extraction or large incision nuclear expression cataract surgery. “Mininuc” technique or manual nucleus expression lens surgery through a small incision.

INTRODUCTION The principles of cataract surgery have changed substantially over the last 10 years. The mainstay of cataract surgery is now phacoemulsification through small corneal incisions, combined with the use of foldable intraocular lenses inserted through these small incisions to correct or minimize astigmatism. The techniques of large incision extracapsular surgery and intracapsular surgery are now used primarily as second line procedures to correct unusual intraoperative problems (e.g., nuclear sclerotic cataracts too dense for phacoemulsification where extracapsular type surgery would be safer or perhaps zonular loss disguised initially by posterior synechiae or otherwise, where conversion to intracapsular would be safer) or as primary procedures when certain conditions have been diagnosed preoperatively and are deemed inappropriate for phacoemulsification (e.g., dislocated lenses due to trauma, or zonular weakness due to congenital or degenerative conditions). The threshold for embarking on these procedures is dependent on the experience of the operating surgeon. The decision about the choice of procedure, in the broader sense, is based on a spectrum of factors related primarily to socioeconomic environment (e.g., equipment) and competence (of the surgeon and the surgical team) on the one hand and to the ophthalmological condition of the patient on the other hand.

HISTORICAL ISSUES Large incision nuclear expression cataract surgery, or extracapsular cataract extraction (ECCE), has been the mainstay of cataract surgery for at least the past two decades. The experiences gained from this form of surgery have in many ways contributed to the development of the smaller incision techniques. Much of the value of the large incision procedure is the lower cost and minimal instrumentation with which the surgery can be performed, a significant factor in third-world care. ECCE is also less demanding in terms of skill yet provides excellent rehabilitation of blindness caused by cataract at the expense of only recovery time and stability of refraction over the first year.1 Intracapsular cataract extraction (ICCE) still has a place in today’s surgical environment, but that place is restricted mainly to eyes with dislocated or subluxed crystalline lenses in the first-world environment. Because cataract is a worldwide problem, particularly in the Third World,

5.10

advanced equipment should not reduce the capacity to treat multitudes of patients who require surgery. It is in conditions of destitution that ICCE remains necessary, and undoubtedly there are ways to improve that operation under such conditions. Before World War II, both ECCE and ICCE were performed, but ECCE was predominant. In 1946 Stallard wrote, “The majority of conservative surgeons favour the extra-capsular method of extraction as being less dangerous from the point of view of vitreous loss.”2 However, the danger existed that lens cortex might remain in the eye after ECCE on an immature cataract, which sometimes excited devastating inflammation, such as severe iritis, phacoanaphylaxis, the development of dense secondary membranes, and glaucoma. Then, as now, ECCE often required secondary capsulotomy, and in those days, this could be very traumatic. In skilled hands, ICCE gave better results. Thus, ICCE held favor until the ECCE method was improved with the introduction of microsurgery in the 1950s and automated infusion-aspiration and phacoemulsification in the 1970s, which enabled the complete removal of lens cortex by peeling from the equator. The improved stability of an intraocular lens (IOL) when placed in the capsular bag encouraged surgeons to return to ECCE. With time, cataract removal became more successful, thanks to complete cortical removal and IOL stabilization against the capsular bag. This was followed by the desire to improve optical outcome by making smaller incisions with consequently less astigmatism and instability. The means of doing this slowly became available with the development of phacoemulsification, but the costs of equipment and the steepness of the learning curve created the need for techniques that reduced the requirement for sophisticated means of decreasing the nuclear size in order to remove fragments through smaller incisions. This led to the development of manual nuclear expression surgery through smaller incisions, or the so-called mininuc technique.3 The development of systems to provide continuous inflow of irrigating fluid while aspirating the lens remnant provided the cornerstones for all forms of extracapsular cataract surgery. These systems reached a high level of technological sophistication in the phacoemulsification techniques. In the mininuc systems, the need for high pressure and high flow for nuclear expression through a smaller incision led to the development of the wide-bore anterior chamber maintainer (ACM), which permitted such an intraocular environment. The independent infusion proved to be advantageous when used throughout the period of surgery because of the continuous flow and resultant positive pressure.4–6 As quoted by the inventor of the procedure:7 Small incision, machine-dependent phacoemulsification of the nucleus,8 which is a common procedure in certain parts of the world, was designed to overcome the need to express the nucleus of the cataract out of the eye through a large incision. Reduction of the size of the nucleus (“mini-nuc”) enables an alternative approach to nuclear expression that uses a manual technique.4 This surgery is best achieved if the operation is performed throughout under positive intraocular pressure9 (IOP), with the utilization of an anterior chamber maintenance system that provides continuous flow from the inside of the eye to the outside. The surgery is best performed through a sclerocorneal tunnel, the major portion of which is in the cornea. The nucleus is separated by hydrodissection and is manipulated manually in part or as a whole into the anterior chamber. Thereafter, nucleus expression is effected by the application of hydrostatic and external pressure, which enables lens implantation under the same conditions. A smaller incision

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5 THE LENS

than used in conventional nuclear expression can be made under topical anesthetic, and no sutures are required. Rehabilitation is rapid and the procedure is cost effective compared to phacoemulsification or any other manual nuclear expression extracapsular cataract extraction using viscoelastic material. In summary, the objective of this procedure is to express the smallest nucleus possible through an intact capsulorrhexis and thereafter through a small sclerocorneal3 tunnel.

LARGER INCISION CATARACT SURGERY Both intracapsular (ICCE) surgery and extracapsular (ECCE) surgery require large incisions, perhaps slightly larger in the ICCE group due to the increased size of the whole lens and the penalty of poor outcome should the capsule break on removal. In both techniques, however, attention to wound construction is vital if a good optical outcome is expected.

Incision

An incision of 8–12 mm of arc length around the limbus (corneal, limbal, scleral, or a combination thereof) is required to manually express the nucleus from the capsular bag in ECCE, whereas an incision of 12–14 mm around the limbus is required in ICCE. Variation in the incision position has a profound influence on the postoperative occurrence of cylindrical error;10 this can be used to benefit the patient. The more corneal the section is placed, the stronger the influence on the cylindrical error. The more scleral the section is placed, the less the cylindrical induction, particularly if a three-plane (Fig. 5-10-1), valve-type incision is utilized. Combinations of both scleral and corneal sections can be used to correct pre-existing cylindrical errors.11 These sections can be rotated appropriately to reduce cylindrical error in any meridian. When the incision is fashioned, the third plane of the incision (see Fig. 5-10-1) should be completed only when the anterior capsulectomy has been performed. This allows the anterior chamber to maintain depth, with or without viscoelastic material, while the anterior capsulectomy is undertaken. Once this is done, the internal incision may be completed.

THREE-PLANE SCLERAL SECTION first part of scleral incision showing incisional gape

second part of incision tunneled 2–3 mm in clear cornea

corneal edge of sectioned conjunctiva

third part of incision into anterior chamber

incised and deflected conjunctiva

Wound Closure

During closure of a wound cut in the three-plane format, the sutures must not be overtightened; the edges are merely opposed (incisional gape; see Fig. 5-10-1).12 The valve effect of the incision seals the wound. In cases in which leakage is excessive, closure can be obtained by intracameral air tamponade in preference to overtightening. A second chance to modify cylindrical effects arises when sutures are removed. This allows controlled dehiscence of the wound. Dehiscence induces negative cylindrical effect on the meridian of the suture removal (e.g., releasing a positive cylindrical effect induced by overly tight wound suturing). A rough guide to timing suture removal is as follows: l After 1 month if major wound dehiscence is required to correct cylindrical error (3–6 diopters) l After 2 months if minor dehiscence is required to correct cylindrical error (2–3 diopters) l At 3–6 months to resume preoperative cylinder l After 6 months to maintain surgically induced cylinder correction if appropriate

INTRACAPSULAR CATARACT EXTRACTION General Technique13

After confirmation that the anesthetized eye is soft and akinetic, a speculum is inserted to retract the lids without pressure being applied to the globe. An incision is made large enough for lens delivery. Endothelial touch must be avoided and a deep anterior chamber maintained during and after the procedure, with the lens removed in an intact capsule with minimal trauma and no disturbance of the vitreous face. Viscoelastic materials facilitate this process. One or two iridectomies (Fig. 5-10-2) are necessary to prevent pupil block, which may result in iris adhesion, incarceration, or prolapse through the wound. Alpha-chymotrypsin (if necessary and if available) is introduced through a cannula to pass behind the lower pupil border. Approximately 0.3 mL of fluid is injected over the zonule to the sides and below it, as well as through an iridotomy over the zonule above it. The fluid serves to weaken the zonule, prove the patency of the iridotomy, and irrigate small amounts of blood or iris pigment from the anterior chamber. This enables removal of the lens without zonular traction on the peripheral retina. With the dramatic reduction in the performance of intracapsular cataract surgery, the production of alpha-chymotrypsin has all but ceased and has thus become very difficult to obtain. However, the cases likely to need intracapsular surgery in today’s indications are likely to be those cases that already have damaged zonules. The lens can be held by capsule forceps, by suction, or by freezing with a cryoprobe; the last is the most reliable. In the cryoprobe technique (Fig. 5-10-3), the cornea is lifted at the incision by a preplaced suture so that the iris can be retracted using a dry cellulose sponge swab to uncover the peripheral lens capsule. The swab must absorb local moisture from the surrounding lens surface before the cryoprobe is applied to the lens capsule. As the probe operates, an ice ball forms and is observed closely until it includes some of the lens substance, while the local dryness prevents inadvertent ice ball linkage to surrounding tissues. This allows traction to be applied with little risk of tearing the capsule or surrounding tissue. There should be no lines of tension showing on the anterior capsule. The lens is then eased through the pupil by a combination of traction and expression. As the lens slides forward and upward, the full equatorial diameter engages and dilates the pupil. As soon as this point is reached, all expressive force is ceased, and the lens is delivered by sliding, using the cryoprobe alone (see Fig. 5-10-3). The vitreous face should be intact after the lens is delivered, but it is exposed fully to the aqueous. Freshly prepared acetylcholine solution is injected to constrict the pupil, protect the vitreous face, and reform the anterior chamber. The section is closed as described above.

Specific Techniques Iris management

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Fig. 5-10-1 Three-plane scleral section. This incision is formed by the use of a sharp microsurgical knife for the initial vertical segment, followed by use of a curved dissecting blade to form the intralamellar section of the incision. The final vertical portion of the incision into the anterior chamber is best cut with corneal microscissors. Tissue elasticity produces the incisional gape evident.

Even with a large cataractous lens, the pupil is sufficiently elastic to permit its extraction. Tears are unlikely except when the iris is atrophic, fibrosed from previous iritis, or chronically constricted from previous pilocarpine therapy. Posterior synechiae are divided using a spatula passed through the iridotomy, behind the iris toward the pupil.

PERIPHERAL IRIDECTOMY Forceps grasp iris and retract corneal lip

Tension on iris forms ridge

5.10 Manual Cataract Extraction

Scissors cut full iris thickness

Open iridectomy retracts to periphery

Fig. 5-10-2 The surgery of peripheral iridectomy. The midzone iris stroma is grasped from below the cornea through the wound lips at the 12 o’clock position, and the iris is drawn out of the incision by about 1 mm to tent its periphery. Curved or angled Vannas’ scissors are introduced from above, with the blades across the tented iris. The blades are closed to cut through the iris. The resultant small iridectomy opens and the iris retracts back through the incision into position as the instruments are removed. Iris pigment should be observed from the excised piece of iris to ensure that the posterior portion of the iris has been cut, confirming patency. (Adapted from Roper-Hall MJ. Stallard’s eye surgery, 7th ed. London: Wright; 1989.)

Fig. 5-10-3 Intracapsular delivery of the lens after it has been brought forward through the pupil with the cryoprobe. (A) The pupil constricts spontaneously as soon as the maximal diameter of the lens is through. In the lower left of the figure, the swab, moistened by aqueous and holding back the iris, is shown, as cryo traction slides the lens out of the eye. (B) The cornea has a concave surface, showing that the eye is soft without forward pressure from the vitreous body. The anterior chamber is reformed with a physiological solution. (From Roper-Hall MJ. Stallard’s eye surgery, 7th ed. London: Wright; 1989.)

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5 THE LENS

The adhesions are usually divided much more easily than their appearance suggests. Use of a cannula and viscoelastic material is an alternative method. Safe delivery of the intact lens is thus facilitated. If the iris is inelastic, a radial iridotomy (keyhole iridotomy − from peripheral iridectomy to pupil) must be performed. A suture can be preplaced before lens extraction so that the radial iridotomy can be repaired after lens extraction without danger to the vitreous face.

Vitreous presentation or prolapse

Vitreous prolapse must be avoided by ensuring that the vitreous volume is reduced during preparation and anesthetic administration and by preventing external pressure on the globe (see Fig. 5-10-3). The hazard is greatest when the maximal diameter of the lens has passed through the pupil. If vitreous prolapses through the pupil, it is essential to prevent its incarceration by sufficient anterior vitrectomy to clear the anterior vitreous from the anterior chamber. An injection of air into the anterior chamber facilitates observation and control.

Intraocular lenses

Because the capsular bag has been removed, the choice of IOL support is limited to the angle, the iris, or to the ciliary sulcus support (fixated by suture). The anterior chamber depth is maintained with viscoelastic material. An angle-supported lens must be fitted carefully to the individual chamber diameter so that it neither distorts nor moves. An iris-supported lens is more stable when placed in an oblique direction and prevented from rotating by suturing the haptic to the midperipheral iris stroma. Ciliary sulcus lens placement requires trans-scleral support by suture fixation and is useful when there is either iris damage (e.g., from trauma) or trabecular damage (e.g., associated with glaucoma). Adequate vitreous clearance is a prerequisite to all these placement sites, but particularly in ciliary sulcus placement.

EXTRACAPSULAR CATARACT EXTRACTION (NUCLEAR EXPRESSION) Extracapsular surgery entails more steps than intracapsular surgery, in that the capsular bag is left in the eye, held in position by the zonules. The loss of the refracting power of the crystalline lens is replaced by a synthetic intraocular lens that can rest either in the capsular bag (preferentially) or in the ciliary sulcus. To initiate the process, a hole is made in the crystalline lens in a central position in the visual axis (anterior capsulectomy). The remainder of the process involves careful removal of the contents. The important variables in this operation are the position and pattern of the incision, the position and method of the anterior capsulectomy, the method of nucleus expression, and the techniques of closure.

Anterior Capsulectomy

The techniques of anterior capsulectomy have changed over the past 20 years.14

“Can-opener” capsulectomy

The simplest type of capsular opening or capsulectomy is the “canopener” type, in which a number of very close, pinpoint perforations are created in a central, circular tract in the anterior capsule. Centri petal traction is placed on the central piece of capsule to create a tear along the perforations. The loose piece is then carefully removed. One advantage of this technique is the relative accuracy that can be achieved when visibility is poor (e.g., for a dense cataract with a poor red reflex or a very small pupil that requires the perforations to be made under the pupillary margin).

Linear capsulectomy (capsulorrhexis) and intercapsular techniques

468

Linear capsulectomy techniques enable external expression while the anterior capsule is utilized to protect the corneal endothelium. In this method, a curvilinear incision is made in the upper third of the anterior lens capsule to create a slit or envelope opening into the lens capsular bag. After nucleus mobilization and expression and cortical material removal, the IOL can be inserted into the remaining capsular bag. The capsulectomy is completed by performing a continuous curvilinear capsulorrhexis across the remaining capsule to effect the circular central opening.

Capsulorrhexis

Capsulorrhexis, or continuous curvilinear capsulectomy, is a quick and, once learned, easy technique for anterior capsule removal; it provides the best security for the IOL within the capsular bag.15 The initial capsulotomy can be made centrally with a cystotome or a bent needle or by utilizing the tip of the capsulorrhexis forceps. Once the capsule has been opened, a piece of anterior capsule is grasped and torn in a circular manner, with continuous change of the tearing vectors to achieve the round opening (capsulotomy) in the anterior capsule.

Size, type, and position of capsulectomy

The capsulectomy needs to be large enough for the passage of the nucleus. The size of the nucleus is age dependent but can be modified by hydrodissection and hydrodelineation using an appropriate cannula.16 If the nucleus is deemed too big for passage through the capsulectomy (e.g., after an unsuccessful hydrodelineation or after too small an initial capsulorrhexis), relaxing incisions in the capsulorrhexis are necessary to reduce the possibility of capsular dislocation and zonular damage during nucleus expression. During hydrodissection, if the anterior capsular opening is large enough, part of the equatorial rim of the nucleus can be expressed into the anterior chamber, then rotated into the anterior chamber and into the incision, and thus removed from the eye. Viscoelastic material between the corneal endothelial surface and the nuclear surface is necessary to prevent endothelial damage. The size and shape of the capsulorrhexis can be varied by the surgeon. A large capsulectomy facilitates surgery, but when this exceeds approximately 6.5 mm in diameter, the capsulorrhexis becomes difficult to control because of the presence of the insertion of the zonules.17 When the anterior capsular ridge is crossed, a peripheral radial tear18 is possible and may be irretrievable particularly if the anterior chamber is not kept deep (a shallow anterior chamber creates tension on the anterior zonules). Peripheral radial tears are usually blocked by the zonules, but extension around the fornix of the capsular bag can occur by this mechanism, causing unwanted posterior capsular tears.

Nuclear expression

The scleral lip of the incision should be depressed to allow the leading pole of the nucleus to present into the incision. Gentle pressure at the 180° opposing limbus then expresses the nucleus. The appropriate pressure may be applied with a broad-based instrument, such as a vectis or squint hook. Alternatively, internal expression using an irrigating vectis is effective, as long as the nucleus has undergone hydrodissection and partial hydroexpression. The space between the nucleus and the posterior capsule or cortex is opened with the irrigation function of the vectis. Viscoelastic material is also very useful in defining and holding these spaces and in preventing posterior capsular and endothelial damage.

Cortical washout

Removal of the remaining cortex using an irrigation-aspiration technique is not difficult, as long as the tip of the irrigation-aspiration cannula is kept in view to avoid unwanted capsular engagement. Difficulties can arise if the posterior globe pressure causes the anterior chamber to become shallow and causes closure of the fornix of the capsular bag. Partial closure of the wound and irrigation produce a deep and safe anterior chamber within which to work. Cleaning of the posterior capsule and removal of remaining resistant cortical remnants can be achieved by aspiration using a fine cannula with a polished tip.

Intraocular lens insertion

Insertion of the IOL is performed under direct vision, with the second haptic inserted either by circular dialing of the IOL or by direct placement using fine forceps.19 When the capsular bag is damaged by complication, the sites of intraocular placement become the same as those noted in the ICCE section. In some circumstances where there is still sufficient capsular support, in spite of capsular damage, posterior chamber implantation can be considered.

Small Incision Nuclear Expression Surgery (Mininuc Technique) Anterior chamber maintainer

An oval anterior chamber maintainer (Fig. 5-10-4) is inserted through clear cornea to the anterior chamber between the 4 o’clock and 8 o’clock positions, parallel to and near the limbus. The height of the infusion

5.10 Manual Cataract Extraction

Fig. 5-10-4 Anterior chamber maintainer located at the 6 o’clock position, parallel and adjacent to the limbus, in clear cornea. A 1.1 mm wide incision is made into the cornea in this position and tunneled approximately 1.5–2.0 mm.

Fig. 5-10-6 The nucleus is lodged in the pocket tunnel and hydroexpressed out of the eye. The glide is located behind the nucleus. External expression is performed on the glide away from the external incision of the pocket tunnel.

POCKET TUNNEL DISSECTION AREA AND BORDERS

Box 5-10-1 Complications of Cataract Surgery

7 mm corneal internal incision present pocket tunnel dimension previous tunnel dimension pocket area

5 mm scleral external incision

1 mm backward extension of scleral incision

Fig. 5-10-5 Pocket tunnel dissection area and borders.

bottle determines the intraocular pressure (IOP). The continuous flow is responsible for the anterior chamber maintenance system.

Capsulorrhexis

The IOP is increased to 40 mmHg (5.3 kPa). This pressure pushes the lens backward, which facilitates the formation of capsulorrhexis and prevents accidental radial capsule tear to the periphery.18 A 5–6 mm capsulorrhexis is preferred.

Sclerocorneal pocket tunnel

The scleral entrance incision to the sclerocorneal pocket tunnel is frown shaped and 5 mm long and is placed 1 mm behind the limbus (Fig. 5-10-5). At both ends of the incision, perpendicular backward continuation incisions 1 mm long are cut. This extension helps accommodate the thickness of the nucleus as it passes through the tunnel. The tunnel is dissected anteriorly for 3–4 mm (1 mm in the sclera, 1 mm in the limbus tissue, and 2 mm in clear cornea). Also, the scleral dissection is enlarged on both sides of the tunnel beyond the 1 mm backward scleral incision to make a pocket-like dissection (hence the term “pocket tunnel” rather than simply “tunnel”). The keratome internal incision is placed parallel to the curvature of the limbus and is 20% longer than the scleral outer incision. The pocket tunnel facilitates nucleus expression.

Nucleus manipulation

Hydrodissection is performed in two separate, anatomically distinct parts of the lens: first, just under the capsule, and second, between the hard-core nucleus and the epinucleus.19 Usually, the hydrodissection under the capsule partially moves the nucleus to the anterior chamber at the 12 o’clock position. If the nucleus does not move anteriorly, the hydrodissector cannula is lodged perpendicularly around the equator of the nucleus and then moved behind the nucleus. The positive IOP in the anterior segment pushes the posterior capsule away, which creates

Optical power aberrations (sphere and cylinder) Capsule rupture without vitreous loss Capsule rupture with vitreous loss Vitreous capture in incisional wound Iris prolapse Iris capture in incisional wound Nuclear loss into the posterior segment Intraocular lens loss into the posterior segment Inability to primarily implant intraocular lens due to above Glaucoma (aphakic, inflammatory, malignant, pupil block) Corneal endothelial damage Chronic inflammatory disease Cystoid macular edema Retinal detachment Hypotony Choroidal edema and effusion Choroidal hemorrhage Infection

a counterforce to the anterior movement of the hydrodissector cannula while the hard-core small nucleus is being separated from the epinucleus and cortex. In this way, the smallest possible hard-core nucleus is isolated, to be delivered through the intact capsulorrhexis. At this stage, the nucleus is ready for expression.

Nucleus expression

A plastic glide (4 mm wide, 0.2 mm thick) is introduced through the tunnel under the nucleus. Slight pressure is induced on the glide at the inner limbal area, which is used to guide the nucleus that is to be engaged in the sclerocorneal pocket tunnel. This pocket is made to accommodate the nucleus at this stage. When the nucleus is well lodged in the pocket, and no leakage of BSS is observed, slight scleral pressure is induced. The further the nucleus is expressed (Fig. 5-106), the more the location of the scleral pressure is moved backward. If the external pressure on the sclera is located near the internal incision throughout, an area of leakage is created rather than prevented, and nucleus expression cannot be completed. The IOP during nucleus expression is 40–45 mmHg (5.3–6.0 kPa), helping hydroexpression of the nucleus.

Cortex removal and intraocular lens implantation

Cortex removal and IOL implantation are facilitated by the deep anterior chamber formation induced by the anterior chamber maintainer system. The capsular bag is inflated during aspiration and during the IOL implantation. Insertion of the IOL is performed under direct vision, similar to ECCE, with the second haptic inserted either by circular dialing of the IOL or by direct placement using fine forceps.20 Once

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again, when the capsular bag is damaged by complication, the sites of intraocular placement become the same as those noted in the ICCE section. With a smaller incision than both ECCE and ICCE, the techniques of foldable lens insertion as per phacoemulsification surgery can be employed.

when lens material has not been completely removed or incisions have been closed poorly. Complications tend to be sequential, increasing the importance of producing a good result at the first surgery. Experience in each technique minimizes complications.

COMPLICATIONS

The drive to smaller incision surgery has continued and with new ideas in the techniques of smaller incision nuclear expression surgery combined with the introduction of anterior capsule staining techniques, advanced grades of cataract surgery have been performed successfully.21 These techniques continue to prove useful in the developing countries where cost constraints are a factor in the delivery of sight-saving cataract surgery.22 The results compare favorably with modern phaco emulsification surgery.23

Complications of cataract surgery tend to be similar, irrespective of the technique used, although the incidence of the different complications varies, depending on the technique (Box 5-10-1). In the majority of cases, these occur in relation to capsule damage with consequential anterior segment vitreous and iris damage, occasionally involving the incision as well. Poor technique may lead to inflammatory conditions

DISCUSSION

REFERENCES 1. Oshika T, Tsuboi S. Astigmatic and refractive stabilisation after cataract surgery. Ophthalmic Surg. 1995;26:309–15. 2. Stallard HB. Eye surgery. 1st ed. Bristol: Wright; 1946:263. 3. Blumenthal M. Manual ECCE, the present state of the art. Klin Monatsbl Augenheilkd. 1994;205:266–70. 4. Blumenthal M, Moisseiev J. Anterior chamber maintainer for extracapsular cataract extraction and intraocular lens implantation. J Cataract Refract Surg. 1987;13:204–6. 5. Blumenthal M, Cahane M, Ashkenazi I. Direct intra operative continuous monitoring of intraocular pressure. Ophthalmic Surg. 1992;23:132–4. 6. Blumenthal M. Manual nucleus expression through a small incision. In: Yanoff M, Duker JS, eds. Ophthalmology, 1st ed. London: Mosby; 1999 . 7. Blumenthal M, Assia E, Neuman D. Lens anatomical principles and their technical implication. J Cataract Refract Surg. 1991;17:211–7. 8. Obstbaum SA. Phacoemulsification, the favoured surgical technique. Editorial. J Cataract Refract Surg. 1991;17:267. 9. Blumenthal M, Assia E, Neuman D. The round capsu lorrhexis capsulotomy and the rationale for 11 mm diameter IOL. Eur Implant Refract Surg. 1990;2:15–9. 10. Storr-Paulsen A, Vangsted P, Perriard A. Long term natural and modified course of surgically induced astigmatism after extracapsular cataract extraction. Acta Ophthalmol (Copenh). 1994;72:617–21.

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11. Howes G. Control of astigmatism in cataract surgery. Presentation at 1986 Annual Meeting of the Ophthalmological Society of South Africa (P.O. Box 339, Bloemfontein 9300, South Africa) 12. Koch P. Incisional gape. Mastering phacoemulsification. 4th ed. Thorofare, NJ: Slack; 1994:23–4. 13. Roper-Hall MJ. Intracapsular cataract extraction. In: Yanoff M, Duker JS, eds. Ophthalmology, 1st ed. London: Mosby; 1999. 14. Apple D, Legler VF, Assia EI. Comparison of various capsulectomy techniques in cataract surgery. An experimental study [in German]. Ophthalmologe. 1992;89:301–4. 15. Gimbel H, Neuhann T. Development, advantages, and methods of the continuous circular capsulorrhexis. J Cataract Refract Surg. 1990;16:31–7. 16. Blumenthal M. Manual ECCE, the present state of the art. Klin Monatsblad Augenheilkd. 1994;205:266–70. 17. Sakabe I, Lim SJ, Apple DJ. Anatomical evaluation of the anterior capsular zonular free zone in the human crystalline lens [in Japanese]. Nippon Ganka Gakkai Zasshi. 1995;99:1119–22. 18. Assia E, Apple D. Mechanism of radial tear formation and extension after anterior capsulectomy. Ophthalmology. 1991;98:432–7.

19. Blumenthal M, Ashkenazi I, Assia E, Cahane M. Small incision manual extra-capsular cataract extraction using selective hydrodissection. Ophthalmic Surg. 1992;23:699–701. 20. Assia EI, Leglar V, Merril JC, et al. Clinicopathologic study of the effect of radial tears and loop fixation on intraocular lens decentration. Ophthalmology. 1993;100:153–8. 21. Venkatesh R, Das M, Prasanth S, Muralikrishnan R. Manual small incision cataract surgery in eyes with white cataracts. Indian J Ophthalmol. 2005;53:173–6. 22. Rao SK, Lam DS. A simple technique for nucleus extraction from the capsular bag in manual small incision cataract surgery. Indian J Ophthalmol. 2005;53:214–5. 23. Gogate PM, Kulkarni SR, Krishnaiah S, et al. Safety and efficacy of phacoemulsification compared with manual small-incision cataract surgery by a randomized controlled clinical trial: six-week results. Ophthalmology. 2005;112:869–74.

PART 5 THE LENS

5.11

Combined Procedures David Allen and David Steel

Key points n n n

n n n

ataract commonly develops in people with glaucoma. C Trabeculectomy increases the incidence of cataract in the target group. Combined surgery for glaucoma and cataract is a valid option in management − nevertheless, the doctor must bear in mind that cataract surgery alone results in lowered (and sustained) intraocular pressure (IOP). There is no rigorous evidence of the superiority of either single-site or two-site combined surgery. Sustained IOP lowering is less with combined surgery than trabeculectomy alone. Closed chamber phacoemulsification can often be used with a deep lamellar keratoplasty (the defect being filled with ophthalmic viscosurgical device to allow clear visualization). Placement of an iris-sutured posterior chamber IOL is an increasingly used option when the surgery is required to replace an anterior chamber IOL. Predictable refractive outcome from combined corneal graft and cataract removal remains problematic. The early incidence of cataract in phacic patients undergoing vitrectomy for most retinal conditions is high. Combined phacovitrectomy is increasingly common as a treatment option for conditions such as macular hole/pucker, even when pre-existing lens opacities are minimal, especially in the presbyopic age group.

INTRODUCTION Cataract develops mainly as a response to aging, but also to chemical or biologic insults to the eye. Frequently, these causative processes are associated with other conditions that may require surgical intervention. With the development of phacoemulsification, and its attendant reduced inflammatory response and early ocular stability, it has become more common to combine this surgical approach with that used for the coexisting disease. The conditions commonly associated with cataract and which lend themselves to such a combined approach are glaucoma, corneal opacity, effects of penetrating trauma, and vitreoretinal disorders.

COMBINED PHACOTRABECULECTOMY PREOPERATIVE EVALUATION AND DIAGNOSTIC APPROACH The prevalence of significant cataract in people aged 65−74 years is >20% and the prevalence of chronic glaucoma is about 4.5% in people over 70 years old.1, 2 The 5-year incidence of nuclear cataract in people with open-angle glaucoma and aged >50 is estimated to be 20%.2 Surgical trabeculectomy results in a 78% increase in the risk of cataract formation.3 For these reasons, combining cataract surgery and glaucoma surgery in a single operation appears to be a valid management option. However, an important consideration is that cataract surgery alone results in an IOP drop of up to 5 mmHg in patients with glaucoma.4

Patient expectation from combined procedures requires careful management. In this situation the use of some form of potential acu ity assessment may be of help. The extent to which the pupil dilates also influences the surgical approach, and enables the surgeon to assess the degree of increased risk of peroperative and early postoperative complications.

SPECIFIC TECHNIQUES Phaco combined with glaucoma surgery probably produces better IOP control with fewer complications than manual extraction plus glaucoma surgery, although there are no large well-controlled, randomized studies on this.4–6 However, the IOP reduction and subsequent control seems to be less effective with combined surgery than with trabeculectomy alone − possibly due to more prolonged breakdown of the blood aqueous barrier associated with cataract surgery.7 If surgeons consider combined surgery, a single-site approach may be less time consuming but a two-site approach allows the surgeon to use the familiar temporal clear corneal approach to the cataract. Debate continues on whether a single-site or two-site approach gives better control: several studies report no significant difference in pressure lowering effect. In a single-site approach a standard 5 mm wide trabeculectomy flap is fashioned, and phacoemulsification and implant insertion is performed through what would become the site of the penetrating sclerectomy. The sclerectomy is then completed with a blade or by using a punch, and this may be followed by peripheral iridectomy (although this is now less common). The scleral flap then is resutured in the normal way for a trabeculectomy (see Chapter 10-30). An alternative approach is to modify the standard self-sealing scleral tunnel phacoincision by removal of part of the posterior internal lip (Fig. 5-11-1) which destroys its self-sealing properties, but still allows a sutureless technique. In this technique, the surgeon creates a standard scleral tunnel incision that commences 2 mm posterior to the limbus. After cataract removal and intraocular lens insertion, a scleral punch is used to create a small sclerectomy. To facilitate this, a relieving incision often is made, either at one end of the phacoemulsification tunnel or in the center to form a ‘T’ incision (Fig. 5-11-2). After sclerectomy, a suture is used to secure the scleral flap if a relieving incision has been made, and the tightness of this or the period before laser suture lysis can be titrated in the standard way, as for a trabeculectomy. Nonpenetrating glaucoma surgery (deep sclerectomy or viscocanalostomy) can be combined with phacoemulsification. There are reports that these relatively new techniques are as effective as trabeculectomy when combined with phacoemulsification,8–10 but more longer term studies are required before their true place in treatment of coexisting cataract and glaucoma can be determined. In a recent series of chronic angle closure glaucoma patients, significant postoperative IOP reduction was obtained after viscodissection of the anterior chamber angle at the end of conventional phacoemulsification surgery for coexisting cataract.11 The authors describe this as viscogonioplasty. Further studies of this technique are required.

COMPLICATIONS The surgical approaches described above demand careful resuture of the conjunctival flap to minimize the possibility of hypotony, and to minimize the risk of intraocular infection. Postoperatively, a visible bleb often is thought to be a sign of successful drainage, but in practice there seems to be little correlation between bleb presence and continued IOP control.12 Nonpenetrating glaucoma surgery avoids the risks of hypotony

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PUNCH USED TO REMOVE CORNEAL FLAP

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cornea iris

sclera

Fig. 5-11-1 Punch used to remove internal corneal lip. Note the position and effect of the punch.

THE ’T‘ INCISION AND SUTURE

Fig. 5-11-2 T incision and suture.

and bleb complications. The incidence of inflammatory response in anterior chamber, fibrinous uveitis, and other complications is reported to be higher with combined surgery than with single operations.13, 14

OUTCOMES IOP reduction following combined surgery is greater than that following cataract surgery alone, although not as great as following trabeculectomy alone.15 The addition of mitomycin C may result in a greater reduction in IOP (although possibly only in those at high risk of surgical failure).16

LENS SURGERY COMBINED WITH KERATOPLASTY Historical Review

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Eyes that require penetrating keratoplasty often have an associated increased risk of cataract due to the underlying pathology (Fig. 5-11-3); this includes corneal perforation as a result of trauma or infection or age-related corneal degeneration, such as Fuchs’ corneal degeneration. Pseudophakic bullous keratopathy associated with the use of closed loop anterior chamber or irisfixated intraocular lenses (IOLs) became apparent during the 1980s and 1990s. These factors resulted in the development of a variety of techniques for combined primary cataract surgery and keratoplasty (the “Triple” procedure), or IOL exchange combined with keratoplasty.

Fig. 5-11-3 Patient with combined corneal and lens opacities. His degree of corneal opacity demands an open-sky approach to cataract removal.

SURGICAL OPTIONS A retrospective analysis of eyes that underwent penetrating keratoplasty for Fuchs’ endothelial dystrophy, with an average follow-up period of 6 years,17 showed an incidence of significant cataract in 75% of patients over 60 years of age. In those who subsequently required lens surgery, 13% lost transplant clarity postoperatively. In addition, those eyes that had significant pre-existing lens opacity had reduced visual benefit from keratoplasty. There are arguments, therefore, for simultaneous lens and corneal surgery. Weighed against these are the problems associated with a combined approach such as delayed visual rehabilitation; the decision in individual cases depends on the balance of the risks and benefits that apply. Choice of IOL depends on the individual circumstances. In the event that cataract surgery is part of the primary procedure, a standard IOL can be placed in the capsular bag. If an IOL is already present, and is considered either to be the cause of or to exacerbate the corneal decompensation, then it should be replaced. If sufficient capsular and/ or zonular support exists, then the best option is a capsule or sulcusplaced posterior chamber IOL. If adequate support is not available, then the choice is a posterior chamber IOL, either transclerally sutured or iris sutured.18, 19 Compared to refractive results within ±1 D of target in >90% with simple cataract removal, reported results from combined cataract extraction and penetrating keratoplasty are within ±2 D for between 26% and 67% of patients20 or ±3 D in 75%.21 Strategies employed to overcome this deficiency have included the use of fellow-eye keratometry readings, analysis of peripheral recipient corneal curvature,20 or retrospective analysis of a series of cases to produce surgeon-specific factors for use in regression formulas.22, 23 In this context, another approach that some surgeons find acceptable is to remove the cataract at the time of keratoplasty, but to insert the IOL as a secondary procedure some 12–18 months later, using the actual postkeratoplasty axial length and central keratometry to calculate the IOL power required. Although there are some reports of good outcomes using this approach, others showed no statistically significant difference in final refractive status using the technique.24

SPECIFIC TECHNIQUES The techniques of keratoplasty are dealt with elsewhere (Chapter 4-32). The surgeon needs to decide whether it is appropriate to retain the benefits of a closed system for phacosurgery or to use an open system and manual extracapsular techniques. Phacoemulsification surgery can be difficult because of the poor visibility as a result of the corneal disease. Selected cases may be suitable for a routine phacoemulsification procedure after deep lamellar keratectomy and use of an ophthalmic viscosurgical device (OVD) in the bed to restore anterior chamber and capsule visibility.25 An alternative is to perform a temporary full-thickness keratoplasty with reject corneal bank tissue, and replace this with a therapeutic graft at the conclusion of intraocular surgery.26 In cases of endothelial disease where the corneal clarity is reasonable, a new approach has been to combine phacoemulsification with Descemet’s stripping and automated deep endothelial keratoplasty. This offers much quicker visual

INDICATIONS AND ADVANTAGES OVER NONCOMBINED SURGERY Fig. 5-11-4 Abnormal reflexes make visualization of the posterior capsule difficult.

rehabilitation and more predictable refractive outcome than combined full-thickness keratoplasty and phaco.27 Such an approach is not always possible, and ‘open-sky’ removal of the lens may be required. The altered anterior chamber and lens−iris diaphragm dynamics, abnormal light reflexes present in the open-sky situation (Fig. 5-11-4),28 and difficulty in controlling the anterior and posterior capsule results in an increased risk of surgical complications. Capsulorrhexis can be difficult because of decreased anterior pressure caused by the open sky. Careful use of scissors can be of help. The nucleus is expressed manually after thorough hydrodissection. Manual irrigation−aspiration of the cortex is carried out using a cannula such as the Simcoe cannula. For surgery on an aphakic or pseudophakic patient, complete clearance of any vitreous from the anterior chamber is mandatory. If a scleral-sutured IOL is to be fixed, then clearance of vitreous from the posterior chamber and from the region of the pars plana−vitreous base is required. As well as the problems of surgical visibility, an open-sky approach to vitrectomy leads to instability of the whole anterior segment, and use of a scleral support ring is helpful.

COMPLICATIONS Apart from the possible inherent complications of keratoplasty, the combined procedure seems to offer an additional risk of cystoid macular edema. Other complications of combined procedures are the variability of refractive outcome and the delayed visual rehabilitation compared to straightforward cataract surgery. Weighed against this, however, is the additional risk of graft failure inherent in the alternative of a two-stage procedure.

OUTCOMES The respective theoretical risks and benefits of a combined approach, a planned staged approach, and a keratoplasty wait-and-see approach have been discussed already. No definitive studies presently exist that provide hard evidence of the benefit of one approach over another.

COMBINED PHACOVITRECTOMY INTRODUCTION Cataract, both age related and secondary, is present in many patients with vitreoretinal disorders. Cataract removal may be necessary to complete posterior segment surgery where cataract is obscuring the fundal view or it may be an integral part of a vitrectomy procedure, for example, in the case of a patient with a ruptured lens and a posterior segment intraocular foreign body (IOFB). Combined phacoemulsification with IOL implant and vitrectomy (phacovitrectomy) is now an established technique to deal with concomitant cataract when vitrectomy is performed.

HISTORICAL REVIEW When pars plana vitrectomy was first introduced in the 1970s, the optimum way to remove associated cataracts was uncertain. Intracapsular and extracapsular cataract surgery required large wounds, with problems of wound leak or even dehiscence during posterior segment surgery.

5.11 Combined Procedures

Pars plana lensectomy with ultrasonic fragmentation allows cataract removal and vitrectomy through small incisions and preserves the anterior capsule, permitting sulcus fixated IOL placement. However, it was the widespread acceptance of phacoemulsification in the late 1980s and 1990s that offered the possibility of efficient combined vitrectomy and cataract surgery, with secure wound construction and stable intracapsular IOL fixation. Newer generations of combined phaco and vitrectomy machines with dual cassettes allowed efficient transition between the two modes of surgery. Studies have shown that combined phacovitrectomy can be carried out with low morbidity and good results.29 As confidence with the technique has grown, indications for combined surgery have expanded.

Phacovitrectomy has now been used in a number of clinical situations including patients with IOFB, retinal detachment, uveitis, diabetes, and a variety of macular pathologies.29 When first introduced, phacovitrectomy was reserved for cases where cataract precluded an adequate fundal view during vitrectomy surgery. However, it is now being considered when lens opacities are mild or even nonexistent, particularly in patients over 60 years old.30 In these cases cataract surgery is not necessary to successfully complete the vitrectomy but is done to avoid the need for subsequent cataract surgery and hasten visual recovery. Vitrectomy surgery, particularly in the 50−60-year age group, often results in the development of significant lens opacities, especially if long-acting gases are used, as in macular hole surgery.31, 32 The practice of what could be called ‘nonessential’ phacovitrectomy in these situations offers a number of advantages over vitrectomy followed by subsequent cataract surgery in two steps. Only one operation is needed and the surgical difficulties and morbidity associated with cataract extraction following vitrectomy are avoided. These include small pupil size, deep anterior chamber with reverse pupil block, and increased mobility of the lens−iris diaphragm with an increased risk of posterior capsule tears. Combining phacoemulsification and vitrectomy also improves postoperative retinal visualization allowing accurate retinal assessment and treatment and visual recovery is not delayed by subsequent cataract development. Phacovitrectomy allows more complete anterior vitrectomy and access to the anterior retina and vitreous base. Arguably a more full vitrectomy allows a better gas fill, improving postoperative retinal tamponade.

DISADVANTAGES The presence of macular hole and macular pucker are the commonest clinical scenarios where nonessential phacovitrectomy is considered because of the high frequency of cataract formation after surgery for these conditions in the age group affected. However, not all patients are ideal candidates for nonessential phacovitrectomy and in some patients vitrectomy followed by sequential cataract surgery, if needed, is a better option. In diabetic patients, lens opacities following vitrectomy are paradoxically less common than in nondiabetic patients.33 Diabetic patients appear to have a higher incidence of posterior synechiae, posterior capsule opacity, and inflammatory anterior uveitis following phacovitrectomy, especially if retinopathy is very active, a large amount of intraoperative laser is needed, or gas tamponade is used.34 Therefore, although phacovitrectomy is frequently carried out successfully in diabetic patients with significant lens opacities,35 such patients do not always form ideal nonessential phacovitrectomy candidates. The absence of accurate preoperative biometry secondary to vitreo retinal pathology could also be regarded as a relative contraindication to nonessential phacovitrectomy. Fellow-eye measurements can be used but incorrect axial length estimations will result in IOL choice errors and potentially significant unplanned ametropia. Similarly, scleral buckling and silicone oil use alter the final refractive outcome in an unpredictable way.

SPECIFIC TECHNIQUES The lens surgery can be carried out successfully via either a clear corneal or scleral tunnel incision. If a corneal incision is used, then the tunnel should be kept relatively short to avoid interference with

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the posterior segment view. A suture can be used to secure the wound to avoid wound leak during scleral indentation. Posterior segment intraocular gas pressure can cause significant problems with phacovitrectomies. Anterior displacement of the optic of the IOL by posterior gas pressure can lead to optic capture by the iris. Similarly, displacement of the anterior capsule onto the iris can lead to postoperative posterior synechiae formation. There are a number of possible strategies to reduce the incidence of these problems. Sustained postoperative dilatation should be avoided, but some clinicians use short-acting mydriatics to discourage synechiae formation. Capsulorrhexis size should be large enough to avoid problems with rhexis phimosis, but should aim to just overlap the optic edges by 0.5 mm to hold the optic posteriorly. Capsulorrhexis can occasionally be difficult in eyes with vitreous hemorrhage and no red reflex. In these cases, capsule staining and use of the endoilluminator in the anterior chamber can assist visualization. IOL optic diameter should be large to reduce the risk of optic capture, and lenses with broad haptic fixation offer advantages in avoiding optic capture and superior IOL centration. Intraocular lens insertion can be performed either before or after vitrectomy is completed. Peripheral vitreous base view can be impaired

in pseudophakic eyes and there is an argument for leaving IOL insertion until after the posterior segment surgery is complete. Lenses with rounded tapering IOL edges and a gradual reduction in optic power offer advantages for ‘trans IOL’ vitrectomy by avoiding the occurrence of “jack-in-the-box” prismatic effects when viewing the posterior segment through the edge of the IOL. Posterior capsule opacity appears to be more common after phacovitrectomy, and primary capsulotomy with the vitrectomy cutter can be performed avoiding another threat to delayed visual recovery.36 Acrylic folding IOLs have several advantages over silicone with less IOL condensation during fluid−air exchange and also a reduced possibility of silicone oil adherence if oil is subsequently used.

CONCLUSION Phacovitrectomy is an effective technique to allow combined cataract extraction and vitrectomy. Its use is now being extended to patients with minimal lens opacities preoperatively undergoing, for example, macular hole surgery, to avoid delaying visual recovery secondary to postoperative cataract.

REFERENCES 1. M itchell P, Cumming RG, Attebo K, et al. Prevalence of cataract in Australia: the Blue Mountains Eye Study. Ophthalmology. 1997;104:581–8. 2. Chandrasekaran S, Cumming RG, Rochtchina E, et al. Associations between elevated intraocular pressure and glaucoma, use of glaucoma medications, and 5-year incident cataract: the Blue Mountains Eye Study. Ophthalmology. 2006;113:417–24. 3. The AGIS Investigators. The Advanced Glaucoma Intervention Study, 8: Risk of cataract formation after trabeculectomy. Arch Ophthalmol. 2001; 119: 1771–9. 4. Friedman DS, Jampel HD, Lubomski LH, et al. Surgical strategies for coexisting glaucoma and cataract: an evidence-based update. Ophthalmology. 2002; 109:1902–13. 5. Shingleton BJ, Jacobson LM, Kuperwaser MC. Comparison of combined cataract and glaucoma surgery using planned extracapsular and phacoemulsification techniques. Ophthalmic Surg Lasers. 1995;26:414–9. 6. Wishart PK, Austin MW. Combined cataract extraction and trabeculectomy: phacoemulsification compared with extracapsular technique. Ophthalmic Surg. 1993;24:814–21. 7. Siriwardena D, Kotecha A, Minassian D, et al. Anterior chamber flare after trabeculectomy and after phacoemulsification. Br J Ophthalmol. 2000;84:1056–7. 8. Gimbel HV, Anderson Penno EE, Ferensowicz M. Combined cataract surgery, intraocular lens implantation and viscocanalostomy. J Cataract Refractive Surg. 1999;25:1370–5. 9. Gianoli F, Schnyder CC, Bovey E, Mermoud A. Combined surgery for cataract and glaucoma: phacoemulsification and deep sclerectomy compared with phacoemulsification and trabeculectomy. J Cataract Refractive Surg. 1999;25:340–6. 10. Carassa RG, Bettin P, Fiori M, et al. Viscocanalostomy versus trabeculectomy in white adults affected by openangle glaucoma: a 2-year randomized, controlled trial. Ophthalmology. 2003;110:882–7. 11. Varma D, Adams WE, Phelan PS, Fraser SG. Viscogonioplasty in patients with chronic narrow angle glaucoma. Br J Ophthalmol. 2006;90:648–9. 12. Simmons ST, Litoff D, Nichols DA, et al. Extracapsular cataract extraction and posterior chamber intraocular lens implantation combined with trabeculectomy in patients with glaucoma. Am J Ophthalmol. 1987;104:465–70.

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13. N aveh N, Kottass R, Glovinsky J, et al. Long term effects on intraocular pressure of a procedure combining trabeculectomy and cataract surgery as compared with trabeculectomy alone. Ophthalmic Surg. 1990; 21:339–45. 14. Siriwardena D, Kotecha A, Minassian D, et al. Anterior chamber flare after trabeculectomy and after phacoemulsification. Br J Ophthalmol. 2000;84:1056–7. 15. Lochhead J, Casson RJ, Salmon JF. Long term effect on intraocular pressure of phacotrabeculectomy compared to trabeculectomy. Br J Ophthalmol. 2003;87:850–2. 16. Shin DH, Ren J, Juzych MS, et al. Primary glaucoma triple procedure in patients with primary open-angle glaucoma: the effect of mitomycin C in patients with and without prognostic factors for filtration failure. Am J Ophthalmol. 1998;125:346–52. 17. Payant JA, Gordon LW, VanderZwaag TO. Cataract formation following corneal transplantation in eyes with Fuchs’ endothelial dystrophy. Cornea. 1990;9:286–9. 18. Hardten DR, Holland EJ, Doughman DJ, Nelson JD. Early postkeratoplasty astigmatism following placement of anterior chamber lenses and transclerally sutured posterior chamber lenses. CLAO J. 1992;18:108–11. 19. Michaeli A, Assia EI. Scleral and iris fixation of posterior chamber lenses in the absence of capsular support. Curr Opin Ophthalmol. 2005;16:57–60. 20. Serdaravic ON, Renard GJ, Pouliquen Y. Videokeratoscopy of recipient peripheral corneas in combined penetrating keratoplasty, cataract extraction and lens implantation. Am J Ophthalmol. 1996;122:29–37. 21. Davis EA, Azar DT, Jakobs FM, Stark WJ. Refractive and keratometric results after the triple procedure: experience with early and late suture removal. Ophthalmology. 1998;105:624–30. 22. Flowers CW, McLeod SD, McDonnell PJ, et al. Evalua tion of intraocular lens power calculation formulas in the triple procedure. J Cataract Refractive Surg. 1996;22:116–22. 23. Viestenz A, Seitz B, Langenbucher A. Intraocular lens power prediction for triple procedures in Fuchs’ dystrophy using multiple regression analysis. Acta Ophthalmol Scand. 2005;83:312–5. 24. Pineros O, Cohen EJ, Rapuano CJ, Laibson PR. Long-term results after penetrating keratoplasty for Fuchs’ endothelial dystrophy. Arch Ophthalmol. 1996;114:15–8.

25. A rdjomand N, Fellner P, Moray M, et al. Lamellar corneal dissection for visualization of the anterior chamber before triple procedure. Eye. 2006;19 May [Epub ahead of print]. 26. Nardi M, Giudice V, Marabotti A, et al. Temporary graft for closed-system cataract surgery during corneal triple procedures. J Cataract Refractive Surg. 2001;27:1172–5. 27. Covert DJ, Koenig SB. New triple procedure: Descemet’s stripping and automated endothelial keratoplasty combined with phacoemulsification and intraocular lens implantation. Ophthalmology. 2007; e-pub 13 April (DOI: 10.1016/j.ophtha.2006.12.030). 28. Groden LC. Continuous tear capsulotomy and phacoemulsification cataract extraction with penetrating keratoplasty. Refractive Corneal Surg. 1990;6:458–9. 29. Chaudhry NA, Cohen KA, Flynn HW Jr, Murray TG. Combined pars plana vitrectomy and lens management in complex vitreoretinal disease. Semin Ophthalmol. 2003;18:132–41. 30. Ling R, Simcock P, McCoombes J, Shaw S. Presbyopic phacovitrectomy. Br J Ophthalmol. 2003;87:1333–5. 31. Cherfan GM, Michels RG, de Bustros S, et al. Nuclear sclerotic cataract after vitrectomy for idiopathic epiretinal membranes causing macular pucker. Am J Ophthalmol. 1991;111:434–8. 32. Thompson JT. The role of patient age and intraocular gas use in cataract progression after vitrectomy for macular holes and epiretinal membranes. Am J Ophthalmol. 2004;137:250–7. 33. Smiddy WE, Feuer W. Incidence of cataract extraction after diabetic vitrectomy. Retina 2004;24:574–81. 34. Shinoda K, O’Hira A, Ishida S, et al. Posterior synechia of the iris after combined pars plana vitrectomy, phacoemulsification, and intraocular lens implantation. Jpn J Ophthalmol. 2001;45:276–80. 35. Lahey JM, Francis RR, Kearney JJ. Combining phacoemulsification with pars plana vitrectomy in patients with proliferative diabetic retinopathy: a series of 223 cases. Ophthalmology 2003;110:1335–9. 36. Jun Z, Pavlovic S, Jacobi KW. Results of combined vitreoretinal surgery and phacoemulsification with intraocular lens implantation. Clin Exp Ophthalmol. 2001;29:307–11.

PART 5 THE LENS

Cataract Surgery in Complicated Eyes

5.12

Gary S. Schwartz and Stephen S. Lane

Key points n n n

onular integrity should be evaluated preoperatively at the slit Z lamp by looking for the presence of phacodonesis or iridodonesis. A capsulorrhexis technique results in stronger capsular support during both nucleus and cortex removal. In the face of zonular laxity, a large capsulorrhexis (at least 5.5 mm in diameter) facilitates removal of nuclear fragments by minimizing zonular stress. A simple technique one can use to stabilize the capsular bag and facilitate completion of the capsulorrhexis when there are large areas of capsular dehiscence utilizes capsular fixation hooks. Zonular dehiscence may be best managed by a polymethyl methacrylate capsular fixation segment or ring during cataract extraction alone or in combination with iris fixation hooks to stabilize the weakened areas. An intact anterior capsulorrhexis may provide adequate support for a posterior chamber intraocular lens even if there is some zonular laxity by prolapsing the optic through the anterior capsulorrhexis, capturing it in the capsular bed while the haptics are placed in the ciliary sulcus. Pachymetry and specular microscopy should be performed as part of the preoperative assessment on any patients with suspect cornea; a history of morning corneal edema predicts a poor prognosis for corneal clarity following even the most atraumatic cataract extraction procedure.

INTRODUCTION Following uncomplicated extracapsular cataract extraction, it is the standard of care that a posterior chamber intraocular lens implant (PCL) be placed within the capsular bag. Most surgeons agree that the intracapsular placement of a PCL minimizes both the incidence of postoperative lens decentration and inflammation secondary to contact between the intraocular lens (IOL) and the iris and ciliary body. Occasionally, a case presents for which the surgeon must determine whether capsular bag placement is truly the preferred way to proceed after cataract extraction. Patients who have a previous history of trauma, pseudoexfoliation syndrome, or Marfan’s syndrome may have areas of zonular dehiscence that preclude safe intracapsular IOL placement. Other patients may experience zonular dehiscence or posterior capsule rupture during cataract extraction, either of which forces the surgeon to rethink the decision of where to place the IOL. A host of other factors, including a history of uveitis, the patient’s age, status of the vitreous and capsule, and prior surgeries, all affect the decision concerning IOL placement after cataract extraction.

PREOPERATIVE EVALUATION AND DIAGNOSTIC APPROACH When cataract surgery and IOL placement are planned, especially for a patient who has a prior history of ocular trauma, surgery, pseudo exfoliation syndrome, or crystalline lens subluxation (e.g., Marfan’s syndrome), it is important to evaluate the status of the zonules. If

a PCL is to be placed into either the capsular bag or the ciliary sulcus, the zonules must hold the implant in place throughout the remainder of the life of that patient. Patients who do not have adequate zonular support may experience postoperative IOL decentration or dislocation following capsule or sulcus placement.1, 2 Zonular integrity should be evaluated preoperatively at the slit lamp by looking for the presence of phacodonesis or iridodonesis. If any ques tion of loss of zonular integrity exists on the basis of slit-lamp evalua tion, the zonules must be evaluated gonioscopically. If a patient has a history of ocular trauma, the eye should also be examined for iridodialy sis and vitreous in the anterior chamber, either of which makes zonular dehiscence more likely. The patient is also evaluated for evidence of uveitis. Both uveitic inflammation and the corticosteroid treatment of uveitis can result in visually disabling cataract. The cause of the uveitis must be elucidated. Some forms of uveitis, such as pars planitis, Fuchs’ heterochromic iridocyclitis, and human leukocyte antigen B27 (HLA-B27)-associated uveitis, tend to heal well with IOL placement after cataract extraction.3 In others, such as uveitis of Vogt-Koyanagi-Harada syndrome, sympa thetic ophthalmia, and juvenile rheumatoid arthritis, the IOL may con tribute to intraocular inflammation, and therefore it may be prudent to leave these patients aphakic.4, 5 However, at least one study discusses the successful implantation of PCLs in older patients who have cataract and a history of juvenile rheumatoid arthritis.6 In vitro and in vivo studies have demonstrated an advantage of heparin surface-modified polymethyl methacrylate (PMMA) lenses compared with regular PMMA lenses when looking at the adhesion of inflammatory cells.7 For this reason, heparin surface-modified PMMA lenses probably have an advantage over regular PMMA lenses in patients with a history of uveitis. However, because of the necessity for a larger incision when using PMMA lenses, it remains to be seen whether heparin surface-modified lenses have an advantage over foldable silicone or acrylic IOLs when otherwise small-incision phacoemulsification is performed. If an IOL is to be placed in a patient who has a history of uveitis, an anterior chamber lens or a sulcus-supported posterior chamber lens should be avoided whenever possible, as increased con tact with the iris and ciliary body may result in increased postoperative inflammation.

GENERAL TECHNIQUES In general, the surgical technique used for cataract extraction in com plicated eyes will depend upon the surgeon’s experience and preference. The surgeon must weigh the advantages and disadvantages of various steps in the surgical technique, notably incision (type, location, length), method for removal of the cataract (phacoemulsification vs. nuclear expression), iris manipulation, and choice of intraocular lens. Phacoemulsification can be performed with continuous-tear capsu lorrhexis, while nuclear expression (NE) extracapsular cataract extraction is often done through either a can-opener capsulectomy or capsulorrhexis with relaxing incisions. The capsulorrhexis technique results in stronger capsular support during both nucleus and cortex removal.8 In addition, because the nucleus is taken out in small pieces during phacoemulsifi cation, its removal causes less stress on the capsule and zonules than does expression of the whole nucleus, as occurs in NE. Several options exist for IOL placement in combination with com plicated cataract surgery (Table 5-12-1). Which procedure is chosen depends upon many factors but mostly on the condition of the zonules

475

TABLE 5-12-1 OPTIONS FOR INTRAOCULAR LENS PLACEMENT AFTER CATARACT EXTRACTION

THE LENS

Procedure

Position of Optic

Position of Haptics

Haptic Fixation

Intracapsular posterior chamber intraocular lens implant

Capsular bag

Capsular bag fornices

Forward-prolapsed optic

Posterior chamber

Capsular bag

Capsular bag fornices

Sulcus-supported posterior chamber intraocular lens implant

Posterior chamber

Ciliary sulcus

Optic bag–haptic sulcus

Capsular bag

Ciliary sulcus

Trans-sclerally sutured posterior chamber intraocular lens implant

Posterior chamber

Ciliary sulcus

Trans-scleral sutures

Iris-sutured posterior chamber intraocular lens implant

Posterior chamber

Ciliary sulcus

Iris sutures

Anterior chamber lens

Anterior chamber

Anterior chamber angle

Aphakia

None

The “forward-prolapsed optic” and “optic bag–haptic sulcus” techniques depend on an intact continuous curvilinear capsulorrhexis.

and capsule and the experience of the surgeon. As a further option, the patient may be left aphakic. For such patients, visual rehabilitation may be achieved with the aid of aphakic spectacles or contact lenses. Epikeratophakia, although uncommon today, is another option for the aphakic patient.

SPECIFIC TECHNIQUES Zonular Dehiscence

476

Aside from a few specific precautions, cataract extraction in compli cated eyes should be performed much as it is for uncomplicated ones. If the eye is compromised by loss of zonular support, as in cases of prior trauma, surgery, or pseudoexfoliation syndrome, care must be taken to preserve as much of the remaining supporting zonules as possible. A large capsulorrhexis (at least 5.5 mm in diameter) is made to facilitate removal of nuclear fragments with minimal zonular stress. Careful and complete hydrodissection is carried out so that the nucleus rotates easily within the capsular bag, which decreases stress on the zonules during removal. If phacoemulsification is to be carried out within the capsu lar bag, the phaco needle tip should be maneuvered to create troughs toward the area of the dehiscence whenever possible. In this way the lens nucleus is pushed toward the weakened area, which preserves the zonules, rather than pushed away from it, which may cause exten sion of the area of zonular dehiscence. If the surgeon feels that zonular support is not adequate for intracapsular manipulation, the nucleus may be subluxed from the capsular bag and phacoemulsification can be performed within the anterior chamber. The surgeon may experience difficulty in performing capsulorrhexis in patients with significant zonular dehiscence because there are no zonules to offer resistance to the tearing forces applied by the surgeon’s instrument.9 A simple technique one can use to stabilize the capsu lar bag and facilitate completion of the capsulorrhexis utilizes capsular fixation hooks.10 If these are not available, nylon iris fixation hooks can be used in a similar manner. After starting the capsulorrhexis, the surgeon gently retracts the capsular edge with hooks in the direction of the area of dehiscence. After the capsulorrhexis is completed, the hooks can be left in place while hydrodissection and phacoemulsification are performed. Once the nucleus and epinucleus have been removed, cortical cleanup must be performed both delicately and completely. With the nucleus re moved, the capsular bag is floppier in nature, and the area of the dehis cence may be drawn toward the aspiration tip. In such cases, it may give the surgeon more control to separate the irrigation and aspiration ports and perform bimanual irrigation-aspiration. In this way, the irrigation tip can be used to hold back the capsular fornix of the area of dehiscence while the aspiration tip safely removes cortex. After complete removal of the cataract, the IOL must be selected. Whenever possible, the IOL is placed within the capsular bag for rea sons described above. Intracapsular IOL placement without a capsular

tension segment or ring may be appropriate for patients who have up to 6 clock hours of zonular dehiscence. In such cases, a PCL with PMMA haptics should be placed so that one of the haptics is aimed toward the area of dehiscence, thus spreading the bag out in that direction (Fig. 5-12-1). If the haptics are rotated so that they are 90° away from the dehiscence, the optic will likely decenter in a direction away from the area of dehiscence. Zonular dehiscence can also be managed by a PMMA capsular fixa tion segment or ring during cataract extraction. Fixation segments and some fixation rings, such as the Cionni ring, have eyelets on them to allow fixation to the scleral wall with a prolene suture.11 These seg ments and rings are left in place after surgery and have been shown to help both expand and center the capsular bag postoperatively, thus keeping the lens implant from migrating away from areas of zonular dehiscence. If the capsular support is felt to be inadequate for intracapsular lens placement, an alternate technique should be performed (see Table 5-12-1). A sulcus-supported PCL can be placed so that the haptics are 90° away from the area of dehiscence (Fig. 5-12-2). This orienta tion prevents the haptic from slipping posteriorly into the vitreous chamber. If a continuous curvilinear capsulorrhexis has been per formed, it may be advantageous to prolapse the optic into the capsular bag while the haptics are kept in the surgical sulcus. This technique often results in more stable optic centration in the presence of zonular dehiscence. If not enough capsule is present to support both haptics, a PCL may be sutured to the iris or held in place with a trans-scleral suture (Fig. 5-12-3).12 Since trans-scleral and iris fixation procedures are technically difficult to perform, the surgeon may opt for placement of an anterior chamber lens instead. Today’s anterior chamber lenses, with their onepiece, PMMA, flexible, open-loop configuration, have proved to be a safe alternative.

Uveitis

Cataract extraction with IOL insertion in uveitic patients is often made more difficult because of small pupils, posterior synechiae, and postoperative inflammation. If possible, a patient should not be oper ated upon until the uveitis has been quiescent for 6 months to a year. Even so, uveitic patients should receive oral prednisone 10 mg/kg daily for up to 1 week prior to surgery followed by a 2–3-week taper. Patients may benefit from intravenous methylprednisolone sodium succinate 125–250 mg during the surgery. Patients with chronic uveitis second ary to herpes simplex virus should be treated with perioperative oral antivirals. Phacoemulsification is usually the procedure of choice for patients who have a history of uveitis.13 This technique normally is performed through a smaller incision and results in less iris manipulation than does large-incision NE, and therefore usually results in less post operative inflammation and faster healing. Making the wound in the avascular clear cornea results in less inflammation than that through

INTRACAPSULAR POSTERIOR CHAMBER INTRAOCULAR LENS IMPLANT PLACEMENT WITH ZONULAR DEHISCENCE Correct placement

5.12

Incorrect placement

iris oval-shaped capsulorrhexis

equator of capsular bag

haptic posterior chamber intraocular lens

zonules

posterior chamber intraocular lens

zonules

equator of capsular bag

area of zonular dehiscence

haptic points away from area of zonular dehiscence area of zonular dehiscence

Cataract Surgery in Complicated Eyes

direction of decentering of posterior chamber intraocular lens

capsulorrhexis

Fig. 5-12-1 Intracapsular posterior chamber intraocular lens implant placement with zonular dehiscence. The intraocular lens is first shown placed properly in the capsular bag with the haptics positioned toward the area of dehiscence. In this way, the bag is stretched toward the dehiscence and the optic does not decenter. Note that the capsulorrhexis is oval shaped because it has been pulled by the haptic in the direction of the dehiscence. The intraocular lens is then shown placed incorrectly in the bag with the haptics oriented 90° away from the dehiscence. A posterior chamber intraocular lens implant placed thus decenters away from the area of dehiscence in the direction of the arrow.

SULCUS PCL WITH ZONULAR DEHISCENCE capsulorrhexis is posterior to PCL optic equator of capsular bag posterior chamber intraocular lens

area of zonular dehiscence

haptic actually lies on top of the zonular ligaments zonules

Fig. 5-12-2 Sulcus PCL with zonular dehiscence. The IOL is properly placed in the ciliary sulcus. The haptics lie away from the area of the dehiscence and therefore are in the areas of greatest support. Placement here will decrease the likelihood that the haptics will prolapse backward into the vitreous cavity.

a scleral pocket incision because the limbal and conjunctival blood vessels are spared. Often, posterior synechialysis must be performed, which can be done with a cyclodialysis spatula or with viscodissection. The pupil may need to be enlarged by stretching it. The surgeon has the choice of stretching the pupil with two instruments usually found on the surgical tray (e.g., Beckert and chopper) or may use an instrument specifically designed for pupillary dilation (e.g., Beehler pupil dilator). If simple stretching

does not provide the surgeon with an adequate pupil size to perform the surgery safely, self-retaining nylon iris hooks or other pupil-enlarging devices may be used. After the cataract has been removed, the surgeon must address the question of which IOL to implant. In uveitic patients, it is best to avoid anterior chamber lenses, iris-supported PCLs, and sulcus-supported PCLs as they have a tendency to cause postoperative inflammation as a result of contact with the iris and ciliary body. Whenever possible,

477

TRANS-SCLERALLY SUTURED POSTERIOR CHAMBER INTRAOCULAR LENS IMPLANT WITH NO ZONULAR SUPPORT

THE LENS

buried knot

eyelet on haptic

posterior chamber intraocular lens haptic with eyelet

peripheral iridectomy iris

iris with peripheral iridectomy

trans-scleral suture posterior chamber intraocular lens haptic with eyelet

posterior chamber intraocular lens

Fig. 5-12-3 Trans-sclerally sutured posterior chamber intraocular lens implant with no zonular support. The intraocular lens has no natural support from the lens capsule and zonules. This implant is a one-piece, polymethyl methacrylate intraocular lens held in place by two trans-scleral 10-0 prolene sutures tied to eyelets on the haptics. The knots are rotated to decrease the risk of long-term complications from knot erosion through the conjunctiva.

a capsule-supported PCL is used. If capsular support is not present at the time of IOL implantation, a trans-sclerally sutured PCL may be used, or the patient may be left aphakic.

Compromised Endothelium

Some patients, specifically those with Fuchs’ endothelial dystrophy, have a compromised endothelium at the time of cataract surgery. They may or may not have symptomatic corneal edema prior to surgery. Regard less, the trauma of intraocular surgery will lead to further endothelial cell loss, and can potentially cause prolonged, and even irreversible, corneal edema. Pachymetry and specular microscopy should be performed as part of the preoperative assessment on any patients with suspected corneal edema. The surgeon should consider altering the surgical technique to

diminish damage to the corneal endothelial cells. Rather than making the incision through temporal clear cornea, the surgeon may wish for a more posterior, scleral tunnel approach. A dispersive ophthalmic viscosurgical device will be more protective to the corneal endothelium than a cohesive one, and the surgeon may wish to periodically refill the anterior chamber with it during the procedure. Phacoemulsification energy and time should be kept to a minimum, and nuclear fragments should be emulsified as posteriorly as possible with the tip of the phaco handpiece aimed away from the cornea. Postoperatively, patients with corneal edema may benefit from topical hyperosmotic agents. Despite all these steps, however, cor neal decompensation may occur and it is critical that adequate informed consent (including a discussion of the possibility of post cataract surgery corneal transplantation) is obtained prior to the procedure.

REFERENCES 1. S mith SG, Lindstrom RL. Report and management of the sunrise syndrome. J Am Intraocul Implant Soc. 1984;10:218–20. 2. Apple DJ, Mamalis N, Loftfield K, et al. Complications of intraocular lenses. A historical and histopathological review. Surv Ophthalmol. 1984;29:1–54. 3. Tessler HH, Farber MD. Intraocular lens implantation versus no intraocular lens implantation in patients with chronic iridocyclitis and pars planitis. Ophthalmology. 1993;110:1206–9. 4. Hooper PL, Rao NA, Smith RE. Cataract extraction in uveitis patients. Surv Ophthalmol. 1990;35:120–44. 5. Fox GM, Flynn HW Jr, Davis JL, Culbertson W. Causes of reduced visual acuity on long-term follow-up after cataract extraction in patients with uveitis and juvenile rheumatoid arthritis. Am J Ophthalmol. 1992;114:708–14.

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6. P robst LE, Holland EJ. Intraocular lens implantation in patients with juvenile rheumatoid arthritis. Am J Ophthalmol. 1996;122:161–70. 7. Ygge J, Wenzel M, Philipson B, Fagerholm P. Cellular reactions on heparin surface-modified versus regular PMMA lenses during the first postoperative month. Ophthalmology. 1990;97:1216–23. 8. Thim K, Krag S, Corydon L. Stretching capacity of capsulorrhexis and nucleus delivery. J Cataract Refract Surg. 1991;17:27–31. 9. Ahmed IIK, Crandall AS. Ab externo scleral fixation of the Cionni modified capsular tension ring. J Cataract Refract Surg. 2001;27:977–81. 10. MacKool RL. Capsule stabilization for phacoemulsification. J Cataract Refract Surg. 2000;26:629.

11. H asanee K, Butler M, Ahmed IIK. Capsular tension rings and related devices. Curr Opin Ophthalmol. 2006;17:31–41. 12. Lane SS, Agapitos PJ, Lindquist TD. Secondary intraocular lens implantation. In: Lindquist TD, Lindstrom RL, eds. Ophthalmic surgery. St Louis: Mosby; 1993:IG1–18. 13. Raizman MB. Cataract surgery in uveitis patients. In: Steinert RF, ed. Cataract surgery: technique, complications, and management, Philadelphia: WB Saunders; 1995:243–6.

PART 5 the lens

Pediatric Cataract Surgery Elie Dahan

Definition: Cataracts occurring in the pediatric age group, arbitrarily birth to adolescence.

Key features n

T wo main approaches are used to remove cataracts in children: pars plana and limbal. Spectacles, contact lenses, and intraocular lenses are the most readily available means to correct aphakia in children. Posterior chamber intraocular lenses supplemented by spectacles are the best option for correction of aphakia in children because most of the correction is permanently situated inside the eye globe.

INTRODUCTION

5.13

of cataracts in childhood or other ocular abnormalities can be relevant. Both parents and all siblings should be examined with a slit lamp to determine any lens abnormalities. When family history is positive, consultation with a geneticist is recommended. A thorough examination by a pediatrician to assess the general health of the child and to elicit information as to other congenital abnormalities is mandatory. Laboratory tests in children who have bilateral cataracts in nonhereditary cases are listed in Box 5-13-1. Most unilateral pediatric cataracts are idiopathic and do not warrant exhaustive laboratory tests. The ophthalmologic part of the evaluation starts with a complete ocular examination, which includes an assessment of visual acuity, pupillary response, and ocular motility. Biomicroscopy follows and might necessitate sedation or even general anesthesia in very young patients. Indirect fundus examination with dilated pupils is made unless the cataract is complete. A- and B-scan ultrasonography is carried out in both eyes to compare axial lengths and to discover any posterior segment abnormalities. Earlier photographs should be examined for the quality of the pupil’s red reflexes. This might help to date the onset of the cataracts.

ALTERNATIVES TO SURGERY

Cataracts in childhood not only reduce vision but also interfere with normal visual development.1–3 The management of pediatric cataracts is, by far, more complex than the management of cataracts in adults. The timing of surgery, the surgical technique, the choice of the aphakic correction, and the amblyopia management are of utmost importance to achieve good and long-lasting results in children.4–10 Children’s eyes are not only smaller than adults’ eyes, but their tissues are also much softer. The inflammatory response to surgical insult seems more pronounced in children, often because of iatrogenic damage to the iris.11 During the past two decades, the refinements that have occurred in adult extracapsular cataract surgery have contributed to the further development of pediatric cataract surgery.2, 4–8 Certain adaptations and modifications in surgical technique are required to achieve results similar to those achieved in adults.2–8 Furthermore, postoperative amblyopia management forms an integral part of visual rehabilitation in children.1–10

The development of metabolic cataracts, such as those found in galactosemia, can be reversed if they are discovered in the early phases. With the elimination of galactose from the diet, the early changes in the lens, which resemble an oil droplet in the center of the lens, can be reversed.13 Later on, lamellar or total cataracts develop, which require surgery. When lens opacities are confined to the center of the anterior capsule or the anterior cortex, mild dilatation of the pupils with homatropine 2% twice daily can improve vision and postpone the need for surgery. Photophobia and partial loss of accommodation are side effects of this measure. This temporary management should be implemented only in bilateral cataracts in which vision is equal in both eyes and better than 20/60 (6/18).

HISTORICAL REVIEW

ANESTHESIA

Discission of soft cataracts was first described by Aurelius Cornelius Celsius, a Roman physician who lived 2000 years ago. Because of its simplicity, discission remained the method of choice until the middle of the twentieth century. The technique consisted of lacerating the ante rior capsule and exposing the lens material to the aqueous humor for resorption and/or secondary washout. Wolfe and Wolfe12 in 1941 refined the technique by introducing the double-barreled aspirating-irrigating cannula, which allowed a one-step procedure. Repeated discissions were often required to manage the inevitable secondary cataracts.2, 11 Many early complications, e.g., plastic iritis, glaucoma, and retinal detachments, were associated with these early techniques.2, 11 With the advent of vitrectomy machines and viscoelastic substances as well as the refinements in extracapsular cataract surgery, these complications have been reduced markedly over the past two decades.2–11

General anesthesia is presently the only anesthetic option in pediatric cataract surgery. It is extremely important to request deep anesthesia with paralysis and ventilation throughout the procedure.5, 7, 8 The extra ocular muscles are the last striated muscles to relax under drugs that cause paralysis. The sclera and cornea are very soft in childhood. Any tension on the extraocular muscles is transmitted to the sclera and results in increased intraocular pressure. A useful marker for anesthesia depth is the position of the eye during surgery. If the cornea moves upwards, the anesthesia is too light and should be deepened. When this advice is followed, surgery is easier to perform and iatrogenic damage to the iris and cornea is diminished.

PREOPERATIVE EVALUATION AND DIAGNOSTIC APPROACH A careful history demonstrates to the clinician the investigations required to determine the cause of cataracts in children.2 Problems during pregnancy (e.g., infections, rashes or febrile illnesses, exposures to drugs, toxins, or ionizing radiation) should be elicited. Family history

GENERAL TECHNIQUES Unlike in adults, pediatric cataracts are soft. Their lens material can be aspirated through incisions that are 1–1.5 mm long at the limbus or can be subjected to lensectomy through pars plana. When intraocular lens (IOL) implantation is intended, a larger wound is needed to introduce the IOL. A scleral tunnel is safer than a clear corneal incision. Unlike in adults, the tunnel should be securely sutured to prevent dehiscence of the wound with iris incarceration – a common complication in children.2, 4, 5, 7, 8, 10

479

BOX 5-13-1 Laboratory Tests for Bilateral Nonhereditary Pediatric Cataracts

teh lens

Full blood count Random blood sugar Plasma calcium and phosphorus Urine assay for reducing substances after milk feeding Red blood cell transferase and galactokinase levels If Lowe’s syndrome is suspected, screening for amino acids in urine Toxoplasmosis titer Rubella titer Cytomegalovirus titer Herpes simplex titer

SPECIFIC TECHNIQUES Two main approaches exist for the removal of cataracts in children: the pars plana approach and the limbal approach. Both techniques have advantages and disadvantages. The pars plana approach was developed with the advent of vitrectomy machines in the late 1970s;14, 15 it was intended to deal mainly with very young infants in whom surgery is more difficult. With the continuing refinements in cataract and implant surgery in adults, the pars plana approach is being abandoned gradually in favor of the limbal approach, because the latter allows better preservation of the capsular bag for in-the-bag IOL placement.2, 5, 7, 8

Pars Plana Approach

The pars plana approach is indicated mainly for neonates and infants under 2 years of age, particularly for those who have bilateral congenital cataracts for whom IOL implantation is not intended immediately.2 The technique requires a guillotine-type vitrectome and balanced salt solution containing epinephrine (adrenaline) 1:500 000. The conjunctiva is opened at the 10 o’clock and 2 o’clock positions to expose the sclera at the level of the pars plana. The location of the pars plana in infants can be 2–3.5 mm from the limbus. Two scleral perforations are made with a 20-gauge stiletto knife at the pars plana level; one for the vitrectomy probe and the second for the infusion cannula. A lensectomy-anterior vitrectomy is completed, sparing a 2–3 mm peripheral rim of anterior and posterior capsule. These capsule remnants are used to create a shelf to support a posterior chamber IOL that may be implanted later on in life.16 It is important to avoid vitreous incarceration in the wounds by turning off the infusion before withdrawing the vitrectome from the eye. This precaution reduces the chances of suffering retinal traction and detachment later in life. The scleral incisions are sutured with 10-0 nylon, and the knots are buried to prevent irritation to the conjunctiva. This technique is rapid and allows a permanently clear visual axis. The postoperative course is normally less complicated than that after the limbal approach, because fewer maneuvers occur in the anterior chamber. Consequently, the iris and the corneal endothelium suffer less iatrogenic damage. In neonates who have bilateral cataracts, for whom the anesthetic risk is great, the two eyes can be operated on at the same sitting using different sets of instruments.2, 6 Simultaneous surgery also reduces the risk of relative amblyopia, which can occur when two operations are undertaken a few days apart.2, 6 A possible occurrence of the pars plana approach is the incarceration of vitreous in the scleral incisions. Subsequent vitreous traction may lead to retinal breaks and/or detachments.2, 17 Another hindrance with the pars plana approach arises when the pupil is dilated insufficiently; the lensectomy has to be performed under partially “blind” conditions, which means either leaving too much lens material in the periphery or too little peripheral capsular support for future posterior chamber IOL implantation.16

Limbal Approach

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With the proper precautions, the limbal approach is the most versatile technique for pediatric cataract surgery.2,4,5,7,8 Many surgeons have not yet recognized the importance of the anterior chamber maintainer (ACM) when operating on eyes in young patients. Although it is possible to use an aspiration-irrigation device or a vitrectome with an irrigation sleeve in order to remove a soft cataract, the use of an ACM makes the

surgery safer. Moreover, although viscoelastic materials maintain space, the ACM provides, in addition, a constant washout of blood, pigment, and prostaglandins that may be released during surgery to leave clear and “clean” media. The ACM also helps to keep the pupil well dilated throughout the procedure because of the positive hydrostatic pressure. It prevents collapse of the globe when the instruments are withdrawn from the eye and thus helps to reduce damage to the iris and corneal endothelium. Two limbal incisions are made with a 20-gauge stiletto knife at the 10 o’clock and 2 o’clock positions; one for the ACM (connected to a balanced salt solution with epinephrine 1:500 000) and the other one for the aspiration cannula. Various techniques have been described by which to open the anterior capsule.2, 4, 14, 15 Capsulorrhexis can be carried out with the help of high-viscosity viscoelastics; however, the younger the child is, the more difficult it is to perform a capsulorrhexis. Infants have a very elastic anterior capsule, which easily tears toward the periphery. A practical alternative to manual capsulorrhexis is to use a vitrectomy probe to create a small central opening in the anterior capsule (Fig. 5-13-1). This initial hole can be enlarged gradually by “biting” into the anterior capsule with the vitrectome until the desired 4–5 mm opening is achieved. The lens material can be aspirated manually or with an automatic aspiration device (Fig. 5-13-2). Once the capsular bag is empty, the decision has to be made as to the management of the posterior capsule. Most authors agree that infants under 2 years of age should receive an elective posterior capsulectomy−anterior vitrectomy.2, 4–8, 14, 15 Posterior capsulorrhexis can be carried out either manually or with the vitrectome, as described for the anterior capsule.2, 4–8, 14, 15, 18 The posterior capsulorrhexis di ameter must be at least 4 mm.One third of the anterior vitreous must be removed to ensure a permanently clear visual axis (Fig. 5-13-3). Smaller posterior capsulectomies with shallow anterior vitrectomies tend to close down, especially in neonates.19 Posterior capsulectomy, either alone or when combined with a shallow anterior vitrectomy, does not guarantee a permanently clear visual axis, because vitreous remnants serve as a scaffold for the lens epithelium to grow on, which results in the formation of new opaque membranes. Furthermore, the immediate postoperative iritis seems markedly reduced when a generous anterior vitrectomy has been performed.2, 4, 5, 7, 8, 14 Mana gement of the posterior capsule in children more than 2 years old remains controversial. Some authors prefer to leave it intact until opacification occurs; others perform an yttrium−aluminum−garnet (YAG) laser capsulectomy immediately after surgery. Experienced pediatric cataract surgeons choose to perform an elective posterior capsulectomy−anterior vitrectomy, routinely, in every child under 8 years of age in order to provide a one-stop treatment in this age group wherein amblyopia is still a risk. This alternative is logical when meti culous follow-up is uncertain.4–10, 14, 15

CHOICE OF APHAKIC CORRECTION IN CHILDREN Spectacles, contact lenses, and IOLs are the most readily available means to correct aphakia in children. Epikeratophakia has been used in limited series, but this option has been abandoned by most surgeons because of complicated postoperative courses and lack of availability of the corneal lenticules.

Spectacles

Aphakic spectacles provide a satisfactory correction only in cases of bilateral aphakia in which anisometropia does not represent a problem.2 Most of these patients develop good visual acuity with spectacles, provided the eyes are not excessively microphthalmic.2 The disadvantages of spectacles are cosmetic blemish and the poor optical quality of high-plus lenses.

Contact Lenses

During the 1970s and 1980s contact lenses were described as the method of choice to correct unilateral and bilateral aphakia in childhood.2 ,9, 10 Contact lenses provide a better optical correction than spectacles, and their dioptric power can be adjusted throughout life. However, the management of contact lenses in children can be very difficult and costly. Frequent loss of lenses, recurrent infections, and poor follow-up turn this theoretically ideal choice into the most impractical option. Most ophthalmologists, therefore, now recommend the use of IOLs supplemented by spectacles in children rather than contact lenses.2, 4, 5, 7, 8, 10, 14

5.13 Pediatric Cataract Surgery

Fig. 5-13-1 Anterior capsulectomy performed using a vitrectomy probe in a congenital cataract. Note the use of the anterior chamber maintainer for a deep anterior chamber and a well-dilated pupil.

Fig. 5-13-2 Completion of lens material aspiration within the capsular bag in a congenital cataract. Note the use of the anterior chamber maintainer, which allows atraumatic maneuvers in a well-formed anterior chamber.

Intraocular Lenses

The IOL option was originally advocated in cases of unilateral pediatric cataracts because it facilitates amblyopia management by providing a more permanent correction.2, 4, 5, 7, 8, 10, 14 Implanting an IOL in a growing eye is not an ideal solution, but it is currently the most practical one. The aim in the IOL option, unlike in the contact lens alternative, is to correct most, but not all, of the aphakia; the residual refractive error has to be corrected using spectacles, which can be adjusted throughout life. The implantation of anterior chamber IOLs in children was discontinued in the mid-1980s. Devastating complications, such as secondary glaucoma and corneal decompensation, were attributed to anterior chamber IOLs, especially in younger patients.20 Posterior chamber IOL implantation represents, by far, the better method for the correction of aphakia in adults, and the same applies in children.

Selection of intraocular lenses

The choice of which IOL of what dioptric power to implant in young children is the main difficulty that faces the ophthalmologist.2 Pediatric IOLs are not yet readily available,21, 22 and the rapid growth of the eye during the first 2 years of life makes an effective choice difficult.2, 4,7, 8, 23–26 Nevertheless, in the 1990s increasingly positive reports were published on the use of posterior chamber IOLs in children and even in neonates. The material from which the IOL is made must have a long track record of safety. Polymethyl methacrylate (PMMA) IOLs have been in use for more than 40 years; PMMA is currently the best material to be used for children, until a similar follow-up is obtained for other biomaterials.21 The optimal size of the capsular bag and the ciliary sulcus in children has been ascertained by the work of Bluestein et al.22 Posterior chamber IOLs, which were originally oversized, have been reduced from 13–14 mm to 12–12.5 mm in diameter in most modern models. In children it is even more important to implant an IOL of correct size.22 Oversized IOLs act like loaded springs in the eye and can dislocate, especially when a child rubs his or her eyes, which can cause damage to intraocular structures. Pediatric IOLs should not exceed 12 mm overall diameter because the average adult ciliary sulcus diameter rarely exceeds 11.5 mm. Ideally, the pediatric IOL should be available in diameters of the range 10.5–12 mm.22 The choice of the IOL size is determined mainly by the site of implantation (i.e., in-the-bag or ciliary sulcus).

Fig. 5-13-3 Elective posterior capsulectomy and a deep anterior vitrectomy. This is performed using a vitrectomy probe, after all the lens material has been aspirated within the capsular bag.

Both the biometry and the age of the child determine the choice of the IOL dioptric power. Two main age groups exist in pediatric cataract surgery: patients younger than 2 years and patients between 2 and 8 years. In the first group the axial length and the keratometric (K) readings change rapidly, whereas in the second group the changes are slower and more moderate.23–26 In order to minimize the need to exchange IOLs later in life, when a large myopic shift occurs, it is advisable to

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BOX 5-13-2 Guidelines for the Choice of Intraocular Lens Dioptric Power

teh lens

CHILDREN LESS THAN 2 YEARS OLD l Do biometry and undercorrect by 20%, or l Use axial length measurements only: Axial length IOL dioptic power 17 mm, 25 D 18 mm, 24 D 19 mm, 23 D 20 mm, 21 D 21 mm, 19 D CHILDREN BETWEEN 2 AND 8 YEARS OLD l Do biometry and undercorrect by 10%

undercorrect children with IOLs so that they can grow into emmetropia or mild myopia in adult life.23–26 Those who are under 2 years of age should receive 80% of the power needed for emmetropia at the time of surgery. Since the K readings also change rapidly during the first 18 months of life, it is practical to rely on the axial length only when the IOL dioptric power is chosen for infants (Box 5-13-2). The postoperative residual refractive error is corrected by spectacles, which can be adjusted at will as the child grows. Infants and toddlers can tolerate up to 6 D of anisometropia, which gradually disappears within 2–3 years.25 Most of the infants who have unilateral pseudophakia need a patch over the sound eye for half their waking hours until 4–5 years of age. Patches alleviate the symptoms of anisometropia but at the same time affect the chances for good binocularity to develop.27 For the age range 2–8 years, the IOL dioptric power should be 90% of that needed for emmetropia at the time of surgery (see Box 5-13-2). The induced anisometropia is moderate and lessens with the expected myopic shift that occurs in adolescence.23–26 The need for spectacles after IOL implantation in pediatric cataract surgery has some positive aspects: l More dependency on the ophthalmologist is needed because spectacles have to be taken care of, adjusted, and repaired periodically; this increases the chances of good follow-up. l The pseudophakic eye is protected from direct trauma by the spectacles. l Spectacles can be used as an adjunct to amblyopia therapy by atropine penalization of the sound eye and alteration of the dioptric power of its lens.

Implantation in children under 2 years of age

In unilateral cases, primary implantation is indicated as soon as the patient is fit for anesthesia, ideally between 2 and 3 months of age. The earlier the surgery is done, the better the chance that deep amblyopia can be overcome. After the cataract has been aspirated, an elective posterior capsulectomy−anterior vitrectomy is performed. The posterior chamber IOL is inserted through a scleral tunnel, which is prepared in advance. The surgeon has to choose between ciliary sulcus and the bag according to the following criteria. Sulcus implantation is easier and also allows an easier explantation in cases where IOL exchange will be needed later in life.25 This option is indicated in neonates and infants less than 1 year of age. The in-the-bag placement is more physiological, but more difficult technically. To facilitate in-the-bag insertion in pediatric cataract surgery, the following technique is used. The IOL haptics are compressed temporarily onto the optics with a suture, which reduces the overall IOL diameter. The compressed IOL is inserted into the bag fornices, and the suture is cut only after the correct position has been verified.28 An in-the-bag IOL is more difficult to explant; this option should be chosen for infants above 1 year of age because they are less likely to need an IOL exchange, provided they are undercorrected by 20%.

Implantation in children above 2 years of age

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For children older than 2 years, the IOL should be inserted in the bag because the eye has reached nearly the adult size, although its sclera is much softer. Gimbel18 has described a special IOL implantation for this group of patients. The technique requires extreme dexterity as both

LENS IMPLANTATION The lens-in-the-bag implantation

A The bag-in-the-lens implantation

Fig. 5-13-4 Schematic drawing of the lens-in-the-bag implantation (A) and the bag-in-the-lens implantation (B).

Fig. 5-13-5 Bag-in-the-lens IOL implanted in a 5-year-old child at 41 months follow-up. Note the perfectly clear visual axis and the capsular rims contained in the IOL peripheral groove. (Reproduced with permission of MJ Tassignon.)

anterior and posterior capsulorrhexises are performed. The IOL haptics are placed in the bag fornices, while the optic is protruded through both capsulorrhexises to be captured beneath the posterior capsule remnants. Tassignon has recently developed a new technique for a special IOL called bag-in-the-lens.20 The technique consists of creating an anterior and posterior capsulorrhexis. The specially designed IOL has, at its periphery, a groove that contains both anterior and posterior capsule rims (Fig. 5-13-4). Although technically demanding, promising early results indicate that this technique might do away with the need for elective anterior vitrectomy (Fig. 5-13-5).20

Postoperative treatment

Topical medications are sufficient when surgery has not been excessively traumatic. A combination of antibiotic-corticosteroid drops every 2 hours with a mild mydriatic agent twice daily is given for the first week. Thereafter, the medications are tapered off during the next 3 weeks. Some authors have used systemic corticosteroids to overcome the intense inflammatory response in young children’s eyes.

COMPLICATIONS A summary of the guidelines used to minimize complications in pediatric cataract surgery is given in Box 5-13-3. Intraoperative complications usually are related to the surgeon’s unfamiliarity with the child’s soft ocular tissues. The anterior chamber tends to collapse, the iris can protrude through the surgical wounds, and the pupil constricts on injury to the iris. These events can be avoided by operating under deep anesthesia and by using an ACM.

BOX 5-13-3 Guidelines for the Surgical Technique Used for Pediatric Cataracts

Immediate postoperative complications include anterior plastic uveitis, high intraocular pressure, incarceration of iris tissue in the wound, and endophthalmitis. Atraumatic surgery, use of an ACM during surgery, thorough removal of viscoelastics at completion of surgery, and meticulous closure of the wound reduce the occurrence of these complications. Late complications include dislocation of the IOL, chronic iritis, glaucoma, and retinal detachment. Close follow-up enables detection of these complications at an early stage. Their treatment is similar to that for the same occurrences in adults.

Amblyopia Management

The child’s parents must understand that visual rehabilitation only starts with surgery and must be continued throughout childhood. The unilateral cases are the most difficult to manage.2, 4, 5, 7–10 Amblyopia treatment starts soon after surgery, after clarification of the media. The initial treatment must be aggressive in order to boost vision in the deprived eye. Full-time occlusion of the sound eye is carried out for a few days − 1 day per month of age. For example, a 3-monthold neonate should be subjected to occlusion for 3 consecutive days, a

Intraocular Lens Exchange and Alternative Options

5.13 Pediatric Cataract Surgery

1. Deep anesthesia by a pediatric anesthesiologist 2. U se an anterior chamber maintainer 3. 5 mm anterior capsulectomy with a vitrectome or by capsulorrhexis 4. Aspiration of all the lens material within the bag remnants 5. Elective posterior capsulectomy 4 mm in diameter 6. Elective deep anterior vitrectomy (In children older than 2 years, steps 5 and 6 are optional) 7. Use one-piece PMMA posterior chamber pediatric IOL (10.5–12 mm) 8. Thorough removal of viscoelastic material 9. Secure suturing of the surgical wound

4-month-old infant for 4 days, etc. Thereafter, occlusion is reduced to half the waking hours. The younger the infant, the easier it is to comply with the patch regimen. Autorefractometers, especially portable ones, help to determine the residual refractive error; retinoscopy is often difficult in pseudophakic children. Spectacles are prescribed from the age of 4 months onward. A bifocal lens with an add of +3.00 is prescribed in the pseudophakic eye from the age of 3 years, when the child becomes verbal. Unilateral pseudophakes should continue with half-day patches until 4−5 years of age. Thereafter, the patch time can be reduced gradually, but should not be abandoned until 10–12 years of age. After that age, amblyopia management is practically superfluous. Cases of bilateral pseudophakia should be followed closely to detect and treat relative amblyopia.

Exchange of IOLs should be considered when a great myopic shift has occurred.23–26 When the pseudophakic eye becomes 7 D more myopic than the sound eye, the IOL should be exchanged, unless contact lens wear is a viable option. Refractive surgery in children is not yet an acceptable option. An experienced anterior segment surgeon who is fami liar with IOL exchange should perform the procedure. An alternative to IOL exchange is to implant, preferably in the posterior chamber, an additional negative dioptric power IOL to correct the myopia. This procedure is easily performed when the primary IOL was inserted in the bag.

OUTCOME The visual outcome depends largely on the type of cataract, the timing of intervention, the quality of surgery, and, above all, the amblyopia management. It is possible to achieve nearly normal vision even in unilateral congenital cataracts, provided amblyopia management is aggressive.2–10, 25 Binocularity is usually poor in these cases, but some gross stereopsis can be expected.27 Aphakic and pseudophakic children certainly should be followed up throughout childhood and preferably throughout life.29

REFERENCES 1. Elston JS, Timms C. Clinical evidence for the onset of the sensitive period in infancy. Br J Ophthalmol. 1992;76:327–8. 2. Lambert SR, Drake AV. Infantile cataracts. Surv Ophthalmol. 1996;40:427–58. 3. Birch EE, Stager DR, Leffler J, Weakley D. Early treatment of congenital cataract minimizes unequal competition. Invest Ophthalmol Vis Sci. 1998;39:1560–6. 4. Ben-Ezra D, Paez JH. Congenital cataract and intraocular lenses. Am J Ophthalmol. 1983;96:311–4. 5. Dahan E. Lens implantation in microphthalmic eyes of infants. Eur J Implant Refract Surg. 1989;1:1–9. 6. Guo S, Nelson LB, Calhoun J, Levin A. Simultaneous surgery for bilateral congenital cataracts. J Pediatr Ophthalmol Strabismus. 1990;27:23–5. 7. Dahan E, Salmenson BD. Pseudophakia in children: Precautions, techniques and feasibility. J Cataract Refract Surg. 1990;16:75–82. 8. Dahan E, Welsh NH, Salmenson BD. Posterior chamber implants in unilateral congenital and developmental cataracts. Eur J Implant Refract Surg. 1990;2:295–302. 9. Neumman D, Weissman BA, Isenberg SJ, et al. The effectiveness of daily wear contact lenses for the correction of infantile aphakia. Arch Ophthalmol. 1993;111:927–30. 10. BenEzra D, Cohen E, Rose L. Traumatic cataract in children: correction of aphakia by contact lens or by intraocular lens. Am J Ophthalmol. 1997;123:773–82. 11. Asrani S, Freedman S, Hasselblad V, et al. Does primary intraocular lens implantation prevent “aphakic” glaucoma in children?. J AAPOS. 2000;4:33–9. Review.

12. Wolfe OR, Wolfe RM. Removal of soft cataract by suction. New double-barreled aspirating needle. Arch Ophthalmol Chicago. 1941;26:127–8. 13. Burke JP, O’Keefe M, Bowell R, Naughten ER. Ophthalmic findings in classical galactosemia − A screened population. J Pediatr Opthalmol Strabismus. 1989;26:165–8. 14. Ahmadieh H, Javadi MA, Ahmadi M, et al. Primary capsulectomy, anterior vitrectomy, lensectomy, and posterior chamber lens implantation in children: limbal versus pars plana. J Cataract Refract Surg. 1999;25:768–75. 15. Koch DD, Kohnen T. Retrospective comparison of techniques to prevent secondary cataract formation after posterior chamber intraocular lens implantation in infants and children. J Cataract Refract Surg. 1997;23:657–63. 16. Dahan E, Salmenson BD, Levin J. Ciliary sulcus reconstruc tion for posterior implantation in the absence of an intact posterior capsule. Ophthalmic Surg. 1989;20:776–80. 17. McLeod D. Congenital cataract surgeries: A retinal sur geon’s viewpoint. Aust NZ J Ophthalmol. 1986;14:79–84. 18. Gimbel HV, Debroff BM. Posterior capsulorrhexis with optic capture: Maintaining a clear visual axis after pediatric cataract surgery. J Cataract Refractive Surg. 1994;20:658–64. 19. Morgan KS, Karcioglu ZA. Secondary cataracts in infants after lensectomies. J Pediatr Ophthalmol Strabismus. 1987;24:45–8. 20. Tassignon MJ, De Groot V, Vrensen G. Bag-in-the-lens implantation of intraocular lenses. J. Cataract Refract Surg. 2002;28:1182–8.

21. Wilson ME, Apple DJ, Bluestein EC, Wang XH. Intraocular lenses for pediatric implantation Biomaterials, designs and sizing. J Cataract Refract Surg. 1994;20:584–91. 22. Bluestein EC, Wilson ME, Wang XH, et al. Dimensions of the pediatric crystalline lens: implications for intraocular lenses in children. J Pediatr Ophthalmol Strabismus. 1996;33:18–20. 23. Spierer A, Desatnik H, Blumenthal M. Refractive status in children after long-term follow-up of cataract surgery with intraocular lens implantation. J Pediatr Ophthalmol Strabismus. 1999;36:25–9. 24. Gordon RA, Donzis PB. Refractive development of the human eye. Arch Ophthalmol. 1985;103:785–9. 25. Dahan E, Drusedau MUH. Choice of lens and dioptric power in pediatric pseudophakia. J Cataract Refract Surg. 1997;23:1–6. 26. Flitcroft DI, Knight-Nanan D, Bowell R, et al. Intraocular lenses in children: changes in axial length, corneal curvature, and refraction. Br J Ophthalmol. 1999;83:265–9. 27. Tytla ME, Lewis TL, Maurer D, Brent HP. Stereopsis after congenital cataract. Invest Ophthalmol Vis Sci. 1993;34:1767–72. 28. Dahan E. Insertion of intraocular lenses in the capsular bag. Metab Pediatr Syst Ophthalmol. 1987;10:87–8. 29. Rabin J, Van Sluyters RC, Malach R. Emmetropization: A vision dependent phenomenon. Invest Ophthalmol Vis Sci. 1981;20:561–4.

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PART 5 THE LENS

Complications of Cataract Surgery Thomas Kohnen, Li Wang, Neil J. Friedman and Douglas D. Koch

INTRODUCTION Phacoemulsification, sutureless, self-sealing tunnel incisions, and foldable intraocular lenses (IOLs) have changed cataract surgery dramatically over the past two decades. Postoperative astigmatism and inflammation are typically minimal; visual recovery and patients’ rehabilitation are accelerated. The published literature indicates that modern cataract surgery, though certainly not free of complications, is a remarkably safe procedure, regardless of which extraction technique is used.1 Using rigid criteria for scientific validity, Powe et al.1 analyzed 90 studies published between 1979 and 1991 that addressed visual acuity (n = 17 390 eyes) or complications (n = 68 316 eyes) following standard nuclear expression cataract extraction with posterior chamber IOL implantation, phacoemulsification with posterior chamber IOL implantation, or intracapsular cataract extraction with anterior chamber IOL implantation. Strikingly, the percentage of eyes with postoperative visual acuity of 20/40 or better was 89.7% for all eyes and 95.5% for eyes with no pre-existing ocular comorbidity. The incidence of sight-threatening complications was less than 2%. In this chapter, the key elements in the prevention, recognition, and management of the major intraoperative and postoperative complications of cataract surgery are discussed.

INTRAOPERATIVE COMPLICATIONS Cataract Incision

The cataract incision serves as more than just the port of access to the anterior segment; it is a critical step of the operation that affects ocular integrity and corneal stability. The traditional limbal or posterior limbal incision has been largely replaced by tunnel constructions, which can be located in the sclera, limbus, or cornea and are characterized by their greater radial length and an anterior entry into the anterior chamber to create the self-sealing internal corneal valve. Advantages of tunnel incisions are increased intraoperative safety, decreased postoperative inflammation and pain, increased postoperative watertightness, and reduced surgically induced astigmatism.2

Tunnel Perforation

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Tearing of the roof of the tunnel predisposes to excessive intra operative leakage, which compromises anterior chamber stability, and to postoperative wound leakage. If the tear occurs at either edge of the roof, surgery usually can be completed using the initial incision, proceeding slowly and observing the wound carefully as instruments are introduced or manipulated in the eye. It usually is preferable to suture the incision at the conclusion of surgery, even if the wound is watertight, to restore a more normal architecture and prevent external wound gape. If, however, the roof is perforated in the center of the flap and this is noted before the anterior chamber is entered, creation of a new incision should be considered. If the cut is extremely small (e.g., < 0.5 mm), sometimes the same procedure as for lateral roof tears (see above) can be used. Before IOL insertion, the opposite margin of the wound is enlarged, and to prevent further tearing, the incision is made larger than normal for IOL insertion. Suture closure usually is advisable to restore normal wound architecture. If the floor of the tunnel is perforated, which can happen during scleral tunnel dissection, surgery usually can be performed through this wound; care must be taken to avoid trauma to any prolapsing uveal tissue. The perforation should be closed with sutures or fibrin glue.

5.14

Descemet’s Detachment

Detachment of Descemet’s membrane can be a major postoperative complication; it results in persistent corneal edema and decreased visual acuity. To prevent Descemet’s detachment, the surgeon should carefully observe the inner lip at each phase of the procedure. To avoid blunt stripping of Descemet’s membrane during enlargement of the wound, a sharp metal or diamond blade is recommended. If detachment is caused by viscoelastic injection, the agent must be removed, such as by using a blunt cannula. Intraoperatively, repositioning of Descemet’s membrane usually can be achieved by injecting balanced salt solution or occasionally air or an ophthalmic viscosurgical device (OVD) through the paracentesis site. If a visually significant Descemet’s detachment is present postoperatively, the authors prefer to intervene after 2–3 weeks; however, late spontaneous reattachment 2–3 months (in one case, 10 months) postoperatively has been reported.3, 4 To reattach Descemet’s membrane, the patient is positioned at the slit lamp after several drops of anesthetic agent and antibiotics have been administered. A paracentesis incision is made inferotemporally. A 27- or 30-gauge cannula is attached to a syringe with a filter, and the syringe is filled with 0.5–1 cm3 of air or, for eyes that have an unsuccessful injection of air alone, an expansive gas (e.g., sulfahexafluoride, SF6). Using the cannula, approximately 50% of the aqueous is drained, and the chamber is reformed with injection of the gas. Another technique for repairing Descemet’s detachments using intracameral gas injection at the slit-lamp microscope has been reported.5 A 25-gauge needle on a 3 ml syringe filled with the gas and another 25-gauge needle are advanced through the corneoscleral limbus at opposite clock hours with the bevel up and the needles oriented parallel to the iris plane. The plunger on the syringe is depressed to inject the gas and fill the anterior chamber while aqueous humor is allowed to egress from the opposing 25-gauge needle. More complicated cases may require direct suturing.6

Thermal Burns

Part of the energy produced by the phacoemulsification tip is dissipated as heat. This heat is conducted into the eye along the titanium tip and then cooled by the ongoing flow of the irrigation-aspiration fluid. If for any reason the flow is blocked, a corneal burn can occur within 1–3 seconds. The most common cause is inadequate flow through the phacoemulsification tip because it has been obstructed by a retentive OVD; this problem arises from using low flow and vacuum settings. The critical warning sign is the appearance of milky fluid that is produced around the tip as emulsification is begun. To avoid corneal burns, phacoemulsification and irrigation-aspiration functions should always be tested before the eye is entered. Some of the viscoelastic material that overlies the nucleus can be aspirated before the start of emulsification to ensure that aspiration is adequate. To prevent constriction of the irrigating sleeve, an incision size that is appropriate for each particular phacoemulsification tip should be selected. If a burn does occur, meticulous suturing of the wound with multiple radial sutures (Fig. 5-14-1) is required. A bandage contact lens may assist with wound closure. Severe postoperative astigmatism can result. The smaller incision size and new-generation phaco tips continue to contribute to a reduction in the incidence of corneal burns.

Anterior Capsulectomy

Preventing radial tears in the anterior capsule

For phacoemulsification, the preferred method of anterior capsulectomy is capsulorrhexis. It is now recognized that radial tears in the anterior capsule can pose significant risks because of their tendency to tear into

Nuclear Expression Cataract Extraction

Complications related to nuclear expression are covered in Chapters 5-9 and 5-10.

Complications During Phacoemulsification Hydrodissection Fig. 5-14-1 Corneal burn following phacoemulsification. In this patient who had an apparent filtering bleb, phacoemulsification was performed through a temporal, clear corneal incision. Posterior capsular rupture was suspected; the surgeon injected a highly retentive ophthalmic viscosurgical device beneath and in front of the nucleus to minimize the risk of posterior dislocation of the nucleus. Phacoemulsification was instituted with low flow and vacuum settings, and a severe corneal burn was immediately produced because of obstruction of the phacoemulsification tip by the viscoelastic material. The incision was closed with several interrupted sutures. Many of these pulled through the injured tissue, and as a result, additional suturing was required several days later. Postoperatively, the patient has 5 D of surgically induced astigmatism that has persisted for more than 5 years.

the equatorial region of the lens7 and extend into the posterior capsule. This causes posterior capsular rupture, loss of lens material, and IOL decentration. The surgeon’s goal, therefore, must be to retain an intact capsulorrhexis. A common cause of radial tears is irretrievable loss of the capsulorrhexis tear peripherally beneath the iris. To prevent this, the following steps should be considered: l The anterior chamber should be reinflated with an OVD. l The vector forces of the tear should be changed to redirect the tear in a more central direction. l If the tear is lost beneath the iris, the capsulorrhexis should be restarted from its origin, proceeding in the opposite direction (if possible, this new capsulorrhexis should finish by incorporating the original tear in an outside-in direction; however, the original tear is often too peripheral to permit this, and a single radial tear is created). An alternative approach to a “lost” capsulorrhexis is to convert to a canopener capsulectomy. It may indeed be safer to have multiple tears rather than a single one, because forces that extend these tears can be distributed to multiple sites, which reduces the likelihood of a tear extending equatorially.

Excessively small capsulorrhexis

If the diameter of the capsulorrhexis opening is excessively small, the tear should be directed more peripherally and continued beyond the original point of origin before completion of the capsulorrhexis; this procedure removes an annulus of capsule and enlarges the opening. If the capsulorrhexis has been terminated and the opening is too small, a new tear can be started by making an oblique cut with Vannas scissors or a sharp needle. It usually is preferable to enlarge the capsulorrhexis after IOL implantation, to minimize the risk of radial tears during lens implantation.

Minimizing complications when radial tears are present

If radial tears are present, several modifications in surgical technique should be considered to minimize the risk of tear extension into the posterior capsule: l Hydrodissection or hydrodelineation is performed gently to minimize distention of the capsular bag. l Cracks during emulsification are made gently away from the area(s) with radial tears. Alternatively, as much of the nucleus as possible is sculpted within the capsular bag, and the rest is removed at the iris plane. The height of the infusion bottle is kept low to prevent overinflation of the anterior chamber (which can cause the tear to extend peripherally). l The IOL should be placed with the haptics 90° away from the tear. One-piece polymethyl methacrylate lenses tend to maintain better centration in these situations. Rotation of the IOL should be minimized. The OVD should be removed in small aliquots, while gentle infusion of balanced salt solution is performed through a side-port incision.

Hydrodissection was developed to permit easy rotation of the nucleus in the capsular bag and to facilitate removal of various layers of the lens by eliminating their adhesion to surrounding tissues. Two major complications of hydrodissection are inadequate hydrodissection and overinflation of the capsular bag. The former results in a nucleus that does not rotate, which predisposes to zonular dehiscence if excessive force is exerted on the nucleus. This can be avoided by making an additional hydrodissection, particularly in quadrants that have not been hydrodissected before. U-shaped cannulas are useful to hydrodissect subincisional regions of the lens not accessible with straight or angulated cannulas. Overinflation of the capsular bag can predispose to nuclear prolapse into the anterior chamber, which might compromise the ease or safety of nucleus emulsification. A serious complication of overinflation is posterior capsular rupture with loss of the nucleus into the vitreous. This is more likely to occur in eyes with long axial lengths, (hyper�) mature cataracts, or with fragile posterior capsules, such as are found in patients who have posterior polar cataracts.8

5.14 Complications of Cataract Surgery

I t is important to avoid anterior chamber collapse at any phase of the operation when radial tears are present. Anterior bulging of the posterior capsule can place increased stress on a radial tear, which predisposes its extension into the equator and posterior capsule. To avoid this, the chamber is deepened each time the phacoemulsification or irrigation-aspiration tip is removed from the eye; this is done by injecting fluid, OVD, or perhaps air through the paracentesis incision with a syringe while the instrument is removed from the incision.

Iris prolapse or damage

Iris prolapse usually is caused when the anterior chamber is entered too posteriorly, such as near the iris root. If this is noted early in the case and interferes with the easy introduction of instruments into the eye, it is advisable to suture the incision and move to another location. A second and more ominous cause of iris prolapse is an acute increase of intraocular pressure (IOP) accompanied by choroidal effusion or hemorrhage. In this instance, the surgeon should attempt to identify the cause and lower the IOP. Sometimes digital massage on the eye, pressing directly on the incision, can successfully lower the pressure. It is useful to examine the fundus to ascertain whether a choroidal effusion or hemorrhage exists. With choroidal effusion, aspiration of vitreous can be helpful, as can the administration of intravenous mannitol. If a choroidal hemorrhage occurs or if the increased IOP from an effusion is resistant to treatment, it usually is best to terminate surgery. The wound is sutured carefully; intraocular miotics are administered, and a peripheral iridectomy may be performed to help reposition the iris. For effusions, surgery can be deferred until later in the day or the next day, when the fluid dynamics of the eye have returned to a more normal state. If a limited choroidal hemorrhage has occurred, it is best to wait 2–3 weeks before attempting further surgery. Trauma to the iris from prolapse or emulsification with a phacoemulsification tip can produce an irregularly shaped pupil and iris atrophy and can predispose to posterior synechiae formation. If iris damage is produced inferiorly through contact with the phacoemulsification tip, loose strands of tissue should be cut to reduce the likelihood of these being aspirated into the phacoemulsification tip. Another option is to use a single iris hook to retract the inferior iris, holding it away from the phacoemulsification tip for the duration of the procedure.

Floppy-iris syndrome

This complication has been observed during phacoemulsification in patients receiving α1-antagonist agents such as tamsulosin (Flomax). The symptoms include iris billowing and floppiness, iris prolapse to the main and side incisions, and progressive constriction to the pupil during surgery.9 When treating patients who receive α1-antagonist agents, the surgeon can try to avoid severe intra- and postoperative complications by preoperative use of atropine, intraoperative epinephrine (adrenaline), lower phacoemulsification vacuum and aspiration settings, the use of supercohesive OVDs, and various iris hooks and pupil dilators.10

485

Trapped nucleus

THE LENS

In this situation, the nucleus seems to be trapped within the capsular bag; it resists rotation, elevation, or both. This usually indicates a nucleus that requires further hydrodissection, which should be repeated in regions not previously hydrodissected (e.g., laterally and inferiorly with angled or straight cannulas, superiorly with U-shaped cannulas; if these cannulas are not available, additional paracentesis sites can be created in strategic locations).11 If this is unsuccessful in achieving adequate mobilization of the nucleus, viscodissection can be performed. An OVD is injected in the plane of the hydrodissection, which usually results in elevation of the nuclear remnant. When re-entering the eye with the phacoemulsification tip, irrigation should not be used until a second instrument has been inserted through the stab incision and placed below the nucleus; when irrigation and aspiration begin and the OVD is removed, the second instrument prevents the nuclear piece from falling back into the posterior chamber. If the capsulorrhexis is small and the nuclear circumference is intact, nuclear elevation through the capsulorrhexis may not be possible. Additional sculpting might be required to thin the nucleus centrally or to remove some of the peripheral nucleus. After the nucleus has been sufficiently thinned, an instrument such as a Sinskey hook or spatula can be teased posteriorly through the remaining nuclear tissue; this enables elevation of a portion of the nucleus and thereby facilitates access to the remainder.

Subluxated lens

The surgical approach for subluxated lenses (Fig. 5-14-2) is determined by lens stability, lens position, and nuclear density.12 In a subluxated lens with adequate zonular support, phacoemulsification (or nuclear expression) can be performed. OVD is injected as needed throughout the surgery to tamponade the vitreous in areas of zonular dehiscence. Extensive hydrodissection and viscodissection should be carried out. Depending on nuclear density, either phacoemulsification in the capsular bag or anterior chamber phacoemulsification under a retentive viscoelastic is performed. Any form of zonular stress should be minimized, particularly with nuclear rotation. If phacodonesis is present but the lens has not fallen posteriorly, a soft nucleus sometimes can be removed by phacoemulsification-aspiration, whereas a hard nucleus should be extracted using an intracapsular approach. Pars plana vitrectomy is an excellent option for these cases as well; it certainly is preferred when the lens is subluxated posteriorly. The location of the IOL placement depends on the status of the capsular bag after cataract removal. If zonular disruption is minimal (fewer than 3 clock hours), the IOL can be implanted into the capsular bag with the haptic orientated in the meridian of the zonular defect. If the zonular disruption is larger, options include: l Ciliary sulcus implantation, possibly with scleral or iris fixation of one or both haptics. l Insertion of one haptic into the capsular bag and suturing of the second haptic into the sulcus. l Endocapsular ring implantation to stabilize the capsular bag or a Cionni-type ring to suture the capsular bag/ring complex to the sclera.13–15 l Anterior chamber lens implantation (angle-supported or iris-fixated).16 An angle-supported anterior chamber lens is acceptable if no anterior chamber angle pathology, glaucoma, or uveitis is present.14

Ruptured Posterior Capsule

Posterior capsule rupture is the most common serious intraoperative complication of cataract surgery;17 however, proper management can result in minimal morbidity to the patient. A posterior capsular rent is more likely to occur in eyes with small pupils, hard nuclei, or pseudoexfoliation syndrome. Recent reports suggest that the visual prognosis of patients who have broken posterior capsules is excellent. The key factors are to minimize ocular trauma, meticulously clean prolapsed vitreous from the anterior segment, if present, and ensure secure fixation of the IOL.

Before nucleus removal

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A capsular break noted before nucleus extraction is a potential disaster. The first objective is to prevent the nucleus from being dislodged into the vitreous cavity. An OVD can be injected posterior and anterior to the nucleus to prevent its posterior displacement and to cushion the corneal endothelium. Another alternative is to insert an instrument

Fig. 5-14-2 Subluxated lens. This patient had a subluxated lens caused by ocular trauma. The crystalline lens was removed using a pars plana approach, and a sulcus-sutured intraocular lens was implanted.

through a pars plana incision 3 mm posterior to the limbus into the vitreous, which Kelman has described as “posterior assisted levitation” (Charles Kelman, personal communication). The nucleus is pushed gently anteriorly, so that it can be captured in front of the iris and safely removed from the eye. Once the nucleus or its remnants have been repositioned in the anterior chamber, the choice is to convert or to continue the emulsification. The latter course can be more hazardous and predisposes to enlarging the rent and possibly losing the nucleus into the vitreous. In most circumstances, the nucleus should be managed by sufficiently enlarging the wound to facilitate easy extraction of the nucleus on a lens loop. However, in the case of a small break or when only a small amount of nucleus is left, it may be possible to cover the posterior capsular opening with a retentive OVD and complete the phacoemulsification. One can also use a Sheets glide as a “pseudoposterior capsule” to facilitate completion of phacoemulsification. Vitreous loss almost always accompanies posterior capsular rupture that occurs before nucleus removal; whenever feasible, vitrectomy should be performed before the nuclear pieces are removed. Clearly, one should not do this if it makes loss of the nucleus into the vitreous more likely.

During cortical irrigation-aspiration

When capsular rupture occurs during aspiration of the cortex (which is, in fact, the most common cause),7, 18 a key factor is the status of the vitreous. If no vitreous is present in the anterior segment, vitreous loss often can be averted. An OVD can be injected through the capsular opening to push the vitreous posteriorly. Cortical removal can be completed using low-flow irrigation. Options include using a manual system; a dry approach, aspirating with a cannula in the chamber filled with OVD; a bimanual approach through two paracentesis openings; and automated irrigation-aspiration with all settings reduced.19 Cortex should be stripped first in the region farthest from the rent, and the direction of stripping should be toward the rent. Because it can be hazardous to remove cortex in the region of the rent, the cortex is sometimes better left in the eye, to avoid the possibility of enlarging the rent and precipitating vitreous loss. One option to prevent extension of the rent is to convert the tear into a small posterior capsulorrhexis, which eliminates any radially orientated tears that could extend with further surgical manipulation. If vitreous is present in the anterior segment, vitrectomy should be performed first, with the necessary caution being taken to prevent extension of the rent. Depending on the type of capsular tear, the vitrectomy is performed through either the limbal incision or the pars plana. The former approach is used when the tear is located near the incision, which permits vitrectomy with minimal risk of enlargement of the tear. A pars plana approach is preferred when the tear is remote from the incision and therefore less accessible anteriorly. In either case, irrigation is provided with an infusion cannula in the paracentesis opening. After a thorough anterior vitrectomy, the remaining cortical material can be removed using one of the techniques described earlier or using the vitrector in the aspiration mode without cutting.

Intraocular lens insertion

5.14 Complications of Cataract Surgery

Careful inspection of the anatomy of the capsule and zonules is required to determine the appropriate site for IOL implantation. There are four choices: capsular bag, ciliary sulcus, sutured posterior chamber, and anterior chamber.

Capsular bag

If the rent is small and relatively central, and if the anterior capsular margins are well defined, the posterior chamber IOL can be implanted into the capsular bag. If possible, conversion of posterior capsule tears to posterior continuous curvilinear capsulorrhexis (CCC) is recommended.20 With the use of an OVD, posterior CCC is initiated by grasping the advancing tear in the posterior capsule with forceps, and then applying CCC principles. This technique is applied to avoid an antici pated extension of the inadvertent linear or triangular tear during maneuvers such as a required vitrectomy or lens placement. The surgeon should ensure that the haptics are orientated away from the rent (to avoid haptic placement or subsequent migration into the vitreous) and that the lens is inserted gently to avoid enlargement of the rent.

Ciliary sulcus

If the rent exceeds 4–5 mm in length or there is extensive zonular loss, the capsular bag probably is not adequate for IOL support. In such cases, the ciliary sulcus is opened with an OVD, and the iris is retracted in all quadrants to assess the status of the peripheral capsule and zonules. The IOL is inserted with its haptics oriented away from the area of the rent and positioned in areas of intact zonules and capsule. Another alternative, if the anterior capsulorrhexis is intact, is sulcus placement of the IOL, with capture of the optic through the capsulorrhexis. Finally, some surgeons advocate iris suture fixation of one or both haptics to prevent IOL decentration. After the IOL optic is captured through the pupil, McCannel sutures are used to secure the haptic(s) to the iris, and then the optic is repositioned through the pupil.

Sutured posterior chamber

If loss of more than 4–5 clock hours of capsule or zonules occurs, the ciliary sulcus may be inadequate for lens stability. The lens can be fixated to the sclera or to the iris using single or dual 10-0 polypropylene sutures. If one region of solid peripheral capsule and zonules exists, one haptic can be inserted into the sulcus in this area, and the opposite haptic can be sutured to the sclera or the iris.

Anterior chamber

A Kelman-type multiflex anterior chamber IOL design is a good option for patients who do not have glaucoma, peripheral anterior synechiae, or chronic uveitis. A peripheral iridectomy should be performed in these patients to prevent pupillary block. Iris-fixated Artisan anterior chamber type IOLs have even less complications.

Dropped Nucleus

Loss of nuclear material into the vitreous cavity (Fig. 5-14-3) is one of the most potentially sight-threatening complications of cataract surgery.21 Clinical and cadaver eye studies implicate posterior extension of breaks in the capsulorrhexis as a common cause of this complication.7, 22 It therefore behooves the surgeon to use increased caution when phacoemulsification is performed with capsulorrhexis tears,23 as noted earlier. Posterior polar cataract, which predisposes to posterior capsular dehiscence, is another risk factor for dropped nucleus.24 Loss of the nucleus into the vitreous cavity can sometimes be avoided by recognizing the early signs of posterior capsular rupture. These include unusual deepening of the anterior chamber, decentration of the nucleus, or loss of efficiency of aspiration, which suggests occlusion of the tip with vitreous. If capsular rupture is noted, the steps outlined earlier should be taken to prevent nucleus loss. Some controversy exists with regard to the appropriate management of loss of the nucleus into the vitreous. Most surgeons recommend completing the procedure with careful anterior vitrectomy and removal of remaining accessible lens material. In general, IOL implantation is permissible; one exception might be loss of an extremely hard, dense nucleus that would require removal through a limbal incision. If a significant amount of nuclear material has been retained, vitreoretinal surgery needs to be performed 1–2 days postoperatively. Patients whose eyes have small residual nuclear fragments may be observed and referred if increased IOP or uveitis refractory to medical treatment develops. Some surgeons advocate

Fig. 5-14-3 Dropped nucleus. B-scan ultrasonography 1 day after dislocation of a lens nucleus into the vitreous cavity in a patient who has high myopia.

irrigating the vitreous with fluid in an attempt to float the nucleus back into position. An obvious concern is that this additional turbulence could increase vitreous traction on the retina and cause retinal tears.

Anterior Segment Hemorrhage

The presence of intraocular blood decreases the surgeon’s view during the procedure, stimulates postoperative inflammation and synechia formation, and accelerates capsular opacification. To minimize the risk of bleeding, discontinuation of anticoagulant therapy before surgery can be considered if it does not pose a significant medical risk to the patient.25 The sites of anterior segment hemorrhage are either the wound or the iris. Steps to minimize or eliminate bleeding from the wound include: l Careful cautery of bleeding vessels in the vicinity of the incision. l Creation of an adequate internal corneal valve to minimize the likelihood of scleral blood entering the anterior chamber. l Performing a clear corneal incision. Iris bleeding is caused by iris trauma. Intraocular bleeding can be stopped by: l Temporarily elevating the IOP with a balanced salt solution or an OVD. l Injecting a dilute solution of preservative-free epinephrine 1:5000 (or a weaker solution). l Direct cautery (if the bleeding vessel can be identified) with a needletipped cautery probe. The direst complication of cataract surgery is expulsive hemorrhage, which is actually a spectrum of conditions that ranges from suprachoroidal effusion to mild hemorrhage to severe hemorrhage with expulsion. A sign of any of these conditions is shallowing of the anterior chamber with posterior pressure that resists further deepening of the chamber, sometimes accompanied by a change in the red reflex. These conditions typically occur intraoperatively but also may occur postoperatively, usually when the IOP is below normal (Fig. 5-14-4). Choroidal effusion also may be a precursor to suprachoroidal hemorrhage, which presumably occurs from the rupture of a blood vessel that is placed under stretch. Risk factors for suprachoroidal hemorrhage include hypertension, glaucoma, nanophthalmos, high myopia, and chronic intraocular inflammation.26 If sudden shallowing of the anterior chamber occurs and the eye becomes firm, the retina is examined, if possible, to ascertain the cause. If a dark choroidal elevation is noted, a choroidal hemorrhage is likely, and the incision should be closed as quickly as possible. The worst scenario is expulsion of intraocular contents through the wound. With tunnel incisions, the wound typically is self-sealing and resists expulsion of a significant amount of tissue. This self-sealing construction can save an eye from complete loss of intraocular contents. However, the surgeon can assist by using a finger tamponade on the wound while hyperosmotic solution is given intravenously. The wound should be closed and the anterior chamber deepened further, if possible, using a balanced salt solution or an OVD. In the event of severe ongoing prolapse of tissue through the incision, a posterior sclerotomy should be performed; this must be done quickly. Time permitting, a conjunctival peritomy is made 3–4 mm posterior to the limbus. Using a microsurgical steel knife, a radial incision approximately

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5 THE LENS Fig. 5-14-4 Choroidal effusion. This patient experienced deep ocular pain 1 day postoperatively. A choroidal hemorrhage was noted on close examination. This resolved over several months, leaving no permanent sequelae.

2 mm in length is made, scratching through the sclera to the level of the suprachoroidal space. Usually, blood begins to ooze from this site. As this occurs, infusion of fluid and OVD into the anterior chamber is commenced in an attempt to restore normal anterior segment anatomy. This bleeding site can be left open, or it can be sutured once the rate of hemorrhage has diminished, the incision has been closed, and the normal anterior chamber depth has been restored. The goal in these cases is to preserve the eye; cataract surgery can always be completed at a later date, typically 2 or more weeks later. It is recommended that postoperative examinations should be performed 1 day, 7–10 days, and 4–6 weeks after cataract surgery.

POSTOPERATIVE COMPLICATIONS Wound Dehiscence

With small-diameter tunnel incisions, wound dehiscence is relatively uncommon. The creation of an internal corneal valve typically prevents the major complications of wound leakage, inadvertent filtering bleb, and epithelial downgrowth. The wound healing process varies according to the site of the posterior entry. Scleral limbal incisions heal by the ingrowth of episcleral vascular tissue. New fibrovascular tissue is deposited with an orientation parallel to the edges of the incision and perpendicular to existing collagen bundles. Over the ensuing few years, collagen remodeling occurs so that the new collagen becomes oriented parallel to existing collagen bundles, which increases the strength of the healed area.27 Ultimately, the strength of the healed area is approximately 70–80% that of the native tissue. For corneal incisions, closure of the external wound takes place by apposition or, in areas of wound gape, by epithelial ingrowth. A gradual process of remodeling then occurs; this consists of fibrocytic metaplasia of keratocytes with deposition of new collagen, again parallel to the incision, followed over a period of years by remodeling similar to that seen with scleral incisions. In the absence of vascular tissue, this process occurs much more slowly than in scleral or limbal tissue. Postoperative abnormalities in wound structure are produced by defects in the tunnel architecture or by defective wound healing because of systemic disorders, pre-existing tissue abnormalities (e.g., excessively thin or weak tissue), or incarceration of material, such as lens, vitreous, or iris, in the wound, which inhibits the normal healing process.

Wound Leakage

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A wound leak that occurs in the immediate postoperative period is usually the result of inadequate suture closure for a specific wound configuration. This entity is rare with tunnel constructions. Scleral pocket incisions have a longer tunnel and can readily be demonstrated to be watertight at the conclusion of surgery. Corneal incisions as small as 3.5 mm in width seal remarkably well, even though intraoperative pinpoint posterior lip pressure in these eyes often can induce a wound leak. Some surgeons perform hydration of the corneal stroma to prevent a wound leak that can be elicited with posterior lip pressure; however, this hydration clears within a few minutes to hours, and it is uncertain whether it has any actual clinical value.

Fig. 5-14-5 Wound dehiscence. This patient had 5 D of against-the-wound astigmatism following nuclear expression. The surgeon resutured the wound 4 weeks postoperatively, but the astigmatism immediately recurred. Note the thin, fragile sclera, sometimes characterized as scleral “melting.”

Wound leaks in scleral incisions typically are covered by conjunctiva and usually resolve within a few days; occasionally, they lead to the formation of a filtering bleb. Medical management of scleral or corneal wound leaks may include the following: l Decreasing or discontinuing corticosteroid therapy. l Administration of prophylactic topical antibiotics. l Pressure patching. l Use of a collagen shield, bandage lens, or disposable contact lens. l Administration of aqueous inhibitors. It usually is necessary to suture a wound if the leak persists after 5–7 days or if there is a flat anterior chamber, iris prolapse, extensive external tissue gape, or excessive against-the-wound astigmatism (Fig. 5-14-5).

Inadvertent Filtering Bleb

Formation of a filtering bleb after cataract surgery occurs if the wound leaks under a sealed conjunctival flap. If early filtration is recognized, progression might be prevented by discontinuation of corticosteroid treatment. If the patient is asymptomatic, the physician can observe the bleb. Elimination of the bleb can be considered if it causes irritation, tearing, or infection. Blebs that tend to be more symptomatic are tall and cystic and encroach over the corneal surface. Options for late closure include cryotherapy, chemical cautery, neodymium:yttrium–aluminum–garnet (Nd:YAG) laser,28 or surgical closure. The latter can be complex because of endothelialization of the fistula. The surgical approach requires excision of the conjunctival bleb, scraping or cryotherapy of the cells that line the fistula, and closure of the fistula, which sometimes requires a scleral patch graft.

Epithelial Ingrowth

Epithelial downgrowth is a rare but serious complication of intraocular surgery. It occurs most commonly after intracapsular cataract extraction and less often following nuclear expression; it is extremely rare after phacoemulsification. Surface epithelium that invades the intraocular structures, such as over the cornea, iris, ciliary body, lens capsule, and Bruch’s membrane,29 can cause corneal decompensation, chronic anterior uveitis, and intractable secondary angle-closure glaucoma. Conditions for the onset of this entity are highly variable, but it appears to be more common in patients who undergo multiple intraocular procedures or have postoperative wound dehiscence. The presence of epithelial downgrowth may be confirmed by irradiation of the affected iris with an argon laser (epithelial tissue turns white with argon ablation, compared with the dark or brown appearance of normal iris) or diagnosed with specular micrography (noting a sheet of abnormal tissue that obliterates the normal endothelial mosaic); however, the definitive diagnosis is dependent on the histopathological confirmation of epithelial tissue in the eye. Treatment consists of complete destruction of all intraocular epithelial tissue using cryotherapy, iridocyclectomy, or pars plana vitrectomy. Unfortunately, the prognosis for this postoperative complication is poor, except for a well-defined cyst that can be excised en bloc.30

Postoperative Astigmatism

Complications related to postoperative astigmatism are covered in Chapters 5-3 and 5-15. Factors that predispose to corneal edema following cataract surgery include the following: l Prior endothelial disease or cell loss. l Intraoperative mechanical endothelial trauma. l Excessive postoperative inflammation. l Prolonged postoperative elevation of IOP. Preoperatively, patients should be carefully examined for evidence of Fuchs’ dystrophy or other conditions that produce a low endothelial cell count. Patients who have marginal corneal endothelial function may complain of poorer vision in the morning because of corneal edema produced by hypoxia overnight. Although most patients who have Fuchs’ dystrophy have guttae that are readily visible with slit-lamp examination, in rare instances, patients can have low endothelial cell counts in the absence of guttae. It is often advisable to obtain an endothelial cell count in the fellow eye. Finally, corneal pachymetry can be helpful to assess such patients, because those with a corneal thickness in excess of approximately 0.63 mm presumably have marginally compensated corneas and are at great risk of developing permanent postoperative corneal edema. If the corneal thickness is greater than 0.63 mm but no corneal edema is evident, the authors generally perform cataract surgery alone and advise patients of the increased risk of developing postoperative corneal decompensation. If frank epithelial and stromal edema is present, a combined cataract extraction with penetrating keratoplasty may be advisable. Several measures can be taken intra- and postoperatively to minimize the risk of corneal injury. For some surgeons, nuclear expression may be safer than phacoemulsification. Techniques to remove the nucleus in the posterior chamber seem to minimize endothelial cell loss,31 and evidence exists that highly retentive OVDs are more protective when surgical removal of the nucleus near the endothelium is carried out. Postoperatively, inflammation should be aggressively treated with topical corticosteroids, and IOP should be controlled below 20 mmHg. Mechanical factors, such as Descemet’s detachment or retained nuclear fragments in the angle touching the endothelium, should be addressed. For symptomatic relief, hypertonic saline ointment is sometimes helpful as a temporary measure. Sequential corneal pachymetry is an excellent way to document the resolution of postoperative corneal edema, which may take up to 3 months; it is usually advisable to wait at least this long before recommending penetrating keratoplasty.

Hyphema

A postoperative hyphema is caused by bleeding from the wound or iris (Fig. 5-14-6). As the hyphema resolves, the IOP should be controlled. Surgical re-intervention to remove a blood clot is indicated if severe,

Endocapsular Hematoma

Endocapsular hematoma is the postoperative entrapment of blood between the posterior surface of the IOL and the posterior capsule.34 It is a variant of hyphema, with the exception that the blood can become entrapped within the capsular bag for months or even permanently. Fortunately, in most instances the amount of blood is minimal and either does not significantly impair vision or is absorbed over a few weeks or months.35 When the accumulation is extensive and persistent, Nd:YAG laser posterior capsulectomy is curative when used to enable the blood to flow immediately into the vitreous, where it can be resorbed.

5.14 Complications of Cataract Surgery

Corneal Edema and Bullous Keratopathy

medically resistant pressure elevation exists for several days. The duration of tolerated pressure elevation depends on the patient’s age and the status of the optic nerve. The incidence of postoperative hyphema is reduced by making clear corneal incisions. Late hyphema or microhyphema most often is caused by chafing of the IOL against the iris or ciliary body (uveitis-glaucoma-hyphema syndrome).32 This most typically occurs because of loss of fixation of the sulcus-fixated posterior chamber IOL; micromovements of the lens cause chafing against a vessel, which produces the postoperative bleeding. Treatment consists of IOL exchange and ensuring that the new lens is well fixated; this might require suture fixation to the sclera or implantation of an anterior chamber lens. A rare cause of postoperative bleeding is hemorrhage from vascularization of the internal margin of the incision (Swan’s syndrome);33 this can be diagnosed by noting neovascularization of the wound using gonioscopy, and it is treated by argon laser photocoagulation.

Intraocular Pressure Elevation

Elevation of IOP following cataract surgery is a common occurrence. Fortunately, it usually is mild and self-limited and may or may not require prolonged antiglaucoma therapy. Causes of acute pressure elevation are retention of viscoelastic substances, obstruction of the trabecular meshwork with inflammatory debris, and pupillary or ciliary block. Patients who have pre-existing glaucoma are at much greater risk of developing acute significant pressure elevation. Prevention of this problem includes careful removal of the OVD at the time of surgery, control of intraocular bleeding, and the use of intra- and postoperative antiglaucomatous agents. Intracameral injection of 0.01% carbachol at the conclusion of surgery is effective, as is the postoperative administration of pilocarpine gel; topical beta blockers; apraclonidine; and topical, intravenous, or oral carbonic anhydrase inhibitors. If marked elevation of IOP is present on the first postoperative day, this can be immediately controlled by “venting” the anterior chamber. After topical anesthetic agents and antibiotics have been administered, a forceps or other fine instrument is used to depress the posterior lip of the paracentesis incision, which allows the egress of a small amount of OVD and aqueous.36 This is repeated as necessary until the IOP is brought into the low-normal range. The patient can then be treated with topical antiglaucoma therapy and followed carefully to ensure that pressure is controlled. Chronic IOP elevation can be caused by corticosteroid use, retained lens (particularly nuclear) material, chronic inflammation, peripheral anterior synechiae formation, endophthalmitis, and ciliary block. The correct diagnosis of the underlying cause is required to institute appropriate therapy.

Capsular Block Syndrome

Fig. 5-14-6 Postoperative hyphema. This hyphema was produced by hemorrhage from the scleral incision in a patient who had a small postoperative wound leak. The hyphema resolved once the incision closed, which led to cessation of ongoing bleeding and restoration of normal intraocular pressure.

Capsular block syndrome (CBS) is initially defined by the entrapment of an OVD in the capsular bag, because of apposition of the anterior rim of the capsulorrhexis with the anterior face of the IOL.37, 38 This may be more common with acrylic IOLs because of their slightly “stickier” surface. Postoperatively, the bag becomes more distended (perhaps through osmotic imbibition of aqueous), and the IOL is pushed anteriorly to create a myopic refractive shift. This can be prevented by meticulous removal of the OVD from the bag at the conclusion of surgery. To accomplish this, it is helpful to gently depress the IOL optic to displace the OVD trapped behind the IOL.39 Treatment requires Nd:YAG laser puncture of the anterior capsule peripheral to the edge of the capsulorrhexis, which permits the OVD to escape into the anterior chamber. Alternatively, if the pupil is relatively small and the anterior capsule is not accessible to laser treatment, a small posterior capsulectomy can be performed, which permits the OVD to drain into the vitreous. A new classification of CBS includes intraoperative CBS, early postoperative CBS, and late postoperative CBS.40 Intraoperative CBS occurs during rapid hydrodissection using a large amount of BSS and has been discussed in the hydrodissection section. Early postoperative CBS represents the initial type of CBS, with accumulation of the OVD in the

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5 THE LENS Fig. 5-14-7 Pupillary capture of the intraocular lens. Predisposing factors in this patient included a can-opener capsulectomy, intraoperative iris trauma, and nonangulated haptics.

capsular bag, as discussed earlier. Late postoperative CBS refers to eyes with accumulation of a milky-white substance in the closed capsular bag.41–43 Reduction of vision with this type of CBS is rare, and Nd:YAG laser capsulectomy can be performed, if necessary.

Intraocular Lens Miscalculation

Complications related to IOL miscalculation are covered in Chapter 5.3.

Intraocular Lens Decentration and Dislocation

Common causes of IOL decentration and dislocation are asymmetrical loop placement, sunset syndrome, loss of zonular support for a lens fixated in the capsular bag, and pupillary capture of the IOL optic.44

Asymmetrical haptic placement

Pathological studies indicate that asymmetrical loop placement is an extremely common occurrence, particularly when can-opener capsulotomies are performed. The incidence of this complication has been greatly reduced with the advent of capsulorrhexis, which permits excellent visualization of the capsular edge and ensures that a lens placed in the capsular bag is retained there. An IOL with asymmetrical loop placement becomes symptomatic if the lens is decentered sufficiently relative to the pupil; symptoms include polyopia, glare, induced myopia (from looking through the peripheral portion of the IOL), and loss of best-corrected acuity. Depending on the severity of the symptoms, treatment includes IOL repositioning or IOL exchange. In some instances, topical miotics can be prescribed; however, few patients prefer this mode of management.

Sunset syndrome

Sunset syndrome occurs when a sulcus-fixated posterior chamber IOL dislocates through a peripheral break in the zonules, typically inferiorly. Sunset syndrome is usually an acute, nonprogressive event. Treatment options again depend on the severity of the patient’s symptoms. The authors have found that simple IOL repositioning is often unsuccessful and predisposes to recurrence. Therefore, several other options are recommended: l Repositioning the lens, combined with iris fixation sutures. l IOL exchange with a larger, more rigid lens. l Scleral fixation of a posterior chamber lens. l Replacement with an anterior chamber lens.

Lens-bag decentration

In rare instances, a lens that is placed in the capsular bag can dislocate as a result of bag decentration caused by zonular rupture or dehiscence. Treatment of this condition, if sufficiently severe, requires IOL exchange with some form of scleral fixation or implantation of an anterior chamber lens.

Pupillary capture

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Pupillary capture of the IOL optic consists of the posterior migration of some portion of the iris beneath the IOL optic (Fig. 5-14-7). Predisposing factors are can-opener capsulectomy and sulcus implantation of the

Fig. 5-14-8 Intraocular lens dislocation. During surgery, a capsular rupture was noted. A lens was, however, implanted in the posterior chamber. On the morning following surgery, the lens was found to be dislocated posteriorly and inferiorly, and the patient was referred for treatment. At the time of lens exchange, it appeared that insufficient capsular support was present, and a new lens was sutured into the ciliary sulcus.

posterior chamber IOL, particularly in the absence of angulated haptics; however, in rare instances, pupillary capture can occur with capsular fixation of the lens after capsulorrhexis, especially when the capsulorrhexis is large.45, 46 Pupillary capture can produce acute and chronic iritis, posterior synechiae formation, visual loss from deposition of inflammatory cells on the IOL surface, and, if the lens is displaced sufficiently eccentrically and anteriorly, chronic endothelial trauma with corneal decompensation. Pupillary capture diagnosed within a few days of its occurrence can be treated pharmacologically or by manually repositioning the optic into the posterior chamber. Chronic pupillary capture may be more difficult to manage, because firm synechiae form between the iris and posterior capsule. In such situations, the IOL should be repositioned if there are visual symptoms, chronic uveitis, or corneal endothelial trauma. Chronic cellular precipitates on the IOL surface can often be managed by the administration of topical corticosteroids and occasional Nd:YAG laser “dusting” of the anterior IOL surface.47

Sulcus-Fixated Intraocular Lens Dislocation

Another subtle but important form of IOL dislocation is loss of fixation of the sulcus-fixated IOL. This can produce recurrent microhyphema or hyphema, as well as chronic iritis and even pigmentary glaucoma. The loss of lens fixation is often subtle, but it can be diagnosed at the slit lamp by observing the third and fourth Purkinje images. If the patient is asked to look eccentrically and then refix centrally, these images can be seen to flutter or wobble excessively (pseudophacodonesis), which indicates lack of adequate IOL fixation. Intraoperatively, this can be verified by touching the IOL with an instrument; there is obvious IOL instability.

Posterior and Anterior Dislocation

In rare instances, a posterior chamber lens can fall posteriorly and either become suspended in the anterior vitreous (Fig. 5-14-8) or dislocate completely into the vitreous cavity. In the former instance, IOL exchange is advisable, because the lens is within reach and can produce visual symptoms or chafe on uveal tissue. Management of a complete posterior IOL dislocation is more controversial. Although in some eyes this condition is well tolerated, in others, the lenses can become entrapped in the vitreous base and cause vitreous traction and retinal tears, or they can produce visual symptoms by intermittently moving into the visual axis. Even more rarely, anterior luxation of a posterior chamber lens into the anterior chamber may occur.48 This can be prevented with a small and continuous capsulorrhexis and in-the-bag implantation of the lens.

5.14 Complications of Cataract Surgery

Fig. 5-14-9 Postoperative endophthalmitis. This patient developed an acute postoperative endophthalmitis after clear cornea cataract surgery and implantation of a polymethyl methacrylate posterior chamber intraocular lens. During cataract surgery, a capsular break occurred, and an anterior vitrectomy was performed. The patient was treated successfully with vitrectomy and injection of intravitreal antibiotics combined with postoperative topical antibiotic therapy. Final visual acuity was 20/50 (6/15).

Fig. 5-14-10 Posterior capsular opacification. Elschnig’s pearl formation and capsular wrinkling causing a severe decrease of visual acuity.

Endophthalmitis

Intraocular Lens Exchange

Several principles of IOL exchange need to be emphasized. It is generally preferable to exchange lenses that have haptics that are poorly designed, too short, or deformed from lens malposition in the eye. Patients who have a marginal corneal endothelium status generally should be subjected to the least traumatic surgery possible, such as iris repositioning with iris fixation sutures rather than IOL exchange, particularly if the latter requires anterior vitrectomy. It is important to distinguish between IOL decentration and pupil displacement. In some instances, the patient’s symptoms result from an eccentrically displaced pupil in the face of a relatively well-positioned IOL. Clearly, surgery, if indicated, should address the underlying problem by reconstructing the pupil. This can be done by suturing the pupil in the peripheral region and opening the pupil centrally with several small sphincterotomies. If certain complications are associated with the site of the dislocated IOL (e.g., recurrent microhyphema with a posterior chamber IOL or peripheral anterior synechiae with an anterior chamber IOL), it may be advisable to place the new lens in a new site. Finally, if sufficient intact posterior capsule exists, an attempt can be made to reopen the capsular flaps to permit fixation of the new lens within the capsular bag; this, clearly, is the most desirable location.

Endophthalmitis can occur in an acute or chronic form. It is characterized by ciliary injection, conjunctival chemosis, hypopyon, decreased visual acuity, and ocular pain. The acute form generally develops within 2–5 days of surgery and has a fulminant course (Fig. 5-14-9). Common causative organisms are gram-positive, coagulase-negative micrococci, Staphylococcus aureus, Streptococcus species, and Enterococcus species.54, 55 Chronic endophthalmitis is caused by organisms of low pathogenicity, such as Propionibacterium acnes or Staphylococcus epidermidis. It typically is diagnosed several weeks or longer after surgery. Signs include decreased visual acuity, chronic uveitis with or without hypopyon formation, and, in some instances, plaque-like material on the posterior capsule. Histopathologically, this material consists of the offending microorganism embedded in residual lenticular tissue. Treatment of endophthalmitis consists of culturing aqueous and vitreous aspirates, followed by administration of intravitreal,56 topical, and subconjunctival antibiotics, as discussed elsewhere. In the Endophthalmitis Vitrectomy Study, no evidence was found of any benefit from the use of systemic antibiotics.57 Pars plana vitrectomy helped increase the final visual outcome only of those patients who had an initial visual acuity of light perception or worse.57 For further discussion of endophthalmitis, see Chapter 7.9.

Cystoid Macular Edema

Posterior Capsular Opacification - see Chapter 5.16

Cystoid macular edema (CME) is the most common cause of unexpected visual loss following cataract surgery.49, 50 Fluorescein angiographic CME can occur in up to 50% of patients at 4–8 weeks postoperatively, but clinical CME occurs in less than 3% of patients. Recent studies have shown that macular swelling can be clinically insignificant, but can be detected, for example, with optical coherence tomography (OCT).51 The typical time of onset of clinical CME is 3–4 weeks postoperatively. Predisposing factors are intraoperative complications (e.g., vitreous loss or severe iris trauma), vitreous traction at the wound, diabetic retinopathy,52 and pre-existing epiretinal membrane. In cases without predisposing factors, CME typically resolves over several weeks, although most surgeons prefer to treat this topically with nonsteroidal and corticosteroid drops.53 Other modes of treatment that have been employed include sub-Tenon’s corticosteroid injection and administration of systemic nonsteroidal anti-inflammatory drugs with corticosteroids. In patients who have epiretinal membranes, CME may take months to resolve. When associated with diabetic retinopathy, CME often is resistant to medical therapy and can persist indefinitely; macular laser photocoagulation is sometimes helpful to document angiographically the leaking vessels and microaneurysms. Patients who have ongoing structural abnormalities, such as vitreous traction or extensive iris chafing, are less likely to experience spontaneous resolution of CME and may benefit from surgical correction of the precipitating factor.

Secondary cataract formation is a major complication of IOL implantation after extracapsular cataract extraction (ECCE or phacoemulsification). The incidence is in the range of 18–50% in adults followed for as long as 5 years; in infants and juveniles, an opacification rate of 44% was found within 3 months of surgery after in-the-bag IOL implantation with an intact posterior capsule.58 Posterior capsular opacification (PCO) is caused by proliferation and migration of residual lens epithelial cells. These can produce visual loss through two mechanisms: l Formation of swollen, abnormally shaped lens cells called Elschnig’s pearls, which migrate over the posterior capsule into the visual axis (Fig. 5-14-10). l Transformation into fibroblasts, which may contain contractile elements (myofibroblasts) and cause the posterior capsule to wrinkle (see Fig. 5-14-8). Standard treatment of PCO consists of opening the capsule with Nd:YAG laser. Complications of this treatment include acute and, in rare instances, chronic IOP elevation, pitting of the IOL, and retinal detachment. Factors that predispose to retinal detachment include an axial length greater than 24.5 mm, male gender, and pre-existing retinal pathology.59–61 A related and unusual abnormality is the formation of striae in the posterior capsule in the absence of abnormal proliferation of lens epithelial cells. In some patients, this produces a Maddox-rod effect; the typical symptoms are linear streaks that radiate from lights, and their

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orientation is 90° from the meridian of the striae. The cause is stretching of the capsular bag by the IOL, which produces the striae aligned with the axis of the lens haptics. Typically, this is present on the first postoperative day but may not be mentioned by the patient until later. In many eyes, the striae resolve in the first week or two after surgery as capsular contraction occurs, which counteracts the stretch forces of the IOL haptics. If the condition persists and is sufficiently symptomatic, it can be corrected readily with a laser posterior capsulotomy. For further discussion of PCO, see Chapter 5-16.

Retinal Detachment

Retinal detachment is a well-recognized complication of cataract surgery; it occurs in 0.2–3.6% of persons after extracapsular cataract surgery. The incidence of retinal detachment increases fivefold if an

intracapsular procedure is performed.62 Predisposing factors include Nd:YAG laser capsulectomy, axial length greater than 24.5 mm, myopic refractive error, lattice degeneration, male gender, intraoperative vitreous loss, postoperative ocular trauma, posterior vitreous detachment, and history of retinal detachment in the fellow eye.60, 63, 64 Steps to prevent retinal detachment include the following: l A careful preoperative fundus examination. l Preservation of the integrity of the posterior capsule at the time of surgery. l Education of patients with regard to the symptoms of retinal tears and detachment. l Regular postoperative dilated fundus examinations.

REFERENCES 1. Powe NR, Schein OD, Gieser SC, et al. Synthesis of the literature on visual acuity and complications following cataract extraction with intraocular lens implantation. Arch Ophthalmol. 1994;112:239–52. 2. Kohnen T, Dick B, Jacobi KW. Comparison of induced astigmatism after temporal clear corneal tunnel incisions of different sizes. J Cataract Refract Surg. 1995;21:417–24. 3. Assia EI, Levkovich-Verbin H, Blumenthal M. Management of Descemet’s membrane detachment. J Cataract Refract Surg. 1995;21:714–7. 4. Iradier MT, Moreno E, Aranguez C, et al. Late spontaneous resolution of a massive detachment of Descemet’s membrane after phacoemulsification. J Cataract Refract Surg. 2002;28:1071–3. 5. Kim T, Hasan SA. A new technique for repairing Descemet membrane detachments using intracameral gas injection. Arch Ophthalmol. 2002;120:181–3. 6. Amaral CE, Palay DA. Technique for repair of Descemet membrane detachment. Am J Ophthalmol. 1999;127:88–90. 7. Kohnen T. Kapsel- und Zonularupturen als Komplikation der Kataraktchirurgie mit Phacoemulsifikation. MD dissertation: University of Bonn; 1989. 8. Osher RH, Yu BC-Y, Koch DD. Posterior polar cataracts: a predisposition to intraoperative posterior capsular rupture. J Cataract Refract Surg. 1990;16:157–62. 9. Chang DF, Campbell JR. Intraoperative floppy iris syndrome associated with tamsulosin (Flomax). J Cataract Refract Surg. 2005;31:664–73. 10. Mamalis N. Intraoperative floppy-iris syndrome. J Cataract Refract Surg. 2006;32:1589–90. 11. Koch DD, Liu JF. Multilamellar hydrodissection in phacoemulsification and planned extracapsular surgery. J Cataract Refract Surg. 1990;16:559–62. 12. Hakin KN, Jacobs M, Rosen P, et al. Management of the subluxated crystalline lens. Ophthalmology. 1992;99:542–5. 13. Cionni RJ, Osher RH. Endocapsular ring approach to the subluxed cataractous lens. J Cataract Refract Surg. 1995;21:245–9. 14. Gimbel HV, Sun R. Clinical applications of capsular tension rings in cataract surgery. Ophthalmic Surg Lasers. 2002;33:44–53. 15. Cionni RJ, Osher RH, Marques DM, et al. Modified capsular tension ring for patients with congenital loss of zonular support. J Cataract Refract Surg. 2003;29:1668–73. 16. Gimbel HV, Condon GP, Kohnen T, et al. Late in-the-bag intraocular lens dislocation: incidence, prevention, and management. J Cataract Refract Surg. 2005;31:2193–204. 17. Ng DT, Rowe NA, Francis IC, et al. Intraoperative complications of 1000 phacoemulsification procedures: a prospective study. J Cataract Refract Surg. 1998;24:1390–5. 18. Cruz OA, Wallace GW, Gay CA, et al. Visual results and complications of phacoemulsification with intraocular lens implantation performed by ophthalmology residents. Ophthalmology. 1992;99:448–52. 19. Brauweiler P. Bimanual irrigation/aspiration. J Cataract Refract Surg. 1996;22:1013–6. 20. Gimbel HV, Sun R, Ferensowicz M, et al. Intraoperative management of posterior capsule tears in phacoemulsification and intraocular lens implantation. Ophthalmology. 2001;108:2186–9. 21. Kim JE, Flynn HW Jr, Rubsamen PE, et al. Endophthalmitis in patients with retained lens fragments after phacoemulsification. Ophthalmology. 1996;103:575–8.

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22. Assia EI, Apple DJ, Barden A, et al. An experimental study comparing various anterior capsulectomy techniques. Arch Ophthalmol. 1991;109:642–7. 23. Chern S, Yung C-W. Posterior lens dislocation during attempted phacoemulsification. Ophthalmic Surg. 1995;26:114–6. 24. Aasuri MK, Kompella VB, Majji AB. Risk factors for and management of dropped nucleus during phacoemulsification. J Cataract Refract Surg. 2001;27:1428–32. 25. Saitoh AK, Saitoh A, Taniguchi H, Amemiya T. Anticoagulation therapy and ocular surgery. Ophthalmic Surg Lasers. 1998;29:909–15. 26. Beatty S, Lotery A, Kent D, et al. Acute intraoperative suprachoroidal haemorrhage in ocular surgery. Eye. 1998;12(Pt 5):815–20. 27. Koch DD, Smith SH, Whiteside SB. Limbal and scleral wound healing. In: Beuerman RW, Crosson CE, Kaufman HE, eds. Healing processes in the cornea, Houston: Gulf Publishing; 1989:165–82. 28. Geyer O. Management of large, leaking, and inadvertent filtering blebs with the neodymium:YAG laser. Ophthalmology. 1998;105:983–7. 29. Küchle M, Green W. Epithelial ingrowth: a study of 207 histopathologically proved cases. Ger J Ophthalmol. 1996;5:211–23. 30. Knauf HP, Rowsey JJ, Margo CE. Cystic epithelial downgrowth following clear-corneal cataract extraction. Arch Ophthalmol. 1997;115:668–9. 31. Koch DD, Liu JF, Glasser DB, et al. A comparison of corneal endothelial changes after use of Healon or Viscoat during phacoemulsification. Am J Ophthalmol. 1993;115:188–201. 32. Johnson SH, Kratz RP, Olson PF. Iris transillumination and microhyphema syndrome. J Am Intraocul Implant Soc. 1984;10:425–8. 33. Swan KC. Hyphema due to wound vascularization after cataract extraction. Arch Ophthalmol. 1973;89:87–90. 34. Hagan JC III, Menapace R, Radax U. Clinical syndrome of endocapsular hematoma: presentation of a collected series and review of the literature. J Cataract Refract Surg. 1996;22:379–84. 35. Hater MA, Yung CW. Spontaneous resolution of an endocapsular hematoma. Am J Ophthalmol. 1997;123:844–6. 36. Laube T, Koch HR, Çubuk H, Kohnen T. Druckentlastung nach Staroperation (abstract). Klin Monatsbl Augenheilkd. 1995;206:59. 37. Davison JA. Capsular bag distension after endophacoemulsification and posterior chamber intraocular lens implantation. J Cataract Refract Surg. 1990;16:312–4. 38. Masket S. Postoperative complications of capsulorrhexis. J Cataract Refract Surg. 1993;19:721–4. 39. Kohnen T, von Ehr M, Schütte E, Koch DD. Evaluation of intraocular pressure with Healon and Healon GV in sutureless cataract surgery with foldable lens implantation. J Cataract Refract Surg. 1996;22:227–37. 40. Miyake K, Ota I, Ichihashi S, et al. New classification of capsular block syndrome. J Cataract Refract Surg. 1998;24:1230–4. 41. Eifrig DE. Capsulorrhexis-related lacteocrumenasia. J Cataract Refract Surg. 1997;23:450–4. 42. Miyake K, Ota I, Miyake S, Horiguchi M. Liquefied aftercataract: a complication of continuous curvilinear capsulorrhexis and intraocular lens implantation in the lens capsule. Am J Ophthalmol. 1998;125:429–35. 43. Namba H, Namba R, Sugiura T, Miyauchi S. Accumulation of milky fluid: a late complication of cataract surgery. J Cataract Refract Surg. 1999;25:1019–23.

44. Tappin MJ, Larkin DF. Factors leading to lens implant decentration and exchange. Eye. 2000;14(Pt 5):773–6. 45. Nagamoto S, Kohzuka T, Nagamoto T. Pupillary block after pupillary capture of an AcrySof intraocular lens. J Cataract Refract Surg. 1998;24:1271–4. 46. Khokhar S, Sethi HS, Sony P, et al. Pseudophakic pupillary block caused by pupillary capture after phacoemulsification and in-the-bag AcrySof lens implantation. J Cataract Refract Surg. 2002;28:1291–2. 47. Brauweiler P, Ohrloff C. Das Polieren eiweißbeschlagener Intraokularlinsen mit dem Nd:YAG-Laser. Fortsch Ophthalmol. 1990;87:78–9. 48. Faucher A, Rootman DS. Dislocation of a plate-haptic silicone intraocular lens into the anterior chamber. J Cataract Refract Surg. 2001;27:169–71. 49. Mentes J, Erakgun T, Afrashi F, et al. Incidence of cystoid macular edema after uncomplicated phacoemulsification. Ophthalmologica. 2003;217:408–12. 50. Ray S, D’Amico DJ. Pseudophakic cystoid macular edema. Semin Ophthalmol. 2002;17:167–80. 51. Jagow B, Kohnen T. Anterior optic neuritis associated with adalimumab. Am J Ophthalmol, in press. 52. Schatz H, Atienza D, McDonald HR, Johnson RN. Severer diabetic retinopathy after cataract surgery. Am J Ophthalmol. 1994;117:314–21. 53. Rho DS. Treatment of acute pseudophakic cystoid macular edema: Diclofenac versus ketorolac. J Cataract Refract Surg. 2003;29:2378–84. 54. Han DP, Wisniewski SR, Wilson LA, et al. Spectrum and susceptibilities of microbiologic isolates in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol. 1996;122:1–17. 55. Montan P, Lundstrom M, Stenevi U, Thorburn W. Endophthalmitis following cataract surgery in Sweden. The 1998 national prospective survey. Acta Ophthalmol Scand. 2002;80:258–61. 56. Mamalis N, Kearsley L, Brinton E. Postoperative endophthalmitis. Curr Opin Ophthalmol. 2002;13:14–8. 57. Group EVS. Results of the Endophthalmitis Vitrectomy Study. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Arch Ophthalmol. 1995;113:1479–96. 58. Apple DJ, Solomon KD, Tetz RM, et al. Posterior capsule opacification. Surv Ophthalmol. 1992;37:73–116. 59. Koch DD, Liu JF, Fill EP, Parke DWI. Axial myopia increases the risk of retina complications after neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol. 1989;107:986–90. 60. Tielsch JM, Legro MW, Cassard SD, et al. Risk factors for retinal detachment after cataract surgery. A population-based case-control study. Ophthalmology. 1996;103:1537–45. 61. Ninn-Pedersen K, Bauer B. Cataract patients in a defined Swedish population, 1986 to 1990. V. Postoperative retinal detachments. Arch Ophthalmol. 1996;114:382–6. 62. Javitt JC, Vitale S, Canner JK, et al. National outcomes of cataract extraction. I. Retinal detachment after inpatient surgery. Ophthalmology. 1991;98:895–902. 63. Koch DD, Liu JF, Fill EP, Parke DWI. Axial myopia increases the risk of retina complications after neodymium-YAG laser posterior capsulectomy. Arch Ophthalmol. 1989;107:986–90. 64. Haddad WM, Monin C, Morel C, et al. Retinal detachment after phacoemulsification: a study of 114 cases. Am J Ophthalmol. 2002;133:630–8.

PART 5 THE LENS

Outcomes of Cataract Surgery Mats Lundstrom

Key features Objective measures of functional vision: n Uncorrected visual acuity n Best-corrected visual acuity n Contrast sensitivity n Glare disability n Visual field n Color vision.

INTRODUCTION Outcomes of cataract surgery can be classified according to objective and subjective findings. Objective measures of functional vision include much more than best-corrected visual acuity – parameters such as uncorrected visual acuity, contrast sensitivity, glare disability, visual field, and color vision are also very important. Subjective findings are best evaluated through interviews or questionnaires. Several questionnaires to help access a patient’s change in functional vision following cataract surgery are now available.1–3

EVALUATION OF OUTCOMES Functional vision assessment implies the ability to characterize parameters of vision and translate these into how well a patient is able to perform daily activities with respect to vision. To do this objectively, the parameters that characterize vision must first be determined. In both clinical practice and research, these parameters can be allocated to five major areas: l Limiting resolution (high contrast visual acuity) l Contrast performance (contrast sensitivity and threshold) l Performance at various background illuminations (glare disability) l Field of view (visual field) l Color performance (color vision) To fully evaluate the visual system using these five parameters in a patient who has a cataract is extremely important. In many cases, the patient does not present to the clinician with the diagnosis of cataract. The patient usually presents with complaints of decreased vision, and it is the clinician’s role to evaluate the patient’s history and examine the patient to determine the cause of the reduced vision. After diagnosis of a cataract – or any other diagnosis – has been made, some of the five parameters that describe visual performance may be found to be less important. To not fully evaluate the patient’s vision in the five areas can be harmful in two major ways: l By rendering therapy when it is not indicated l By not rendering therapy when it is indicated To translate the visual performance or functional vision of a patient into the ability to perform a specific activity necessitates knowledge of the visual requirements needed to carry out that activity. The visual requirements needed to perform specific daily life activities are poorly mapped out. Difficulty in determining the visual requirement of various activities and the variation in daily activities from one individual to another (variation in preferences and abilities) results in difficulty in correlating the significant improvement in visual performance in the five areas with improvement in the patient’s quality of life (QoL).4–6 Therefore, the patients’ self-assessed visual function in daily life is an important part of the outcomes evaluation. It has been suggested that

5.15

self-assessed visual function is the most important part of the outcomes evaluation.7 However, the subjective findings can only be made by asking the patient. To do this, an interview or a self-administered questionnaire can be used. A structured interview or questionnaire usually contains fixed questions and fixed response options. In the evaluation of outcomes of cataract surgery in daily practice, a proper follow-up time after surgery is crucial. Just as status 1 day after surgery may reflect whether the surgery was traumatic or not, sufficient time must elapse before the final refraction and patient satisfaction can be evaluated. The visual outcome depends on the surgical procedure, the age of the patient, ocular comorbidities, and surgical complications, among other things. The refractive outcome depends on the surgical procedure, the preoperative status and examination, and the intended target refraction. The type of intraocular lens (IOL), pupil size, and surgical procedure are important for contrast sensitivity, glare, halos, and other visual disturbances. The patient’s satisfaction with vision after surgery depends on the preoperative information given and the patient’s expectations, as well as the visual outcome.

FIVE PARAMETERS THAT DESCRIBE VISUAL FUNCTION Visual Acuity Testing

Standardized visual acuity testing

Standardized visual acuity tests measure the ability of a patient to recognize standardized optotypes (usually Snellen acuity letters) at a specified visual angle, illumination, and contrast.8 Visual acuity can be recorded in various notations, in which normal vision would be Snellen units 20/20 or 6/6, decimal notation 1.0, or logarithm of minimum angle of resolution (LogMAR) 0.0.

Potential retinal acuity testing

A special type of acuity test used in cataract patients is the assessment of potential retinal acuity. This test is essential for patients who have pigment mottling in the macula and reduced vision, particularly in the presence of a cataract or other optical aberrations of the eye. In the cataract age group, the incidence of macular degeneration is at least 10% and may exceed 15%, depending on the age of the patient.9 It is important that both the surgeon and the patient have a realistic expectation of the quality of postoperative vision, which helps both parties to accurately assess the risk-benefit ratio. It is true that there are different modalities, such as laser interferometry, super pinholes, the entoptic phenomenon, and projected retinal acuity charts, and all have been shown to be helpful in various situations. In dense, mature cataracts, the entoptic phenomenon is the only test expected to function, because the others require some small optical window or windows for the transmission of coherent light. Removal of a significant cataract should always be considered, even in the presence of an abnormal macula or if the predicted acuity is low. Cataracts are progressive, affecting contrast sensitivity and glare, and even if the patient does not gain an improvement in acuity after cataract removal, perversely a subjective improvement may occur along with protection from vision degradation through progression of the cataract.

Contrast Sensitivity Testing

Contrast sensitivity testing is important for the assessment of both sensory disease and media opacities. With media opacities, such as cataracts, there is a general depression in contrast sensitivity at all points, with a slightly greater depression at the lower contrasts.10–12

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Contrast sensitivity testing is an area of active research, in which types of stimuli (letter targets, and sinusoidal and square-wave gratings), number of sample points, and methods of reporting are being standardized. There are still large discrepancies in the test results bet ween different contrast sensitivity testing methods, especially under different lighting conditions.13 However, for the clinician, there is no question about the value of testing contrast sensitivity.

Glare Testing

Glare testing is most important in the assessment of media opacities such as cataracts. The effects are negligible in sensory disorders, except for a few macular disorders, such as cystoid macular edema (CME), in which intraocular light scatter occurs in the superficial layers of the retina.14, 15 Even with this disorder, the changes in glare disability are minimal. Glare testing can be very sensitive and specific to media opacities, but more importantly, it gives visual acuity values or equivalents that relate to a person’s vision in daylight, as opposed to vision in a testing room with high-contrast letters. Glare and contrast sensitivity testing have not yet been completely standardized and remain an area of active research and development. The value of glare testing to the clinician, both in the evaluation of a patient’s vision (as part of the diagnostic assessment) and in demonstrating the improvement following cataract surgery, is considerable. It is also important to realize that a patient’s history of glare symptoms is very difficult to interpret, because the meaning of the word “glare” is ambiguous to most patients. A patient often uses “glare” to describe unwanted images on spectacles or windshield, or originating from the sidewalk surface, which have nothing to do with the patient’s visual symptoms, much less a cataract. The value of both glare testing and contrast sensitivity testing is to provide the clinician with objective data to corroborate both examination and history. Without these tests, the patient’s history may be very misleading.

Visual Fields

The integrity of visual fields is particularly important in patients with sensory disorders, such as glaucoma and optic neuropathies, and patients who have suffered strokes that have affected the visual pathways.16, 17 Unfortunately, these disorders are also common in the age group that suffers from cataracts and may go undetected until after the cataract surgery. In most cases, a patient will be unaware of the loss of visual field until an accident occurs. Patients also may have trouble describing the difficulties encountered by the loss of peripheral vision; they may use terms such as “reduced vision,” which may be misinterpreted by the clinician as being caused by the cataracts. Also, visual field defects that result from strokes may change the risk-benefit ratio for cataract surgery, particularly if the stroke is recent.

Color Vision

Uncorrected Visual Acuity

“Uncorrected visual acuity” refers to the patient’s vision in standard conditions with no extraocular optical correction. Unlike best corrected visual acuity, there are several additional factors (such as pupil size, degree of refractive error, and amount of regular astigmatism) that also influence the measured visual acuity.24–26 Uncorrected visual acuity is most useful in the evaluation of specialty lenses, such as multifocal and toric intraocular lenses (IOLs). The goal when using these lenses is to reduce or eliminate the patient’s dependence on glasses, and to achieve good uncorrected distance and near visual acuity. To achieve target refraction is crucial when using multifocal IOLs. Unfortunately, multifocal IOLs have a tendency to give more glare and halo compared with monofocal IOLs.27 This applies to most types of IOLs with more than one focus, and to construct the optimal IOL for both near and distant vision is an area of active research. Uncorrected visual acuity can also be used as a quality characteristic of the surgical procedure, especially on the day after surgery.28 For this purpose, however, it is relevant to use the target refraction if, for instance, postoperative myopia is planned.

Target Refraction Prediction Error

Another factor in the determination of uncorrected visual acuity is the ability to achieve the target postoperative refraction. Most surgeons target the majority of their patients for postoperative refractions in the range of 0.0 to –0.50 D. With newer IOL formulas, personalization of lens constants, and improvements in surgical technique, at least 90% of patients should have spheroequivalent refraction within ±1.00 D of the intended target.29 In routine cataract surgery, this may be difficult to achieve and there is also a problem with measurement errors in keratometry, bulb length measurements, and precision of the IOL power. In recent publications on routine cataract surgery, between 75% and 80% of surgeries resulted in a final refraction within ±1.0 D of the intended target refraction.9, 19, 22 Surgically induced astigmatism (SIA) may be intended or not intended. Modern small-incision cataract surgery results in less SIA than earlier surgical technique did, with larger incisions.19, 30, 31 The magnitude of SIA may be less than 0.5 D on average, depending on incision site and incision size.32–34 The best outcome of cataract surgery with respect to astigmatism is usually to achieve as low a postoperative astigmatism as possible. Surgically induced astigmatism can be used to achieve this result by varying the placement of the incision. Surgically induced astigmatism can thereby counteract preoperative astigmatism and give a reduced postoperative astigmatism.35, 36

Color vision is specifically important in sensory disease, such as retino pathies and optic neuropathies, which often show characteristic color vision changes that help in making the differential diagnosis and in monitoring the effect of therapy. In patients who have ocular media disorders, such as cataracts, the changes in color vision can usually be correlated with the color of the cataract. For example, a patient who has a brunescent (yellow-brown) cataract has significant deficiencies in the blue end of the visual spectrum (shorter wavelengths).18 When color deficiencies do not correlate, sensory disorders should be suspected. Although color vision testing is very sensitive in disorders such as central serous maculopathy and CME, by “bleaching” or reducing the apparent brightness, other parameters, such as visual acuity, visual field, and contrast sensitivity, are also affected, which makes routine color testing unnecessary.

Contrast Sensitivity

OBJECTIVE FINDINGS OF CATARACT SURGERY OUTCOMES

Color Vision

Best-Corrected Visual Acuity

494

achieved best spectacle-corrected visual acuity equal to, or better than, 20/40 (6/12; 0.5).9, 19–23 The corresponding figures for all routine cataract patients including cases with ocular comorbidity were 84% to 90% in recent reports.9, 19–23

The term “best-corrected visual acuity” implies that the patient’s eye has been optically corrected to achieve the best visual acuity. In most cases, this value is obtained with best spectacle refraction. In cases of irregular corneal astigmatism, the best-corrected visual acuity may be attained with a rigid contact lens, not with spectacles. In recent studies with known preoperative pathology excluded (best case analyses), between 92% and 96% of the patients who had received cataract surgery

Following cataract surgery, in the absence of other ocular disease, the contrast sensitivity returns to normal.37, 38 Binocular contrast sensiti vity may not be normalized until second eye surgery has been performed given the occurrence of cataract in both eyes.39

Glare

Studies have documented the correlation of most of the instruments used for glare testing and outdoor vision testing, and show a dramatic improvement following cataract surgery.11, 12, 40–43

Visual Fields

The visual field returns to normal after cataract surgery in the absence of ocular comorbidity. Following cataract surgery in patients who have blue color deficiencies caused by the cataract, the return to normal color vision is very important to some patients, but is not even noticed by others. The artist, the decorator, and the individual who appreciates the color of the blue sky on a clear day all feel such an improvement to be remarkable; they experience the ability to continue in their chosen profession or the recovery of good-quality vision as a gift. In a patient who has a cataract and unusual color vision complaints, the results of color vision testing can be very helpful in the diagnosis and treatment of the concomitant disease. Color vision returns to normal in the absence of other ocular disease.

SUBJECTIVE FINDINGS OF CATARACT SURGERY OUTCOMES A large number of questionnaires for use in cataract surgery care have been published. They usually cover physical and functional dimensions and are therefore disease-specific questionnaires for establishing the health-related (vision-related) QoL for cataract patients. To describe the psychometric properties of the different questionnaires is beyond the scope of this chapter, but there are a number of review articles that have detailed this subject.1–3 On average, 80–90% of patients undergoing cataract surgery achieve improved self-assessed visual function, according to the questionnaires. Results of cataract surgery, as defined by some frequently used questionnaires,44–46 are detailed in Table 5-15-1. Older patients (> 85 years) also benefit from cataract surgery.47, 48 The positive impact of cataract surgery on patients’ self-assessed visual function seems to be long lasting, provided that no other ocular disease appears in the operated eye.49 Poor self-assessed visual function after cataract surgery may be caused by an ocular comorbidity, a disturbing cataract in the fellow eye, or anisometropia.50

CATARACT SURGERY OF ONE OR BOTH EYES Patients with bilateral cataract benefit from bilateral cataract extraction. Studies have shown that second-eye cataract surgery adds QoL for such patients.51, 52 A remaining cataract in the fellow eye after first-eye surgery may have a poor effect on binocular vision.39, 50 A bilateral cataract extraction can be performed sequentially with a varying interval between the two surgeries, so that some patients receive immediately sequential cataract surgery (ISCS), while others have delayed sequential cataract surgery (DSCS) with an interval between the surgeries of weeks or months. However, same-day bilateral cataract surgery requires a strict set of operating rules whereby each eye is treated as an entirely new operative procedure to avoid any possibility of cross contamination. Rapid rehabilitation of the patient is a worthy goal and a more economic process for all concerned.

Number of cases

Improved (%)

Steinberg et al., 199444

552

89*

199445

420

81.2

1933

83.7

Questionnaire

Publication

VF-14 ADVS† Catquest‡

Mangione et al.,

Lundström et al.,

199846

*Only first-eye surgery. †Activities of Daily Vision Scale. ‡Self-assessment questionnaire for cataract patients.

CATARACT SURGERY IN EYES WITH OCULAR COMORBIDITY

5.15 Outcomes of Cataract Surgery

Patients’ Self-Assessment of the Visual Outcome

TABLE 5-15-1 RESULTS FROM QUESTIONNAIRES FOLLOWING CATARACT SURGERY

In routine cataract surgery, a substantial number of patients have co existing eye diseases. A sight-threatening ocular comorbidity is the most frequent reason for a poor outcome after cataract surgery.19, 20, 50, 53–55 However, this does not mean that cataract extraction is unnecessary when there is an ocular comorbidity. Studies have shown that many patients with age-related macular degeneration and cataract benefit from cataract extraction.56, 57

SUMMARY All clinicians realize that good history taking, a thorough examination, and quantification of the five areas that describe functional vision are all important in the determination of indications for surgery and outcome of surgery. Furthermore, it is extremely important to evaluate the indications for, and outcomes of, cataract surgery with respect to health-related QoL. This is in the interests of patients, but it should also be done because of the significant costs to health-care linked to this procedure.

REFERENCES 1. Massof RW, Rubin GS. Visual function assessment questionnaires. Surv Ophthalmol. 2001;45:531–48. 2. Margolis MK, Coyne K, Kennedy-Martin T, et al. Visionspecific instruments for the assessment of health-related quality of life and visual functioning. Pharmacoecono mics. 2002;20:791–812. 3. de Boer MR, Moll AC, de Vet HCW, et al. Psychometric properties of vision-related quality of life questionnaires: a systematic review. Ophthal Physiol Opt. 2004;24:257–73. 4. Prager TC, Urso RG, Holladay JT, Stewart RH. Glare testing in cataract patients: instrument evaluation and identification of sources of methodological error. J Cataract Refract Surg. 1989;15:149–57. 5. Miller ST, Graney MJ, Elam JT, et al. Predictions of outcomes from cataract surgery in elderly persons. Ophthalmology. 1988;95:1125–9. 6. Graney MJ, Applegate WB, Miller ST, et al. A clinical index for predicting visual acuity after cataract surgery. Am J Ophthalmol. 1988;105:460–5. 7. Cataract Management Guideline Panel. Cataract in adults: management of functional impairment. Rockville, MD: US Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research; 1993 (AHCPR pub. No. 93–0542; Clinical practice guideline No. 4). 8. National Research Council Committee on Vision. Recommended standards for the clinical measurement and specification of visual acuity. Adv Ophthalmol. 1980;41:103–48. 9. Lundström M, Barry P, Leite H, et al. U. The 1998 European Cataract Outcome Study. Report from the European Cataract Outcome Study. J Cataract Refract Surg. 2001;27:1176–84. 10. Williamson TH, Strong NP, Sparrow J, et al. Contrast sensitivity and glare in cataract using the Pelli-Robson chart. Br J Ophthalmol. 1992;76:719–22. 11. Levin ML. Opalescent nuclear cataract. J Cataract Refract Surg. 1989;15:576–9. 12. Koch DD. Glare and contrast sensitivity testing in cataract patients. J Cataract Refract Surg. 1989;15:158–64. 13. Buhren J, Terzi E, Bach M, et al. Measuring contrast sensitivity under different lighting conditions: comparison of three tests. Optom Vis Sci. 2006;83:290–8.

14. Barrett BT, Davison PA, Eustace PE. Effects of posterior segment disorders on oscillatory displacement thresholds, and on acuities as measured using the potential acuity meter and laser interferometer. Ophthalmic Physiol Opt. 1994;14:132–8. 15. Alio JL, Artola A, Ruiz-Moreno JM, et al. Accuracy of the potential acuity meter in predicting the visual outcome in cases of cataract associated with macular degeneration. Eur J Ophthalmol. 1993;3:189–92. 16. Frisen L. High-pass resolution perimetry and agerelated loss of visual pathway neurons. Acta Ophthalmol. 1991;69:511–5. 17. Ball KK, Beard BL, Roenker DL, et al. Age and visual research: expanding the useful field of view. J Optom Soc Am Assoc. 1988;5:2210–9. 18. Cooper BA, Ward M, Gowland CA, McIntosh JM. The use of the Lanthony New Color Test in determining the effects of aging on color vision. J Gerontol. 1991;46: 320–4. 19. Lundström M, Stenevi U, Thorburn W. The Swedish National Cataract Register: a 9-year review. Acta Ophthalmol Scand. 2002;80:248–57. 20. Desai P, Minassian DC, Reidy A. National cataract surgery survey 1997–8: a report of the results of the clinical outcomes. Br J Ophthalmol. 1999;83:1336–40. 21. Schein OD, Steiberg EP, Javitt JC, et al. Variation in cataract surgery practice and clinical outcomes. Ophthalmology. 1994;101:1142–52. 22. Murphy C, Tuft SJ, Minassian DC. Refractive error and visual outcome after cataract extraction. J Cataract Refract Surg. 2002;28:62–6. 23. Wegener M, Alsbirk PH, Hojgaard-Olsen K. Outcome of 1000 consecutive clinic- and hospital-based cataract surgeries in a Danish county. J Cataract Refract Surg. 1998;24:1152–60. 24. Holladay JT. A prospective, randomized, double-masked comparison of a zonal-progressive multifocal IOL. A discussion. Ophthalmology. 1992;99:860. 25. Steinert RF, Post CT Jr, Brint SF, et al. A prospective, randomized, double-masked comparison of a zonalprogressive multifocal intraocular lens and a monofocal intraocular lens. Ophthalmology. 1992;99:853–60.

26. Lindstrom RL. Food and Drug Administration update. One-year results from 671 patients with the 3M multi focal intraocular lens. Ophthalmology. 1993;100:91–7. 27. Javitt JC, Steinert RF. Cataract extraction with multifocal intraocular lens implantation: a multinational clinical trial evaluating clinical, functional, and quality of life outcomes. Ophthalmology. 2000;107:2040–8. 28. Osher RH, Barros MG, Marques DMV, et al. Early uncorrected visual acuity as a measurement of the visual outcomes of contemporary cataract surgery. J Cataract Refract Surg. 2004;30:1917–20. 29. Holladay JT, Prager TC, Ruiz RS, Lewis JW. Improving the predictability of intraocular lens calculations. Arch Ophthalmol. 1986;104:539–41. 30. Rainer G, Menapace R, Vass C, et al. Surgically induced astigmatism following a 4.0 mm sclerocorneal valve incision. J Cataract Refract Surg. 1997;23:358–64. 31. Naeser K, Knudsen EB, Hansen MK. Bivariate polar value analysis of surgically induced astigmatism. J Cataract Refract Surg. 2002;18:72–8. 32. Kohnen S, Neuber R, Kohnen T. Effect of temporal and nasal unsutured limbal tunnel incisions on induced astigmatism after phacoemulsification. J Cataract Refract Surg. 2002;28:821–5. 33. Alio J, Rodriguez-Prats JL, Galal A, Ramzy M. Outcomes of microincision cataract surgery versus coaxial phacoemulsification. Ophthalmology. 2005;112:1997–2003. 34. Borasio E, Mehta JS, Maurino V. Surgically induced astigmatism after phacoemulsification in eyes with mild to moderate corneal astigmatism: temporal versus on-axis clear corneal incisions. J Cataract Refract Surg. 2006;32:565–72. 35. Ben Simon GJ, Desatnik H. Correction of pre-existing astigmatism during cataract surgery: comparison between the effects of opposite clear corneal incisions and a single clear corneal incision. Craefes Arch Clin Exp Ophthalmol. 2005;243:321–6. 36. Qammar A, Mullaney P. Paired opposite clear corneal incisions to correct pre-existing astigmatism in cataract patients. J Cataract Refract Surg. 2005;31:1167–70. 37. Pfoff DS, Werner JS. Effect of cataract surgery on contrast sensitivity and glare in patients with 20/50 or better Snellen acuity. J Cataract Refract Surg. 1994;20:620–5.

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38. Hard AL, Beckman C, Sjostrand J. Glare measurements before and after cataract surgery. Acta Ophthalmol Scand. 1993;71:471–6. 39. Lundström M, Albrecht S, Nilsson M, Åström B. Patients benefit from bilateral same-day cataract extraction – a randomized clinical study. J Cataract Refract Surg. 2006;32:826–30. 40. Sunderraj P, Villada JR, Joyce PW, Watson A. Glare testing in pseudophakes with posterior capsule opacification. Eye. 1992;6:411–3. 41. Masket S. Relationship between postoperative pupil size and disability glare. J Cataract Refract Surg. 1992;18:506–7. 42. Masket S. Reversal of glare disability after cataract surgery. J Cataract Refract Surg. 1989;15:165–8. 43. Hirsch RP, Nadler MP, Miller D. Clinical performance of a disability glare tester. Arch Ophthalmol. 1984;102:1633–6. 44. Steinberg EP, Tielsch JM, Schein OD. National study of cataract surgery outcomes. Variation in 4-month postoperative outcomes as reflected in multiple outcome measures. Ophthalmology. 1994;101:1131–40. 45. Mangione CM, Russell SP, Lawrence MG, et al. Improved visual function and attenuation of declines in healthrelated quality of life after cataract extraction. Arch Ophthalmol. 1994;112:1419–25.

46. Lundström M, Stenevi U, Thorburn W, Roos P. Catquest questionnaire for use in cataract surgery care: assessment of surgical outcomes. J Cataract Refractive Surg. 1998;75:688–91. 47. Lundström M, Stenevi U, Thorburn W. Cataract surgery in the very elderly. J Cataract Refractive Surg. 2000;26:408–14. 48. Mönestam E, Wachmeister L. Impact of cataract surgery on the visual ability of the very old. Am J Ophthalmol. 2004;137:145–55. 49. Lundström M, Wendel E. Duration of self-assessed benefit of cataract extraction – a long-term study. Br J Ophthalmol. 2005;89:1017–20. 50. Lundström M, Brege KG, Florén I, et al. Impaired visual function following cataract surgery. An analysis of poor outcomes as defined by the Catquest questionnaire. J Cataract Refractive Surg. 2000;26:101–8. 51. Laidlaw DA, Harrad RA, Hopper CD, et al. Randomised trial of effectiveness of second eye cataract surgery. Lancet. 1998;352:925–9. 52. Lundström M, Stenevi U, Thorburn W. Quality of life after first- and second-eye cataract surgery. Five-year data collected by the Swedish National Cataract Register. J Cataract Refract Surg. 2001;27:1553–9.

53. Mangione CM, Orav EJ, Lawrence MG, et al. Prediction of visual function after cataract surgery: a prospectively validated model. Arch Ophthalmol. 1995;113:1305–11. 54. Schein OD, Steinberg EP, Cassard SD, et al. Predictors of outcome in patients who underwent cataract surgery. Ophthalmology. 1995;102:817–23. 55. Lundström M, Stenevi U, Thorburn W. Outcome of cataract surgery considering the preoperative situation: a study of possible predictors of the functional outcome. Br J Ophthalmol. 1999;83:1272–6. 56. Lundström M, Brege KG, Florén I, et al. Cataract surgery and quality of life in patients with age-related macular degeneration. Br J Ophthalmol. 2002;86:1330–5. 57. Armbrecht AM, Findlay C, Aspinall PA, et al. Cataract surgery in patients with age-related macular degeneration: one-year outcomes. J Cataract Refract Surg. 2003;29:686–93.

PART 5 THE LENS

5.16

Secondary Cataract Liliana Werner

Definition: Secondary cataract, also known as posterior capsule

opacification (PCO), is the most common complication after cataract surgery, resulting from migration and proliferation of residual lens epithelial cells (LECs) onto the central posterior capsule, leading to decrease in visual function, and ultimately in visual acuity. Opacification within the capsular bag may also present as anterior capsule opacification (ACO) or interlenticular opacification (ILO).

Key features n n n

nderstanding of the PCO pathogenesis. U Understanding of surgery-related factors for PCO prevention. Understanding of intraocular lens-related factors for PCO prevention.

Associated features n�� n��

nderstanding of the ACO pathogenesis. U Understanding of the ILO pathogenesis.

INTRODUCTION Secondary cataract or posterior capsule opacification (PCO) is the most common postoperative complication of cataract surgery. Its incidence has decreased over the past few decades as the understanding of its pathogenesis has evolved. Advances in surgical technique, intraocular lens (IOL) design, and materials have all contributed to the gradual decline in PCO incidence. However, it remains a major cause of decreased visual acuity after cataract surgery occurring at a rate of between 3% and 50% (less in recent years) in the first 5 years postoperatively.1, 2

PATHOGENESIS PCO results from migration and proliferation of residual lens epithelial cells (LECs) onto the central posterior capsule. When the cells invade the visual axis as pearls, fibrotic plaques, or wrinkles, the patient experiences a decrease in visual function, and ultimately in visual acuity.3 The epithelium of the crystalline lens consists of a sheet of anterior epithelial cells (“A” cells) that are in continuity with the cells of the equatorial lens bow (“E” cells). The latter cells comprise the germinal cells that undergo mitosis as they peel off from the equator. They constantly form new lens fibers during normal lens growth. Although both the anterior and equatorial lens epithelial cells stem from a continuous cell line and remain in continuity, it is useful to divide these into two functional groups. They differ in terms of function, growth

patterns, and pathologic processes. The anterior or “A” cells, when disturbed, tend to remain in place and not migrate. They are prone to a transformation into fibrous-like tissue (pseudofibrous metaplasia). In contrast, in pathologic states, the “E” cells of the equatorial lens bow tend to migrate posteriorly along the posterior capsule; e.g., in posterior subcapsular cataracts, and the pearl form of PCO. In general, instead of undergoing a fibrotic transformation, they tend to form large, balloon-like bladder cells (the cells of Wedl). These are the cells that are clinically visible as “pearls” (Elschnig’s pearls). These equatorial cells are the primary source of classic secondary cataract, especially the pearl form of PCO. In a recent clinical study by Neumayer et al. significant changes in the morphology of Elschnig’s pearls were observed within time intervals of only 24 hours. Appearance and disappearance of pearls as well as progression and regression of pearls within these short intervals illustrate the dynamic behavior of regeneratory PCO.4 The “E” cells are also those responsible for formation of a Soemmerring’s ring, which is a doughnut-shaped lesion composed of retained/ regenerated cortex and cells that may form following any type of disruption of the anterior lens capsule. This lesion was initially described in connection with ocular trauma. The basic pathogenic factor of the Soemmering’s ring is the anterior capsular break, which may then allow exit of central nuclear and cortical material out of the lens, with subsequent Elschnig’s pearl formation. A Soemmering’s ring forms every time any form of extracapsular cataract extraction (ECCE) is done, whether manually, automated, or with phacoemulsification. For practical purposes it is useful to consider this lesion as the basic precursor of classic PCO, especially the “pearl” form. The LECs have higher proliferative capacity in the young compared with the old; therefore, the incidence of PCO formation is higher in younger patients. The same cell types mentioned above are also involved in other processes of opacification within the capsular bag (Fig. 5-16-1). These include anterior capsule opacification (ACO)5, 6 and interlenticular opacification (ILO).7, 8 The latter involves opacification of the space between two or more IOLs implanted in the bag (piggy-back implantation).

TREATMENT AND PREVENTION The treatment of PCO is typically neodymium:yttrium–aluminum– garnet (Nd:YAG) laser posterior capsulectomy. This is a simple procedure in most cases, but is not without risks. Complications include IOL damage, IOL subluxation or dislocation, retinal detachment, and secondary glaucoma.9 Therefore, prevention of this complication is important, not only because of the risks associated with its treatment, but also because of the costs involved in the procedure. Extensive research has been performed on the inhibition of LEC proliferation and migration by pharmacologic agents through various delivery systems or IOL coatings – in vitro and in vivo animal studies.10–12 Physical techniques to kill the LECs, as well as immunotherapy and gene therapy, have also been investigated.13, 14 While basic research into the most effective mechanism for PCO eradication evolves, the practical surgeon can already apply some principles to prevent it.15 Studies carried out in our laboratory together with clinical studies done in other centers enabled the definition of three surgery-related factors that help in the prevention of PCO: (1) hydro dissection-enhanced cortical clean-up; (2) in-the-bag IOL fixation; and (3) performance of a capsulorrhexis slightly smaller than the diameter of the IOL optic (Fig. 5-16-2). The same studies helped in the definition of

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5 THE LENS A

Fig. 5-16-1 Different forms of opacification within the capsular bag. (A) Human eye obtained postmortem (posterior or Miyake-Apple view) implanted with a rigid lens, showing asymmetric fixation, and decentration. A doughnut-shaped, white lesion can be seen for 360° in the equatorial region of the capsular bag (Soemmering’s ring), and the posterior capsule is fibrotic. (B) Human eye obtained postmortem (posterior view) implanted with a rigid lens. Soemmering’s ring is also present. A posterior capsulotomy had been performed for posterior capsule opacification, and proliferation of Elschnig’s pearls can be seen at the edges of the capsulotomy (arrow). (C) Human eye obtained postmortem (posterior view) implanted with a foldable, plate silicone lens. The anterior capsule is fibrotic (arrow). Although Soemmering’s ring formation can be seen, the posterior capsule is not opacified. (D) Pair of foldable, hydrophobic acrylic lenses explanted because of interlenticular opacification. The lenses are fused together through the material within the interlenticular space.

Fig. 5-16-2 Human eyes obtained postmortem (posterior view) implanted with silicone (A) and hydrophobic acrylic (B) lenses. These are examples of application of the three surgery-related factors for prevention of posterior capsule opacification. The lenses were symmetrically implanted in the bag, via capsulorrhexis smaller than the optic diameter of the lenses (ideally, the capsulorrhexis margin should cover the edge of the lens for 360°). No significant Soemmering’s ring formation is present.

498

5.16 Secondary Cataract

three IOL-related factors for PCO prevention: (1) use of a biocompatible IOL to reduce stimulation of cellular proliferation; (2) enhancement of the contact between the IOL optic and the posterior capsule; and (3) use of an IOL with a square, truncated optic edge.

HYDRODISSECTION-ENHANCED CORTICAL CLEAN-UP Dr Howard Fine introduced this technique and coined the term cortical cleaving hydrodissection.16 The edge of the anterior capsule is slightly tented up by the tip of the cannula, while injecting the fluid. This technique is used by many surgeons to facilitate removal of the cortex and equatorial lens epithelial cells; it also enhances the safety of the operation. We emphasize that complete removal of the cortex is critical, which has a beneficial influence on the prevention of PCO. Once cortical cleaving hydrodissection has been carried out successfully, the following operation is easier and faster.17 Various solutions (e.g., preservative-free lidocaine 1%, antimitotics, etc.) for the hydrodissection step of the phacoemulsification procedure have been studied.18, 19 Further studies are necessary to establish the safety and utility of these solutions in terms of PCO prevention. It is especially important to remove all cortical material and “E” cells from the equatorial region of the capsular bag, which contribute to the formation of the Soemmering’s ring. While a careful cortical clean-up and elimination of as many “E” cells as possible is fundamental to reducing the incidence of this complication, the role of anterior capsule polishing and elimination of “A” cells remains to be demonstrated. Indeed, Sacu et al. have recently performed a study to evaluate the effect of anterior capsule polishing on PCO.20 In this randomized, prospective study, 26 patients received a silicone IOL with a truncated optic in both eyes. The anterior capsule was extensively polished in one eye and was left unpolished in the other eye. Digital slit-lamp photographs taken 1 year postoperatively using a standardized photographic technique showed that anterior capsule polishing caused no significant difference in the outcome of PCO. The same group of authors obtained similar results in another clinical study, with a 3-year follow-up.21 Some authors actually believe that the postoperative fibrous metaplasia of remaining “A” cells push the IOL against the posterior capsule, and that would explain the relatively low PCO rates of eyes implanted with silicone lenses having rounded optic edges.22

IN-THE-BAG IOL FIXATION The hallmark of modern cataract surgery is the achievement of consistent and secure in-the-bag or endocapsular IOL fixation. The most obvious advantage of in-the-bag fixation is the accomplishment of good lens centration. However, endocapsular fixation functions primarily to enhance the IOL-optic barrier effect, as will be discussed later. In a large series of human cadaver eyes implanted with different IOLs analyzed in our laboratory, both central PCO and Nd:YAG rates were influenced by IOL fixation, i.e., less PCO and Nd:YAG capsulectomies in eyes where the IOLs were in the bag.23 Dr Marie-José Tassignon proposed a variation of the in-the-bag IOL fixation concept for PCO prevention, named “bag-in-the-lens” implantation.24 This involves the use of a twin-capsulorrhexis IOL design, and performance of anterior and posterior capsulorrhexis of the same size. The biconvex lens has a circular equatorial groove in the surrounding haptic, for placement of both capsules after capsulorrhexis. In theory, if the capsules are well stretched around the optic of this lens, the LECs will be captured within the remaining space of the capsular bag and their proliferation will be limited to this space, so the visual axis will remain clear (Fig. 5-16-3). In studies performed in human eyes obtained postmortem and in rabbits, bag-in-the-lens implantation was highly effective in preventing PCO, when the anterior and posterior capsules were properly secured in the IOL groove.

CAPSULORRHEXIS SIZE There is evidence that PCO is reduced if the capsulorrhexis diameter is slightly smaller than that of the lens optic, so that the anterior edge rests on the optic. This helps provide a tight fit of the capsule around

Fig. 5-16-3 Clinical photograph taken 6 months after cataract surgery with “bag-in-the-lens” implantation in a 64-year-old patient. The area corresponding to the optic of the lens is completely free of opacities. (Courtesy of Dr Marie-José Tassignon, Belgium.)

the optic analogous to “shrink-wrap,” which has beneficial effects in maximizing the contact between the lens optic and the posterior capsule. Another advantage may be the sequestration of the interior compartment of the capsule containing the IOL from the surrounding aqueous humor and any potentially deleterious factors within it, such as inflammatory mediators. In a retrospective clinical study performed at the John A. Moran Eye Center, University of Utah on patients implanted with different IOLs, including lenses with round or square optic edges, the degree of postoperative PCO was correlated with the degree of anterior capsule overlap.25 Considering all patients, but also considering the patients distributed in different IOL groups, there was always a significant negative, linear correlation between the degree of overlap and PCO.

BIOCOMPATIBLE IOL There are many definitions for the term “biocompatibility.” With regards to PCO, materials with the ability to inhibit stimulation of cell proliferation are more “biocompatible.” The “Sandwich” theory states that a hydrophobic acrylic IOL with bioadhesive surface would allow only a monolayer of lens epithelial cells to attach to the capsule and the lens, preventing further cell proliferation and capsular bag opacification. We performed two immunohistochemical studies on the adhesion of proteins to different IOLs that had been implanted in human eyes obtained postmortem.26, 27 Analyses of histological sections demonstrated that fibronectin mediates the adhesion of hydrophobic acrylic lenses to the anterior and posterior capsules. Analyses of explanted lenses confirmed the presence of greater amounts of fibronectin on the surfaces of the same lens. However, even though differences among materials exist, in terms of PCO prevention it appears that the geometry of the lens, i.e., having a square, posterior optic edge, is the most important factor (see section on “IOL Optic Geometry”). The adhesiveness of the material may have a more direct impact on the development of ACO. This generally occurs much earlier in comparison to PCO, sometimes within 1 month postoperatively. When the continuous curvilinear capsulorrhexis (CCC) is smaller than the IOL optic, the anterior surface of the optic’s biomaterial maintains contact with the adjacent posterior aspect of the anterior capsule. Any remaining anterior lens epithelial cells (A cells) in contact with the IOL have the potential to undergo fibrous proliferation; thus, ACO is essentially a fibrotic entity. Studies in our laboratory using pseudophakic human eyes obtained postmortem showed that ACO is more common with silicone IOLs, especially the plate designs, because of the larger area of contact between these lenses and the anterior capsule (Fig. 5-16-1C).5 However, the same studies showed that the plate design resists contraction forces within the

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5 THE LENS

capsular bag better than three-piece silicone lenses with flexible haptics (polypropylene).6 The latter showed the higher rates of capsulorrhexis phimosis and IOL decentration as a result of excessive capsular bag fibrosis. There is, therefore, a tendency in IOL manufacture favoring haptic materials with higher rigidity, such as polymethyl methacrylate (PMMA), polyimide (Elastimide), and poly(vinylidene) fluoride (PVDF). In the same studies, ACO was less significant with hydrophobic acrylic lenses having an adhesive surface. ACO has been considered a clinical problem when anterior capsular shrinkage associated with constriction of the anterior capsulectomy opening (capsulorrhexis contraction syndrome or capsular phimosis) accompanies excessive anterior capsule fibrosis. This has been especially observed in conditions associated with zonular weakness, e.g., pseudoexfoliation and advanced age, and with chronic intraocular inflammation. Besides phimosis of the CCC opening, excessive zonular traction and its sequelae, IOL dislocation and retinal detachment, can also occur because of excessive capsular fibrosis. Excessive opacification of the anterior capsule is problematic in that it hinders visualization of the peripheral fundus during retinal examination. Otherwise, a certain degree of ACO is sometimes considered an advantage, as it can prevent potential dysphotopsia phenomena caused by the square edge of some IOL optic designs. Also, anterior capsule fibrosis with contraction of the capsular bag will push the IOL optic against the posterior capsule, helping in the prevention of PCO according to the “no space, no cells” theory. This mechanism would explain the relatively low PCO rates with some silicone lenses, in the absence of a square optic edge profile, as noted above.22 The adhesiveness of the IOL material may also have an influence on ILO formation. To date, all cases of ILO we analyzed in our laboratory seemed to be related to two hydrophobic acrylic IOLs being implanted in the capsular bag through a small capsulorrhexis, with its margins overlapping the optic edge of the anterior IOL for 360°.7 When these lenses are implanted in the capsular bag through a small capsulorrhexis, the bioadhesion of the anterior surface of the front lens to the anterior capsule edge and of the posterior surface of the back lens to the posterior capsule prevents the migration of the cells from the equatorial bow onto the posterior capsule. This migration may be directed towards the interlenticular space. In this scenario, the two IOLs are sequestered together with aqueous and lens epithelial cells in a hermetically closed microenvironment. In addition, the adhesive nature of the material seems to render the opacifying material very difficult to remove by any surgical means (Fig. 5-16-1D). Analyses of the above-described cases of ILO in our laboratory allowed us to conclude that the opacification within the interlenticular space is derived from retained/regenerative cortex and pearls, which is similar to the pathogenesis of the pearl form of PCO. Based on the common features of different cases of ILO, some surgical methods were proposed for its prevention. The first option would be to implant both IOLs in the capsular bag but with a relatively larger diameter capsulorrhexis. In this scenario, there is a possibility that the cut edge of the rhexis may fuse with the posterior capsule. This should help sequester the retained/proliferated equatorial lens epithelial cells within the equatorial fornix. The other possibility is to implant the anterior IOL in the sulcus and the posterior IOL in the bag with a small rhexis. The rhexis margin will adhere to the anterior surface of the posterior IOL and the cells within the equatorial fornix will also be sequestered. Reassessment of factors leading to ILO formation is important because of the development of dual-optic accommodating IOLs to be implanted in the capsular bag.8 Also, piggy-back implantation for correction of residual refractive errors appears to be increasing in popularity, including implantation of a multifocal IOL in pseudophakic patients. However, in these cases the second (anterior) IOL is generally fixated in the ciliary sulcus.

CONTACT BETWEEN THE IOL OPTIC AND THE POSTERIOR CAPSULE

500

Different factors can help maximize the contact between the IOL and the posterior capsule, contributing to the so-called “no space, no cells” concept. Optic/haptic angulation displacing the optic posteriorly and stickiness of the IOL optic material are the most important lens features to obtain a tight fit between lens and capsule. Threepiece lenses manufactured from the different haptic materials currently available today have in general a posterior optic/haptic

a ngulation ranging from 5° to 10°. To keep the advantages of the two above-mentioned factors, it is important to achieve endo capsular lens fixation and to create a capsulorrhexis smaller than the diameter of the lens optic. According to the “no space, no cells” theory, capsular tension rings may also have a role in the prevention of PCO.28, 29 Equatorial capsular tension rings have the ability to maintain the contour of the capsular bag and to stretch the posterior capsule. They have thus primarily been used in cases of zonular rupture or dehiscence, secondary to trauma, or when inherent zonular weakness is present, such as in pseudoexfoliation syndrome. In the latter case, they also provide countertraction to prevent excessive postoperative shrinkage of the capsular bag secondary to fibrosis. It has been demonstrated by highresolution laser interferometric studies that there is a space between the IOL and the posterior capsule with various lens designs. With a capsular tension ring in place, this space was found to be smaller or nonexistent. Thus, lens epithelial cells would not find a space to migrate and proliferate onto the posterior capsule. Capsular tension rings also produce a circumferential stretch on the capsular bag, with the radial distention forces equally distributed. Formation of traction folds in the posterior capsule, which may be used as an avenue for cell ingrowth, is thus avoided. Capsular tension rings may also have a role in the prevention of opacification of the anterior capsule. The presence of a broad bandshaped capsular ring would keep the anterior capsule leaf away from the anterior optic surface and the posterior capsule. This would ultimately lead to less metaplasia of lens epithelial cells on the inner surface of the anterior capsule with less fibrous tissue formation, and thus less opacification and contraction of this structure. IOLs with design features that help to maintain the anterior capsule away from the anterior surface of the lens have also been evaluated in our laboratory.8, 30 A capsular tension ring designed to prevent opacification within the capsular bag was evaluated in two centers, one in Japan (Nishi et al.) and the other in Austria (Menapace et al.). Both centers reported a significant reduction in PCO and ACO with the rings, in comparison to the contralateral eyes implanted with the same lens design.

IOL OPTIC GEOMETRY The square, truncated lens optic edge may act as a barrier, preventing migration of proliferative material from the equatorial region onto the posterior capsule.31 The barrier effect is absent with lenses having rounded edges, and proliferative material from the equatorial region has a more free access to the posterior capsule, opacifying the visual axis. The barrier effect of the square optic edge is functional when the lens optic is fully in the bag, in contact with the posterior capsule. When one or both haptics are out of the bag, a potential space exists that allows an avenue for cellular ingrowth toward the visual axis. A number of modern lenses on the market manufactured from different materials present this important design feature. Some of them have a square edge on the posterior optic surface, while the anterior optic edge remains round in order to prevent disphotopsia. Evidence from rabbit studies shows that the optic-haptic junctions of square-edged, single-piece lenses may represent a site for cell ingrowth and PCO formation.32, 33 At the level of those junctions, the barrier effect of the square edge appears to be less effective. We obtained better results regarding PCO formation with a hydrophilic acrylic singlepiece lens having an “enhanced” square edge than with the standard model of the same design.32 The enhanced edge provided the lens with a peripheral ridge around the lens optic for 360°. In the standard model, the square edge profile appeared to be absent at the level of the optic-haptic junctions (Fig. 5-16-4). Therefore, the square optic edge is probably the most important IOL design feature for PCO prevention. It appears, however, that it should be present for 360° around the IOL optic in order to provide an effective barrier.

EXPERIMENTAL DEVICES: SEALED CAPSULE IRRIGATION FOR PCO PREVENTION As noted above, prevention of PCO relies on removal of lens epithelial cells from the anterior and equatorial regions of the capsular bag after cataract removal. Use of pharmacological and non pharmacological agents for this purpose in an unsealed system may increase the risk of toxicity to surrounding intraocular structures,

5.16 Secondary Cataract

Fig. 5-16-4 Foldable, hydrophilic acrylic lenses with square optic and haptic edges. The lens in (B) was modified to incorporate an extra ridge all around the optic (enhanced square edge; arrow). (C) and (D) are photographs obtained from rabbit eyes (posterior view), experimentally implanted with the lenses in (A) and (B), respectively. Soemmering’s ring formation is observed in both eyes. The arrow in (C) shows the opacification of the posterior capsule, which started at the level of the optic-haptic junction. (Reproduced from Werner L, Mamalis N, Pandey SK, et al. Posterior capsule opacification in rabbit eyes implanted with hydrophilic acrylic intraocular lenses with enhanced square edge. J Cataract Refract Surg. 2004;30:2403–9.)

especially corneal endothelial cells. Dr Anthony Maloof has developed a new concept in irrigation of the human lens capsule following lens surgery called sealed capsule irrigation (SCI), which may allow the isolated safe delivery of irrigating solutions containing pharmacological or nonpharmacological agents into the capsular bag following cataract surgery. 34 Any device providing SCI needs to meet the following requirements: it should be minimally invasive, easy to use, fit through a small incision, be relatively inexpensive, provide a safe and repeatable seal of the lens capsule, and its use should not add significantly to the duration of routine cataract surgery. Milvella (Sydney, Australia) has recently developed a device called PerfectCapsule, a sealed delivery system made of biomedical grade soft silicone, which allows the surgeon to reseal the capsular bag. The device consists of a rounded plate containing a suction ring, which abuts the anterior capsule, and an extension arm that passes

through a phacoemulsification wound of 2.9 mm. This extension arm carries a vacuum channel, which supplies vacuum to the suction ring, and a combined irrigation and aspiration channel. The irrigation and aspiration channel allows for communication between the sealed capsular bag and the external eye. The overall diameter of the device is 7 mm, with an inner diameter of 5 mm. It was designed to temporarily seal a capsulorrhexis of less than 5 mm, enabling selective and specific irrigation of the internal capsular bag with different solutions (Fig. 5-16-5). Animal and clinical studies demonstrated the effectiveness of PerfectCapsule for SCI, without any leakage of the irrigating solutions used into the anterior chamber. Ongoing studies will ascertain the definitive solution(s) to be used in conjunction with this device. If proved definitively useful for the prevention of capsular bag opacification, this technology may eventually be incorporated as a step of the cataract/lens exchange surgical procedure.

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5 THE LENS A

Fig. 5-16-5 Device for sealed capsule irrigation (PerfectCapsule, Milvella). (A) Schematic drawing showing the device sealing the anterior capsulorrhexis, to allow injection of solutions within the internal compartment of the capsular bag. (B) Photograph showing the device implanted in a human eye, after complete evacuation of the capsular bag. (Courtesy of Dr Anthony Maloof, Australia.)

SUMMARY In summary, development of PCO is multifactorial, and its eradication depends on the quality of the surgery, as well as on the quality of the IOL implanted. Each factor described here does not act in isolation, and it is their interaction that produces the best results. Research on the prevention of any form of opacification/fibrosis within the capsular

bag is increasing in importance, especially with the advent of specialized IOLs such as accommodative lenses, which are designed to enable a forward movement of the optic upon efforts of accommodation. The functionality of such lenses will probably require long-term trans parency and elasticity of the capsular bag.

REFERENCES

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1. Apple DJ, Solomon KD, Tetz MR, et al. Posterior capsular opacification. Major review. Surv Ophthalmol. 1992;37:73–116. 2. Schaumberg DA, Dana MR, Christen WG, Glynn RJ. A systematic overview of the incidence of posterior capsule opacification. Ophthalmology. 1998;105:1213–21. 3. Meacock WR, Spalton DJ, Boyce J, Marshall J. The effect of posterior capsule opacification on visual function. Invest Ophthalmol Vis Sci. 2003;44:4665–9. 4. Neumayer T, Findl O, Buehl W, Georgopoulos M. Daily changes in the morphology of Elschnig pearls. Am J Ophthalmol. 2006;141:517–23. 5. Werner L, Pandey SK, Escobar-Gomez M, et al. Anterior capsule opacification: A histopathological study comparing different IOL styles. Ophthalmology. 2000;107:463–71. 6. Werner L, Pandey SK, Apple DJ, et al. Anterior capsule opacification: correlation of pathological findings with clinical sequelae. Ophthalmology. 2001;108:1675–81. 7. Werner L, Apple DJ, Pandey SK, et al. Analysis of elements of interlenticular opacification. Am J Ophthalmol. 2002;133:320–6. 8. Werner L, Mamalis N, Stevens S, et al. Interlenticular opacification: Dual-optic versus piggyback intraocular lenses. J Cataract Refract Surg. 2006;32:656–62. 9. Charles S. Vitreoretinal complications of YAG laser capsulotomy. Ophthalmol Clin N Am. 2001;14:705–10. 10. Fernandez V, Fragoso MA, Billote C, et al. Efficacy of various drugs in the prevention of posterior capsule opacification: Experimental study of rabbit eyes. J Cataract Refract Surg. 2004;30:2598–605. 11. Werner L, Legeais JM, Nagel MD, Renard G. Evaluation of Teflon-coated intraocular lenses in an organ culture method. J Biomed Mater Res. 1999;46:347–54. 12. Okajima Y, Saika S, Sawa M. Effect of surface coating an acrylic intraocular lens with poly(2-methacryloyloxyethyl phosphorylcholine) polymer on lens epithelial cell line behavior. J Cataract Refract Surg. 2006;32:666–71. 13. Meacock WR, Spalton DJ, Hollick EJ, et al. Doublemasked prospective ocular safety study of a lens epithelial cell antibody to prevent posterior capsule opacification. J Cataract Refract Surg. 2000;26:716–21.

14. Malecaze F, Decha A, Serre B, et al. Prevention of posterior capsule opacification by the induction of therapeutic apoptosis of residual lens cells. Gene Ther. 2006;13:440–8. 15. Apple DJ, Werner L. Complications of cataract and refractive surgery: A clinicopathological documentation. Trans Am Ophthalmol Soc. 2001;99:95–109. 16. Fine IH. Cortical cleaving hydrodissection. J Cataract Refract Surg. 1992;18:508–12. 17. Peng Q, Apple DJ, Visessook N, et al. Surgical prevention of posterior capsule opacification. Part II. Enhancement of cortical clean up by increased emphasis and focus on the hydrodissection procedure. J Cataract Refract Surg. 2000;26:188–97. 18. Vargas LG, Escobar-Gomez M, Apple DJ, et al. Pharmacologic prevention of posterior capsule opacification: In vitro effects of preservative-free lidocaine 1% on lens epithelial cells. J Cataract Refract Surg. 2003;29:1585–92. 19. Chew J, Werner L, Stevens S, et al. Evaluation of the effects of hydrodissection with antimitotics using a rabbit model of Soemmering’s ring formation. Graefes Arch Clin Exp Ophthalmol. 2006; 34:449–456. 20. Sacu S, Menapace R, Findl O, et al. Influence of optic edge design and anterior capsule polishing on posterior capsule fibrosis. J Cataract Refract Surg. 2004;30:658–62. 21. Menapace R, Wirtitsch M, Findl O, et al. Effect of anterior capsule polishing on posterior capsule opacification and neodymium:YAG capsulotomy rates: three-year randomized trial. J Cataract Refract Surg. 2005;31:2067–75. 22. Spalton DJ. In reply to: Nishi O. Effect of a discontinuous capsule bend. J Cataract Refract Surg. 2003;29:1051–2. 23. Ram J, Apple DJ, Peng Q, et al. Update on fixation of rigid and foldable posterior chamber intraocular lenses (IOLs). Part II. Choosing the correct IOL designs to help eradicate posterior capsule opacification. Ophthalmology. 1999;106:891–900. 24. Tassignon MJBR, De Groot V, Vrensen GFJM. Bag-in-thelens implantation of intraocular lenses. J Cataract Refract Surg. 2002;28:1182–8.

25. Smith SR, Daynes T, Hinckley M, et al. The effect of lens edge design versus anterior capsule overlap on posterior capsule opacification. Am J Ophthalmol. 2004;138:521–6. 26. Linnola RJ, Werner L, Pandey SK, et al. Adhesion of fibronectin, vitronectin, laminin and collagen type IV to intraocular lens materials in human autopsy eyes. Part I: histological sections. J Cataract Refract Surg. 2000;26:1792–806. 27. Linnola RJ, Werner L, Pandey SK, et al. Adhesion of fibronectin, vitronectin, laminin and collagen type IV to intraocular lens materials in human autopsy eyes. Part II: explanted IOLs. J Cataract Refract Surg. 2000;26:1807–18. 28. Menapace R, Findl O, Georgopoulos M, et al. The capsular tension ring: designs, applications, and techniques. J Cataract Refract Surg. 2000;26:898–912. 29. Nishi O, Nishi K, Sakanishi K. Inhibition of migrating lens epithelial cells at the capsular bend created by the rectangular optic edge of a posterior chamber intraocular lens. Ophthalmic Surg Lasers. 1998;29:587–94. 30. Werner L, Hickman MS, LeBoyer RM, Mamalis N. Experimental evaluation of the Corneal Concept 360 intraocular lens with the Miyake-Apple view. J Cataract Refract Surg. 2005;31:1231–7. 31. Peng Q, Visessook N, Apple DJ, et al. Surgical prevention of posterior capsule opacification. Part III. The IOL barrier effect functions as a second line of defense. J Cataract Refract Surg. 2000;26:198–213. 32. Werner L, Mamalis N, Pandey SK, et al. Posterior capsule opacification in rabbit eyes implanted with hydrophilic acrylic intraocular lenses with enhanced square edge. J Cataract Refract Surg. 2004;30:2403–9. 33. Werner L, Mamalis N, Izak AM, et al. Posterior capsule opacification in rabbit eyes implanted with single-piece and three-piece hydrophobic acrylic intraocular lenses. J Cataract Refract Surg. 2005;31:805–11. 34. Maloof A, Neilson G, Milverton EJ, Pandey SK. Selective and specific targeting of lens epithelial cells during cataract surgery using sealed capsule irrigation. J Cataract Refract Surg. 2003;29:1566–8.

PART 5 THE LENS

Epidemiology, Pathophysiology, Causes, Morphology, and Visual Effects of Cataract

5.17

Mark Wevill

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I n the next 20 years there will be a doubling of cataract visual morbidity. Developing countries face the greatest challenge because they have a higher incidence of cataract and resources are more scarce. Oxidation of lens proteins and mitochondrial function are key factors in cataract pathogenesis. Failure of protective mechanisms, protein modification, and abnormalities of calcium metabolism, cellular proliferation and differentiation also play important roles. Chronic accumulation of environmental insults (e.g., ultraviolet [UV] light, toxins, drugs, and systemic diseases) induce structural and physiological changes that result in age-related cataracts. Knowledge about the causes of cataracts is incomplete. Minor risk factors such as UV-B exposure and smoking can be modified. Other nutritional, pharmacological, and genetic interventions need to be developed. Anomalies of lens growth are usually associated with other ocular or systemic disorders.

EPIDEMIOLOGY OF CATARACTS In 2002, the World Health Organization calculated that the number of visually impaired people worldwide was in excess of 161 million. Cataract is the leading cause, accounting for 47.8% of all cases.1 The estimated global costs of blindness and low vision in 2000 was estimated at US$42 billion.2 There are also hidden costs of cataract blindness. Each person who is blind requires a caregiver, placing demands on one tenth of their time so reducing their economic activity.3 Over the next 20 years it is estimated that the world’s population will increase by about one third, this growth occurring predominantly in developing countries. During the same period, the number of people over the age of 65 years will more than double. Therefore, there will be approximate doubling in the incidence of cataract, visual morbidity, and need for cataract surgery. But questions remain, such as, how much cataract is enough to warrant surgery, how should it be performed and delivered, and how should it be paid for? In the developed world, the threshold for cataract surgery is now 20/30 (6/9) or less, which has resulted in a three- to fourfold increase in patients receiving surgery with an associated increased need for resources and funding. The challenge is to determine at what visual acuity level a government or insurer should pay for surgery, and how to allocate resources appropriately.4 Without trivializing the challenges for developed nations, the real challenges are in developing countries, which will bear an increased burden for cataract blindness. Cataracts occur earlier in life in developing countries, and the incidence is higher. In India, visually significant cataract occurs 14 years earlier than in the United States, and the age-adjusted prevalence of cataract is three times that of the United States.5, 6 In addition there are fewer ophthalmologists to carry out the surgery. It is possible for governmental and nongovernmental organization programs to reduce the prevalence of blindness, as illustrated by the Gambian Eye

Care program, which reduced the prevalence of blindness from 0.7% to 0.42% between 1986 and 1996.3 However, in the developing world, the shift from intracapsular to extracapsular cataract surgery has also resulted in a lower visual threshold for surgery and increased the number of operations that need to be done. Developing countries also face other challenges such as poor uptake of services because of a lack of patient information, misinformation from traditional healers, superstition, poor quality of services, monetary costs, distance to services, and the need for an escort. Even where facilities are available, there is often a lack of surgeons, instruments, and other equipment (exacerbated by poor maintenance), and a shortage of consumables and medications. Developing intraocular lens manufacturing facilities in these countries (such as the Fred Hollows Foundation in Eritrea and Nepal), will reduce costs and improve access to surgery.4

Genetics

Recent developments in cataract epidemiology have identified a strong genetic component. Population-based studies have implicated dominant genes in the development of cortical cataracts; genetics also plays a role in nuclear cataracts.7 Increased or decreased gene expression of a few groups of genes in the lens epithelial cells may play an important role in cataract formation. Of the genes whose expression is increased in cataract, many are associated with ionic transport and extracellular matrix proteins, e.g., calcium-ATPase controls calcium channels, copine III is involved in calcium binding, and adducin, a cytoskeletal protein, interacts with epithelial sodium channels. Extracellular matrix proteins include claudin, a component of tight junction filaments that binds adjacent epithelial cells; supervillin, bamacan, and osteonectin are also increased.8 But most genes involved in cataract formation show decreased expression. These genes function in diverse processes including protein synthesis, oxidative stress, structural proteins, chaperones, and cell cycle control proteins. Many of these processes represent metabolic systems designed to preserve lens homeostasis and their decreased expression may reflect the inability of the lens to maintain its internal environment in the presence of stress and/or cataract. Specific examples of these genes include those for: multiple ribosomal protein subunits involved in protein synthesis, which are decreased in cataract relative to clear human lenses; selenoprotein W1, a glutathionedependent antioxidant which could play a role in defending the lens against oxidative stress; glutathione peroxidases and important oxidative stress enzymes, which are likely to play major roles in lens protection and maintenance; multiple crystallins and other lens structural components; heat shock proteins; and α-crystallin, which in addition to its structural role in the lens, is also a small heat shock protein that can prevent protein aggregation in the lens. Individual changes in gene expression are informative, but further gene identification is needed to define those functional gene clusters that could elucidate major pathways associated with cataract.8 Despite increasing evidence of a genetic component to the development of cataracts, no genes have been identified that are associated with any form of isolated, adult onset cataract. It is likely that multiple loci will be involved. Genetic studies might identify people at greater risk for cataract, who could then modify behaviors (smoking, sun exposure) known to contribute to lens opacity. At present nothing can be done

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to alter an individual’s genetic make-up in relation to cataract. In the future, identification of the genes controlling age-related cataract may facilitate the repair of specific abnormalities at critical loci or may result in the discovery of specific anticataract agents.9

THE LENS

Nutrition, Health, and Diabetes

A number of health-related factors − diabetes, hypertension, and body mass index − have been shown to be associated with an increased risk of various forms of lens opacity, and they may be interrelated. A high body mass index in humans increases the risk of developing posterior subcapsular, nuclear, and cortical cataracts.10 Diabetes is associated with cortical cataracts, as is hypertension. These conditions can be treated but the effectiveness of treatment on cataract progression is unproven.9 Severe diarrhea and dehydration have also been associated with an increased risk of developing cataracts in some studies,11 but not in others,12 and severe protein-calorie malnutrition is more common in people with cataract.5 Therefore, a moderate calorie intake may be optimal to reduce the risk of developing cataract.

Antioxidants

The role and mechanisms of action of antioxidant vitamins and minerals in the biochemistry and metabolism of the lens are not clear. Comparing results of the studies is difficult as the study designs differ. Studies may be retrospective or prospective; the duration of the studies vary; some studies report dietary intake, but definitions and measures vary; other studies report the effect of supplements to the normal diet; and cataract classifications vary. Ascorbate, a water-soluble antioxidant, was not shown to reduce the incidence of cataract in most studies. Vitamin E is a lipid-soluble antioxidant, which inhibits lipid peroxidation, stabilizes cell membranes, is affected by ascorbate, and enhances glutathione recycling. Vitamin E had no effect on cataract incidence in most studies. Carotenoids are lipid-soluble antioxidants. Beta-carotene is the bestknown carotenoid; it is a vitamin A precursor and is one of 400 naturally occurring carotenoids. There are mixed reports in the literature with some studies showing no benefit and others showing some benefit with vitamin A, carotenoids, and combinations of vitamins C and E and beta-carotene supplements.13 Further longitudinal and intake studies are necessary to establish the effect of nutrients on cataract.

Sunlight and Irradiation

There is much evidence that UV-B light has an effect on cataractogenesis, presumably on the basis of increased oxidative damage. Aging eyes are more susceptible to UV damage because the level of free UV filters decreases with age and breakdown products of the filters can also act as photosensitizers, which promote the production of reactive oxygen species and oxidation of proteins. The risk of cortical and nuclear cataract has been shown to be highest among those with high sun exposure at younger ages. Exposure later in life resulted in weaker associations. Wearing sunglasses, particularly during the early years, affords some protective effect.14 Unfortunately, the proportion of risk attributable to sunlight exposure is small,15 and cortical cataracts are less debilitating than nuclear or posterior subcapsular cataracts. Therefore, reducing sunlight exposure may have a limited benefit in delaying the onset of cataracts. Animal and retrospective studies have shown that exposure to high levels of x-rays and whole body irradiation causes cataracts.

Smoking and Alcohol

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Smoking causes a threefold increase in the risk of developing nuclear cataracts. There is evidence of a dose-response, temporal relationship, and partial reversibility of effect with cessation of smoking. There is limited evidence of an association between smoking and posterior subcapsular cataract, and little or no association with cortical cataract. Smokers also have a higher prevalence of other healththreatening habits such as poor diet and high alcohol consumption, which are risk factors for cataract. Smoking causes a reduction in endogenous antioxidants and tobacco smoke contains heavy metals such as cadmium, lead, and copper, which accumulate in the lens and cause toxicity. Potential weaknesses of the studies are varying definitions of current and ex-smokers, categorizing intensity of smoking, self-reported data from the smokers, and potential change of smoking status during the study period. No association between passive smoking and cataract has been demonstrated.16

Chronic alcoholism is associated with a significantly increased risk of cataract.17 Consumption of alcohol, particularly hard liquor and wine, is associated with nuclear opacities. Wine drinking was inversely related to cortical opacity.18 Some studies have not shown an association between alcohol consumption and cataracts.19

Age, Education, and Other Factors

Increasing age is the greatest risk factor for cataract due to cumulative exposure to risk factors together with an age-related decline in antioxidants and antioxidant enzymes.20 Increasing age is also associated with an increased incidence of diseases such as diabetes.21 The chronic cumulative effect of taking medications (such as steroids) that may cause cataracts increases the risk of developing cataracts in older people. The incidence of steroid-induced cataract is expected to increase further as life expectancy increases and more people develop conditions that can benefit from steroid therapy.22 A higher level of education is associated with a lower risk of age-related cataract; however, this may be related to smoking, alcohol intake, and increased sun exposure in people with less education.

Myopia

Refractive errors and cataracts are common conditions. A third of the population over the age of 40 is myopic, and cataract is the commonest cause of visual impairment in the elderly. The relationship between refractive errors and cataracts has been difficult to establish because of inconsistencies in definitions, populations studied, and methods. After controlling for age, gender, and other cataract risk factors (diabetes, smoking, and education), posterior subcapsular cataracts were found to be associated with myopia, deeper anterior chambers, and longer vitreous chambers, suggesting that the refractive association with posterior subcapsular cataract is axial. Nuclear cataracts were not associated with a biometric component, but are associated with myopia suggesting that the myopia is due to the increased refractive index of the sclerotic lens only.23

Pharmacological Prevention of Cataracts

In the future compounds may be developed that reduce the risk factors for cataracts. Potential anticataract compounds include aldose reductase inhibitors, pantethine, and aspirin-like drugs such as ibuprofen. Population studies have also revealed a decreased risk of nuclear sclerosis with estrogen replacement therapy. However, none of these agents has demonstrated efficacy in the prevention of human lens opacity in a trial setting. New drugs are under investigation. An anticataract agent would need to be safe for long-term use and sufficiently inexpensive to compete with increasingly cost-effective cataract surgery.9 Understanding the causes of age-related cataract will be helpful in preventing or delaying cataract formation but our knowledge is incomplete. Minor risk factors such as UV-B exposure and smoking can be modified but are not likely to result in large reductions in visual disability. Aging, the most important risk factor cannot be modified. Other strategies such as nutritional, pharmacological, and specific medical and genetic interventions have to be developed, but are of unproved benefit. Integrated and innovative approaches to the provision of surgery, management of resources, training, supply of start-up capital equipment and consumables, and cost recovery mechanisms are required.4

PATHOPHYSIOLOGY OF CATARACTS The lens transmits, filters, and focuses light onto the retina. The lens has a high refractive index and is transparent because of the high concentration and orientation of structural proteins: α, β, and γ crystallins. Lens cells are epithelial in origin. A single layer of cuboidal cells is found on the anterior surface of the lens, below the capsule. They are nucleated, actively divide, and account for almost all the metabolic activity of the lens. Cuboidal cells in the equatorial zone of the lens differentiate and elongate into lens fiber cells, and lose their nuclei and intracellular organelles such as mitochondria. Thus, most of the lens consists of mature lens fibers, which lack the ability to perform metabolic functions such as protein synthesis and energy production. The fibers are forced toward the interior of the lens and are compressed as new fibers are deposited over them. As the lens fibers age, other biochemical, physiological, and structural changes occur. Aging changes share some similarities with age-related cataract changes, however, there are also unique cataract changes.22, 24 The transparency of the lens is dependent on the regular organization of the lens cells and intracellular lens proteins. Genetic, metabolic,

Cell Proliferation and Differentiation

The proliferation and differentiation of the epithelial cells are under the control of growth factors present in the media that bathe the lens. Fibroblast growth factor (FGF), which stimulates epithelial proliferation, is produced in the ciliary epithelium and is present in low concentrations near the anterior lens surface. Higher concentrations near the lens equator induce differentiation into lens fibers. Other growth factors, such as epidermal growth factor (EGF), insulin-like growth factor (IGF), platelet-derived growth factor (PDGF), and transforming growth factor (TGF-β) are also involved in these processes. If the concentration of FGF is too low, the concentrations of other growth factors are incorrect, or differentiation is inhibited by a cytokine, differentiation of epithelial cells into fiber cells in the equatorial zone will not occur. The undifferentiated cells continue to migrate to the posterior pole. Therefore, incorrect cell maturation, differentiation, and proliferation can result in posterior subcapsular cataract formation.22

Metabolic Disturbance and Osmotic Regulation Failure

Altered gene expression causes changes in enzyme, growth factor, membrane protein, and other protein levels. This causes a reduction in energy production, cytokine fluctuations, changes in ion transport, calcium metabolism and antioxidant pathways, and a breakdown in protective mechanisms.22 The lens maintains ion differentials between intra- and extracellular fluids (high potassium and low sodium internally; low potassium and high sodium externally) via the action of the sodium-potassium ATPase pump. Pump inactivation causes increased intracellular osmolality, which with membrane leakiness results in localized water accumulation and light scatter.22 The lens epithelial cells are bathed in aqueous humor, a source of nutrients and mineral ions including calcium (Ca2+). Ca2+ is a versatile intracellular signal that regulates many functions including the permeability of the cell membranes. The extracellular Ca2+ concentration is 10 times the intracellular Ca2+ concentration, and this gradient drives Ca2+ into the epithelial cell. Ca2+ pumps on the plasma and intracellular organelle membranes regulate cytoplasm Ca2+ levels. Within the cell, very little Ca2+ is free; most is bound to complex proteins including crystallins or sequestered in the intracellular organelles (the endoplasmic reticulum, golgi apparatus, and mitochondria). Extracellular Ca2+ can be bound to lipid molecules in the outer layer of the cell membrane. Reduced capacity of membrane lipids to bind Ca2+ affects cell membrane permeability and causes a deterioration of intracellular Ca2+ homeostasis, a rise in intracellular Ca2+ levels, the formation of calcium oxylate crystals, the formation of strong bonds between Ca2+ and insoluble lens proteins, increased light scattering, and nuclear cataract formation. Increased intracellular Ca2+ levels also affect lens epithelial cell terminal differentiation causing posterior subcapsular cataracts. Steroids have been shown to mobilize intracellular Ca2+ in other tissues. It is hoped that in the future Ca2+-regulating drugs will be developed that prevent cataracts.25

Calpains

Calpains are a group of intracellular cysteine proteases, which are activated by Ca2+. The physiological roles of calpains in the lens are poorly understood, but they may be needed to degrade damaged lens proteins that accumulate during the life of the lens. Calpains can contribute to cataract in two ways. First, a lack of calpains can lead to pathologically elevated levels of damaged proteins, reduced optical performance, and cause cataract. Second, excessive stimulation of calpain activity by Ca2+

can also lead to unregulated proteolysis and cataract. Calpain inhibitors could therefore be useful in the nonsurgical treatment of cataract. However, calpain inhibitors of high molecular weight are unable to cross membranes and are of no therapeutic use at present, while others have poor water solubility or are toxic to lenses.26

Protein Modification

Post-translational modifications (PTMs) of lens proteins can be additive, neutral, or subtractive, which increase, cause no change, or decrease the molecular weight of lens proteins, respectively. Additive modifications are numerous and typically involve covalent bonding of small molecules to polypeptides. Methylation, acetylation, carbamylation, glycation in diabetics, and binding of ascorbate are examples of PTMs and may be responsible for the coloration of the lens. The addition of these small molecules to proteins occurs especially in disease and can alter the function or properties of a protein. Diabetes (reducing sugars), renal failure (cyanate generated from urea), aging (photo-oxidation products), and steroid use (ketoamines) have been linked to cataracts. PTMs can cause further protein reactions such as polymerization and make proteins more susceptible to photo-oxidation by UV light.22, 24 Subtractive PTMs include proteolysis of crystallins and other lens proteins by enzymes including calpains. Crystallin cleavage causes precipitation of lens proteins. Cleavage of channel proteins can affect intercellular communication or create the lens barrier. Neutral PTMs such as isomerization affects the function of the protein and can result in denaturation. Deamidation changes the charge and affects protein−protein interactions. Proteins in the center of the lens are as old as the individual; therefore, despite being very stable, they can be modified over several decades. Protein modification causes conformational changes (unfolding) that expose thiol groups, which are usually “hidden” in the folds of the protein (Fig. 5-17-1). These groups are oxidized to form disulfide bonds such as oxidized glutathione (GSSG) causing aggregation of proteins. Further conformation changes and aggregation occur, which result in scattering and absorption of light.

Oxidation

Oxidation is a key feature in the pathogenesis of most cataracts and low oxygen levels (O2) are important for maintaining a clear lens. There is a steep oxygen gradient from the outer part of the lens to the center. Mitochondria in the lens cortex remove most of the oxygen, thus keeping nuclear O2 levels low. However, in older people mitochondrial function diminishes and superoxide production by the mitochondria increases resulting in increased nuclear oxygen and superoxide levels. As the lens ages, a lens barrier develops at approximately the cortex−nuclear interface, which impedes the flow of molecules such as antioxidants (including glutathione) into the nucleus. Unstable nuclear molecules such as H2O2, which are generated in the nucleus or which penetrate the barrier, therefore have more time to cause protein oxidation. Also there is a lower concentration of antioxidants. Decomposition of UV filters in the nucleus also produces unstable, reactive molecules that bind to proteins, especially if glutathione (GSH) levels are low. Ascorbate also becomes reactive with proteins in the absence of GSH. These oxidative changes can be detected even in the earliest cataracts and are progressive. Elevated levels of superoxide or peroxide (H2O2) in the aqueous (exogenous H2O2) may play more of a role in the development of cortical cataracts since the cortex is closest to the aqueous. Copper and iron also play a role in oxidative damage. They are present in higher concentrations in cataract lenses, and both are involved in redox reactions, which produce hydroxyl radicals.24

5.17 Epidemiology, Pathophysiology, Causes, Morphology, and Visual Effects of Cataract

utritional, and environmental insults and ocular and systemic diseases n cause cataracts by affecting lens clarity. These factors disrupt cellular organization and intracellular homeostasis, eventually causing spatial density fluctuations, light scattering, and absorption, which compromise vision. Cataract is not a single disease. There are different causes, morphologies, and rates of opacification. Once damaged, the lens has limited means of repair and regeneration, and may lose its transparency by the formation of opaque lens fibers, fibrous metaplasia, epithelial opacification, accumulation of pigment, or formation of extracellular materials. Several interlinked mechanisms for cataract formation have been proposed, and no single theory completely explains age-related cataract (the commonest form).24 Although much is still unknown about cataractogenesis, many of the important components are becoming clearer.

Defensive Mechanisms

Primary defenses are provided by antioxidant enzymes and antioxidants such as ascorbate, glutathione, tocopherols, and carotenoids, which maintain lens proteins in the reduced state. A decrease in nuclear concentration of GSH can occur while the cortical levels remain normal even in advanced age-related nuclear cataracts. In advanced agerelated nuclear cataracts more than 90% of protein sulfhydryl groups and almost half of all methionine residues in the nuclear proteins become oxidized. Secondary defenses include proteolytic and repair processes, which degrade and eliminate damaged proteins, UV filters, and other molecules such as glutathione reductase and free radical scavenging systems. Failure of these protective mechanisms, a shortage of antioxidants, and increased free radicals result in cell membrane and protein damage.22, 24

505

CONFORMATIONAL CHANGES IN LENS PROTEINS

THE LENS

unfolding

oxidation protein thiol groups (–SH) disulphide bonds (–S–S–)

Fig. 5-17-1 Conformational changes in lens proteins (unfolding) exposes thiol groups (−SH). Oxidization to disulfides (−S−S−) causes protein aggregation and scatters light.

Other Factors

Crystallins may have a number of functions. For example α-crystallin may be a chaperone that binds to other lens proteins to prevent precipitation. Decreased crystallin levels cause proteins to precipitate, which leads to cataract formation. Phase separation of proteins refers to the hydrophobic aggregation of lens proteins causing reversible protein rich and poor regions in the lens fibers, which results in light scatter. The lipid composition of the cell membranes alters dramatically with age. PE plasmalogen and phosphatidylcholine levels decrease and sphingolipid levels increase, which may have functional consequences.

CAUSES OF CATARACT Cataract may be hereditary, associated with systemic disorders or risk factors as detailed above, or caused by a number of insults (physical trauma or toxins). Certain types of cataract are distinctive and are associated with a specific cause, but many are the result of a combination of factors, develop according to the pathways described above, and have a nonspecific morphology.

Age

Many factors cause age-related cataract. The cumulative effect of environmental factors (UV light, x-irradiation, toxins, metals, steroids, drugs, and diseases including diabetes) plays a role. Gene expression changes result in altered enzyme, growth factor, and other protein levels. Protein modification, oxidation, conformational changes, aggregation and phase separation, formation of the nuclear barrier, increased proteolysis, defective calcium metabolism, and defense mechanisms are also important factors. Compromised ion transport leads to osmotic imbalances and intercellular vacuolation. Abnormal cellular proliferation and differentiation also produces opacities (Fig. 5-17-2).

Trauma

506

Blunt trauma, which does not result in rupture of the capsule, may cause an anterior and/or posterior subcapsular cataract, or both. Initially, fluid influx causes swelling and thickening of the lens fibers. Later the fibers become less swollen; the anterior subcapsular region whitens and may develop a characteristic flower-shaped pattern (Fig. 5-17-3), or an amorphous or punctate opacity. A Vossius ring of iris pigment may be present on the anterior capsule. If the capsule is ruptured, it usually ruptures posteriorly; the lens is rapidly hydrated forming a white cataract. A small capsular penetrating injury may result in a localized lens opacity. A larger rupture results in rapid hydration and complete opacification. Penetrating injuries can be caused by accidental or surgical trauma such as a peripheral iridectomy or during a vitrectomy. Electric shocks as a result of lightning or an industrial accident cause coagulation of proteins or osmotic changes. These cataracts are typically fern-like with a grayish white anterior and posterior subcapsular opacities.27 Sources of ionizing radiation, such as from x-rays, damages

Fig. 5-17-2 Age-related cataract. Nuclear sclerosis and cortical lens opacities are present.

the capsular epithelial cell DNA, affecting protein and enzyme transcription and cell mitosis. An enlarging posterior pole plaque develops. Nonionizing radiation, such as infrared, is the cause of cataract in glassblowers and furnace workers working without protective lenses. A local ized rise in the temperature of the iris pigment epithelium causes a characteristic posterior subcapsular cataract, which may be associated with exfoliation of the anterior capsule. The effect of ultraviolet light has been discussed above.

Systemic Disorders

In uncontrolled type 1 diabetes mellitus, a bilateral diabetic snowflake cataract may occur in young people. Hyperglycemia causes glucose to diffuse into the lens where it is converted to sorbitol by the enzyme aldose reductase. The cell membrane is impermeable to sorbitol, therefore it accumulates in the lens fiber. Water enters the lens to correct the osmotic imbalance and the lens fibers swell then rupture. The onset is usually quick with the development of white, anterior and posterior subcapsular and cortical opacities with vacuoles and water clefts. In type 2 diabetic adults, an earlier onset age-related type of cataract occurs. They are more prevalent with longer duration of the diabetes, occur earlier, and progress more rapidly than other age-related cataracts. Many mechanisms are involved and include sorbitol accumulation, protein glycosylation, increased superoxide production in the mitochondria, and phase separation. During hyperglycemia, glucose is reduced to sorbitol using up antioxidant reserves, so less glutathione can be maintained in the reduced form, which causes oxidative stress. In diabetic cataractogenesis, levels of lens Ca2+ are elevated, which

Dermatological Disorders

Fig. 5-17-3 Traumatic cataract. (A) Typical flower-shaped pattern with coronary lens opacities. (B) Seen in retroillumination in anterior subcapsular region.

a ctivates calpains causing unregulated proteolysis of crystallins. In animal models, aldose reductase inhibitors have been shown to prevent the development of cataracts, but no benefit has been demonstrated in humans. The cataracts are usually cortical or posterior subcapsular or less frequently nuclear.28, 29 Galactosemia is an autosomal recessive disorder where a lack of one of the three enzymes involved in the conversion of galactose into glucose causes a rise in serum galactose levels. There is an accumulation of galactitol within the lens and in a similar process to diabetes, the osmotic imbalance is corrected by water inflow. Anterior and posterior subcapsular opacities occur during infancy, which later become nuclear. Galactose 1-phosphate uridyltransferase galactosemia is also associated with failure to thrive, mental retardation, and hepatosplenomegaly. Progression of the cataract can be prevented if galactose is removed from the diet. Galactokinase deficiency is associated with galactosemia and cataract but without the systemic manifestations.30 Fabry’s disease is an X-linked lysosomal storage disorder that results in accumulation of the glycolipid ceramide trihexoside. The patient suffers from episodic fever, pains, hypertension, renal disease, and a characteristic rash. In the affected man and the carrier woman, a typical mild, “spoke-like,” visually insignificant cataract develops. Lowe’s or oculocerebrorenal syndrome is a severe X-linked disorder that results in mental retardation, renal tubular acidosis, aminoacidosis, and renal rickets. Associated congenital glaucoma, congenital cataracts, and corneal keloids can all lead to blindness. The cataract is total, the lens being small and discoid. Female carriers may show focal dot opacities in the cortex. Alport’s syndrome is a dominant, recessive, or X-linked trait disease causing hemorrhagic nephropathy and sensorineural deafness. Ocular features include congenital or postnatal cortical cataract, anterior or posterior lenticonus, and microspherophakia. Dystrophia myotonica is a dominantly inherited disorder and results in muscle wasting and tonic relaxation of skeletal muscles. Other features include premature baldness, gonadal atrophy, cardiac defects, and mental retardation. Cataract is a key diagnostic criterion and may

Both the skin and the lens share a common embryological origin, the ectoderm. Therefore, skin disorders may be associated with cataract formation. Atopic dermatitis and eczema may affect any part of the body, especially the limb flexures. Cataract develops in some atopic adults, usually as a bilateral, rapidly progressive “shield cataract.” This is a dense, anterior subcapsular plaque with radiating cortical opacities, and wrinkling of the anterior capsule because of localized proliferation of lens epithelium. Posterior subcapsular opacities may also occur. Ichthyosis is an autosomal recessive disorder that features hyper trophic nails, atrophic sweat glands, cuneiform cataracts, and nuclear lens opacities. Incontinentia pigmenti is an X-linked dominant disorder that affects skin, eyes, teeth, hair, nails, and the skeletal, cardiac, and central nervous systems. Blistering skin lesions occur soon after birth, followed by warty outgrowths. Ocular pathology includes cataract, chorioretinal changes, and optic atrophy.

Central Nervous System Disorders

Neurofibromatosis type II is an autosomal dominant disorder causing numerous intracranial and intraspinal tumors and acoustic neuromata. Ocular features include combined hamartoma of the retina and retinal pigment epithelium, epiretinal membranes, Lisch nodules (a diagnostic sign), and cataracts that develop in the second or third decade of life. The cataracts are posterior subcapsular, or cortical. Zellweger syndrome, also known as hepatocerebrorenal syndrome, is an autosomal recessive disorder, characterized by renal cysts, hepatosplenomegaly, and neurological abnormalities. Ocular features include corneal clouding, retinal degeneration, and cataracts. Norrie’s disease is an X-linked recessive disorder that causes leuko koria, congenital infantile blindness, and is associated with mental retardation and cochlear deafness. In the eye, vitreoretinal dysplasia, retinal detachment, vitreous hemorrhage, and formation of a white retrolental mass occur. Eventually, a cataract forms.

5.17 Epidemiology, Pathophysiology, Causes, Morphology, and Visual Effects of Cataract

develop early, but usually occurs after 20 years of age and progresses slowly, eventually becoming opaque. Early cataract consists of polychromatic dots and flakes in the superficial cortex. As the opacities mature, a characteristic stellate opacity appears at the posterior pole. Other ocular features include hypotony, blepharitis, abnormal pupil responses, and pigmentary retinopathy. Rothmund-Thompson syndrome is an autosomal recessive disorder characterized by poikiloderma, hypogonadism, saddle-shaped nose, abnormal hair growth, and cataracts, which develop between the second and fourth decades of life and progress rapidly. Werner’s syndrome is an autosomal recessive disorder with features that include premature senility, diabetes, hypogonadism, and arrested growth. Juvenile cataracts are common. The condition usually leads to death at about 40 years of age. Cockayne’s syndrome causes dwarfism, but with disproportionately long limbs with large hands and feet, deafness, and visual loss from retinal degeneration, optic atrophy, and cataracts.

Ocular Disease and Cataracts

Inflammatory uveitis (e.g., Fuchs’ heterochromic cyclitis and juvenile idiopathic arthritis) usually results in posterior subcapsular or posterior cortical lens opacities. Infective uveitis (e.g., ocular herpes zoster and toxoplasmosis, syphilis, and tuberculosis) can cause cataracts, but the organism does not penetrate the lens. However, in maternal rubella infection, after 6 weeks of gestation, the virus can penetrate the lens capsule causing unilateral or bilateral lens opacities at birth or they may develop several weeks or months later. The opacity is nuclear and has a dense, pearly appearance. Corticosteroid treatment can also cause cataracts. Retinal pigment degenerations such as retinitis pigmentosa, Usher’s syndrome, and gyrate atrophy are associated with cataracts, which are usually posterior subcapsular opacities and may be caused by toxic retinal breakdown products or from the deficiency of a product necessary for normal retinal and lens metabolism. Retinal detachment and retinal surgery may cause a posterior subcapsular cataract particularly in association with silicone oil injection and tamponade or an anterior subcapsular form may develop because of metaplasia of the lens epithelium after vitreoretinal surgery. Degenerative myopia is associated with posterior cortical, subcapsular, and nuclear cataracts. Ciliary body tumors may be associated with cortical or lamellar cataract in the affected quadrant. Anterior segment ischemia may cause a subcapsular or nuclear cataract, which progresses rapidly.

507

Toxic Causes

THE LENS

Topical, inhaled, and systemically administered steroids can cause posterior subcapsular cataracts. The mechanisms are poorly understood but direct and indirect mechanisms are involved. Direct interaction of steroids with enzymes may affect their function, e.g., steroid modulation of Na+,K+-ATPase may cause sodium-potassium pump inhibition affecting osmotic regulation. Steroids may induce crystallin conformational changes causing aggregation and may affect intracellular Ca2+ homeostasis causing protein bonding. Indirectly, steroids affect DNA/ RNA synthesis of proteins and enzymes causing metabolic changes, and may also affect ciliary body growth hormone levels responsible for lens cellular differentiation causing posterior subcapsular opacities.22 Chronic use of long-acting anticholinesterases previously used in the treatment of chronic open-angle glaucoma may cause anterior subcapsular vacuoles and posterior subcapsular and nuclear cataracts. Pilocarpine, a shorter acting agent, causes less marked changes. The mechanism of action is unknown. Phenothiazines, such as chlorpromazine, may cause deposition of fine, yellow-brown granules under the anterior capsule in the pupillary zone and may develop into large stellate opacities but are not usually visually significant. The development of the opacities may be related to the cumulative dose of the medication, and photosensitization of the lens may play a role. Allopurinol used in the treatment of gout is also associated with cataracts.31 Psoralen-UV-A therapy for psoriasis and vitilligo has been shown to cause cataracts in very high doses in animal studies, but is rare in humans; concomitant UV exposure may be a risk factor. Antimitotic drugs, such as busulfan, used in the treatment of chronic myeloid leukemia, may cause posterior subcapsular cataract. The antimalarial chloroquine (but not hydroxychloroquine), which is also used in the treatment of arthritis, may cause white, flake-like posterior subcapsular lens opacities. Amiodarone is used to treat cardiac arrhythmias and causes insignificant anterior subcapsular opacities and corneal deposits.32 Siderosis, which follows retention of a foreign body, causes iron deposits in the lens epithelium and iris, and results in a brown discoloration of the iris and a flower-shaped cataract may occur. Wilson’s disease, an autosomal recessive disorder of copper metabolism, causes a brown ring of copper deposition in Descemet’s membrane and the lens capsule, resulting in a sunflower cataract − an anterior and posterior capsular disc-shaped polychromatic opacity in the pupillary zone with petal-like spokes that is not usually visually disabling.33 Hypocalcemia in hypoparathyroidism is associated with cataracts. In children, the cataract is lamellar; in adults it produces an anterior or posterior punctate subcapsular opacity.

Congenital and Juvenile Cataracts

Congenital cataracts are noted at birth, infantile cataracts occur in the first year, and juvenile cataracts develop during the first 12 years of life. Hereditary cataracts may be associated with other systemic syndromes, such as dystrophia myotonica. About one third of all congenital cataracts are hereditary and unassociated with any other metabolic or systemic disorders. Trisomy 21, or Down’s syndrome, is the most common autosomal trisomy, with an incidence of 1 per 800 births. Systemic features include mental retardation, stunted growth, mongoloid facies, and congenital heart defects. Ocular features include visually disabling lens opacities in 15% of cases, narrow and slanted palpebral fissures, blepharitis, strabismus, nystagmus, light-colored and spotted irides (Brushfield spots), keratoconus, and myopia.34 Cataract is also associated with trisomy 13 (Patau’s syndrome), trisomy 18 (Edwards’ syndrome), Cri du chat syndrome (deletion of short arm of chromosome 5), and Turner’s syndrome (X chromosome deletion). A total cataract is a complete opacity present at birth. It may be hereditary (autosomal dominant or recessive) or associated with systemic disorders such as galactosemia, rubella, and Lowe’s syndrome. Infantile cataracts cause amblyopia if unilateral and may cause strabismus and nystagmus if bilateral. The incidence is about 0.4% of newborns, but the majority of cases are not associated with poor vision. Amblyopia depends on the size, location, and density of the cataract. The causes of infantile cataracts are many and include maternal infections (such as rubella), systemic diseases, hereditary disorders, and ocular disease.

MORPHOLOGY

508

Age-related changes in the lens affect the lens power and light transmissibility causing fluctuations in vision and scattering of light. Slit-lamp biomicroscopy, the usual method used to observe the lens, can be used

to grade and differentiate lens opacities. Each type of opacity has different clinical effects, and combinations of the different types occur. Nuclear opacities are caused by a gradual increase in the optical density of the deepest layers of the nucleus, progressing slowly to involve more superficial layers (see Fig. 5-3-1). The nucleus may also change color from clear to yellow to brown and sometimes to black. Patients may experience increased myopia (because of the increased refractive index of the lens) and a progressive, slow reduction in visual acuity and loss of contrast sensitivity. Cortical opacities cause few symptoms initially since the visual axis remains clear, but later the opacities involve most of the cortex of the lens (Fig. 5-3-2). The changes evolve as follows: 1. Hydration of the cortex with development of subcapsular vacuoles. 2. Formation of ray-like transparent spaces filled with liquid, which become opaque. 3. Formation of cuneiform opacities that originate at the periphery of the lens and spread toward the center. Posterior subcapsular opacities begin at the posterior polar region, then spread toward the periphery. Patients have significant glare disability because of light scattering at the nodal point of the eye. Complete opacification of the lens eventually occurs. The crystalline lens may then swell (intumescent cataract; see Fig. 5-3-3). The cortical material may liquefy (Morgagnian cataract; see Fig. 5-3-4) and then re-absorbed causing the solid nucleus to “sink” to the bottom of the capsular bag.

ASSESSMENT AND GRADING OF CATARACTS Grading and classifications of cataracts (Box 5-17-1) are useful in cataract research, in studies to explore causation, and in trials of anticataract drugs. Direct ophthalmoscopy with retroillumination can be used to assess and grade cataracts.35 The Lens Opacification Classification System II (LOCS-II) slit-lamp grading system is reproducible and has been validated. Using slit-lamp direct and retroillumination, nuclear, cortical, and posterior subcapsular cataracts are graded by comparison with a set of standard photographs.36 Devices for quantifying lens opacification have also been developed (such as the Kowa Early Cataract Detector and the Scheimpflug Photo slit lamp).

VISUAL EFFECTS OF CATARACTS The effect of cataract on vision varies according to the degree of the cataract and the cataract morphology.

Visual Acuity

Visual acuity has been the standard tool by which to measure the visual effect of cataracts. However, visual acuity can remain good despite other lens opacity related effects on vision, which compromise the patient’s ability to function. Therefore, visual acuity should not be assessed in isolation when considering the functional effect of a cataract in a particular patient.

Contrast Sensitivity, Glare, and Wavefront Aberrometry

Patients who have a cataract-related reduction in contrast sensitivity notice difficulty with detailed visual tasks at low ambient light levels because of loss of contrast at higher spatial frequencies. Contrast sensitivity measurements based on linear sine-wave gratings have resulted in improved understanding and quantifying of visual quality and function. Contrast sensitivity measures the total visual system quality in terms of contrast. Wavefront aberrometry measures the optical quality in terms of spatial distortion. Both measurements are useful to understand the effects of cataracts on vision.37 Contrast sensitivity data can be processed by digital imaging software to demonstrate the quality of a patient’s vision. Glare, which occurs as a result of forward scatter of light, may be produced by opacities that do not lie within the pupil diameter and therefore also affects visual function.38

Other Effects

The natural aging of the human lens produces a progressive hyperopic shift. Nuclear changes induce a modification of the refractive index of the lens and produce a myopic shift, which improves uncorrected near vision. Cortical opacities may cause localized changes in the refractive index of the lens, which may result in monocular diplopia or even polyopia. As the lens nucleus becomes more yellow, it absorbs blue light.

5.17

BOX 5-17-1 Infantile Cataracts ANTERIOR POLAR CATARACT l Dominantly inherited, well-defined opacities of the anterior capsule may affect the vision. l Caused by imperfect separation of lens from surface ectoderm, by epithelial damage, or by incomplete reabsorption of the vascular tunic of the lens. l May have anterior or posterior conical projections; if it extends into the cortex in a rod shape, it is called a “fusiform” cataract. SPEAR CATARACT l Dominantly inherited, polymorphic cataract with needle-like clusters of opacities in the axial region, which may not affect vision. CORALLIFORM CATARACT l Dominantly inherited cataract, which consists of round and oblong opacities, grouped toward the center of the lens; they resemble coral. FLORIFORM CATARACT l A rare, ring-shaped, bluish white, flower-shaped cataract in the axial region. LAMELLAR CATARACT A common, bilateral and symmetrical, round, gray shell of opacity that surrounds a clear nucleus; usually dominantly inherited cataract, which may have a metabolic or inflammatory cause. l Fibers become opacifed in response to a specific insult during their most active metabolic stage and are pushed deeper into the cortex as normal lens fibers are laid down around it. l

CATARACTA CENTRALIS PULVERULENTA l Dominantly inherited, nonprogressive cataract consisting of fine, white, powdery dots within the embryonic or fetal nucleus. (Fig. 5-17-4) CONGENITAL PUNCTATE CERULEAN CATARACT l Bilateral, nonprogressive, small, bluish dots scattered throughout the lens with little effect on vision. CONGENITAL SUTURE (STELLATE) CATARACT l Dominantly inherited bluish dots or a dense, chalky band around the sutures affecting one or both fetal sutures, especially posteriorly and may interfere with vision. MITTENDORF’S DOT l A small (about 1 mm diameter), nonprogressive, white condensation occurs on the posterior pole of the lens capsule; it may be decentered slightly inferonasally and may be attached to a free-floating thread in the vitreous gel, which represents the anterior part of the hyaloid artery remnant. CONGENITAL DISCIFORM CATARACT l Central thinning creates a doughnut shape, which may arise from failure of development of the embryonic nucleus.

The slow change is not apparent to the patient until after cataract surgery. The morphology, density, and location of lens opacities may cause changes in the visual field. These changes may be progressive and may obscure the disc; therefore, diagnosis and monitoring of glaucoma may be compromised.

Fig. 5-17-5 Marfan syndrome. A retroillumination slit-lamp photograph of ectopia lentis associated with Marfan syndrome.

ANOMALIES OF LENS GROWTH The lens is ectodermal and the vascular capsule is mesodermal in origin. A number of exogenous or endogenous influences can affect ectodermal or mesodermal development and can have multiple manifestations in the eye.

Aphakia

Aphakia is the absence of the lens. Primary aphakia is a rare condition associated with a primary defect in the surface ectoderm and is associated with other abnormalities of the anterior segment such as microphthalmos, microcornea, and nystagmus. Secondary aphakia is more common and is characterized by the presence of lens remnants. The cause is unknown. It may be associated with the same malformations, or may be found in an otherwise normal eye.39

Microspherophakia

Microspherophakia is the presence of a small, usually relatively spherical crystalline lens. It has an increased anteroposterior thickness and steeper than normal anterior and posterior lens curvatures. Hypoplastic zonules may cause the lens to be small and spherical, or the hypoplastic zonules may develop as a consequence of the lens changes. It is a bilateral condition that may be familial, may occur as an isolated defect, or may be associated with other mesodermal defects, such as the Weill-Marchesani and Marfan syndromes. The condition causes lenticular myopia and may be associated with lens dislocation (which is usually downward) and pupil block.39, 40

Epidemiology, Pathophysiology, Causes, Morphology, and Visual Effects of Cataract

Fig. 5-17-4 Cataracta centralis pulverulenta. Opacification of fetal nucleus.

Lenticonus and Lentiglobus

Abnormalities of the central lens curvature include lenticonus (conical) and lentiglobus (spherical), and may be anterior or posterior. They may be associated with abnormalities of the lens epithelium, by traction from hyaloid remnants or by localized areas of capsule weakness, which causes bulging. They may be inherited as an autosomal recessive trait or associated with other abnormalities, such as Alport’s syndrome (familial hemorrhagic nephritis) or Lowe’s oculocerebral syndrome (associated with posterior lenticonus). They can cause lenticular myopia with irregular astigmatism. Lens umbilication is a depression in the lens surface (usually posteriorly).39, 41

Lens Coloboma

Lens coloboma is a unilateral, congenital indentation of the lens periphery, which occurs as a result of a localized absence of the zonules. The condition may be associated with coloboma of the iris, ciliary body, or choroid, or with ectopia lentis, sperophakia, or localized lens opacities. It may occur because persistence of mesodermal vascular capsules in an area of the lens prevents the development of zonules in that area.

Ectopia Lentis

Ectopia lentis, or displaced lens, is usually a bilateral condition caused by extensive zonular malformation. The lens is displaced in the opposite direction to the weak zonules (usually superomedially) and usually

509

5 THE LENS

presents in childhood or young adulthood. The lens may sublux completely into the anterior chamber or vitreous or become cataractous. It may be an autosomal dominant or recessive trait or may be associated with other developmental abnormalities of the eyes such as iris coloboma, microspherophakia, aniridia, and ectopia pupillae congenita. It may also be associated with systemic disorders such as Marfan syndrome (Fig. 5-17-5), Weill-Marchesani syndrome, homocystinuria,

s ulfite oxidase deficiency, and hyperlysinemia. The clinical features of a subluxed lens include iridodinesis (tremulous iris), fluctuating anterior chamber depth and vision, and phacodinesis (a visibly mobile lens). Vitreous may herniate into the anterior chamber. Pupil block may occur with iris apposition to the vitreous face or an anterior subluxated lens (into the anterior chamber).

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