Northeast Florida Medicine - Summer 2011 - Ophthamology by Duval County Medical Society

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Inside this issue of

VOLUME 62, NUMBER 2 Ophthalmology Summer 2011 MANAGING EDITOR Leora Legacy ASSOCIATE EDITORS Raed Assar, MD Steven Cuffe, MD Ruple Galani, MD Kathy Harris (Alliance) Sunil Joshi, MD James Joyce, MD Neel Karnani, MD Mobeen Rathore, MD James St. George, MD

Executive Vice President Jay W. Millson DCMS FOUNDATION BOARD OF DIRECTORS Benjamin Moore, MD, President Todd L. Sack, MD, Vice President Kay M. Mitchell, MD, Secretary J. Eugene Glenn, MD, Treasurer Guy I. Benrubi, MD, Immediate Past President Mohamed H. Antar, MD Raed Assar, MD Ashley Booth Norse, MD J. Bracken Burns, DO LT Orlando Cabrera, MC, USN, Resident Malcolm T. Foster, Jr., MD Jeffrey M. Harris, MD Mark L. Hudak, MD Sunil N. Joshi, MD Daniel Kantor, MD Neel G. Karnani, MD Heather Kearney, MD, Resident John W. Kilkenny III, MD Harry M. Koslowski, MD Eli N. Lerner, MD Jeannine Mauney, MD, Resident Jesse P. McRae, MD Jason D. Meier, MD, Resident Nitesh N. Paryani, MD, Resident Nathan P. Newman, MD Mobeen H. Rathore, MD Ronald J. Stephens, MD Jeffrey H. Wachholz, MD David L. Wood, MD Northeast Florida Medicine is published by the DCMS Foundation, Jacksonville, Florida, on behalf of the County Medical Societies of Duval, Clay, Nassau, Putnam, and St. Johns. Except for official announcements from the County Medical Societies, no material or advertisements published in NEFM are to be seen

Northeast Florida Medicine

Features

Focus on the Eye

Janet A. Betchkal, MD, Guest Editor

Ocular Signs of Non-ocular Cancers in Children and Adults

David A. Kostick, MD

15 Advances in Cataract Surgery: A Review for the Non-ophthalmic Physician Walter R. Gilbert, Jr., MD

The History of Refractive Surgery

Jerry W. Maida, MD 25 Taking on Glaucoma: The Role of the Primary Care Physician Tina N. Tillis, MD

32 Use of Vascular Endothelial Growth Factor Inhibitors for Retinal Disease

Fred H. Lambrou, Jr., MD and Gregory M. Lewis, MD

37 Evaluation and Treatment of the Low Vision Patient Diane Cates, OD and Kim Rigdon, CLVT

Special Articles

Insert Impact of HIV on Vision Michael W. Stewart, MD (CME)

as representing the policy or views of the DCMS Foundation or its colleague Medical Societies. All advertising is subject to acceptance by the Editor in Chief. Address correspondence and advertising to: 555 Bishopgate Lane, Jacksonville, FL 32204 (904-355-6561), or email: llegacy@dcmsonline.org. COVER: Image courtesy of Abbott Medical Optics, Inc.

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Departments

4 5 8 9

From the EVP’s Desk From the President’s Desk Trends in Public Health Residents’ Corner

Northeast Florida Medicine Vol. 62, No. 2 2011 3

From the EVP’s Desk

WHTDFYL? - A 2011 Legislative Recap The language my kids and those across the country use to communicate is a dizzying array of acronyms that leave most adults dazed, confused, and maybe feeling even a little bit insulted. That is, of course, until they tell us that ‘TMI’ has to do with information and not our waist line and ‘LOL’ hopefully means they are laughing with us, not at us. What does this have to do with the 2011 Florida Legislative Session? Suffice it to say, the term ‘WHTDFML’ is the most accurate description of what the Florida Medical Association (FMA), state specialty and your county medical societies (DCMS) accomplished on behalf of the medical profession when the legislature adjourned on May 7. So, next time you ponder payment of your membership dues, take a look at exactly “What Have They (organized medicine) Done For You Lately”.

Medical Liability Reform (HB 479)

Arguably the most significant piece of legislation passed by organized medicine in over 20 years, HB 479 goes a long way in the battle to achieve meaningful tort reform in Florida. The legislation: 1) Requires MD, DO, or DDS, licensed in another state, to obtain an expert witness certificate before being able to provide expert testimony in Florida; 2) Gives the Boards of Medicine, Osteopathic Medicine, and Dentistry the specific authority to discipline any expert witness, both those licensed in state and those with an expert witness certificate, who provide deceptive or fraudulent expert witness testimony; 3) Requires the Board of Medicine and the Board of Osteopathic Medicine to create a standard informed consent form that sets forth the recognized risks related to cataract surgery. Provides that an incident resulting from a recognized specific risk is not considered an adverse incident; 4) Deletes the provision in current law that prohibits an insurance company from selling a malpractice insurance policy to a physician that gives the physician the authority to control settlement decisions; 5) Excludes from evidence in Jay W. Millson Executive Vice President/DCMS any medical negligence action any information regarding an insurer’s reimbursement policies or reimbursement determinations; 6) Provides that the breach of, or failure to comply with, any federal requirement is not admissible as evidence in a medical negligence case; 7) Provides that the expert witness who submits the pre-suit verified expert medical opinion is no longer immune from discipline; and 8) Provides that volunteer team physicians are immune from suit when gratuitously rendering care at a school athletic event or screening.

Medicaid Reform (HB 7107 & 7109)

Florida Medicaid is growing at an uncontrollable pace, with approximately 35% of the entire state budget being dedicated to the program ($21 of $59 billion). With estimates of over $25 billion in costs by 2014, the Florida legislature passed HR 7107 and 7109 transitioning Medicaid into a managed care system by October 2013. Although there are some carve outs for medically needy and disabilities, the program will be broken into 11 regions utilizing capitated payments to control costs. Beneficiaries will select or be assigned a PCP and the plans must promote healthy lifestyle behaviors (e.g., proper nutrition, smoking cessation, exercise, etc.). The most significant negatives come in the way of unknown physician payment rates and the prospect of an increasing beneficiary population. Positives include the fact that physicians are not required to participate in the program, Provider Service Networks (PSN) like UF&Shands Jacksonville were maintained to compete with for-profit plans, and the inclusion of a $200,000 (individual) or $300,000 (group) medical liability cap on noneconomic damages for practitioners (physicians and hospitals). More importantly, the evidentiary standard was raised to “clear and convincing standard” rather than a “preponderance of the evidence”. Implementation will depend upon receipt of a federal waiver from CMS to transition matching funds into a managed care model. Other key provisions: • Sovereign Immunity for teaching hospitals and extension clinics • Pill Mills/Pain Clinics (HB 7095) - 1) Maintains Prescription Drug Monitoring Program database posting requirement of seven days, will help prevent doctor shopping; 2) Limits physician office dispensing most abused narcotics, except surgical procedures, clinical trials, methadone clinics and hospice; and 3) New registration processes for practitioners and pharmacies prescribing controlled, most abused substances • Gun Bill – Boards of Medicine determine if asking about gun ownership is medically necessary, not the civil court system • Scope of Practice (bills defeated) - 1) ARNP independent practice and ability to prescribe controlled substances; 2) Optometrists being able to prescribe oral medications; and 3) Pharmacists being able to provide immunizations beyond influenza (e.g., shingles) Should you want more details regarding any aspect of the legislative session, send an email to jmillson@dcmsonline and I’ll get back to you ASAP (even us old folks understand this one!) 4 Vol. 62, No. 2 2011 Northeast Florida Medicine

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From the President’s Desk

Reflecting on Healthcare Improvements Recently I was reflecting on the improvements made in healthcare in our country since I began practicing medicine. Many of them improvements are due to the discovery of vaccines and the development of public health efforts. For example, DPT, measles, mumps, varicella, and rubella have nearly disappeared as well as smallpox. A new vaccine for Rotavirus is now recommended as is a vaccine to prevent certain meningococcal infections. BCG has not been particularly successful, but perhaps it prevents miliary tuberculosis in children. Pneumovax has not proven to be effective although it may prevent invasive pneumococcal disease. Influenzae vaccination is 80% effective, although it loses some effectiveness in older patients, and other vaccines are used selectively such as rabies for animal handlers, anthrax for the military, and still others for international travelers. There have also been key public health measures over the decades. These include: 1) The control of hookworm in the South, starting in the late 1930s, by an education program and the use of outdoor toilets; 2) The reduction of syphilis after World War II by rapid treatment centers, required screening blood tests and later by epidemiologic investigations; 3) Improvement in food safety through inspection of food establishments, education of food handlers, refrigeration and most recently irradiation of food. (These efforts must be continued—think E. coli, E. coli, E.coli); 4) During the great depression the WPA and CCC drained the swamps in the southeastern United States virtually eliminating malaria and elephantiasis; 5) Oral rehydration programs reduced the death rate in Cholera victims, particularly children; 6) Fluorination of the public water supply helped to prevent dental carries; 7) The addition of iodine to salt to prevents goiters, and the Malcolm T. Foster, Jr., MD addition of vitamin D in milk to prevents Ricketts. In fact, vitamin deficiency is rarely seen now; 2011 DCMS President 8) Tuberculosis control has been set back by HIV and in persons born outside the United States. Direct Observed Treatment (DOT) has been a successful program; and 9) As of yet, we have not been successful in controlling most venereal diseases. These public health efforts should be celebrated and continued when appropriate, however, we have to address many chronic conditions in a population that continues to age. These conditions include: 1. COPD is still growing as a major problem. Cigarette smoking should be Public Enemy #1 and air pollution should be #2; 2. Diabetes mellitus, sometimes disguised as the “metabolic syndrome” is a growing problem. The root casues are genetics, obesity, and sedentary lifestyle. We should embrace all efforts to fight obesity and inactivity. The more diabetics, the more renal failure and dialysis we will have; 3. Atherosclerosis requires an entire article, but the efforts to treat hypercholesterolemia are bearing fruit as is the recognition and treatment of hypertension; 4. Dementia is just entering our medical radar scope, but over the next 30 years it will become a major societal problem; 5. As the population ages, more and more patients will have oncological diseases. The MKSAP suggests that 60 or greater percent of these malignancies are environmentally related; 6. Osteoarthritis - everyone seems to have OA; 7. HIV is still a major health and societal concern. The only effective control for viral diseases has been vaccination. It is true that HIV has been converted from a “death sentence” to a chronic disease that requires continuous therapy. Recently two new vaccines were introduced: Zostavax for patients over 60 years of age. It promises to reduce clinical Herpes Zoster infections by 50% and lessening post hepatic neuralgias will justify the vaccine’s expense. In addition, Medicare will pay us to administer the vaccine. Also, Gardisil for girls and women age 9-26 promises to prevent HP viral infections and therefore presumably carcinoma of the cervix. This vaccine is a major public health advance. There are many questions to be answered about this vaccine, most notably is should we administer it to men as well and will booster immunizations be needed? The significance of this vaccine for women’s health rivals the introduction of the birth control pill 50 years ago. All of these problems call out for prevention, early diagnosis,and aggressive treatment, including lifestyle changes. What can DCMS as an organization do? What can you as an individual practitioner do? Certainly we can continue to educate our members, the public, and our legislators.

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Northeast Florida Medicine Vol. 62, No. 2 2011 5

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Trends in Public Health

Vision Screening in Duval County Niketa Walawalkar, MD, MPH; Thomas Bryant III, MSW and Robert Harmon, MD Vision screening is a cost-effective and efficient public health preventive technique to identify people with vision impairments early in the course of the disease. It is especially important in young children, since they are often unaware that they are not seeing as well as others and their vision problems can go undetected. Vision screening is most effective when performed periodically throughout infancy and childhood to detect conditions such as amblyopia, strabismus, and defects in visual acuity. The first vision screening must take place in the newborn period at the nursery, with the doctor checking the eyes, pupil and the red reflex. In 2009, there were more than 12,000 clinic visits due to eye or vision related problems in Duval County. Of these visits, 75% of clinic visits in Duval County both adults and children were for cataracts. Florida Statute 381.0056(5) (2002) requires a documented vision screening or comprehensive eye examination before children begin school. It requires the county health department to partner with the district school board and the local school health advisory committee to develop a comprehensive school health services plan, which must include vision screening. Health departments are also required to arrange referrals and follow-ups for children diagnosed with vision problems after consulting the student’s parent or guardian and maintain records regarding the problem, the corrective measures taken, and other information. The Duval County Health Department (DCHD) has initiated partnerships to address vision screening for children in Duval County. DCHD clinics have established protocols requiring that vision screening be conducted during all wellchild exams for children ages 5 and older. In 2010, DCHD clinic staff conducted more than 5,300 of these exams. Duval County Public Schools (DCPS) partner with the DCHD to provide school health services in Jacksonville in accordance with Florida Statutes. A critical health service is the DCPS Vision Screening Program, under the leadership of Dot Mathias, which screened almost 70,000 students in Duval County during 2009-2010. During this period, more than1,500 volunteers were trained to conduct vision screening and provided free eye exam and/or glasses to ~300 referred students from financially 8 Vol. 62, No. 2 2011 Northeast Florida Medicine

disadvantaged families. In addition, the program notified parents and referred more than 6,000 of these students for further evaluation. DCHD nurses provided follow-up services for all the students referred for further care and maintained health records. DCHD pediatricians and clinic staff received training for vision acuity screening through the Nemours Children’s Clinic Jacksonville and its “See by Three” program. This program was started by American Association for Pediatric Ophthalmology and Strabismus (AAPOS) and has succeeded in Florida and West Virginia by screening almost 10,000 children in 2009-2010. A similar program is the Northeastern Early Steps program through the University of Florida College of Medicine–Jacksonville, which provides vision services, along with other developmentally supportive services, for infants and toddlers from birth to 36 months who have or may be at risk for developmental delay. This program serves families living in Duval, Clay, St. Johns, Nassau, Baker, and Bradford counties. Vision screening and eye examinations are an important part of health maintenance for everyone. They are recommended by the U.S. Preventive Services Task Force as a key component of the periodic health exam. Adults should have their eyes checked to keep their vision prescriptions current and to catch early signs of eye diseases like cataracts. For children, vision screenings and eye exams are critical not only to prevent permanent blindness, but also to ensure normal vision development and academic achievements. Vision screening is closely linked to learning skills. Children who have difficulty seeing and interpreting what they see, can start their education at a disadvantage and are often inappropriately labeled as having a learning disability and sometimes placed in Special Education. Vision screening will help ensure that children’s visual issues are identified and treated early, helping them to advance academically, athletically and socially. It is important that schools, daycares, medical practices and hospitals incorporate vision screening into routine care. It is also the responsibility of parents and families to take advantage of community programs and their insurance benefits. www . DCMS online . org

Residents’ Corner: Mayo Clinic’s Graduate School of Education Editor’s Note: In an effort to connect more Duval County Medical Society members with residents, in each 2011 issue, there will be a “Residents’ Corner” with information about a residency program in the area, details about research being done and a list of achievements/ accomplishments of the program’s residents. This “Residents’ Corner” features Mayo Clinic Jacksonville’s Graduate School of Education.

Overview of Residency Program

Mayo Clinic is a three-campus academic medical center with a distinguished history of preparing physicians and scientists to succeed as leaders in their chosen fields. Mayo’s practices in Phoenix/Scottsdale, Arizona; Jacksonville, Florida, and Rochester, Minnesota, offer residency and fellowship programs in virtually all medical and surgical specialties. More than 1,500 residents and fellows participate in Mayo Clinic graduate medical education programs each year. At the Jacksonville campus, there are 160 residents and fellows spanning 38 specialties. Mayo Clinic Hospital, which opened in April 2008, integrates inpatient and outpatient services on the Mayo campus in Jacksonville. It has 214 beds and 22 operating rooms and offers care in 20 medical and 15 surgical specialties. It also includes a full-service Emergency Department. Residents and fellows rotate through virtually every part of the hospital, as well as through outpatient clinics on the Mayo campus, the primary care center in Jacksonville Beach, and at the student health center at the University of North Florida. Several residents also participate in rotations at the Nemours Children’s Clinic as well as the Wolfon Children’s Hospital in downtown Jacksonville. The campus is also home to two large research buildings. The Birdsall Medical Research Building has 10 laboratories where scientists investigate neurological diseases such as Alzheimer’s. The Griffin Cancer Research Building was completed in 2002 and is the first building on the Jacksonville campus devoted primarily to cancer research.

Resident Leadership Roles

Mayo residents are involved in many leadership roles both internally at the Clinic as well as on national committees. Some of the national leadership roles are: • • • •

Neurology residents Rachel DiTrapani, MD and Ryan Walsh, MD, are involved with a national Clinical Skills Examination Committee, a workgroup aiming to improve the training available to administrators of the American Board of Psychiatry and Neurology Clinical Skills Examination. Nicole Chiota, MD, also a resident in the department of neurology, plays an active role in the Florida Society of Neurology, serving on their executive board as well as their advocacy and education committees. Ross Goldberg, MD, a fellow in the department of surgery, takes an active role in shaping national legislative policy. He serves on the Board of Directors for the American College of Surgeon’s Political Action Committee (SurgeonsPAC). He also serves on the Legislative Committee for the Society of American Gastrointestinal and Endoscopic Surgeons. Radiation Oncology resident Katherine Tzou MD, serves on the Annual Meeting and Program Committee for the American Society for Radiation Oncology. Here she works with physicians from across the country to plan the annual convention attended by over 12,000 oncologists, medical physicists, dosimetrists, and nurses from all over the world.

Resident Research

Mayo trainees are also heavily involved in research activities and are constantly publishing cutting edge research articles across many different specialties. Publishing the titles alone of all of the articles authored by residents and fellows in the last year would take more space than this entire journal! Nevertheless, highlighted are just a few of the many impressive accomplishments of residents and fellows: • • •

Family Medicine residents Ramon Cancino, MD and Scott Simmons, MD, have authored several abstracts focusing on quality improvement projects in diabetes, resident education, and Medicare/Medicaid PQRI initiatives. Radiation Oncology Chief Resident Jennifer Peterson, MD, has authored three publications, one book chapter, and more than six abstracts during her four-year residency. Her publications focus on topics including breast cancer, prostate cancer, and treatment of liver metastases. She has even received several institutional grants to support her research efforts. Internal Medicine Chief Resident Lynsey Cassidy, MD, recently published an article in The Journal of General Internal Medicine focusing on asymptomatic patent ductus arteriosis (PDA) in adults.

Mayo residents are always looking for new research projects and leadership opportunities, including opportunities to partner with community physicians. They appreciate the continued support and mentorship of the Duval County Medical Society physicians. Residents’ Corner written by: Dr. Nitesh Paryani, a transitional year resident at Mayo Clinic Jacksonville. He will begin his radiation oncology residency at Mayo in July. Dr. Paryani serves as Mayo’s resident representative to the DCMS Board of Directors and is also on the Board of Governors of the Florida Medical Association. He is a graduate of the University of Florida College of Medicine. www . DCMS online . org

Northeast Florida Medicine Vol. 62, No. 2 2011 9

Keep an eye out in 2012 for the DCMS History Book What you will see in its pages?

Watch for 200+ great historic photographs Focus on 8 intriguing chapters with facts from bygone days Look for interesting tidbits in numerous sidebars View DCMS from its past and gaze into its future

Special thanks to Mrs. Lee-Margaret Borland for her photograph entitled “Flirt.” Taken in the Tucson, Arizona desert, it shows an injured owl who was recuperating in a desert animal hospital. The owl had a broken wing and was on a perch, so Mrs. Borland could get close to it for this great photo. She watched the owl for a long time and saw it close one eye and then the other, turn its head and then close both eyes. For more of Mrs. Borland’s photographs, go to www.throughthelensoflee-margaret.com. 10 Vol. 62, No. 2 2011 Northeast Florida Medicine

www . DCMS online . org

This Issue’s Focus: Ophthalmology

Focus on the Eye While the eye seems so small, it makes up an entire organ system of the human body. Yet when I was in medical school I think spent only one half day studying the embryology of the eye and another half day on the visual system. The rest of the time relegated to the other organ systems of the body. No wonder ophthalmologists’ reports seem like a “foreign” language to other areas of medicine. A recent survey of 4,352 people in 7 countries found that twice as many people fear blindness as they do a premature death or heart disease, so it is important that physicians understand diseases that affect sight. The purpose of this issue of Northeast Florida Medicine is to provide insight into some of the more common ophthalmic diseases and procedures, help identify some of the causes and manifestations, explain how they are treated and discuss how they affect the overall health of the patient.

Janet A. Betchkal, MD The Gilbert Cataract Center Jacksonville, FL

David A. Kostick, MD, describes “Ocular Signs of Non-Ocular Cancers in Children and Adults.” It is important that both ophthalmologists and other medical providers be aware of these important findings as they may represent the earliest or only occult sign of some of these cancers. Walter R. Gilbert, Jr., MD, gives a brief history of cataract surgery in “Advances in Cataract Surgery: A Review for the Non-ophthalmic Physician.” He provides an excellent summary of the current state of cataract surgery commonly performed in the Medicare population, and also describes the many choices that patients now have when it comes to “customizing” their functional visual outcomes.

Jerry W. Maida, MD, discusses the evolution of the specialty of refractive surgery in “The History of Refractive Surgery.” A pioneer in refractive surgery, Dr. Maida has performed refractive surgery from the early days of radial keratotomy (RK) up to present day LASIK procedures. Tina N. Tillis, MD, takes some of the mystery out of glaucoma in “Taking on Glaucoma: The Role of the Primary Care Physician”. She describes how the non-ophthalmologist can help identify risk factors, understand treatment options, and help make the glaucoma diagnosis.

Fred H. Lambrou, Jr., MD, and Gregory M. Lewis, MD, write in “Use of Vascular Endothelial Growth Factor Inhibitors for Retinal Disease” about how VEGF inhibitors can safely be injected intravitreally in the treatment of many potentially blinding retinal diseases, including diabetic retinopathy and age-related macular degeneration. In “Evaluation and Treatment of the Low Vision Patient,” Diane Cates, OD, and Kim Rigdon, CLVT, provide important functional and legal definitions and descriptions of the various types of visual impairment from minor decreases in visual acuity to total blackness. They describe visual aides, local resources and assistance available to visually-impaired children and adults. The CME article for this issue also focuses on the eye. Michael W. Stewart, MD, in “Impact of HIV on Vision,” provides a historical perspective of AIDS and the eye as well as a comprehensive discussion of current causes of vision loss in HIV patients since the introduction of anti-retroviral therapy (HAART). It is my hope that after reading this Ophthalmology issue you will not only be able to spell “ophthalmology” correctly (everyone leaves out the first “h”), but will have a better understanding of some the more common ocular conditions affecting your patients. Note: See a related Trends in Public Health article on page 8 entitled “Vision Screening in Duval County.”

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Northeast Florida Medicine Vol. 62, No. 2 2011 11

Ocular Signs of Non-ocular Cancer in Children and Adults David A. Kostick, MD, FACS Abstract: Systemic malignancies may cause a variety of ocular symptoms, resulting from either direct invasion of ocular tissue by the tumor cells or by secondary phenomena related to tumor-induced pathological processes. Both ophthalmologists and non-ophthalmologist should be aware of the clinical findings during the ophthalmic evaluation that may suggest systemic malignancies.

Introduction

Cicero (106-43 B.C.) is quoted as saying, “Ut imago est animi voltus sic indices oculi”…The face is a picture of the mind as the eyes are its interpreter. The topic of this paper is an example of this generalization. Many systemic malignancies may produce ocular manifestations, either from direct invasion of the tumor or from complex neuro-physiologic responses.1 This article will help ophthalmologists and nonophthalmologists recognize findings during the ophthalmic evaluation that may suggest underlying systemic malignancy in either the adult or the pediatric patient.

Eyelid Findings

An “S-shaped”eyelid as shown in Figure 1 suggests a lacrimal gland fossa tumor. The most common malignancy in this area is lymphoma which has a typical appearance on either computed tomography (CT) or magnetic resonance imaging (MRI).2 The oblong mass conforms to the surrounding structures without soft tissue or bone destruction. The lymphoma may be localized or systemic. To confirm the diagnosis a tissue biopsy is required. Depending on the locations involved with lymphoma, the lacrimal gland fossa lesion may be the best choice for obtaining tissue to biopsy. Periocular lesions are common findings. The risk of malignancy is greater if the lesion displays the classic triad: loss of lashes, lid margin destruction, and increased vascularity (Figure 2). Basal cell carcinoma is the most common malignancy of the eyelid. It is rare for a basal cell carcinoma to be associated with systemic disease. However, if present in a patient under age of 30 years old, then the Nevoid Basal Cell Carcinoma (Gorlin’s syndrome) should be considered.3 The palms of these patients should be carefully inspected because approximately 80% will have palmar pits or cysts. Another common feature is odontogenic cysts. It is also important to remember that brain cancer (medulloblastoma) may occur in 1- 4% of patients with Gorlin’s syndrome.4 Signet cell carcinoma (Figure 3) will often have similar clinical findings of basal cell carcinoma, but, if present, requires systemic evaluation for adenocarcinoma elsewhere.5

Address Correspondence to: David A. Kostick, MD, FACS, Mayo Clinic, Department of Ophthalmology, 2-West Davis Building, 4500 San Pablo Road, Jacksonville, Florida 32224. Email:kostick. david@mayo.edu. 12 Vol. 62, No. 2 2011 Northeast Florida Medicine

Another example of eyelid lesions indicating a systemic malignancy is the Muir-Torre syndrome. This autosomal dominant disorder is characterized by sebaceous gland tumors that are associated with gastrointestinal malignancies (Figure 4).6 If multiple periocular sebaceous-appearing lesions are present, a biopsy should be performed to exclude local sebaceous gland carcinoma. In addition, referral for evaluation of possible visceral malignancies is indicated.6,7,8 Figure 1 A. “S-Shaped” eyelid in patient with left lacrimal gland fossa lesion.

B. CT scan showing enlarged lacrimal gland with oblong mass conforming to adjacent structures. Biopsy of lesion proved to be lymphoma.

Figure 2 Clinical photograph showing basal cell carcinoma involving the margin of the left lower eyelid. Note: triad of irregular eyelid margin, loss of lashes, and increased vascularity (arrow). Figure 3 Photograph of specimen showing multiple “signet cells”. (H&E stain)

Figure 4 Muir-Torre Syndrome: multiple periorbital sebaceous adenomas (white arrows) in a patient with known colon cancer.

www . DCMS online . org

Xanthelasma are common periocular lesions that can be associated with systemic hypercholesterolemia. These benign lesions are characterized by their yellow color, sharply demarcated edge, consistent thickness and relatively smooth surface. However, not all yellow periorbital lesions are benign. If the yellow lesion has a nodular-like appearance with irregular thickness and texture, then necrobiotic xanthogranuloma (NXG) should be considered.1 These NXG lesions are often associated with a systemic dysproteinemia such as multiple myeloma.9 Once the diagnosis is established, evaluation for hematologic malignancy and life-long follow-up is indicated.9,10

Paraneoplastic Syndrome

A bitemporal quadrant visual field deficit suggests a lesion in the pituitary gland fossa area; an example of direct involvement of a tumor into the visual pathways. However, there are several unusual neurologic disorders that have symptoms and/ or clinical findings anatomically unrelated to the site of the tumor. The suspected mechanisms in these “Paraneoplastic Syndromes” are auto-immune and antibody abnormalities.11,12 These complex neurophysiologic responses to the cancer may involve the retina, visual pathways and/or brain stem.11-15 Multiple tumor types have been reported including lung cancer and melanoma.11-15 Paraneoplastic syndromes should be considered in any patient with unexplained visual loss, optic neuropathy and/or ocular motility disorders since often in these situations there is an occult malignancy. The common serologic markers for paraneoplastic syndromes are listed in Table 1. (p.14) Cancer-Associated Retinopathy (CAR) is an example of an ocular paraneoplastic syndrome. The clinical findings in CAR include decreased visual acuity, decreased color perception, and central scotomas (blind spots). Fundus findings include arteriolar narrowing, optic nerve pallor, and abnormal pigmentation of the posterior pole.1,11,13 Opsoclonus, unusual, jerking type movements of the eye, is another example of an ocular paraneoplastic syndrome. Opsoclonus has been associated with various malignancies including neuroblastoma in children. Myasthenia-like syndromes with fatigable ptosis and strabismus are another example of paraneoplastic syndromes affecting ocular motility.11-15

Ophthalmic Manifestations of Pediatric Cancers

Leukemia is the most common malignancy of childhood. When compared to adults, children are more likely to have acute forms of the disease rather than chronic forms. Furthermore, in children acute lymphoblastic leukemia (ALL) is more common than acute myelogenous leukemia (AML). Ophthalmic manifestations of ALL in children are more likely to have intra-ocular and optic nerve involvement rather than orbital involvement. These ophthalmic manifestations typically occur in patients with known ALL disease. Pediatric patients who develop recurrence of ALL with ophthalmic manifestations have a much lower 5-year survival rate (21%) compared to those who have recurrence of ALL www . DCMS online . org

without ophthalmic manifestations (46%).16 Children with AML commonly have orbital involvement (versus intra-ocular or optic nerve involvement) and this may be the initial presentation of the disease.17 A “chloroma” is a greenish-colored mass from primitive myeloblast deposits in AML.18 This may occur in the orbital bone or soft tissues. Neuroblastoma is the most common metastatic lesion to the orbit in children. The age of onset may range from birth to 16 years with the average age 1.5-3 years. The primary lesion is typically adrenal, retroperitoneal, or from the sympathetic ganglion. Twenty percent of neuroblastoma patients will have ophthalmic findings and in approximately 10% of these patients the ophthalmic findings represent the initial presentation of the disease. Facial flushing may indicate the abnormal catecholamine production associated with neuroblastoma. The mass effect of the metastatic lesion to the orbital bone may cause proptosis, periorbital ecchymosis, and ptosis. Indication of orbital involvement portends a worse prognosis with a 3-year survival of approximately 11%.19 The presence of Horner’s syndrome (triad of ptosis, miosis, and unilateral anhidrosis) is suggestive of mediastinal or cervical sympathetic ganglia involvement which is associated with a better 3-year survival of approximately 79%.19 As mentioned earlier, opsoclonus is a paraneoplastic phenomenon that can occur in patients with neuroblastoma. Since the finding of opsoclonus may lead to an earlier diagnosis, the 3-year survival rate is almost 100% in these patients.19

Summary Systemic malignancies may cause a variety of ocular symptoms, resulting either from tumor cells directly invading the ocular tissues or from a paraneoplastic response. Both ophthalmologists and non-ophthalmologist should be aware of the ophthalmic findings and symptoms that may suggest an underlying systemic malignancy as the ability to diagnose the condition early often leads to an overall increased survival rate.

References

Robertson DM. Non-cancerous ophthalmic clues to nonocular cancer. Surv Ophthalmol. 2002; 47(5):397-430.

Jakobiec FA, Yeo JH, Trokel SL et al. Combined clinical and computed tomographic diagnosis of primary lacrimal fossa lesions. Am J Ophthalmol. 1982; 94:785-807.

Gorlin RJ. Nevoid basal-cell carcinoma syndrome. Medicine. 1987; 66(2):98-113.

Evans DG, Farndon PA, Burnell LD, Gattamaneni HR, Birch JM. The incidence of Gorlin syndrome in 173 consecutive cases of medulloblastoma. Br J Cancer. 1991; 64(5):959-61.

Langel DJ, Yeatts RP, White WL. Primary signet ring cell carcinoma of the eyelid: report of a case demonstrating further analogy to lobular carcinoma of the breast with a literature review. Am J Dermatopathol. 2001; 23(5):444–449. Northeast Florida Medicine Vol. 62, No. 2 2011 13

Table 1 Paraneoplastic Auto-antibodies and Associated Cancers and Syndromes Antibody Anti-Hu

Associated Cancer Small cell lung

Anti-Yo

Anti-CV2

Gynecologic Breast Breast Gynecologic Small cell lung Hodgkin lymphoma

Anti-Ma

Small cell lung

Anti-amphiphysin

Small cell lung

AVGCC*

Small cell lung

ACHR** AVGPC***

Thymoma Thymoma

Anti-Ri

Paraneoplastic Syndrome Encephalomyelitis Cerebellar degeneration Sensory neuropathy Cerebellar degeneration Cerebellar degeneration Opsoclonus-myoclonus Encephalomyelitis Cerebellar degeneration Sensory neuropathy Limbic encephalitis Cerebellar degeneration Stiff-man syndrome Encephalomyelitis Lambert-Eaton myasthenic syndrome Cerebellar degeneration Myasthenia gravis Limbic encephalitis

*AVGCC = Anti-variable-gated calcium channel **ACHR = Anti-acetylcholine receptor ***AVGPC = Antivariable-gated potassium channel Adapted from Braik T, “Paraneoplastic Neurological Syndromes: Unusual Presentations of Cancer. A Practical Review”. The American Journal of the Medical Sciences; Volume 340, Number 4, October 2010

Demicri H, Nelson CC, Shields CL, et al. Eyelid sebaceous carcinoma associated with Muir-Torre syndrome in two cases. Ophthal Plast Reconstr Surg. 2007; 23(1):77-78.

Dores GM, Curtis RE, Toro JR, et al. Incidence of cutaneous sebaceous carcinoma and risk of associated neoplasms: insight into Muir-Torre syndrome. Cancer. 2008; 113:3372–3381.

14. Ray D, Nigam A. Paraneoplastic effects on neurophthalmologic function. Otol Neurotol. 2007; 28:860-2.

Ko CJ. Muir-Torre syndrome: facts and controversies. Clinic Dermatol. 2010; 28(3):324-9.

15. Leavitt JA. Myasthenia gravis with a paraneoplastic marker. J Neuro-Ophthalmol. 2000; 20(2):102-5.

Ugurlu S, Bartley GB, Gibson LE. Necrobiotic xanthogranuloma: long-term outcome of ocular and systemic involvement. Am J Ophthalmol. 2000; 129(5):651-7.

16. Kishiko O, William GT. Prognostic importance of ophthalmic manifestations in childhood leukaemia. Br J Ophthalmol 1992; 76: 651-655.

10. Guo J, Wang J. Adult orbital xanthogranulomatous disease: review of the literature. Arch Pathol Lab Med. 2009; 133(12):1994-7. 11. Solomon SD, Smith JH, O’Brien J. Ocular manifestations of systemic malignancies. Curr Opin Ophthalmol. 1999; 10:447–451. 12. Braik T, Evans AT, Telfer M, et al. Paraneoplastic

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neurological syndromes: unusual presentations of cancer: a practical review. Am J Med Sci. 2010; 340(4):301–308. 13. Chan JW. Paraneoplastic retinopathies and optic neuropathies. Surv Ophthalmol. 2003; 48:12–38.

17. Sharma T, Grewal J, Gupta S, Murray PI. Ophthalmic manifestations of acute leukaemias: the ophthalmologist’s role. Eye 2004; 18:663–672. 18. Zimmerman LE, Font RL. Ophthalmologic manifestations of granulocytic sarcoma (myeloid sarcoma or chloroma). Am J Ophthalmol 1975; 80(6):975-90. 19. Musarella MA, Chan HS, DeBoer G, Gallie BL. Ocular involvement in neuroblastoma: prognostic implications. Ophthalmol 1984; 91:936 –940. www . DCMS online . org

Advances in Cataract Surgery: A Review for the Non-ophthalmic Physician Walter R. Gilbert, Jr., MD, FACS Abstract: More than 3 million cataract operations are performed

The last decade has brought even more refinements and advances. The most significant of these have been in areas of more efficient ultrasonic energy delivery, improved surgical control of anterior chamber (AC) stability, new and more refined microsurgical instruments, improved IOL designs, and more accurate IOL power calculations.

Introduction

Advances in Phacoemulsification Technology

annually in the United States.1 The rapid visual rehabilitation of these patients has been one of the most spectacular achievements of modern medicine. The two developments most responsible for this advance are small incision surgery using phacoemulsification and intraocular lens implants (IOL). This is a review for the non-ophthalmic physician of the advances in cataract surgery in the last few decades.

Just forty years ago cataract patients were hospitalized for 5-7 days. The entire cataract was removed through a 12 mm superior corneal-scleral incision that required 6-10 sutures and caused astigmatism. The eyes were vulnerable to hemorrhage and/or wound dehiscence. Patient activities were restricted for weeks. Complications such as retinal detachment, macular edema and corneal clouding were far more prevalent. Following surgery, “best” visual acuity was achieved with either thick glasses or contact lenses which caused optical aberrations that often precluded returning to a normal lifestyle.

The energy for breaking up cataracts is usually delivered by a blunted titanium needle attached to an ultrasonic transducer. The needle tends to become hot and is cooled by the continuous inflow of saline as well as by the movement of aspirated fluid and lens emulsion up the needle bore and out of the eye. Many advances have been made in this ultrasonic technology over the last decade. These include modulating power delivery to reduce heat and improve lens aspiration as well as precisely controlling fluid inflow, outflow and pressure to preserve AC stability during the operation.

The move toward small incision cataract extraction began with the invention of ultrasonic emulsification and aspiration in 1967.2 The technology became commercially available in 1970.3 However, it was slow to be accepted and was not being used by more than 50% of cataract surgeons until 1990.4-5 Today it is preferred by an overwhelming majority of surgeons throughout the industrialized world.6

Modulating Power Delivery – Early machines ran continuously when activated by the foot switch and it was necessary to rapidly tap the foot switch causing interruptions in power delivery in order to keep the needle cooler. Recent advances enable machines to deliver extremely short duration pulses of energy interrupted by extremely brief cooling periods. These alternating periods are typically in the range of 30-70 msec and the time “on” to time “off” ratio can be customized (“WhitestarTM” Abbott Medical Optics) to reduce heating, retain cutting ability and improve flowability of lens particles into the needle bore. Cataracts can now be removed more efficiently by delivering less energy and minimizing corneal endothelial damage and trauma.

Incisions are now constructed to self-seal so that sutures are rarely needed, thus eliminating foreign body sensations, fluctuating astigmatism and refractive instability. This outpatient surgery is most often done under either topical or local injection anesthesia.7 Patients are often discharged without an eye patch and may return to normal activities in 1-2 days. Small incisions have also reduced or eliminated the need to discontinue anticoagulants preoperatively. A review of 11,685 cataract surgical patients receiving sharp needle or subtenon anesthesia while taking anticoagulants and/or antiplatelet medications, showed no increase in serious sight-threatening hemorrhagic complications.8 The first IOL was implanted in England in 1949 and in the US in 1958, but it was not until after FDA approval in 1978 that IOLs moved into the main stream. Early IOLs were made of hard plastic and insertion required relatively large incisions, negating some of the benefits of phacoemulsification. Soft, foldable IOL usage surpassed hard plastic IOLs by 1998.9 Small incisions with foldable IOLs led to the almost instant visual rehabilitation achieved today. Address Correspondence to: Walter R. Gilbert, Jr., M.D., F.A.C.S., Gilbert Cataract Center,3 Shircliff Way Suite 122, Jacksonville, FL 32204. Email:wrgilbert@comcast.net.

www . DCMS online . org

Traditional longitudinal needle movements are inefficient because they only cut on the forward stroke. Forward strokes tend to repel or knock away small lens particles which may damage the cornea and increase inflammation. Torsional (OzilTMAlcon Laboratories) and horizontal or elliptical needle movements (EllipsTMAbbot Medical Optics) allow cutting in both directions eliminating the inefficiency of the backstroke. OzilTM has been reported to emulsify hard nuclei more efficiently than longitudinal ultrasound.9,10 These developments reduce energy requirements, reduce repulsion of particles and require less time than traditional ultrasound. Preserving AC Stability – Sensors that regulate and control vacuum and aspiration can be programmed to reduce vacuum upon occlusion of the needle tip thus minimizing the sudden inflow or “surge” that may occur when an occluding particle is suddenly sucked through the small needle bore. This reduces the frequency of AC collapse and forward bouncing of the posterior capsule. The technology improves efficiency, lessens Northeast Florida Medicine Vol. 62, No. 2 2011 15

thermal damage, avoids post-occlusion surges, and produces clearer eyes.

Figure 1 IOL Implantation (Reprinted with permission from Advanced Medical Optics)

Advances in Surgical Instruments and Techniques

Most cataract surgery in the developed world is now done by phacoemulsification through a self-sealing < 3mm temporal corneal incision. Preexisting astigmatism may require changing the incision location. Even smaller incision surgery uses separate incisions (0.9 – 1.5 mm) for an infusion cannula and a sleeveless ultrasonic needle.11,12 Such small incisions must be enlarged to admit conventional foldable IOLs but an implant (Akreos M160 AO) has been developed to pass through a 1.8 mm incision. Advocates of this micro-incision cataract surgery (“MICS”) claim better AC stability as well as reduction in astigmatism and refractive corneal aberrations.13 The trend is toward further reduction in incision size.

Lens implant placed within the capsule of the natural lens

Figure 2 Malyugen Ring (Reprinted with permission from Advanced Medical Optics)

The opening in the lens anterior capsule has traditionally been made with the bent tip of a 23-27 gauge needle or forceps. Newly developed smaller forceps and scissors can enter the AC through 1 mm incisions improving chamber stability for intraocular maneuvers such as iridectomy or iris suturing. “Viscoelastics”, including hyaluronic acid, chondroitin sulfate and methylcellulose, are transparent, clear, jelly-like substances that now come in a variety of viscosities. They are useful in protecting the corneal endothelium and deepening the AC for delicate surgical maneuvers including IOL implantation (Figure 1). Cataracts are best removed through a widely dilated pupil for good visualization of the peripheral lens. Small pupils increase the risks of tearing the capsule or iris. Flomax and other alpha-adrenergic blockers are now known to cause poor pupil dilation and (possibly) atrophy of the iris dilator muscle leading to a loss of iris rigidity (“floppy iris”) and a significantly increased risk of iris damage during cataract surgery. The Malyugen Ring (Figure 2), a collapsible plastic square shaped ring for insertion into the pupil through a small incision is now being used in these “floppy iris” cases. It creates a 6 mm pupil, prevents pupil contraction, and reduces complications. Pupil size, shape, and contractility are usually not permanently altered by this device.

Advances in Lens Implant Design

In addition to ultraviolet filtering capability and injection systems for inserting IOLs through small incisions, three major developments have occurred in the optics of lens implants. These include toric lenses to correct astigmatism; aspheric optic design to improve contrast sensitivity; and more presbyopia-correcting IOLs to allow better near vision. Astigmatism Correction – Corneal astigmatism is consequent to different surface curvatures present in different meridians. The globe is not a perfect sphere, causing light to be refracted differently in different meridians. Astigmatism causes blurring because rays of light are not brought to a single focal point on the retina. It can be corrected by glasses, contact lenses or 16 Vol. 62, No. 2 2011 Northeast Florida Medicine

Pupil dilated by a Malyugen plastic ring in phacoemulsification cataract surgery

refractive surgery. A very effective toric IOL (different curves in different meridians) has been developed by Alcon Laboratories.14,15 It maintains position in the eye better than prior toric implants. Although it cannot always completely correct pre-existing corneal astigmatism, it improves uncorrected vision better than other IOL types. It is more predictable than corneal surgery for correcting astigmatism and requires no additional incisions. Patients see better and require less optical correction postoperatively. Aspheric Optics – The normal cornea bends parallel rays of light entering its periphery to a shorter focal length than rays of light entering its center. This phenomenon is known as positive spherical aberration. It can decrease image quality and reduce contrast sensitivity particularly in dim lighting conditions when the pupil dilates. The crystalline lens of a young person normally offsets this corneal effect with negative spherical aberration (bending peripheral rays to a longer focal length than central rays). A standard spherical IOL has positive spherical aberration and adds to the total spherical aberration of the eye. Aspheric lens implants have negative or neutral spherical aberration and reduce overall positive spherical aberration in the eye. Visual benefits from these can be shown by contrast sensitivity testing.16,17,18 These aspheric implants accounted for 70% of implanted lenses in a recent survey.19 www . DCMS online . org

Presbyopia Correction – The lens is focused at distance when the eye is in the resting state. It can quickly re-focus on a near object by changing its shape and moving anteriorly in response to contraction of the ciliary muscle, called “accommodation”. Patients lose the ability to accommodate and start requiring reading glasses at approximately age 43, a process known as presbyopia. By age 72, the average age of cataract surgery patients in the US, the patient has lost almost all ability to accommodate. Presbyopia-correcting IOLs have been gaining in popularity since the first multifocal IOL was FDA approved in 1997. The FDA approved presbyopia-correcting IOLs fall into three basic types: refractive multifocal; diffractive multifocal; and accommodating IOLs.

Refractive Multifocal IOLs

The most popular of this group have been the first generation silicone AMO ArrayTM(1997) and the second-generation refractive hydrophilic acrylic AMO ReZoomTM (2005). The optic of the ArrayTM lens is designed so that 4 different optical zones are arranged within the central 4.7 mm of the 6mm lens as 4 concentric rings around a small central zone powered for distance. The first and third surrounding rings are for near while the second and fourth are for distance causing visual function to be dependent upon pupil size. The zonal refractive rings of the ArrayTM were modified in the ReZoomTM in an effort to reduce glare and improve near vision. FDA studies show that eyes with either of these lenses have equally good distant vision and much better reading vision than eyes with standard monofocal IOLs. The result is less spectacle (glasses) dependence and high levels of patient satisfaction.20, 21 Patients must accept some halos and glare, reported by >50% of patients, in exchange for improved reading ability. After six months fewer than 10% of patients still were bothered by glare.20, 21

Diffractive Multifocal Lens Implants

The two most popular diffractive multifocal lenses in the US are the Alcon ReSTORTM and the AMO Technis ZM900TM. The ReSTORTM is a single piece hydrophyllic acylic lens with a 3.7mm central ringed diffractive zone containing 12 rings on the front surface. In an FDA trial, 80% of patients bilaterally implanted with this lens achieved total spectacle independence (versus 20% with standard monofocal IOLs) and 96.9% said they would have the same lens again. 22 The Technis ZM900TM, an aspheric silicone lens with 36 concentric diffractive rings on the posterior surface, is less pupil size dependent than the ReSTORTM. Both of these lenses tend to give excellent reading vision which is usually better than that achieved with the refractive multifocals. Reports on intermediate vision vary from equivalent to not as good as with the refractive multifocals.23,24 Halos and glare are present with diffractive just as with the refractive multifocals and reports comparing the two multifocal types are at variance as to which style produces fewer photic phenomena.24,25 Patients must be willing to tolerate some glare and reduced contrast sensitivity for enhanced reading ability. www . DCMS online . org

Accommodating Lens Implants

Although other IOLs are being implanted abroad, the only accommodating FDA-approved IOL to date is the silicone CrystalensTM, (Eyeonics) with a 5 mm optic which is 1 mm smaller than the 6 mm optic on most other lenses. It has two solid silicone plate haptics for fixation in the capsular bag. These extend out from the optic to give it an 11.5 or 12 mm overall length dependent upon the power required (longer implant for the larger near-sighted eyes). Each of the silicone plate haptics is scored by a transverse groove that “hinges” the haptic allowing the lens to move posterior to anterior inside the eye. When the lens optic moves forward toward the cornea with ciliary muscle contraction, its effective power increases making it truly “accommodating”. However, studies of forward movement have generally not shown sufficient movement to allow for reading at the most popular reading distances.26,27 This is especially true for lower powered lenses which must move farther than higher powered IOLs to achieve a comparable optical effect. This accommodative effect might be achieved by an increase in anterior curvature of the IOL with ciliary contraction, so called “accommodative arching”. There is no consensus about how the CrystalensTM works. However, FDA studies have shown that these patients do read better than those with standard monofocal IOLs. 28 They usually have good intermediate vision but near reading vision lags behind those with multifocals. Unlike multifocal IOLs, the CrystalensTMrarely causes halos or glare. Although no IOL can approach the optical performance of the natural crystalline lens in a healthy young eye, these new developments are allowing more patients to be less-spectacle dependent than in the past.

Advances in Lens Implant Power Calculations

Refractive outcome depends on preoperative IOL power selection. This requires accurate measurement of both the optical power of the central 3mm of the cornea and of the axial length of the eye (cornea to retina). These power measurements have been automated and computerized in recent years to produce more data points and even to produce elaborate detailed maps of the corneal surface (corneal topography) leading to greater accuracy. Errors of 0.5 mm in axial length may result in postoperative refractive errors up to 1.4 diopters. Until recently, axial length was measured with ultrasound which required corneal contact, was less reproducible, and more operator-dependent than a newer technique, partial coherence interferometry. It requires no physical contact, is easy for the patient, is operator-friendly and the results are highly reproducible, making it possible for ophthalmologists all over the world to compare results. The major difficulty with IOL power calculations is that the distance from corneal surface to IOL, critical for determining accurate power of the IOL, cannot be determined preoperatively. Statistical average values and other measurements which correlate with and help us to predict this distance Northeast Florida Medicine Vol. 62, No. 2 2011 17

(such as axial length, corneal diameter, and preoperative AC depth) are employed. A deviation from expected of 0.5 mm in corneal to IOL distance can result in a 1.25 diopter postoperative refractive error. The mathematical formulas for predicting required IOL power have been replaced by empirical linear regression formulas using constants derived from large case series. Even with current prediction accuracy (error < 0.5 diopter), 10% of eyes have residual refractive errors> 1 diopter.29 These eyes, as well as some of those having refractive errors between 0.50 and 1.00 diopter, will need glasses if they desire to obtain “best-corrected” distance vision. All patients cannot expect to see without glasses after cataract surgery. If being free of glasses is the goal, refractive corneal surgery may be required after the cataract operation.

Laser Cataract Surgery

Much excitement today is being generated in ophthalmology by talk of “laser cataract surgery”. Laser cataract surgery is misleading terminology because lasers cannot remove cataracts. The excimer laser can be used to make surgical excisions, anterior capsulotomies, and to break up or soften cataracts in preparation for surgical removal. However, using the laser to perform these portions of the cataract surgery does not eliminate a trip to the operating room.30,31,32,33

Conclusion

Small incision surgery and lens implants have been the two most important developments of modern cataract surgery. Patients today have outpatient surgery, usually without a stitch or patch, and may return to work in 1-2 days. Improvements in ultrasonic technology and fluid dynamics as well as more refined surgical instruments, have enabled cataracts to be removed with less energy, less heat production, better AC stability and greater safety. Continuing improvements in IOLs have included aspheric lenses as well as newer multifocal and accommodating lens implants which improve the ability to read without glasses and lessen spectacle dependence. The result of these advances is that cataract surgery is more safe and effective today than ever before.

References

Leaming D. Highlights of the 2008 ASCRS member practice style survey. www.leamingsurveys.com. Accessed April 2008.

Kelman C D. Phacoemulsification and aspiration; a new technique of cataract removal: a preliminary report. Am J Ophthalmol. 1967; 64:23-35.

Kelman C D. The genesis of phacoemulsification. Cataract & Refractive Surgery Today. 2004; 4: 57-58.

Leaming D V. Practice styles and preferences of ASCRS members – 1985 survey. J Cataract Refract Surg. 1986; 12:380-384.

Leaming D V. Practice styles and preferences of ASCRS members 1990 survey. J Cataract Refract Surg. 1991; 17:495-502.

Jaycock P, Johnston RL, Taylor H, Adams M, et al. The Cataract National Dataset electronic multi-centre audit of 55,567 operations: updating benchmark standards of care

18 Vol. 62, No. 2 2011 Northeast Florida Medicine

in the United Kingdom and internationally. Eye. Advance online publication. November 23, 2007; doi:10.1038/ sj.eye.6703015. www.medscape.com/viewarticle/587071. Accessed January 2009. 7.

El-Hindy N, Johnston R L, Jaycock P, et. al. The Cataract National Dataset electronic multicenter audit of 55,567 operations: anesthetic techniques and complications. Eye. 2009; 23:50-55.

Benzimra J D, Johnston R L, Jaycock P, et al. The Cataract National Dataset electronic multicenter audit of 55,567 operations: antiplatelet and anticoagulant medications. Eye. 2009; 23:10-16.

Leaming D V. Practice styles and preferences of ASCRS members 1998 survey. J Cataract Refract Surg. 1999; 25: 851-859.

10. Zeng M. Liu X, Liu Y, et al. Torsional ultrasound modality for hard nucleus phacoemulsification cataract extraction. Br J Ophthalmol. 2008; 92:1092-1096. 11. Agarwal A, Agarwal A, Agarwal S. et al. Phakonit: phacoemulsification through a .9 mm corneal incision. J Cataract Refract Surg. 2001; 27:1548-1552. 12. Weikert M P. Update on bimanual microincisional cataract surgery. Curr Opin Ophthalmol. 2006; 17:62-67. 13. Denoyer A, Denoyer L, Marotte D, et al. Intraindividual comparative study of corneal and ocular wavefront aberrations after biaxial microincision versus coaxil small-iincision cataract surgery. Br J Ophthalmol. 2008; 92:1679-1684. 14. Mendicute J, Irigoyen C, Aramberri J, et al. Foldable toric intraocular lens for astigmatism correction in cataract patients. J Cataract Refract Surg. 2008 34:601-607. 15. Bauer NJ, deVries NE, Webers CA, et al. Astigmatism management in cataract surgery with the AcrySof toric intraocular lens. J Cataract Refract Surg. 2008; 34:1483-1488. 16. Kershner RM. Retinal image contrast and functional visual performance with aspheric , silicone, and acrylic intraocular lenses. Prospective evaluation. J Cataract Refract Surg. 2003; 29:1684-1694. 17. Shentu X, Tang X, Yao K. Spherical aberration, visual performance and pseudoaccommodation of eyes implanted with different aspheric intraocular lens. Clinical and Experimental Ophthalmol. 2008; 36:620-624. 18. Bellucci R, Scialdone A, Buratto L, et al. Visual acuity and contrast sensitivity comparison between Tecnis and AcrySof SA60AT intraocular lenses: A multicenter randomized study. J Cataract Refract Surg. 2005; 31: 712-717 19. Harmon D, Thomas D. “Market Scope”, The Ophthalmic Surgeon’s Quarterly Survey Report. September 30, 2010, p.14. 20. Steinert RF, Aker BL, Trentacost BS, et al. A prospective comparative study of the AMO ARRAY zonal-progressive multifocal silicone intraoculaar lens and a monofocal intraocular lens. Ophthalmology. 1999; 106:1243-1255. 21. Mester U, Hunold W, Wesendahl T, Kaymak H. Functional outcomes after implantation of Tecnis ZM900 and Array SA40 multifocal intraocular lenses. J Cataract Refract Surg. 2007; 33:1033-1040. 22. Davison, JA. Managing Cataract Patients’ Refractive Expectations: Six Areas to Emphasize for Success. Cataract Refract Surg Today. March 2006;3:71-78.

www . DCMS online . org

23. Lane, SS, Morris M, Nordan L, et al. Multifocal intraocular lenses. Ophthalmol Clin N Am. 2006; 19: 89-105. 24. Cillino S, Casuccio A, Di Pace F, et al. One year outcomes with new-generation multifocal intraocular lenses. Ophthalmology. 2008; 115:1508-1516. 25. Goes F. Visual results following implantation of a refractive multifocal IOL in one eye and a diffracive multifocal IOL in the contralateral eye. J Refract Surg. 2008; 24:300-305. 26. Findl O, Leydolt C. Meta-analysis of accommodating intraocular lenses. J Cataract Refract Surg. 2007; 33:522-527. 27. Menapace R, Findl O, Kriechbaum K, Leydold-Koeppl, Ch. Accommodating intraocular lenses: a critical review of present and future concepts. Graefe’s Arch Clin Exp Ophthalmol. 2007; 245:473-489. 28. Olsen T. Calculation of intraocular lens power: a review. Acta Ophthalmologica Scand. 2007; August 85(5):472-85. 29. Alio JL, Pinero DP, Plaza-Puche AB. Visual outcomes and Optical Performance with a Monofocal Lens and a New Generation Single-optic Accommodating Intraocular Lens. J Cataract Refract Surg. October 2010; 36(10):1656-64. 30. Nanevicz TM, Prince MR, Gawande AA, Puliafito CA. Excimer laser ablation of the lens. Arch Ophthalmol. 1986; 104: 1825-1829. 31. Maguen E, Martinez M, Grundfest W, et al. Excimer laser ablation of the human lens at 308 nm with a fiber delivery system. J Cataract Refract Surg. 1989; 15: 409-414. 32. Dodick JM, Sperber LTD, Lally JM. Neodymium YAG laser phacolysis of the human cataractous lens (letter). Arch Ophthalmol. 1993; 111:903-904. 33. Kanellopoulos AJ, and the Photolysis Investigative Group. Laser Cataraact Surgery: A prospective clinical evaluation of 1000 consecutive laser cataract procedures using the Dodick photolysis Nd:YAG system. Ophthalmology. 2001; 108:649-655.

3rd Annual Quality & Safety Forum Attracts 160 Participants

Over 160 participants attended the 3rd Annual Quality & Safety Forum on The Engines of Excellence: Professionalism, Collaboration & Leadership, at the University of North Florida University Center, April 26, 2011. Keynote addresses were given by Jo Shapiro, MD, FACS and David Pryor, MD. Dr. Shapiro, Director, Center for Professionalism and Peer Support at Brigham & Women’s Hospital in Boston, MA, focused on the importance of professionalism. Dr. Pryor, Chief Medical Officer for Ascension Health, spoke about leadership and the creation of a culture of excellence, quality and accountability. The forum was sponsored jointly by the Center for Global Health and Medical Diplomacy at the University of North Florida and Duval County Medical Society. The photo above shows (L to R) Yank D. Coble, Jr., MD, Director of the Center and Capt. Lynn Welling, MD, Commanding Officer at Naval Hospital Jacksonville. www . DCMS online . org

The DCMS needs YOUR help with the

Student Athletic Screenings Share your expertise at the JSMP Athletic Screenings Saturday, August 6 – high school boys and middle and high school girls

Saturday, August 13 – middle school boys

Nemours Children’s Clinic & Wolfson Children’s Hospital JSMP coordinates free pre-participation athletic screenings for studentathletes in Duval County. Primary care physicians, orthopedic surgeons, cardiologists, pulmonologists, other medical specialists, physician assistants, and allied health professionals participate in the screenings. Physician and PA volunteers are coordinated through the DCMS. These screenings are provided at no charge to student athletes, most from homes with limited means, and are not intended to replace annual physical exams performed by pediatricians and primary care physicians. Follow up care with individual physicians is encouraged when screenings indicate potential problems which may impact the athlete’s participation in sports activities.

Want to Help?

Watch your email or fax for registration forms, visit our website, or contact Barbara Braddock at membership@dcmsonline.org or 355-6561 ext. 107. Northeast Florida Medicine Vol. 62, No. 2 2011 19

The History of Refractive Surgery: Past, Present and Future Jerry W. Maida, MD, MBA Abstract: Scientists have been trying to understand the basis for refractive errors since the time of Leonardo DaVinci. Now, with the latest innovations, over a period of fifty years, myopia, hyperopia and astigmatism can be treated with safety and predictability using lasers. Presbyopia, the last great challenge, is on the brink of being conquered. Extensive research has provided invaluable refinements and advancements of laser technology and diagnostic tools to develop safe and appropriate treatment options for patients with a myriad of refractive disorders. Laser-assisted in situ keratomileusis (LASIK) is presently the most performed elective procedure in the modern world. This review will discuss the history of refractive surgery, past and present technological advances, surgical procedures, risks, complications and the future of refractive surgery.

Introduction

The function of a normal cornea is to refract incoming light rays onto the retina. In a myopic (near-sighted) eye, light rays are focused in front of the retina causing blurring at a distance, whereas in a hyperopic (far-sighted) eye, the light rays are focused behind the retina causing blurring at close distance. During the last half century, several laser and non-laser refractive procedures have been experimented with and developed to correct these vision abnormalities. The procedures that were developed through the years change the shape of the cornea to focus light rays sharply on the retina. In myopia, correction is achieved by flattening the surface of the cornea, while in hyperopia the corneal surface is steepened.

History of Refractive Surgery

The first person to utilize incisional surgery to correct ammetropia (refractive error) was Hjalmar Schiotz in 1885.1 In the 1940s, Tatsuhiko Sato attempted to refine his technique.1 In 1948, Jose Barraquer of Bogotá, Colombia, considered by many to be the father of refractive surgery, first performed corneal lamellar surgery to reshape the cornea.1 Barraquer removed a portion of the cornea, froze and reshaped it in a lathe, and then sutured it to the eye with very fine sutures, the precursor to LASIK surgery. Few surgeons other than Barraquer were able to master that technique. Today, lasers with accuracy to a millionth of an inch, replace the lathe and the need for sutures. In the 1970s and 1980s, there was a rapid infusion of new technologies for treating refractive errors including radial keratotomy (RK). Slava Fyodorov of Russia developed RK, a procedure in which 4 to 16 equally distanced incisions were made into the anterior cornea at a depth of approximately 90% leaving a clear central zone.2 Fyodorov noted, after treating a myopic boy who had an accidental corneal penetrating injury, that when the cornea healed, nearsightedness was corrected. Address Correspondence to: Jerry W. Maida, MD, MBA, Director – MAIDA CustomVision, 11945 San Jose Blvd., Suite 102, Jacksonville, FL 32223. Email: maida@maidalaser.com.

20 Vol. 62, No. 2 2011 Northeast Florida Medicine

In 1978, the procedure was introduced into the U.S. and first performed by Leo Bores in Santa Fe, New Mexico.3 During the 1980s, there was a revolutionary change in treatment of refractive errors departing from incisional to laser-assisted refractive surgery with the inception of excimer laser technology. Argon lasers had been used to treat glaucoma and retinal disorders and the neodymium YAG laser to treat post-cataract surgical complications, but lasers had never been used to treat the clear, transparent cornea. In 1983, Stephen Trokel utilized the excimer laser to ablate (vaporize) corneal tissue.4 Argon and fluoride gases mix creating an unstable bond called an “excited dimer” – hence the acronym, Excimer laser – that releases UV light in the 193nm spectrum. Unlike other lasers, it does not penetrate the cornea or have any thermal affects. It separates the bonds that hold the corneal cells together with sub-micrometer precision removing 0.25 microns of tissue with each pulse. It is so precise that it can etch a clean pattern into a human hair (Figure 1). The first studies with the excimer laser were performed by photo-chemist, R. Srinivasan, at IBM. He was experimenting with excimer lasers to etch plastics and realized that fine cuts could be made into a human hair.4 Since he applied for the first patent, most laser companies must license this technology from IBM.5 Summit Technology and VISX also had patents, so to resolve lawsuits over the patents, they formed Pillar Point Partnership which sub-licenses the technology to ophthalmologists. To this day, refractive surgeons, even after they have purchased an excimer laser, are required to pay a royalty fee, i.e., a per use fee for each eye that is treated.5

Figure 1 Laser Pattern in a Human Hair

(Reprinted with permission from Slack Incorporated) Citation: Krueger, RR, Rabinowitz, YS and Binder, PS. The 25th Anniversary of Excimer Lasers in Refractive Surgery: Historical Review. The Journal of Refractive Surgery. 26(10):749-760.

Theo Seiler, a physicist and ophthalmologist from Berlin, Germany, whose course this author attended in early 1989, performed the first excimer laser treatment on a blind eye in the mid-1980s.6 This was followed in 1988 in the U.S. by Marguerite McDonald who performed the first treatment on a sighted-eye with myopia.7 FDA trials began a few months later. In 1989, this author, participating in an FDA study, www . DCMS online . org

Table 1 FDA Approved Lasers for PRK and Other Refractive Surgeries (Adapted from FDA website)

Company & Model

Approval Number & Date

Approval Indications (D = diopters)

Summit -Apex & Apex Plus

P930034 10/25/95

PRK; Myopia from -1.5 to -7.0D

VISX -Model B & C (Star & Star S2)

P930016 3/27/96

PRK; Myopia from 0 to -6.0D

performed the first excimer laser procedure (for glaucoma) in Florida.

Photo Refractive Keratectomy

Michael Gordon performed the first Photo Refractive Keratectomy (PRK)8 procedure in the U.S. with the Summit Excimer Laser in 1989.8 In PRK, the anterior surface (epithelium), is removed and then the excimer laser removes Bowman’s membrane and a few microns of anterior stroma (depending on the degree of myopia). In those early years, refractive surgeons were not aware of the importance of pupil size, corneal thickness, curvature of the cornea, dry eye syndrome or even the degree of refractive error. And, in most cases, they did not have the technology to evaluate those parameters. PRK obtained FDA approval for treating myopia in late 1995 (Table 1). It is still performed today in 10-20% of refractive surgery patients.

LASIK

Laser Assisted In-Situ Keratomileusis (LASIK) is currently the predominant type of refractive surgery in the U.S., while PRK is more popular in some European countries. (See further discussion in later section.) Concurrent with the development of PRK, various techniques not involving the corneal surface were being developed. Barraquer’s three-hour intralamellar corneal surgery preserved the corneal surface. Luis Ruiz, modified Dr. Barraquer’s technique by developing a geared automated instrument to create a flap in preparation for the refractive surgery (insitu keratomileusis).9 This hand-held microkeratome used an oscillating razor blade to make a lamellar cut into the corneal stroma. In the early 1990s, Lucio Buratto of Italy described a technique combining the two technologies, i.e., using the blade of the microkeratome to make a corneal flap (an advance of Barraquer’s work in the 1950s), with the micron accuracy of the excimer laser to remove tissue,10 instead of removing a button of corneal stromal tissue with a blade. Ioannis Pallikaris coined the name LASIK, which means removing tissue within the cornea.11 An advantage of LASIK is the avoidance www . DCMS online . org

of the corneal haze and pain associated with PRK. It leaves the corneal epithelium intact, avoiding the majority of nerve endings and the necessity for anterior corneal remodeling. In LASIK, the removal of tissue is within the corneal stroma (intralamellar), so vision is often improved the day of surgery compared to one to two weeks for PRK.

Femtosecond Laser Use in LASIK

The hand-held microkeratome is still in use today for 3040% of the refractive surgery cases performed; however, it is gradually being replaced by the femtosecond laser. LASIK was approved by the FDA in 1999 (Table 2, p. 22), although it had been performed earlier in the U.S. by surgeons (including this author in 1996) as an off-label procedure. The mechanical microkeratome uses an oscillating razor blade that is not as dependable or accurate as the microprecision of a femtosecond laser. On rare occasions, it malfunctions due to loss of suction, poor blade oscillation or operator error resulting in a loose, torn, or perforated flap, which can be sight-threatening. Even though the microkeratome was ingenious and the risk of perforating the eye was eliminated with the evolution of the fixed plate, the femtosecond laser resolved many of its potential complications. Due to its high cost ($400,000 and $160/eye), in comparison to the microkeratome($30,000 and blade $30/eye), and its inherent early complications, the acceptance of the femtosecond laser has been particularly slow. The femtosecond laser, however, rarely has problems with irregular cuts or perforated or loose flaps. The femtosecond laser is the fastest laser in the world,12,13 working in a billionth of a trillionth of a second. In that time, light will travel only 13 inches. The femtosecond laser was first utilized in the U.S. in the early 2000s and in Jacksonville in 2003. This laser etches a treatment plane within the corneal stroma at a desired depth accurate to within a few millionths of an inch. It is not dependent on corneal curvature, diameter or thickness, and it produces consistent flaps. The early models, due to their high energy level, occasionally caused diffuse lamellar keratitis (inflammation of the corneal flap) and transient light sensitivity syndrome (TLSS), which are treated with anti-inflammatory agents.14,15 These problems have been reduced with advances in femtosecond technology.16 Northeast Florida Medicine Vol. 62, No. 2 2011 21

Table 2 FDA Approved Lasers for LASIK (Adapted from FDA website)

Company & Model

Approval Number & Date

Approval Indications(D = diopters)

VISX - Star S2

P990010 11/19/99

Myopia less than -14.0D with or without Astigmatism between -0.5 and -5.0D

WaveLight - Allegretto Wave

P020050 10/07/03

Myopia up to -12.0D with or without Astigmatism up to -6.0D

Summit -Apex Plus

P930034/S13 10/21/99

Myopia less than -14.0D with or without Astigmatism from 0.5 to 5.0D

LASIK/ PRK Techniques and Improvements

During LASIK, a flap is created with the femtosecond laser or microkeratome, and a hinge is maintained. The flap is lifted and the programmed excimer laser is focused directly on the eye.The flap is then repositioned and held in place by the natural osmotic gradient and endothelial pump inherent in the cornea, which results in a detergescent affect (without stitches).The excimer laser has a tracking device to adjust for micro-saccadic eye movements up to 200/second. Nomograms and algorithms are developed for the computer-driven treatment based on the individual surgeon’s technique and takes into account humidity, temperature, oxygen concentration, altitude and other variables. Hyperopia, myopia and astigmatism can be treated.

PRK is more popular than LASIK in some European countries. Even though PRK maintains the integrity of the cornea by avoiding any stromal cuts as in LASIK, it involves a more complex and slower healing process with stromal remodeling. Visual recovery is slower and more uncomfortable than with LASIK. Patients that have PRK must wear a bandage lens for several days and mild steroid drops are often utilized for a few months. In PRK, alcohol now enables easy removal of the epithelium and decreased post-operative discomfort. Although LASIK has virtually replaced PRK, there is still a place for PRK today. It is the procedure of choice for patients with thin corneas, potential irregularities in vision, epithelial basement membrane disease and for aviators in the US military and sports figures exposed to trauma since there is no flap as in LASIK, thereby decreasing the risk of corneal rupture. However, LASIK has now taken the world by storm with more than 28 million procedures performed worldwide since 1996.17 Many corneas have minor irregularities that may be exacerbated by traditional refractive procedures. Wavefront-guided and wavefront-optimized treatments have improved the LASIK and PRK procedures by further refining the patient’s vision often leading to a result as good or better than they had with contacts or glasses.18,19 22 Vol. 62, No. 2 2011 Northeast Florida Medicine

Pre-Operative Assessment

Not everyone is a candidate for refractive surgery. Technology to measure the curvature or subtle irregularities in the cornea (corneal topography), the thickness of the cornea (pachymetry), and the pupil size in dim light (pupillometry) was not available 10-20 years ago. These measurements are critical to the proper patient selection and long-term success of the refractive surgery. Corneal topography reveals which corneas are too steep, flat, or irregular. Surgery on these eyes may lead to serious corneal abnormalities 5-10 years later. Ultrasound pachymetry measures corneal thickness. Surgery on an excessively thin cornea can destabilize the eye resulting in keratoconus. The first excimer lasers only treated a small central area of the cornea with resultant glare and halos for many patients. These problems are now rectified with the advanced technologies available in the computer programming of the excimer laser. Tear production, which can decrease with age especially in the menopausal female, must be assessed. Dry eyes must be treated pre-operatively with artificial tears, Restasis, or punctual occlusion. This problem is not simply a lack of tearing, but often a mild immune or inflammatory problem.20 Sjorgen’s Syndrome (dry mucus membranes) is often a contraindication along with auto-immune illnesses such as: Lupus, Hashimoto’s, and Rheumatoid Arthritis. Patients having these illnesses need to be evaluated on a case-by-case basis. Patients with previous or concurrent eye diseases including glaucoma, retinal detachment, herpes simplex, and keratitis are questionable candidates for treatment. Furthermore, there are medications that can cause corneal melting such as Acutane for acne or Amiodarone for atrial fibrillation, so careful histories must be obtained from the prospective candidates. Good candidates are usually between 21 and 70 years of age and in relatively good health. The lifestyle of the patient will lead the surgeon to prefer one procedure over another.

Complications

As safe as laser refractive surgery is, complications may still occur. Loose, irregular or torn flaps are issues associated with the microkeratome.21 Intra-operative difficulties with the femtosecond laser are uncommon, yet, post-operatively, www . DCMS online . org

Impact of HIV on Vision

Background - Benefits that Matter!

The Duval County Medical Society (DCMS) attempts to provide its members with the benefits that consistently meet your professional needs. One example of how this is being accomplished is by providing to DCMS members free Continuing Medical Education (CME) opportunities in the subject areas mandated/and or suggested by the State of Florida Board of Medicine to obtain and retain medical licensure. The DCMS would like to thank the St. Vincent’s Healthcare (SVHC) Committee on CME for reviewing and accrediting this activity in compliance with the Accreditation Council on Continuing Medical Education (ACCME). Helena Karnani, MD, Chair of the CME Committee; Betsy Miller, Director, Medical Staff, Quality Management; and Cindy Williamson, CME Coordinator, from SVHC deserve special recognition for their work on behalf of DCMS. This issue of Northeast Florida Medicine includes an article, “Impact of HIV on Vision” authored by Michael W. Stewart, MD (see pp. 3-8), which has been approved for 1.0 AMA PRA Category 1 credit(s).™ For a full description of CME requirements for Florida physicians (MD/DO), please visit the DCMS website (http://www.dcmsonline.org/cme_requirements.aspx).

Faculty/Credentials: Michael W. Stewart, MD, is an Assistant Professor and Chair of the Department of Ophthalmology at Mayo Clinic Florida in Jacksonville, FL. Dr. Stewart received his MD degree from the McGill University School of Medicine after completing an AB degree in chemistry at Harvard University. He did residencies in the Department of Medicine at University of Miami and the Department of Ophthalmology at Emory University. He also did fellowships in vitreoretinal diseases at the Retina Research Foundation and the University of California. Objectives for CME Journal Article 1. Understand the major reasons for vision loss in patients with HIV/AIDS 2. Understand the treatment options for the most common ocular opportunistic infections 3. Know the relationship between HIV activity and likelihood of vision loss

Date of Release: June 3, 2011 Date Credit Expires: June 3, 2013 Estimated time to complete: 1 hr.

Methods of Physician Participation in the Learning Process 1. Read the “Impact of HIV on Vision” article on pages 3-8 2. Complete the Post Test and Evaluation on page 2 3. Fax the Post Test and Evaluation to DCMS (FAX) 904-353-5848 OR members can also go to www.dcmsonline.org & submit test online

CME Credit Eligibility

In order to receive full credit for this activity, a minimum passing grade of 70% must be achieved. Only one re-take opportunity will be granted if a passing score is not made on the first attempt. DCMS members and non-members have one year to submit the post test and earn CME credit. A certificate of credit/completion will be emailed, faxed or USPS mailed within 4-6 weeks of submission. If you have any questions, please contact the DCMS at 355-6561, ext. 103, or llegacy@dcmsonline.org.

Faculty Disclosure Information

Dr. Stewart reports no significant relationships to disclose, financial or otherwise with any commercial supporter or product manufacturer associated with this activity.

Disclosure of Conflicts of Interest

St. Vincent’s Healthcare (SVHC) requires speakers, faculty, CME Committee, and other individuals who are in a position to control the content of this educational activity to disclose any real or apparent conflict of interest they may have as related to the content of this activity. All identified conflicts of interest are thoroughly evaluated by SVHC for fair balance, scientific objectivity of studies mentioned in the presentation and educational materials used as basis for content, and appropriateness of patient care recommendations.

Joint Sponsorship Accreditation Statement

This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of St. Vincent’s Healthcare and the Duval County Medical Society. St. Vincent’s Healthcare is accredited by the Florida Medical Association to provide continuing medical education for physicians. The St. Vincent’s Healthcare designates this educational activity for a maximum of 1.0 AMA PRA Category 1 credit(s) .TM Physicians should only claim credit commensurate with the extend of their participation in the activity.

Insert

Northeast Florida Medicine

Vol. 62, No. 2 2011

(Return by June 3, 2013 by FAX: 904-353-5848, by mail: 555 Bishopgate Lane, Jacksonville, FL 32204 OR online: www.dcmsonline.org) 1. Which of the following is true? a. Microvasculopathy occurs in all AIDS patients b. Retinopathy occurs in all AIDS patients c. Retinopathy occurs in the early stage of HIV infection d. Retinopathy usually causes significant loss of vision 2. An induction/maintenance treatment schedule is used for each of the following drugs EXCEPT: a. Intravenous ganciclovir b. Intravenous foscarnet c. Ganciclovir implant (Vitrasert) d. Valganciclovir 3. Which of the following is true about valganciclovir? a. It is taken orally b. Venous and tissue drug levels are comparable to those achieved with intravenous ganciclovir c. Major side effects are neutropenia and gastrointestinal disturbances d. All of the above 4. Which of the following drugs has NOT been administered intravitreally? a. Valganciclovir b. Ganciclovir c. Foscarnet d. Cidofovir 5. Which of the following is true about HAART therapy? a. It does not change the immune status in most patients b. It fails to increase the CD4+ lymphocyte counts



Impact of HIV on Vision CME Questions & Answers (Circle Correct Answer) /Free-DCMS Members/$50.00 charge non-members*

c. It improves immune status without changing the HIV viral load d. It decreased the prevalence of CMV retinitis by 80% 6. For patients receiving HAART, which of the following is true? a. CMV retinitis tends to be more aggressive in patients who are HAART naÏve b. CMV retinitis appears clinically different compared to HAART naÏve patients c. Development of CMV retinitis signifies a greater risk of death than for HAART naÏve patients d. They are more likely to develop CMV retinitis than are HAART naÏve patients 7. Which of the following is true regarding the selection of anti-CMV therapy? a. The ganciclovir implant should be used in all patients b. Valganciclovir is the drug of choice for most patients c. Due to their high complication rates, intravitreal injections should never be used d. Systemic therapy (oral or intravenous) alone is sufficient for all patients 8. Which of the following is true about immune recovery uveitis? (IRU) a. It is caused by the immune system’s recognition of residual CMV DNA with the retina b. It occurs in 15-25% of patients with previous CMV retinitis c. It is usually accompanied by an increase in the CD4+ T-lymphocyte count and a decrease in HIV load d. All of the above



Evaluation questions & CME Credit Information (Please evaluate this article. Circle one number using this scale: 1= Strongly Agree to 5= Strongly Disagree) The article met the stated objectives: 1 2 3 4 5 The article was appropriate to my practice: 1 2 3 4 5 The topic was current and well presented: 1 2 3 4 5 Comments:______________________________________________________________________________________ ____________________________________________________________________________________________ Name (Print)___________________________________________Email_____________________________________ Address/City/State/Zip_____________________________________________________________________________ Phone__________________________Fax_____________________DCMS Member (circle)

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2 Vol. 62, No. 2 2011

Northeast Florida Medicine

Insert

Impact of HIV on Vision Michael W. Stewart, MD Abstract: The human immunodeficiency virus (HIV) and its associated opportunistic infections frequently target the visual system. Cytomegalovirus (CMV) retinitis, despite an 80% decrease in incidence following the introduction of highly active anti-retrovirus therapy (HAART), remains the most frequent reason for vision loss in AIDS patients. Other major causes of vision loss include cataracts and immune recovery uveitis. Herpetic retinitis (H. simplex, H. zoster), toxoplasma retinitis, pneumocystis choroiditis, and microsporidium keratitis comprise less important causes of vision loss. Optimal care of patients with HIV related vision loss requires the coordinated efforts of both the ophthalmologist and infectious disease specialist. Treatment of patients requires both reconstitution of the immune system by optimally suppressing HIV replication and targeted therapy for opportunistic infections. Successful reconstitution of the immune system, with elevation of CD4+ lymphocyte counts, enables the discontinuation of CMV therapy in many patients.

Introduction

The first description of patients with the acquired immunodeficiency syndrome included those with opportunistic infections that resulted in blindness. During the early years of the AIDS epidemic, cytomegalovirus (CMV) retinitis developed in up to 40% of patients. The introduction of highly active anti-retroviral therapy (HAART) reduced the incidence of CMV retinitis by 80% but caused other problems such as immune recovery uveitis. Current causes of vision loss in HIV patients include CMV retinitis, cataracts, immune recovery uveitis with secondary macular edema, epiretinal membranes, and HIV retinopathy. Successful management of HIV patients with co-existing ocular disease requires close communication between the ophthalmologist and infectious disease specialist to coordinate anti-HIV therapy with specific anti-microbial therapy directed against opportunistic infections.

HIV Microvasculopathy

HIV-related microvasculopathy causes histopathological changes similar to those seen in diabetic retinopathy. Though autopsy studies demonstrate this finding in all AIDS patients,7 only 50% have the retinal hemorrhages and cotton wool spots characteristic of HIV retinopathy (Figure 1).6 Factors responsible for advancement from HIV microvasculopathy to clinical retinopathy remain unknown. However, retinopathy occurs with advanced immunodeficiency, generally with CD4+ T-cell lymphocyte counts <200 cells/µL.8 Though HIV retinopathy usually does not decrease visual acuity, it predisposes patients to CMV retinitis, possibly by altering local blood flow and vascular endothelial integrity, thereby allowing blood borne CMV to access the retina. 9

Cytomegalovirus Retinitis

CMV accounts for 99% of HIV-related opportunistic retinal infections in the United States. CMV enters the eye through the bloodstream and, in contrast with other infectious agents, spreads from a single focus. Despite continued viremia, additional seeding of the retina is uncommon.10 In untreated patients without reconstitution of the immune system, CMV retinitis inexorably marches across the entire retina, resulting in full thickness necrosis and total loss of vision (Figure 2).

Figures 1 & 2 HIV Retinopathy and Retinitis

Numerous cotton wool spots typical of HIV retinopathy.

The 1981 reports of 5 homosexual men with unusual opportunistic infections (pneumocystis carinii pneumonia, cytomegalovirus (CMV) infections and candidiasis) ushered in the AIDS era.1,2 A subsequent manuscript that included two additional patients described both a non-infectious, occlusive retinal microvasculopathy and a progressive, necrotizing retinitis due to cytomegalovirus.3 Thus, retinal abnormalities were quickly recognized as the most common HIV-related ocular findings. Over the next 14 years, CMV retinitis affected 25%-42% of AIDS patients4,5 and caused more than 90% of HIV-related vision loss. Though CMV retinitis accounted for the majority of vision loss in AIDS patients, other opportunistic infections (Herpes simplex, Herpes zoster, toxoplasmosis and pneumocystis) in the aggregate accounted for substantial ocular morbidity.6

Retinitis is progressing from top to bottom: Solid line - areas of necrotic retina following retinitis; Dashed line - area of active retinitis; Dotted line area of normal retina.

Address Correspondence to: Michael W. Stewart, MD, Assistant Professor and Chairman, Dept. of Ophthalmology, Mayo Clinic Florida, 4500 San Pablo Rd., Jacksonville, FL 32224. Phone: 904953-2232. FAX: 904-953-7040. Email: stewart.michael@mayo.edu. Insert

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Anti-CMV Drugs

Most CMV treatment strategies – those including ganciclovir, foscarnet and valganciclovir - begin with a 2-3 week period of high-dose drug administration (induction) to control the infection, followed by an indefinite period of lower dosing (maintenance) to suppress viral replication. Invariably patients experience reactivation of the retinitis, necessitating another course of induction therapy. Generally each subsequent round of maintenance therapy is shorter than the preceding period. Compared to intravenous ganciclovir or foscarnet, oral valganciclovir is the drug of choice for most cases of CMV rentinitis. Due to its high bioavailability (60%) and not needing an indwelling catheter is the primary reason why valgancicolir is preferred. Serious and potentially lethal side effects occur with each of the anti-CMV drugs: severe neutropenia (neutrophil count <1000 cells/µL) due to ganciclovir(34%)11 and valganciclovir (16%)12; renal toxicity due to foscarnet (17%-23%) and cidofovir (50%).

The repetitive induction/maintenance/reactivation treatment and disease cycle enables the emergence of drug resistant CMV. The incidence of viral resistance increases with larger areas of retinitis, increased loss of vision13 and longer duration of therapy (from 2.2% at 3 months to 15.3% at 18 months).14 Though the incidence of viral resistance appears to have dropped in the HAART era, (0.05 cases/patient year)15 some patients will need treatment with foscarnet or cidofovir if resistance to ganciclovir develops.

Intravitreal Therapy

Weekly intraocular injections (Figure 3) of ganciclovir or foscarnet suppress retinitis for periods that range from 8 to 20 weeks.16,17 To eliminate the need for inconvenient weekly injections, the ganciclovir implant (Vitrasert™), a semipermeable polymer reservoir that steadily releases ganciclovir for 9 months, was developed. (Figure 4, p. 5) Patients with vision threatening zone 1 (near the macula or optic nerve) retinitis benefit most from the implant, as opposed to those with zone 3 (peripheral) disease whose vision results do not surpass standard systemic therapy alone.18 To lessen the incidence of contralateral retinitis and non-ocular end organ disease when receiving local therapy, patients are usually given oral (valganciclovir or ganciclovir) or intravenous (ganciclovir, foscarnet, cidofovir) anti-CMV therapy.

HAART and CMV Retinitis

The development of highly active anti-retroviral therapy (HAART) became a watershed event in the treatment of HIV-infected patients. HAART, defined by the Department of Health and Human Services/Kaiser panel to include protease inhibitors (PI), a non-nucleoside reverse transcriptase inhibitor (NRTI), one of the NRTIs (abacavir or tenofovir), an integrase inhibitor (e.g., raltegravir), or an entry inhibitor (e.g., Maraviroc or enfuvirtide).19 This drug regimen usually clears HIV from the blood, increases the levels of circulating CD4+ T-lymphoctyes and partially restores cell-mediated immunity. Despite the institution of HAART, however, patients

4 Vol. 62, No. 2 2011

Northeast Florida Medicine

Figure 3 Intravitreal Injection of Ganciclovir Through the Pars Plana

remain at risk for new opportunistic infections since immune restoration may not occur for at least 3 months. Following HAART introduction, many centers saw the incidence of CMV retinitis decrease by 80%20 to 5.6/100 person-years (PY).21 This initial decline appears to have leveled off, with new cases continually being reported.20,22 Sixty-nine percent of new CMV retinitis infections occur in patients with HAART failure or persistently elevated HIV titers.10 Most patients with newly diagnosed CMV retinitis have low CD4+ T-cell lymphocyte counts but with greater variability than in the pre-HAART era.10 Though the diagnosis of CMV retinitis indicates HAART failure, the milder ocular disease suggests that HAART beneficially modulates disease severity and vision loss. In patients on HAART therapy with CMV, retinitis recurs less frequently,23 affects contralateral eyes less, and causes fewer retinal detachments.24 Newly diagnosed retinitis appears similar to that in the pre-HAART era, though the severity tends to be less in HAART-failure patients compared to HAART-naïve patients.10 Despite having less aggressive ocular disease, HAART patients with CMV retinitis, especially those with lower CD4+ T-lymphocyte counts, have an increased mortality rate. Since the introduction of HAART, the focus of retinitis treatment has shifted from short-term suppression of the acute infection to long-term management of chronic CMV/ HIV disease. For patients with newly diagnosed CMV retinitis, the first therapeutic intervention should concentrate on reconstituting the immune system, since this may permanently suppress CMV retinitis in some patients. For patients already receiving HAART, optimization of the drug regimen should occur as these patients have usually been inadequately treated due to either ineffective medications or non-compliance. For HAART naïve patients, initiation of anti-HIV therapy should be considered, though many infectious disease specialists recommend delaying HAART institution to avoid precipitating acute immune-mediated uveitis. Communication between the ophthalmologist and infectious disease specialist, regarding factors such as location and extent of retinitis, helps balance the risk of vision loss due to retinitis with that due to immune-mediated uveitis. If HAART therapy is deferred in favor of anti-CMV therapy alone, patients must be carefully monitored since they face an increased risk of death during this period.25 Insert

Figure 4 Sustained Release Ganciclovir Implant Sutured to the Pars Plana (as seen through the pupil)

When initiating anti-CMV therapy, drug selection depends upon the location of the retinitis and the patient’s HAART status. Unless otherwise contraindicated, oral valganciclovir is the systemic drug of choice for most patients. For patients with zone 1 retinitis – threatening the macula or optic nerve – or HAART failure, intraocular ganciclovir, either in the form of injections or the ganciclovir implant is also recommended (Table 1, p.6). Since CMV retinitis adversely affects patients’ quality of life, prevention becomes increasingly important.26 Prior to the introduction of HAART, more than 90% of vision loss in AIDS patients could be attributed to CMV retinitis.27 In the postHAART era the longitudinal rates of vision loss among AIDS patients without baseline CMV retinitis are 1.5/100 eye-year (EY) to <20/50 (loss of reading and driving vision), 0.8/100 EY to <20/200 (legal blindness) and 2.1/100 EY for doubling of the visual angle (e.g. 20/30 to 20/60). The rate of vision impairment in patients with newly developed CMV retinitis patients is 21.0 cases/100 EY and of blindness is 8 cases/100 EY, with most of the improvement from the pre-HAART era attributed to improvement in immune status. Over a 3.5 year period, 1.9% of eyes lost vision to < 20/200. Interestingly, even CMV retinitis patients not receiving HAART have lower rates of visual impairment (0.36 cases/100 EY) and blindness (0.16 cases/100 EY) than in the pre-HAART era.28 Much of the vision loss in eyes with CMV retinitis can be attributed to the same factors (zone 1 disease involving the optic nerve or macula, retinal detachment) as in the pre-HAART era.29 Patients who develop CMV retinitis have rates of vision loss 8-10 times higher than those that do not. Successful immune recovery allows many patients to discontinue anti-CMV therapy without rebound CMV reactivation. Long-term studies show that patients with non-sight threatening, quiescent retinitis for 6 months and reconstitution of the immune system may discontinue anti-CMV medications. The decision to stop CMV therapy depends upon many factors: rising CD4+ T-lymphocyte counts, falling systemic HIV loads (preferably to undetectable levels), duration of HAART (at least 3 months) and inactivity of CMV lesions. The United States Centers for Disease Control (CDC) recommends that the CD4+ T-lymphocyte count be at least 100-150 cells/µl Insert

for 3-6 months before CMV therapy is discontinued.30 Most authors, however, require more robust evidence of immune reconstitution (i.e. CD4+ T-lymphocyte counts > 200 cells/ µl and a 100-fold drop in HIV blood levels) before discontinuing therapy.31,32 Contradicting studies report successful discontinuation of therapy despite HIV blood levels exceeding 30,000 copies/ml.33 The immune-reconstitution inflammatory syndromes, unseen before HAART, frequently complicate HAART therapy. Though these disorders have been given several names, immune reconstitution inflammatory syndrome (IRIS) is the most widely accepted general term34whereas patients with ocular inflammation are said to have immune recovery uveitis (IRU). IRU occurs in 15%-25% of CMV retinitis patients receiving HAART, with the highest incidence between 8 and 16 weeks after initiation of treatment.35 IRU occurs when the recovered immune system, as measured by an increase in the CD4+ T-lymphocyte count, recognizes a large load of residual CMV DNA at the edge of previous retinitis36and then initiates a cell-mediated immune reaction. Patients with low CD4+ T-lymphocyte counts (fewer than 50 cells/µl),37 large areas of CMV retinitis (25%-30% of the retina),38 and a history of cidofovir use39 have the greatest risk of IRU. A small percentage of patients develop IRU without a CD4+ T-lymphocyte increase, suggesting that improved immunity against CMV may occur by some as yet unrecognized mechanism.40,41 CMV DNA in the blood and vitreous specimens of IRU patients becomes undetectable, though rare cases with partial immune reconstitution develop IRU in the presence of persistent CMV retinitis.41 The clinical spectrum of IRU ranges from asymptomatic vitritis, through a persistent uveitis with floaters, decreased vision, cystoid macular edema (12.3x increased risk) and epiretinal membrane (3.7x increased risk) formation.38,42 Infrequent complications include neovascularization, disc edema, proliferative vitreoretinopathy, cataract and posterior synechiae.40 Though some patients experience severe vision loss (20/200 or worse), most patients maintain visual acuities between 20/50 and 20/200.The rate of visual impairment in IRU patients is 0.17 cases/EY and the rate of blindness is 0.06 cases/EY.40 HAART treated patients diagnosed with IRU need to have other inflammatory conditions (syphilis, herpetic retinitis, drug toxicity) excluded. PCR testing of intraocular fluids may help rule out infectious etiologies (CMV, H. simplex, H. zoster, toxoplasmosis).43 The Longitudinal Study of AIDS38 reported a CMV retinitis prevalence of 22%, while other AIDS-related ocular conditions, including opportunistic infections, were found in <1% of patients. Of the patients noted to have CMV retinitis, 22% of them were newly diagnosed upon enrollment into the study. Of the patients with CMV retinitis, 59% had CD4+ T-lymphocyte counts >100 and 48% had discontinued anti-CMV therapy following reconstitution of the immune system. Groups both with and without CMV retinitis had Northeast Florida Medicine

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Table 1 Suggested Treatment Strategy for Patients with Newly Diagnosed CMV Retinitis

good (20/20) median and average visual acuities, but patients with CMV retinitis had a higher prevalence of VA worse than 20/40 (23.5%) and worse than 20/100 (14.4%). Patients with other opportunistic infections or non-infectious ocular conditions – such as retinal vein occlusions – had high rates of vision <20/40 (50.9%) and worse than 20/100 (35.1%). Among all AIDS patients, CMV retinitis accounted for 40% of vision loss (<20/200), cataracts were responsible for 25%, and in 10% the reason for vision loss could not be determined.29 Risk factors for vision loss were a low CD4+ T-cell count (<50 cells/µl) and a low Karnofsky (functional ability) score. The use of HAART decreases the incidence of vision loss by 50%, even after excluding patients with infectious retinopathies. CMV retinitis patients had relatively high prevalences of IRU (9.6%), cataracts (20%) and previous cataract surgery (21%).

Other Causes of Vision Loss

Nine percent of AIDS patients have abnormalities in color vision, contrast sensitivity, visual fields and electrophysiology sufficient to impair reading. Histopathologic analysis of affected eyes show damaged retinal ganglion cells with loss of optic nerve axons,44 possibly due to the cumulative effect of nerve fiber layer infarctions coupled with prolonged HIV infection. Despite the introduction of HAART therapy, the incidence of this optic neuropathy has not decreased;45 this may account for the unexplained vision loss seen in many AIDS patients. Most other chorioretinal opportunistic infections (pneumocystis, toxoplasmosis, varicella zoster retinitis) also occur with advanced immune deficiency. Opportunistic ocular surface disorders, caused by microsporidium, Kaposi’s sarcoma, Herpes zoster and Molluscum contagiosum, contribute to further visual morbidity. Not surprisingly, the incidence of all these diseases has dropped in the HAART era.21 HIV patients also continue to be plagued by lesser problems such as blepharitis and dry eyes.

Conclusion

The prevalence of vision loss in AIDS cohorts equals that found in general population-based studies, but when

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compared to age-matched populations, AIDS patients have a higher risk of vision loss.46 The introduction of HAART converted AIDS into a chronic disease with many patients surviving more than 15 years. The evolving need for long-term patient management makes controlling ocular complications increasingly important.

References

Gottlieb MS, Schroff R, Schanker HM, et al. Pneumocystis carinii pneumonia and mucosal candidiasis in previously healthy homosexual men: evidence of a new acquired cellular immunodeficiency. N Engl J Med. 1981; 305:1425-1431.

Masur H, Michelis MA, Greene JB, et al. An outbreak of community-acquired Pneumocystis carinii pneumonia: Initial manifestation of cellular immune dysfunction. N Engl J Med. 1981; 305:1431-1438.

Holland GN, Gottlieb MS, Yee RD, et al. Ocular disorders associated with a new severe acquired cellular immunodeficiency syndrome. Am J Ophthalmol. 1982; 93:393-402.

Holland GN, Buhles WC, Mastre B, Kaplan HJ. A controlled retrospective study of ganciclovir treatment for cytomegalovirus retinopathy. Use of a standardized system for the assessment of disease outcome. UCLA CMV Retinopathy Study Group. Arch Ophthalmol. 1989; 107:1759-1766.

Studies of Ocular Complications of AIDS Research Group in collaboration with the AIDS Clinical Trials Group. FoscarnetGanciclovir Cytomegalovirus Retinitis Trial. 5. Clinical features of cytomegalovirus retinitis at diagnosis. Am J Ophthalmol. 1997; 124:141-157.

Jabs DA. Ocular manifestations of HIV infection. Trans Am Ophthalmol Soc. 1995; 93:623-683.

Pepose JS, Holland GN, Nestor MS, et al. Acquired immune deficiency syndrome. Pathogenic mechanisms of ocular disease. Ophthalmology. 1985; 92:472-484.

Kuppermann BD, Petty JG, Richman DD, et al. Correlation between CD4+ counts and prevalence of cytomegalovirus retinitis and human immunodeficiency virus-related noninfectious retinal vasculopathy in patients with acquired immunodeficiency syndrome. Am J Ophthalmol. 1993; 115(5):575-582. Insert

Holland GN. AIDS and Ophthalmology: the first quarter century. Am J Ophthalmol. 2008; 145:397-408.

10. Holland GN, Vaudaux JD, Shiramizu KM, et al. Characteristics of untreated AIDS-related cytomegalovirus retinitis. II. Findings in the era of highly active antiretroviral therapy (1997 to 2000). Am J Ophthalmol. 2008;145:15-22. 11. Walmsley S, Tseng A. Comparative tolerability of therapies for cytomegalovirus retinitis. Drug Saf. 1999; 21(3):203-224. 12. Lalezari J, Lindley J, Walmsley S, et al. A safety study of oral valganciclovir maintenance treatment of cytomegalovirus retinitis. J Acquir Immune Defic Syndr. 2002;30(1):392-400. 13. Jabs DA, Martin BK, Forman MS, et al. Cytomegalovirus resistance to ganciclovir and clinical outcomes of patients with cytomegalovirus retinitis. Am J Ophthalmol. 2003:135:26-34. 14. Boivin G, Gilbert C, Gaudreau A, et al. Rate of emergence of cytomegalovirus (CMV) mutations in leukocytes of patients with acquired immunodeficiency syndrome who are receiving valganciclovir as induction and maintenance therapy for CMV retinitis. J Infect Dis. 2001;184:1598-1602.

25. Kempen JH, Jabs DA, Wilson LA, et al. Mortality risks for patients with cytomegalovirus retinitis and acquired immune deficiency syndrome. Clin Infect Dis. 2003; 37:1365-1373. 26. Kempen JH, Martin BK, Wu AW, et al. The effect of cytomegalovirus retinitis on the quality of life of patients with AIDS in the era of highly antiretroviral therapy. Ophthalmology. 2003; 110:987-995. 27. Holbrook JT, Jabs DA, Weinberg DV, et al. Visual loss in patients with cytomegalovirus retinitis and acquired immunodeficiency syndrome before widespread availability of highly active antiretroviral therapy. Arch Ophthalmol. 2003; 121:99-107. 28. Ortega-Larrocea G, Espinosa E, Reyes-Teran G. Lower incidence and severity of cytomegalovirus-associated immune recovery uveitis in HIV-related patients with delayed highly active antiretroviral therapy. AIDS. 2005; 19(7):735-738. 29. Thorne JE, Holbrook JT, Jabs DA, et al. Effect of cytomegalovirus retinitis on the risk of visual acuity loss among patients with AIDS. Ophthalmology. 2007; 114:591-598.

15. Martin BK, Ricks MD, Forman MS, Jabs DA. Change over time in incidence of ganciclovir resistance in patients with cytomegalovirus retinitis. Clin Infect Dis. 2007; 44(7):10011008.

30. Benson CA, Kaplan JE, Masur H, et al. Treating opportunistic infections among HIV-infected adults and adolescents: recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association/Infectious Diseases Society of America. MMWR Recomm Rep. 2004; 53:1-112.

16. Cochereau-Massin I, Lehoang P, Lautier-Frau M, et al. Efficacy and tolerance of intravitreal ganciclovir in cytomegalovirus retinitis in acquired immune deficiency syndrome. Ophthalmology. 1991; 98:1348-1353.

31. Holland GN. Discussion of MacDonald JC, Karavellas MP, Torriani FJ, et al. Highly active antiretroviral therapy-related immune recovery in AIDS patients with cytomegalovirus retinitis. Ophthalmology. 2000; 107:877-833.

17. Diaz-Llopis M, Espana E, Munoz G, et al. High dose intravitreal foscarnet in the treatment of cytomegalovirus retinitis in AIDS. Br J Ophthalmol. 1994; 78:120-124.

32. Wohl DA, Kendall MA, Owens S, et al. The safety of discontinuation of maintenance therapy for cytomegalovirus (CMV) retinitis and incidence of immune recovery uveitis following potent antiretroviral therapy. HIV Clin Trials. 2005; 6:136-146.

18. Kempen JH, Jabs DA, Wilson LA, et al. Risk of vision loss in patients with cytomegalovirus retinitis and the acquired immunodeficiency syndrome. Arch Ophthalmol. 2003; 121:466-476. 19. Johns Hopkins School of Public Health, http://statepiaps.jhsph. edu/wihs/Invest-info/Def-haart.pdf. Accessed September 2009. 20. Jabs DA. AIDS and Ophthalmology in 2004. Arch Ophthalmol. 2004; 122:1041-1042. 21. Jabs DA, van Natta ML, Holbrook JT, et al. Longitudinal study of the ocular complications of AIDS. 1. Ocular diagnoses at enrollment. Ophthalmology. 2007;114:780-786. 22. Jacobson MA, Stanley H, Holtzer C, et al. Natural history and outcome of new AIDS-related cytomegalovirus retinitis diagnosed in the era of highly active antiretroviral therapy. Clin Infect Dis. 2000; 30:231-233. 23. Jabs DA, van Natta ML, Thorne, et al. Course of cytomegalovirus retinitis in the era of highly active antiretroviral therapy: 1. Retinitis progression. Ophthalmology. 2004; 111:2224-2231. 24. Jabs DA, van Natta ML, Thorne JE, et al. Course of cytomegalovirus retinitis in the era of highly active antiretroviral therapy: 2. Second eye involvement and retinal detachment. Ophthalmology. 2004; 111:2232-2239.

Insert

33. Walmsley SL, Raboud J, Angel JB, et al. Long-term followup of a cohort of HIV-infected patients who discontinued maintenance therapy for cytomegalovirus retinitis. HIV Clin Trials. 2006; 7:1-9. 34. Murdoch DM, Venter WD, Van Rie A, Feldman C. Immune reconstitution inflammatory syndrome (IRIS): review of common infectious manifestations and treatment options. AIDS Research and Therapy. 2007; 4:9. 35. Kempen JH, Min YI, Freeman WR, et al. Risk of immune recovery uveitis in patients with AIDS and cytomegalovirus retinitis. Ophthalmology. 2006; 113:684-694. 36. Schrier RD, Song MK, Smith IL, et al. Intraocular viral and immune pathogenesis of immune recovery uveitis in patients with healed cytomegalovirus retinitis. Retina. 2006; 26:165-169. 37. Hirsch HH, Kaufmann G, Sendi P, et al. Immune reconstitution in HIV infected patients. Clin Infect Dis. 2004; 38:1159-1166. 38. Jabs DA, Van Natta ML, Holbrook JT, et al. Longitudinal study of the ocular complications of AIDS. 2. Ocular examination results at enrollment. Ophthalmology. 2007;114:787-793.

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39. Kempen JH, Min YI, Freeman WR, et al. Risk of immune recovery uveitis in patients with AIDS and cytomegalovirus retinitis. Ophthalmology. 2006; 113:684-694. 40. Thorne JE, Jabs DA, Kempen JH, et al. Incidence of and risk factors for visual acuity loss among patients with AIDS and cytomegalovirus retinitis in the era of highly active antiretroviral therapy. Ophthalmology. 2006; 113:1423-1440. 41. French MA. The immunopathogenesis of mycobacterial immune restoration disease. Lancet Infect Dis. 2006; 6:461-462. 42. Karavellas MP, Plummer DJ, MacDonald JC, et al. Incidence of immune recovery vitritis in cytomegalovirus retinitis patients following institution of successful highly active antiretroviral therapy. J Infectious Dis. 1999; 179:697-700. 43. Westeneg AC, Rothova A, De Boer JH, Groot-Mijnes JD. Infectious uveitis in immunocompromised patients and the diagnostic value of polymerase chain reaction and GoldmannWitmer coefficient in aqueous analysis. Am J Ophthalmol. 2007; 144:781-785. 44. Tenhula WN, Xu S, Madigan MC, Heller K, Freeman WR, Sadun AA. Morphometric comparisons of optic nerve axon loss in acquired immunodeficiency syndrome. Am J Ophthalmol. 1991; 113(1):14-20. 45. Freeman WR, Van Natta ML, Jabs D, et al. Vision function in HIV-infected individuals without retinitis: report of the Studies of Ocular Complications of AIDS Research Group. Am J Ophthalmol. 2008; 145(3):453-462. 46. Eye Diseases Prevalence Research Group. Causes and prevalence of visual impairment among adults in the United States. Arch Ophthalmol 2004;122:4787-485.

it’s time for the 2011 BeAls & shAhin AwArds! John A. BeAls AwArd for medicAl reseArch

Articles submitted for the Beals Award must have been written by a member of the Duval County Medical Society, based on work done in Duval County. They must have been published between January 2010 and December 2010 in a peer reviewed periodical listed in the MEDLINE / PubMed journal database.

G. shAhin AwArd

for reseArch By A physiciAn in trAininG in duvAl county

Articles submitted for the G. Shahin Award must have a resident or fellow in training in Duval County as the lead author. The majority of the work must have been done while the resident or fellow was training in Duval County. They must have been published between January 2010 and December 2010 in a peer reviewed periodical listed in the MEDLINE / PubMed journal database.

Beals and Shahin Awards will be considered in three categories: • Original Investigation • Clinical Observation • Review Articles

suBmission deAdline is August 5, 2011. All winners will be recognized and receive plaques at the DCMS / Navy Meeting in late September. Winners in the Original Investigation categories also receive monetary awards. Please visit the DCMS website (www.dcmsonline.org) and follow the Beals / Shahin link (under “Quick Links”) to submit your article for consideration. You will be asked to complete a brief form with contact information, award category, and publication details, and if available, email a PDF file of your article as it appeared in print or electronically.

If you have questions, please contact Marigrace Doran at 355-6561 ext. 101 or mdoran@dcmsonline.org. 8 Vol. 62, No. 2 2011

Northeast Florida Medicine

Insert

one can have inflammation of the cornea or Transient Light Sensitivity Syndrome (TLSS). Epithelial in-growth (an extension of epithelium into the stroma),22 infection, glare, and halos can occur. The most common postoperative complaint is dry eye. This is best prevented by performing proper analysis pre-operatively. Regression, a return toward the original refractive error, is infrequent with current lasers. The worst late-onset (rare) complication, is corneal ectasia (keratoconus). If the cornea is too thin, there can be loss of its biomechanical stability due to bowing of the cornea and decreased vision. This risk is reduced with preoperative corneal topography which measures thickness throughout the cornea, and demonstrates any subtle irregularities. Ectasia is treated with rigid contact lenses, corneal surgery (intacs), corneal transplant, or a new treatment developed in Europe, but not yet FDA approved, called collagen cross-linking.23 The average onset of this complication is normally 12 to 14 months after surgery, but can take years.24

Presbyopia

affect and increases the depth of focus. An advantage of this technique is that it is reversible and interchangeable28 and can treat patients with excellent distance vision who wish to be spectacle free for reading.

Conclusion

Over the past decade, refractive surgery has improved the quality of life in over 28 million patients with a > 95% patient satisfaction rate29 and made it one of the most popular elective surgery procedures in all of medicine. It is considered safe and has been approved by the military for Navy pilots and NASA astronaut candidates.30 Presbyopia treatment will continue to improve. If the present direction and volume of research is any guide, a large proportion of tomorrow’s femtosecond technological advances and discoveries will be based on our mastery of treating refractive errors without even touching the cornea. All treatment will be intrastromal.

References

Sakimoto T, Rosenblatt, MI, Axar DT. Laser eye surgery for refractive errors. Lancet. 2006, 367(9520):1432-47.

Dr. Slava Fyodorov, Sante Fe, New Mexico, Nov. 1980, Personal conversation.

Dr. Leo Bores, Sante Fe, New Mexico, Nov. 1980, Personal conversation.

Presbyopia is a condition of the eye in which the ability to focus on nearby objects is gradually lost beginning around age 40. The treatment for presbyopia has long been monovision. Monovision is a state in which the dominant eye is often treated for distance and the non-dominant eye is treated for both reading and computer vision. Roughly 75% of patients adjust to monovision quite well. Occasionally night driving is problematic due to loss of stereopsis or depth perception. If it is noticeable, glasses for night driving are a viable option. With advancing age, the degree of presbyopia increases and this can affect the eye corrected for near vision.

Trokel SL, Srinivasan R, Braren B. Excimer laser surgery of the cornea. AM J Ophthalmol. 1983, 96:710-15.

Arons I. Summit Technology, Visx and Pillar Point Partners. Iry Arons Journal. May 2006.

Seiler T, Kahle G, Kriegrowski M. Excimer laser (193 nm) myopic keratomileusis in sighted and blind human eyes. Refract. Corneal Surg. 1990, 6:383-85.

The Final Frontier

McDonald MB, Kaufman HE, Frantz JM et al. Excimer laser ablation in a human eye. Arch Ophthalmol. 1989 107:641-42.

Krueger Ronald R, Rabinowitz, Yaron S, Binder Perry S. The 25th Anniversary of Excimer Lasers in Refractive Surgery, J Refract. Surg. Oct 2010, 26:749-60.

Ruiz L, Rowsey JJ. In-situ keratomileusis, Invest. Ophthalmol. Vis. Sci. 1988, 29:5392.

The final frontier is finding a better treatment for presbyopia. There are several procedures on the horizon to treat presbyopia. The objective is to have good distance and near vision in each eye rather than monovision in which one eye is for distance and the other eye is for near vision. Roberto Pinelli of Italy described his technique for presbyLASIK, an excimer laser-based procedure to create a multifocal cornea to improve distance and near vision.25,26 It can be performed with PRK or LASIK. A myopic treatment with a smaller, central treatment zone is combined with a hyperopic treatment of a larger zone resulting in a multifocal cornea. Although this procedure is presently being performed by some eye surgeons, it is not yet FDA approved. Another area of research for presbyopia is intrastromal laser refractive surgery with the femtosecond laser. This involves the removal of a lenticle of corneal stroma without creating a flap or touching the surface of the cornea (intraCOR) creating a multifocal cornea by making circular intrastromal rings that steepen the central cornea improving the patients reading vision and depth of focus. Ruiz treated 245 eyes with the intraCOR and reported 100% improvement of near vision.27 The intracorneal Inlay, a 10 micron thick device placed in the mid-cornea under a LASIK type flap creates a pinhole www . DCMS online . org

10. Buratto L, Ferrari M, Genisi C. Myopic keratomileusis with the excimer laser: one-year follow up. Refract Corneal Surg. 1993, 9:12-19. 11. Pallikaris IG, Papatzanaki ME, Stathi EZ, Frenschock O, Georgiadis A. Laser in-situ keratomileusis. Lasers Surg Med. 1990, 10:463-68. 12. Juhasz T, Loesel FH, Kurtz RM, et al. Corneal refractive surgery with femtosecond lasers. J Sel Topics Quantum Electron. 1999, 5: 902-10. 13. Ratkay-Traub I, Ferincz IE, Juhasz T, et al. First clinical results with the femtosecond neodymium-glass laser in refractive surgery. J Refract Surg. 2003, 19:94-102. 14. McLeod SD, Tham V, M-B, Phan ST. Bilateral difuse lamellar keratitis following bilateral simultaneous versus sequential laser in-situ keratomileusis. Br. J. Ophthmol. 2003, 87:1086-87. 15. Stoncipher KG, Dishler JG, Ignacio TS, et al. Transient light sensitivity after femtosecond laser flap creation: clinical findings and management. J Cataract Refract. Surg. Jan 2006, 32:91-94. 16. Binder Perry. AMO’s New IFS Advanced Femtosecond Laser – Faster, Safer, More Versatile. Refractive Eye Care. May 2008, 12:16-21. Northeast Florida Medicine Vol. 62, No. 2 2011 23

17. Soloman KD, Fernandez LE, Sandoval HP, et al. Lasik world literature review. Ophthalmology Annual. 2009, 119:691-701. 18. Chalita MR, Xu M, Krueger RR. Correlation of aberrations with visual symptoms using wavefront analysis in eyes after laser in-situ keratomileusis. J Refract. Surg. 2003, 19:S682-86. 19. Stonecipher KG, Kezirian GM. Wavefront-optimized versus wavefront-guided LASIK for myopic astigmatism with the ALLEGRETTO WAVE; three-month results of a prospective FDA trial. J Refrac. Surg. 2008, 24:S424-30. 20. Donnefield E. Ocular surface management for the cataract and refractive surgeon. Ocular Surg News. June 25, 2009, pp. 12-13. 21. Nakano K, Nakano E, Oliveira M. Intraoperative microkeratome complications in 47,094 laser in-situ keratomileusis surgeries. J Refract Surg. 2004, 20:S723-25. 22. Wang M, Maloney R. Epithelial ingrowth after laser in-situ keratomileusis. Am J Opthal. 2000, 129:746-51. 23. Witting-Silvac, Whiting M, Lamoureux E, et al. A randomized controlled trial of corneal collagen cross-linking in progressive keratoconus: preliminary results, J Refract Surg. 2008, 24(7): S720-25. 24. Rad AS, Jabbarvand M, Saifl N. Progressive keratectasia after laser in-situ keratomileusis. J Refract. Surg. 2004, 20(5):S71822. 25. Pinelli R, Ortiz D, Simonetto A, et al. Correction of presbyopia in hyperopia with a center-distance paracentral-near technique. J Refract. Surg. 2006, 22(5):49V-50V.

In a MEDICaL MaLPRaCTICE CLaIM: Be ready for anything and everything.

26. Gordon M. Laser presbyopic corrections with the wavelight laser. Cat. and Refract Surg. Mar 2010, 10(3): 71-72. 27. Ruiz LA, Cepeda LM, Fuentes VC. Intrastromal correction of presbyopia using a femtosecond laser system, J Refract. Surg. 2009, 25:847-54. 28. Binder P. WOC debates the future of refractive surgery. Eurotimes. June 29, 2008, pp. 3-4. 29. Soloman KD, Fernandez LE, Sandoval HP, et al. Lasik world literature review. Ophthalmology Annual. 2009, 116:691-701. 30. Stanley PF, Tanzer DJ, Schallhorn SC. Laser refractive surgery in the United States Navy. Curr. Opin. Ophthalmol. 2008, 19(4):321-324.

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Contact Barbara Braddock at membership@dcmsonline.org 24 Vol. 62, No. 2 2011 Northeast Florida Medicine

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Taking on Glaucoma: The Role of the Primary Care Physician Tina N. Tillis, MD Abstract: The goal of this article is to give an overview of glaucoma and describe how this disease and its treatment might affect other disease processes or organ systems. Armed with this information the primary care physician (PCP) should be able to recognize patients at greatest risk of developing glaucoma and better understand their role in the glaucoma patients’ maintenance of continuity of care with ophthalmologists.

Introduction

The diagnosis of glaucoma brings about a sense of dread and almost immediately stimulates visions of complete blindness – no pun intended. It is one of the leading causes of irreversible blindness worldwide.1-4 While currently there is no cure, glaucoma is treatable and does not need to lead to blindness in most cases. With appropriate treatment, glaucoma patients are likely to keep their vision or at least slow the progression of the disease and live relatively normal lives.5 The key, like most disease processes, is early detection and treatment. Except for acute angle closure glaucoma (ACG), glaucoma is largely a “silent” disease with few symptoms or signs before it has reached an advanced stage.5,6 As such, the PCP has a critical role in screening and referring patients to the ophthalmologist as part of their overall health care.

Epidemiology

Primary Open Angle Glaucoma (POAG) – It is estimated that 45 million people have OAG worldwide.5 Glaucoma (combined OAG and ACG) is the second leading cause of blindness worldwide (8.4 million people).5 In the US, the prevalence of POAG in adults over the age of 40 is 2%.7,8 It is estimated that in 2010 there were 2.2 million people in the U.S. with glaucoma and that with the aging population, this number will increase to 3.3 million by 2020.5 There are definite differences in the prevalence of glaucoma among ethnic groups.5,9-12 In the U.S. the prevalence of glaucoma in African Americans is three to four times greater than in Whites.11 It is the leading cause of blindness in African Americans.5 Hispanics and Latinos have similar prevalence rates as African Americans.5,9,10 Glaucoma is a more “aggressive” in Blacks where it tends to occur at an earlier age and is more refractory to treatment.11 Hyper-vigilance is warranted in screening African Americans and Hispanics.9,12-14 Primary Angle Closure Glaucoma (PACG) – Of the nearly 67 million patients with glaucoma worldwide, it has been estimated that 50% have ACG,2 making it the most common form of glaucoma and the leading cause of bilateral blindness in the world (but not in the U.S.).2 There is considerable difference in the prevalence of ACG among ethnic groups.6 PACG, the overwhelming predominant form of glaucoma Address Correspondence to: Tina N. Tillis, MD, University of Florida Eye Institute, 580 West 8th Street, Jacksonville, FL 322096533, Phone: (904) 244-9390. Email: tina.tillis@jax.ufl.edu. www . DCMS online . org

in East Asia, is responsible for 1.5 million or 91% of the bilateral blindness cases in China.2 The rates are lower among African Americans and people of European decent.2,6 PACG may equal POAG in prevalence in some Asian populations.6 Worldwide, 0.7% of people over the age of 40 have ACG, and it is estimated that by 2020 21 million people worldwide will have ACG.6

Risk Factors for Glaucoma

Below is a listing of some of the accepted risk factors for glaucoma: • •

• •

•

• •

•

Intraocular Pressure (IOP): For every 1mmHg rise risk increased 10%15-20 Central Corneal Thickness (CCT): The thinner (especially <550 microns) the greater risk; African Americans tend to have thinner corneas21-27 Optic Disc Cupping: Increased (vertical >horizontal) cup-disc ratio28-31 Diabetes Mellitus (DM): It remains controversial as to whether DM is associated with an increased risk of developing glaucoma32-36 Hypertension (HTN): Acute hypertension increases the risk of glaucoma while chronic HTN is less clearly associated with an increased risk of developing glaucoma37-41 Race: African Americans are much more likely to have POAG and rarely, have PACG (but when present in African Americans is much more likely to be chronic); Inuits and Asians are more likely to have PACG42,43 Age: Ocular Hypertension Treatment Study (OHTS) showed increased risk of POAG with age per decade of 22-43% (in the univariate and multivariate analyses, respectively);2 PACG is rare < 40 years old but prevalence increases each decade thereafter2,44 Gender: PCAG is 2-4 times more common in women than in men2,10 Family History: First degree relative with POAG increases risk up to 13%;5,45 First degree relative with PACG risk is different among racial groups with 1-12% prevalence in Whites and > 6 times risk in Chinese patients with any family history2 Refraction Error: Myopia (nearsightedness) risk factor for POAG; Hyperopia (farsightedness) = risk factor for PACG2,46,47

Definition

Over the years the definition of glaucoma has evolved from the simple “elevated eye pressure that causes blindness” to a more comprehensive definition: “a multi-factorial group of diseases that have in common a characteristic ‘optic Northeast Florida Medicine Vol. 62, No. 2 2011 25

Figure 1 Optic Disc Evaluation with OCT

neuropathy’ with associated ‘visual field loss’ for which elevated ‘intraocular pressure (IOP)’ is one of the primary risk factors.”2 The range for normal IOP is not a perfect bell-shaped Gaussian curve but is skewed to the right. Ninety-five percent of the general population has IOPs of 10-22mmHg with a mean of 16.2 There are patients with high IOPs who do not have glaucoma and patients who have always had low IOPs who do have glaucoma. Despite low IOPs, these patients still go on to develop optic neuropathy leading to blindness (Normal or Low Tension Glaucoma — NTG or LTG). While it is generally accepted that the etiology of glaucoma is multi-factorial, we do know that IOP plays a major role in its effect on the Optic Nerve (ON). Historically (and currently), lowering the IOP (regardless of high or low base IOP) to prevent progressive neuropathy and ganglion cell loss with resultant visual field loss has been the basis for glaucoma treatment. Clinical research studies have proven the validity of lowering the IOP in preventing or slowing the progression of visual field (VF) loss.2,5 When one hears the diagnosis of cancer, the next logical question is, what type of cancer? Similarly, the diagnosis of glaucoma should prompt the question, what type of glaucoma does the patient have? There are three basic categories of glaucoma, and while they all share some common characteristics, they also differ from one another in key areas. The categories are (1) congenital (or developmental); (2) open angle; and (3) angle closure glaucomas. Congenital glaucoma will not be discussed here for the sake of brevity. Adult glaucoma is generally divided into Primary Open Angle Glaucoma (POAG) and Primary Angle Closure Glaucoma (PACG). When there is a known underlying etiologic disease process it is categorized as a secondary glaucoma.

Clinical Glaucoma Evaluation

The elements of a good glaucoma evaluation consist of a thorough history (family, medical, medications, allergic drug reactions and review of systems). The ocular exam includes determination of best-corrected visual acuity, pupillary exam, IOP measurement, gonioscopy slit lamp

26 Vol. 62, No. 2 2011 Northeast Florida Medicine

exam, CCT measurement and careful retinal and optic nerve examination. Imaging studies of the nerve fiber layer (NFL) and optic disc head are often performed (GDX, HRT and OCT) (Figure 1).48,49 The visual field (Figure 2, p.27) is used to check for actual loss of field of vision (sometimes referred to as “peripheral vision”).

Open Angle vs. Angle Closure Glaucoma

The eye can be divided into posterior and anterior chambers separated by the lens-iris diaphragm. Aqueous humor (AH) produced by the ciliary body (CB) located in the posterior chamber (PC) (Figure 3, p.28) of the eye helps maintain the shape and firmness of the eye, provides nutrients, and clears out by-products of various biochemical reactions. AH flows from the PC around the lens, through the pupil into the anterior chamber (AC) and out through the trabecular meshwork (TM) (i.e “angle”). It is the anatomic status of this angle that determines whether glaucoma is “open” or “closed”. Anything that obstructs the TM (either by covering it or by pushing the peripheral iris against it) causes the angle to close – hence the term, angle closure (glaucoma). POAG has an “open” angle. PACG and POAG are usually hereditary. Secondary forms of OAG and ACG are the result of other factors. POAG, including LTG/NTG and pigmentary glaucoma accounts for approximately two thirds of all cases of glaucoma while PACG only accounts for 5% of U.S. cases of glaucoma.

Primary Angle Closure Glaucoma

Because of the internal reflection of light, the angle cannot be directly visualized. A mirrored goniolens(gonioscopy) allows visualization of the angle. (Figure 4, p.29) Anyone with >1800 of iridotrabecular contact (ITC) in primary gaze is at risk of angle closure.6 Ideally we would prefer to prevent an attack rather than treat an attack. IOP can be dangerously high and must be reduced as quickly as possible to avoid irreversible loss of vision. Classic signs and symptoms of acute ACG are severe pain, decreased vision, headache, tearing, halos around lights, nausea, vomiting, conjunctival hyperemia, mid-dilated pupil, shallow AC, corneal edema and extremely high IOP (>50-60 mmHg). www . DCMS online . org

Figure 2 Humphrey Visual Fields

Oral, topical and IV medication may be necessary to manage the attack initially, but unlike POAG the definitive treatment of PACG is surgical. PACG is commonly associated with pupillary block caused by anterior movement of the aging lens against the iris and “occluding” the pupil, thus blocking the flow of AH from the PC into the AC. Once blocked, a larger pressure gradient is created between the PC and AC resulting in further forward movement of the lens. A vicious cycle occurs, compounding the problem, elevating the pressure and leading to optic nerve damage. In order to break the “attack”, flow must be established between the PC and AC. This is usually accomplished by creating a small hole in the iris most commonly with a laser – laser peripheral iridotomy (LPI). This is almost always a bilateral condition despite the fact that 90% of acute cases are unilateral, so LPIs are done in both eyes.6

Primary Open Angle Glaucoma Treatment

Medical – In the U.S., initial therapy for POAG is usually medical in the form of drops since glaucoma medicines are generally more effective when applied directly to the ocular surface. Medical treatment for glaucoma (Table 1, p.30) consists of beta-blockers (Timolol, Betimol, Betagan, Betaxolol, Betoptic S), prostaglandin analogs (Lumigan, Travatan, Xalatan), alpha-agonists (Brimonidine, Alphagan P), carbonic anhydrase inhibitors (Azopt, Trusopt), and cholinergic (Pilocarpine) medications. In the last decade the prostaglandins have beaten out the beta blockers to become the most commonly prescribed class of drugs with the other classes more often used as adjunctive therapy. Combination medications such

www . DCMS online . org

as Combigan (timolol + brimonidine) and Cosopt (timolol + trusopt) have been developed in hopes of helping with patient compliance. Oral carbonic anhydrase inhibitors such as Diamox (acetazolamide) and Neptazane(methazolamide) are used in conjunction with drops for recalcitrant glaucoma and in emergency situations.5,50,51 It is important for PCPs to be aware of potential interactions of topical eye and systemic medications. Some medications prescribed by the PCP can also exacerbate glaucoma. Steroids in particular have a propensity to cause elevation of intraocular pressures even in patients who are not known to have glaucoma. These patients are referred to as “steroid responders”. Ninety-five percent of POAG patients and first-degree relatives of POAG patients are steroid responders, while only 5% of the general population are steroid responders. While the increased IOP can occur with any mode of steroid dosing (nasal, depo-injection, topical, oral), it is much more common with topical medications. Eye drops should be considered when unexplained systemic symptoms occur; specifically CNS, cardiac and pulmonary side effects or allergic reactions. Surgical – While initial therapy of POAG is usually medical, there are some cases best treated with initial laser surgery or a combination of medications and laser. More severe cases are usually treated with incisional surgery. All of these treatments are geared towards lowering the intraocular pressure either by decreasing aqueous production and/or increasing the outflow of AH from the eye. The two most common Laser Trabecloplasty (LTP) procedures are Selective Laser Trabeculoplasty (SLT) and Argon Northeast Florida Medicine Vol. 62, No. 2 2011 27

Figure 3 Anatomy of the Eye and Flow of Aqueous

Laser Trabeculoplasty (ALT). The application of the laser beam directly to the TM has been shown to increase outflow of the AH from the eye.

there is an increased risk of complications. The post-operative care is long and labor-intensive. It is not uncommon for some patients to require more than one procedure in their lifetime.

Incisional surgery is indicated when patients are on maximal tolerated medications with failure to achieve lowered target IOP; medicines are not well-tolerated; progression of visual field loss and/or optic nerve damage has occurred; or poor patient compliance is present.2

Summary

Several different surgical procedures are done to lower the intraocular pressure. They can be divided into nonpenetrating, penetrating (trabeculectomy or filtering procedure, Express Mini Shunt), various drainage tube implants (Ahmed, Molteno, Baerveldt tubes) (Figure 5, p.31) and ciliary body ablation.2 The goal of filtering surgery is to create a new pathway (fistula) for the flow of AH from the AC through the surgical defect in the sclera into the subconjunctival and sub-Tenons spaces.2 The guarded-trabeculectomy uses the sclera of the patient’s eye to create a trap door through which aqueous can escape and be absorbed by the circulatory system. Shunts or tubes of varying sizes (with or without valves) are used as external drains. With any penetrating procedure 28 Vol. 62, No. 2 2011 Northeast Florida Medicine

Glaucoma can be a devastating disease. The morbidity associated with it affects all of us from a socio-economic perspective. Those patients blinded by glaucoma become less independent and less productive citizens. When patients lose their independence, such as their ability to drive or take care of themselves, the entire family is affected. This is a chronic disease with no known cure, however treatment has been shown to be effective in slowing or preventing progression to blindness. Therefore, we have to be more proactive in fighting this disease until we find a cure. Collaboration between PCPs and Ophthalmologists is the key to taking on glaucoma and having some measure of success.

References

Congdon N, O’Colman B, Klaver CC, et al. Causes and Prevelance of Visual Impairment Among Adults in the United States. ArchOphthalmol. 2004; 122(4):477-85.

American Academy of Ophthalmology. Basic and Clinical Science Course: Glaucoma. 2005-2006; 10:3-209. www . DCMS online . org

Figure 4 Gonioscopy

Use of a gonio-lens allows visualization of the “angle” and determination of whether the angle is open or closed. (Figure, left) © 2008 American Academy of Ophthalmology. Used by permission. (Figure, right) © 2006 American Academy of Ophthalmology. Used by permission. 3.

Leibowitz HM, Krueger DE, Maunder LR, et al. The Framingham Eye Study monograph: An ophthalmological and epidemiological study of cataract, glaucoma, diabetic retinopathy, macular degeneration, and visual acuity in a general population of 2631 adults, 1973-1975. Surv Ophthalmol. 1980; 24(Suppl):335-610.

Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypetension Treatment Study: A randomized trial determines that topical ocular hypertensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002; 120:701-713.

American Academy of Ophthalmology Glaucoma Committee. Preferred Practice Patterns® Guidelines. Primary Open Angle Glaucoma. San Francisco, CA: American Academy of Ophthalmology, 2010.

American Academy of Ophthalmology Glaucoma Committee. Preferred Practice Pattern® Guidelines. Primary Angle Closure Glaucoma. San Francisco, CA: American Academy of Ophthalmology. 2010. Tsai JC, Forbes M. Epidemiology: Primary Open Angle Glaucoma. Medical Management of Glaucoma. 2nd ed. West Islip, NY: Professional Communications, Inc. 2004; pp.55-61. Klein BE, Klein R, Sponsel WE, et al. Prevalence of Glaucoma. The Beaver Dam Eye Study. Ophthalmology. 1992 Oct.; 99(10):1499-504. Varma R, Ying-Lai M, Francis BA, et al. Prevalence of open angle glaucoma and ocular hypertension in Latinos: The Los Angeles Latino Eye Study. Ophthalmology. 2004; Aug.,111(8):1439-48.

10. Rudnicka AR, Mt-Isa S, Owen CG, et al. Variations in primary open-angle glaucoma prevalence by age, gender, and race:A Bayesian Meta-Analysis. Invest. Ophthalmol. Vis. Sci. 2006 Oct.;47(10):4254-4261. 11. The Eye Diseases Prevalence Research Group. Prevalence of open-angle glaucoma among adults in the United States. Arch Ophthalmol. 2004; 122 (4):532-538. 12. Racette L, Liebmann JM, Girkin CA, et al. African Descent

www . DCMS online . org

and Glaucoma Evaluation Study (ADAGES):III. Ancestry Differences in Visual Function in Healthy Eyes. Arch Ophthalmol. 2010; 128(5):551-559. 13. Sample PA, Girkin CA, Zangwill LM. The African Descent and Glaucoma Evaluation Study (ADAGES): Design and Baseline Data. Arch Ophthalmol. 2009; 127(9):1136-1145. 14. Ryskulova A, Turczyn K, Makuc DM, et al. Self-reported age-related eye diseases and visual impairment in the United States: Results of the 2002 National Health Interview Survey. AJPH 2008; 98:454-461. 15. Leske MC, Heijl A, Hussein M, et al. Factors for glaucoma progression and the effect of treatment: The Early Manifest Glaucoma Trial. Arch Ophthalmol. 2003; 121:48-56. 16. Gordon M, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: Baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002; 120:714-720. 17. Asrani S, Zeimer R, Wilensky J, et al. Large diurnal fluctuations in intraocular pressure are an independent risk factor in patients with glaucoma. J Glaucoma. 2000 Dec; 9(6):487-8. 18. Nemesure B, Honkanen R, Hennis A, et al. Incident openangle glaucoma and intraocular pressure. Ophthalmology. 2007 Oct; 114(10);1810-5. 19. Prata TS, De Moraes CGV, Kanadani FN, et al. Posture induced intraocular pressure changes:considerations regarding body position in glaucoma patients. Surv of Ophthalmol. 2010; 55(5):445-453. 20. Bengtsson B, Leske CM, Hyman L. Fluctuation of intraocular pressure and glaucoma progression in the Early Manifest Glaucoma Trial. Ophthalmology, 2007; 114:205-209. 21. Herndon LW, Weizer JS, Stinnett SS. Central corneal thickness as a risk factor for advanced glaucoma damage. Arch Ophthalmol. 2004; 122:17-21. 22. Wu RY, Zheng YF, Wong TY, et al. Relationship of central corneal thickness with optic disck parameters: The Singapore Malay Eye Study. Invest. Ophthalmol. Vis. Sci. 2011 March; 52(3):1320-1324. Northeast Florida Medicine Vol. 62, No. 2 2011 29

Table 1 Glaucoma Medications

23. Xu L, Zhang H, Wang YX, et al. Central Corneal Thickness and Optic Disc Hemorrhages: The Beijing Eye Study. Arch Ophthalmol. 2008; 126(3):435-436. 24. Brandt JD. Corneal thickness in glaucoma screening, diagnosis and management. Curr Opin Ophthalmol. 2004 Apr;15(2);85-89. 25. Touboul D, Roberts C, Kerautret J, et al. Correlations between corneal hysteresis, intraocular pressure and corneal central pachymetry. J Cataract Refract Surg. 2008; 34(4);616-22. 26. Doughty MJ, Zaman ML. Human corneal thickness and its impact on intraocular pressure measures: a review and meta-analysis approach. Surv Ophthalmol. 2000 Mar-Apr; 44(5):367-408. 27. Shah S, Chatterjee A, Mathai M, et al. Relationship between corneal thickness and measured intraocular pressure in a general ophthalmology clinic. Ophthalmology. 1999 Nov; 106(11):2154-60. 28. Hoffmann EM, Zangwill LM, Crowston JG. Optic disc size and glaucoma. Surv Ophthalmol . 2007; 52(1):32-49. 29. Spaeth GL, Lopes JF, Junk AK, et al. Systems for staging the 30 Vol. 62, No. 2 2011 Northeast Florida Medicine

amout of optic nerve damage in glaucoma: a critical review and new material. Surv Ophthalmol. 2006; 51(4):293-315. 30. Martus P, Stroux A, Budde WM, et al. Predictive factors for progressive optic nerve damage in various types of chronic open-angle glaucoma. AJO; 139(6):999-1009. 31. Jonas JB, Budde WM, Panda-Jonas S. Ophthalmoscopic Evaluation of the optic nerve head.SurvOphthalmol; 43(4):293-320. 32. Chopra V, Varma R, Francis BA, et al. Type 2 diabetes mellitus and the risk open angle glaucoma the Los Angeles Latino Eye Study. Ophthalmology. 2008 Feb; 115(2):227232. 33. Gordon MO, Beiser JA, Kass MA. Is the history of diabetes mellitus protective against developing primary open-angle glaucoma? Arch Ophthalmol,. 2008; 126(2):280-281. 34. Kass MA, Gordon MO. Diabetes and Glaucoma. Arch Ophthalmol. 2008;126: 746-747. 35. De Voogd S, Ikram MK, Wolfs RCW, et al. Is Diabetes Mellitus a Risk factor for open-angle glaucoma?: The Rotterdam Study. Ophthalmology; 113(10):1827-1831. 36. Bonovas S, Peponis V, Filioussi K. Diabetes mellitus as a risk www . DCMS online . org

Figure 5 Tube Shunts

Various tube shunts: 1a Molteno, single and double; 1b Baerveldt; 1c Krupin; 1d Ahmed AAO. (Figures ÂŠ 2002 American Academy of Ophthalmology. Used by permission.)

factor for primary open-angle glaucoma: a meta-analysis. Diabetic Medicine. 2004; 21(6):609-614. 37. Costa VP, Arcleri ES, Harris A. Blood pressure and glaucoma. Br J Ophthalmol 2009; 93:1276-1282 doi:10.1136/bjo. 2008. 14947. 38. Bonomi L, Marchini G, Marraffa M, et al. Vascular risk factors for primary open angle glaucoma: The EgnaNeumarkt Study. Ophthalmology. 2000; 107(7): 1287-1293. 39. Werne A, Harris A, Moore D, et al. The circadian variations in systemic blood pressure, ocular perfusion pressure, and ocular blood flow: risk factors for glaucoma? Surv Ophthalmol. 2008; 53(6):559-567. 40. Sultan MB, Mansberger SL, Lee PP. Understanding the importance of IOP variables in glaucoma: a systemic review. Surv Ophthalmol. 2009; 54 (6):643-662. 41. Muskens R, Voogd S, Wolfs RC, et al. Systemic antihypertensive medication and incident open-angle glaucoma. Ophthalmology. 2007; 114(12):2221-2226. 42. Tielsch JM, Sommer A, Katz J, et al. Racial variations in the prevalence of primary open-angle glaucoma: The Baltimore Eye Survey. JAMA. 1991; 266:369-374. 43. Racette L, Wilson MR, Zangwill LM, et al. Primary openangle glaucoma in Blacks: a review. Surv Ophthalmol. 2003; 48(3): 295-313. 44. Chauhan BC, Mikelberg FS, Artes PH. Canadian Glaucoma Study: 3. Impact of risk factors and intraocular www . DCMS online . org

pressure reduction on the rates of visual field change. Arch Ophthalmol. 2010; 128(10):1249-1255.doi:10.1001/ archophthalmol.2010.196. 45. Leske CM, Connell AMS, Wu SY, et al. Risk factors for open-angle glaucoma:The Barbados Eye Study. Arch Ophthalmol. 1995; 113(7):918-924. 46. Khawaja AP. Primary open angle glaucoma. Eye Wiki.1-11. Available from: http://eyewiki.aao.org/Primary Open-Angle Glaucoma. Accessed: November 29,1010. 47. Grodum K, Heijl A, Bengtsson B. Refractive error and glaucoma. ActaOphthalmol Scand. 2001; 79:560-6. 48. Pablo LE, Ferreras A, Schlottmann PG. Retinal nerve fiber layer evaluation in ocular hypertensive eyes using optical coherence tomography and scanning laser polarimetry in the diagnosis of early glaucomatous defects. Br J Ophthalmol. 2011; 95:51-55. 49. Kim NA, Lee ES, Seong GJ, et al. Spectral domain optical coherence tomography for detection of localized retinal nerve fiber layer defects in patients with open-angle glaucoma. Arch Ophthalmol. 2010; 128(9);1121-1128. 50. Karmel M. Glaucoma Drops: Rx for Success or Trouble? EyeNet. 2009;13(3):39-43 51. Pasquale LR. Optimizing therapy for newly diagnosed openangle glaucoma: Lessons learned from the Collaborative Initial Glaucoma Treatment Study. Arch Ophthalmol. 2008; 126(1):125-127. Northeast Florida Medicine Vol. 62, No. 2 2011 31

Use of Vascular Endothelial Growth Factor Inhibitors for Retinal Disease Fred H. Lambrou, Jr., MD and Gregory M. Lewis, MD Abstract: In this paper, we will discuss the use of vascular endothelial growth factor (VEGF) inhibitors (See “Introduction” for definitions/ descriptions) for the treatment of retinal vascular occlusive disease, diabetic retinopathy, and age-related macular degeneration. Bevacizumab and ranibizumab are the most commonly used intravitreally injected VEGF inhibitors. We will review the rational and the clinical evidence supporting the use of these medications.

Introduction

Vascular endothelial growth factor (VEGF) is elevated intraocularly in many blinding retinal diseases. Bevacizumab and ranibizumab are VEGF inhibitors that can be safely injected intravitreally. They have been shown to be effective in treatment of retinal vein occlusions, diabetic retinopathy and age-related macular degeneration. In these conditions, VEGF inhibitors cannot only reduce the risk of blindness but also improve vision. Patients must be followed carefully with possible monthly injections. Vascular endothelial growth factor (VEGF) inhibitors have been used for retinal diseases since 2004. They have revolutionized the treatment of many macular diseases and have given us treatments for blinding diseases for which we previously had no therapy. VEGF contributes to retinal vascular angiogenesis, tortuosity and hyperpermeabiltiy.1

Bevacizumab (Avastin) is a full-length humanized monoclonal antibody that binds to all subtypes of VEGF.2 Ranibizumab (Lucentis) developed for intraocular use, is an antigen-binding fragment (Fab) derived from the same parent molecule as bevacizumab that also binds to all subtypes but with greater affinity than bevacizumab.

Intravitreal Injections

The thought of an intravitreal injection is disconcerting and most patients’ first response is often “You’re going to stick a needle in my eye?” However, most patients tolerate the injection extremely well. The technique involves the use of topical anesthetic drops followed by placement of a lid speculum. Following this, some practitioners give a subconjunctival injection of 2% lidocaine, while others use viscous tetracaine and/or a 4% lidocaine-soaked pledget. The eye is then sterilized with 5% povidone iodine and often flushed with antibiotic drops. A 30-gauge needle is inserted through the pars plana into the vitreous cavity and 0.05 mL of solution of ranibizumab (0.5 mg) or bevacizumab (1.25 mg) is injected. The needle is removed and the optic nerve is checked for adequate perfusion by indirect ophthalmoscopy, or the intraocular pressure is checked. The patient is allowed Address Correspondence to: Dr. Fred H. Lambrou, Jr., or Dr. Gregory M. Lewis, Retina Associates, PA, 2 Shircliff Way, Suite 715, Jacksonville, FL 32204. Phone: 904-388-8446. 32 Vol. 62, No. 2 2011 Northeast Florida Medicine

to go home resuming normal activities. Injections are given monthly or as needed and careful follow-up is required to maintain vision. Complications of intravitreal injections are rare. The most feared complication is endophthalmitis. This has been reported to occur in approximately 1 per 2000 injections. Other complications, such as intraocular inflammation, retinal detachment, retinal tear or vitreous hemorrhage, are also uncommon and occur in less than 1% of injections. The most common complication seen is subconjunctival hemorrhage. This can be upsetting for the patient as the conjunctiva turns beet red. However, it clears spontaneously and causes no permanent sequelae. Another feared complication is the occurrence of a cardiovascular event. In patients receiving bevacizumab intravenously for metastatic colon cancer, cardiovascular events have been shown to occur at a higher frequency than patients on placebo. With intravitreal injections, however, there does not seem to be an increased risk of cardiovascular events with treatment versus sham injection. 3

Diabetic Retinopathy

Diabetic retinopathy is the most common cause of blindness among working age adults in the United States,4 causing 12,000 to 24,000 new cases of blindness annually.5 Mild to moderate vision loss from diabetic retinopathy is usually due to diabetic macular edema (DME).6 Diabetic vision loss can also occur from proliferative diabetic retinopathy when vitreous hemorrhage or traction retinal detachment occurs. Microvascular damage occurs in diabetics as hyperglycemia causes apoptosis of glial cells, pericytes, and endothelial cells. Hyperglycemia also causes leukostasis, increased production of VEGF, and loss of tight junction proteins. Subsequently, retinal vessels develop occlusions and leaky microaneurysms, leading to DME.7 Until recently, the mainstay of treatment of DME was laser photocoagulation, studied in the Early Treatment Diabetic Retinopathy Study (ETDRS).8 In this study laser was applied directly to leaking microaneurysms and in a grid pattern to areas of microaneurysm clusters or capillary nonperfusion when macular thickening was seen near the center of the macula. Treatment was repeated 4 months later if edema persisted. Photocoagulation reduced the risk of moderate visual loss from diabetic macular edema by half, from 24% to 12%, 3 years after initiation of treatment; however, visual improvement was minimal. The past few years have seen an increase in the number of treatment options available for treating diabetic macular edema. In the early 2000’s many retina specialists began using intravitreally injected triamcinolone as an adjunct to laser for macular edema. Corticosteroids inhibit inflammation and www . DCMS online . org

leukostasis, upregulate production of tight junction proteins, and suppress production of VEGF.9,10 Recently, however, this treatment has begun to fall out of favor based on the results of the Diabetic Retinopathy Clinical Research Network (DRCR.net) study, a randomized, multicenter clinical trial. The DRCR.net Steroid vs. Laser Study for DME study compared 1 mg and 4 mg preservative-free triamcinolone intravitreal doses to macular laser photocoagulation, all repeated every 4 months, as needed.11,12 Although the steroid groups did better in the first few months, laser was superior thereafter. At 3 years, 26% percent of patients in the photocoagulation group gained 15 or more letters of vision (on an ETDRS chart), vs. 21% of patients treated with triamcinolone. Only 8% of patients treated with laser lost 15 or more letters of vision, as opposed to 16% of patients treated with triamcinolone. The incidence of cataract and increased intraocular pressure (IOP) was lower with laser compared to triamcinolone. Unlike intravitreal triamcinolone, intravitreal injection of anti-VEGF medications has shown superiority to laser.13 The BOLT study, reporting in 2010, is a 2-year clinical trial supporting the use of intravitreal bevacizumab in patients with DME compared to focal laser.14 Patients receiving bevacizumab gained a median of 8 ETDRS letters, compared with the a median loss of 0.5 ETDRS letters for the laser group (P=.0002). At 12 months, central macular thickness decreased from baseline significantly more in the bevacizumab group than in the laser group. The DRCR.net trial studied intravitreal ranibizumab, either with prompt or deferred (24 weeks) focal/grid laser, as compared with laser alone and with triamcinolone plus prompt laser.13 At both 1 and 2 years follow-up, nearly 50% of DME patients who received 0.5 mg intravitreal ranibizumab plus laser experienced > 10 ETDRS letters of visual improvement, vs. only 28% in the laser plus sham group and about 30% in the intravitreal triamcinolone plus laser group. Patients receiving triamcinolone also had a high frequency of increased IOP (50%) and cataracts requiring surgery (60%). The subgroup of pseudophakic patients receiving triamcinolone, plus laser, had similar visual gains to the ranibizumab groups, but increased IOP was still a major concern. The RESTORE Phase 3 trial is a randomized, double-blinded, multicenter, laser-controlled trial comparing ranibizumab monotherapy with laser monotherapy and with ranibizumab plus laser.15 The study includes 345 patients. Treatment initiation with ranibizumab includes three consecutive monthly injections with subsequent injections given as needed. At 12 months there is no significant difference in morphologic or functional response between the ranibizumab mono-and combination therapy groups. Thirty-seven percent of the ranibizumab monotherapy group and 43% of the combination therapy group have gained >10 ETDRS letters of visual acuity, vs. only 16% in the laser monotherapy group. Bevacizumab is occasionally also used off-label to treat neovascularization in diabetic retinopathy when opaque www . DCMS online . org

ocular media such as cataract, cloudy cornea, or vitreous hemorrhage, prevent panretinal photocoagulation. This is often helpful in preparation for vitrectomy surgery to remove vitreous hemorrhage.16

Retinal Vein Occlusions

Retinal vein occlusions (RVO) are the second most common type of retinal vascular disease behind diabetic retinopathy.17 They include branch retinal vein occlusion (BRVO), hemiretinal vein occlusion (HRVO), and central retinal vein occlusion (CRVO). Intraocular VEGF levels have been found to be elevated in RVO.18,19 CRVO is the most debilitating type of vein occlusion. It has been known as giving a “blood and thunder” picture of the fundus, as there is marked intraretinal hemorrhaging in all quadrants. It occurs in 0.1% to 0.5% of adults and is further subcategorized into ischemic versus non-ischemic CRVO. Visual loss is often caused in ischemic central retinal vein occlusions by the development of retinal or iris neovascularization, leading to vitreous hemorrhage or neovascular glaucoma. In non-ischemic CRVO, the altered capillary network of the macula leads to significant vascular leakage and macular edema. Prior to the development of VEGF inhibitors, therapy was performed by photocoagulation. In ischemic central vein occlusion, ischemic retina could undergo panretinal photocoagulation (PRP) leading to regression of neovascularization. An injection of a VEGF inhibitor can markedly and quickly cause regression of neovascularization. These patients may require multiple injections at monthly intervals in order to keep the neovascularization regressed.20 The treatment of macular edema in CRVO has been revolutionized by the development of VEGF inhibitors. Photocoagulation is of no benefit in improving visual acuity in patients with macular edema from CRVO.20 The CRUISE study, “Ranibizumab for the Treatment of Macular Edema After Central Retinal Vein Occlusion Study: Evaluation and Efficacy and Safety”, was a phase III, multicenter trial comparing intravitreal ranibizumab with sham injection.21 The CRUISE randomized patients between sham injection, 0.3 mg of ranibizumab and 0.5 mg of ranibizumab. Patients received injections monthly for 6 injections, followed by monthly follow-up in the observation period. After 6 months, patients could receive additional ranibizumab injections if they had evidence of macular edema. The results of this study showed a significant improvement in visual acuity in patients receiving ranibizumab versus sham injections, with approximately 50% of patients having improved greater than 15-letter improvement in visual acuity from baseline in treated patients versus 33% in untreated patients. Bevacizumab has also been shown to be of help for the treatment of macular edema in CRVO. In one study, 86 eyes had 24 months of follow-up, with 57% showing improvement in visual acuities.22 BRVOs are also a common cause of visual loss. Traditional therapy in patients with macular edema from BRVO includes Northeast Florida Medicine Vol. 62, No. 2 2011 33

photocoagulation or observation.17,23 The natural history of BRVO indicates that 74% may improve spontaneously by two lines within 6 months. In patients whose vision does not spontaneously improve, the Branch Vein Occlusion Study showed that grid laser treatment to the macula could decrease macular edema and improve visual acuity.24 This improvement was very slowly achieved and only modestly beneficial. Since the publication of this study in 1984, grid photocoagulation has been the mainstay of therapy for this condition. More recently, the BRAVO study has shown that ranibizumab injections dramatically improve visual acuity. Like the CRUISE study, patients were randomized between sham injection, 0.3 mg of ranibizumab and 0.5 mg of ranibizumab. They received monthly injections for 6 months followed by a 6-month observation period where they could obtain additional monthly treatment if they demonstrated macular edema. The results indicated that both doses of ranibizumab cause an increase in visual acuity in approximately 60% of patients. This was a statistically significant increase above the 44% increase in sham injections at 12 months. Like the CRUISE study, complications were rare.24

Age Related Macular Degeneration

Perhaps the most dramatic use of VEGF inhibitors is in the treatment of age-related macular degeneration (AMD). AMD causes severe, irreversible vision loss and is the leading cause of blindness in Americans over the age of 65.25,26 It is divided into two subtypes, dry macular degeneration and neovascular macular degeneration (“wet” AMD). In neovascular AMD, choroidal neovascularization breaks through Bruch’s membrane and the retinal pigment epithelial cells to get into the subretinal space. There the neovascularization can leak serous fluid or bleed into the retina. VEGF inhibitors have revolutionized our treatment of neovascular AMD. Left untreated, this neovascularization would grow, bleed and form a large, permanent scar in the central portion of the macula (Figure 1). This leads to a large central scotoma with severe visual loss and is responsible for

Figure 1 Disciform Macular Scar

80% of severe visual loss from AMD. Prior to 2000, there was no treatment which could prevent visual loss in patients with neovascular AMD in which the neovascularization was growing in the subfoveal location. In 2000, the Food and Drug Administration approved verteporfin (Visudyne) for use in photodynamic therapy. Using this technique, the choroidal neovascular membrane could be destroyed and prevent visual loss in approximately 60% of patients. However, visual improvement was rare, occurring in only 4%.27 In 2004, pegaptanib sodium (Macugen) was approved. This is an intravitreally injected selective VEGF inhibitor of the 165 isoform of VEGF–A. Because of its selectivity, it did not have profound inhibitory effect. Its results were an improvement over photodynamic therapy, but it was still lacking. In 2006, ranibizumab was approved for the treatment of neovascular macular degeneration. Two pivotal studies demonstrated the dramatic effect of ranibizumab on neovascular AMD, the MARINA study and the ANCHOR study.3,28 Both studies compared ranibizumab with photodynamic therapy and both showed a dramatic improvement in vision in 40% of patients with ranibizumab as compared to 4% of photodynamic therapy patients. It also showed that 95% of patients had a stabilization of vision with ranibizumab. Both studies showed very few serious adverse effects of intravitreal ranibizumab. Similarly in 2006, bevacizumab was first used intravitreally for the treatment of neovascular AMD. Small studies have shown similar results to the ranibizumab studies. In both the ANCHOR and MARINA studies, patients were treated monthly with intravitreal injections. Through the years, however, the general feeling of retina surgeons was that monthly injections were not always needed. Consequently, surgeons around the world have experimented with altering the dosing schedule, and, currently, the most common method of dosing is to follow patients monthly and to treat only if there is evidence of active neovascularization. Patients are examined clinically as well as with Optical Coherence Tomography (OCT) to look for evidence of activity such as, the presence of subretinal or intraretinal fluid, or the presence of hemorrhage (Figure 2,p.35). If any of these findings are present, patients are given an injection; otherwise, they are observed and followed. Another study called the PIER study looked at giving patients three monthly injections followed by quarterly injections.29 This study showed that, although patients could initially get an improvement in visual acuity, the improvement was lost by the end of 12 months. For this reason, it is vitally important to follow patients closely with clinical examination and OCT to monitor their visual and retinal status.

Retinal photo showing a disciform macular scar in a patient with neovascular age-related macular degeneration.

34 Vol. 62, No. 2 2011 Northeast Florida Medicine

Another controversy in the use of VEGF inhibitors is whether bevacizumab is equivalent to ranibizumab. The Comparison of Age-related macular degeneration Treatment Trials (CATT study) compared ranibizumab and bevacizumab www . DCMS online . org

Figure 2 Optical Coherence Tomograph (OCT)

(Top, left) OCT showing the presence of sub-retinal fluid in a patient with neovascular AMD. Visual acuity is 20/200. (Top, right) OCT in the same patient following treatment with ranibizumab showing resolution of sub-retinal fluid. Visual acuity has improved to 20/30. (Left) OCT in the same patient showing recurrence of sub-retinal fluid. Visual acuity has dropped to 20/50.

and showed that bevacizumab is equivalent to ranibizumab when given monthly for 12 months. It also compared the as needed dosing schedule with monthly injections. In this arm of the study, as needed bevacizumab was slightly inferior to as needed ranibizumab. However, the difference was not clinically significant. The data comparing the safety of both drugs showed no difference although the numbers studied were too small to make any definitive conclusion as serious complications are rare.30 This study will give retina surgeons confidence to use bevacizumab as it costs 40 times less than ranibizumab. Another VEGF inhibitor has just completed phase III trials. It is a VEGF trap (Afibercept, Regeneron Pharmaceuticals, Inc.) which binds VEGF and prevents it from attaching to its receptors.31 The advantage of the VEGF trap is that it has a dosing schedule allowing for injections every two months. The phase III study has shown it to be “non-inferior” to monthly ranibizumab.

Retina Study Group at 6-month follow-up. Ophthalmology. 2007;114:743-750. 2.

Emerson MV, Lauer AK. Emerging therapies for the treatment of neovascular age-related macular degeneration and diabetic macular edema. BioDrugs. 2007;21:245-257.

Rosenfeld PJ, Brown DM, Heier JS, et al. Ranibizumab for neovascular age-related macular degeneration. New England J Med 2006; 355:1432-44.

Practice Patterns: Diabetic Retinopathy. San Francisco, CA: American Academy of Ophthalmology; 2003.

National Diabetes Statistics, 2007. National Diabetes Information Clearinghouse, 2008.

Bhagat N, Grigorian RA, Tutela A, Zarbin MA. Diabetic macular edema: pathogenesis and Treatment. Surv Ophthalmol. 2009;54(1):1-Preferred 32.

Singh A, Stewart JM. Pathophysiology of Diabetic Macular Edema. International Ophthalmology Clinics. 2009;49(2):1-11.

Early Treatment Diabetic Retinopathy Study Research Group. Treatment techniques and clinical guidelines for photocoagulation of diabetic macular edema. Early Treatment Diabetic Retinopathy Study Report Number 2. Early Treatment Diabetic Retinopathy Study Research Group. Ophthalmology. 1987;94(7):761-74.

Audren F, Tod M, Massin P, et al. Pharmacokineticpharmacodynamic modeling for the effect of triamcinolone acetonide on central macular thickness in subjects with diabetic macular edema. InvestOphthalmol Vis Sci. 2004;45(10):34353441.

Conclusion

VEGF inhibitors have dramatically altered retinal treatment. In the 1980s and 1990s, laser was the mainstay for slowing vision loss from retinal vascular diseases, but it rarely led to visual improvement. VEGF inhibitors are a tremendous breakthrough because study after study shows improving visual acuity. They have also allowed us to treat blinding conditions which had no treatment prior to their development, such as macular edema in central retinal vein occlusion. Currently used VEGF inhibitors are very safe, both systemically and ophthalmologically, but the need for monthly injections is a significant obligation for many patients. Advances will continue to be made with longer-acting drugs on the horizon. 1.

References

Arevalo, JF, Fromow-Guerra J, Quiroz-Mercado H, et al. Primary intravitreal bevacizumab (Avastin®) for diabetic macular edema: results from the Pan-American Collaborative

www . DCMS online . org

10. Kuo C, Gillies M Role of Steroids in the Treatment of Diabetic Macular Edema International Ophthalmology Clinics. 2009;49(2):121-134. 11. Diabetic Retinopathy Clinical Research Network. A randomized trial comparing intravitreal triamcinolone acetonide and focal/grid photocoagulation for diabetic macular edema. Ophthalmology. 2008;115:1447-1459. 12. Diabetic Retinopathy Clinical Research Network, Beck RW, Edwards AR, et al. Three-year follow-up of a randomized trial comparing focal/grid photocoagulation and intravitreal triamcinolone for diabetic macular edema. Arch Ophthalmol. 2009;127:245-251. Northeast Florida Medicine Vol. 62, No. 2 2011 35

13. Diabetic Retinopathy Clinical Research Network. Randomized trial evaluating ranibizumab plus prompt or deferred laser or triamcinolone plus prompt laser for diabetic macular edema. Ophthalmology. 2010;117:1064-1077. 14. Michaelides M, Kaines A, Hamilton RD, et al. A prospective randomized trial of intravitreal bevacizumab or laser therapy in the management of diabetic macular edema (BOLT Study): 12-month data report 2. Ophthalmology. 2010;117:1078-1086. 15. Lang G. on behalf of the RESTORE study group. Safety and efficacy of ranibizumab as monotherapy or adjunctive to laser photocoagulation in diabetic macular edema: 12-month results of the RESTORE study. Late-breaker presentation at EASDec Meeting. May 22, 2010. 16. Nicholson BP, Schachat AP A review of clinical trials of antiVEGF agents for diabetic retinopathy.Graefes Arch Clin Exp Ophthalmol. 2010;248(7):915-30. 17. Klein R, Moss SE, Meuer SM, Klein BE. The 15-year cumulative incidence of retinal vein occlusion: The Beaver Dan Eye Study. Arch Ophthalmol 2008;126:513-8. 18. Noma H, Funatsu H, Yamanstu M, et al. Pathogenesis of macular edema with branch retinal vein occlusion and intraocular levels of vascular endothelial growth factor and interleukin-6. AM J Ophthalmol 2005;140:256-61. 19. Campachiaro PA, Hufiz G, Shah SM, et al. Ranibizumab for macular edema due to retinal vein occusions: Implications of VEGF as a critical stimulator. Mol Ther 2008; 16:791-9. 20. Evaluation of grid pattern photocoagulation for macular edema in central vein occlusion. The Central Vein Occlusion Study Group M report. Ophthalmology 1995; 102:1425-33. BW ad:ad 4/19/11 4:16 PA, PM Sinch Page 21. Brown DM, Campochiaro RP,1et al. Ranibizumab

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for Macula Edema following Central Retinal Vein Occlusion: Six Month Primary End Point Results of a Phase III study. Ophthalmology 2010;117(6):1124-1133. 22. Lihteh, W, Arevalo F, Berrocal M, et al. Comparison of Two Doses of Intravitreal Bevacizumab as Primary Treatment for Macular edema Secondary to Central retinal Vein Occlusion Results of the Pan American Collaborative Retina Study Group at 24 Months; Retina 2010; 30:1002-1011. 23. Branch vein occlusion Study Group. Argon laser photo coagulation for macular edema in branch retinal vein occlusion. Am J Ophthalmol 1984;98-271-82. 24. Campochiaro PA, Heier JS, Feiner L, et al. Ranibizumab for Macular Edema following Branch Retinal Vein Occlusion. Six-month Primary End Point Results of a Phase III Study; Ophthalmology 2010;117:1102-1112. 25. Bressler, NM. Age-related macula degeneration is the leading cause of blindness. JAMA 2004;291:1900-1. 26. Friedman DS, O’Colmain BJ, Monoz B, et al. Prevalence of age-related macular degeneration in The United States. Arch Ophthalmol. 2004;122:564-72. 27. Treatment of Age-related Macular Degeneration with Photodynamic Therapy (TAP) Study Group. Photodynamic Therapy of subfoveal choroidal neovascularization in age-related macular degeneration with Vereporfin: One-year results of 2 randomized clinical trials – TAP report. Arch. Ophthalmol. 1999;117:1329-45. 28. Brown DM, Michels M, Kaiser PR, et al. Ranibizumab versus verteporfin photodynamic therapy for neovascular age-related macular degeneration: Two-year results of the ANCHOR study. Ophthalmology 1009; 116:57-65. 29. Regillo CD, Brown DM, Abraham P, et al. Randomized, double masked, sham - controlled trial of ranibizumab for neovascular age-related macula degeneration: PIER study 1. AmJ Ophthalmol. 2008;145:239-248. 30. The CATT Research Group Ranibizumab and Bevacizumab For Age-Related Macular Degeneration. www.nejm.org/doi/ full/10.1056/NEJMoa1102673. Accessed May 2011. 31. Regeneron Pharmaceuticals, non-published data.

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36 Vol. 62, No. 2 2011 Northeast Florida Medicine

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Evaluation and Treatment of the Low Vision Patient Diane Cates, OD and Kim Rigdon, CLVT Abstract: Many patients, as well as health care providers, are un-

aware of the specialty service known as Low Vision (LV). The purpose of this article is to give the reader insight into the field of low vision while defining the difference between visual impairment and “legal” blindness. This will enable the reader to understand who is a candidate for a low vision evaluation while giving a glimpse of the various aspects of the low vision evaluation, devices, and services that are available to the visually-impaired patient.

Figures 1-3 Normal Vision, Central Vision Loss and Peripheral Vision Loss

Visual Impairment vs. Legal Blindness

Knowing the difference between visual impairment and the legal definition of blindness is important. It is estimated that there are approximately 300,000 visually impaired children and between 1.5 and 3.4 million visually impaired adults in the United States. That number is expected to increase as the first baby boomers turn 65 this year. There is a direct correlation between aging and the increased incidence of eye disease. 1-6 More than two-thirds of persons with low vision are over the age of 65, so the need for low vision services will increase as the largest proportion of our population hits the golden years.7 As people live longer, more will be living with eye disease and some degree of visual impairment. Visual impairment is a functional limitation of the eyes or visual system due to hereditary or acquired eye disease, advancing age, or trauma that cannot be corrected by conventional eyeglasses, contact lenses, medication, or surgery. This loss in vision results in the patient’s inability to perform routine activities of daily living such as reading, cooking, cleaning, maintaining personal hygiene, employment, and/ or driving. 8-10 In contrast, the definition of legal blindness takes into account the specific level of central and peripheral vision. The Social Security Act defines legal blindness: (1) remaining vision in the better eye, after best correction, < 20/200 or (2) contraction of the peripheral visual field (VF) in the better eye either to < 10o from the point of fixation; or widest diameter subtends an angle <20o.11 It is difficult to understand and conceptualize what visually impaired persons see when they look through eyes that have been affected by macular degeneration, glaucoma, diabetic retinopathy, stroke or other retinal or neurological diseases. The Lighthouse International website (www. lighthouse.org), provides an excellent means of “experiencing” what your patient sees on a daily basis. Adapted from the website are Figures 1, 2, 3 which represent normal vision, central vision loss and peripheral vision loss respectively. Address Correspondence to: Diane M. Cates, OD, or Kim Rigdon, CLVT, Low Vision Center of Northeast Florida, 2519 Riverside Avenue, Jacksonville, FL 32204. Emails: Dr.DianeCates@yahoo. com, and kimrigdon@hotmail.com. Website: www.jacksonvillelowvision.com www . DCMS online . org

Who Benefits From a Low Vision Evaluation?

Patients as young as 3 years old and as old as 100+ years of age, (average age 75), can benefit from a low vision evaluation. The most commonly seen eye conditions responsible for the decrease in vision are macular degeneration, glaucoma, Northeast Florida Medicine Vol. 62, No. 2 2011 37

cataracts, diabetic retinopathy, and other retinal disorders. Although some patients suffering from profound vision loss are legally blind, others are less severely visually-impaired, but all share the same goals of trying to maintain independent lifestyles and positive self-esteem. Anyone who has vision loss that cannot be corrected with conventional glasses and/or contact lenses can be a candidate for a LV evaluation. A patient with 20/50 vision can be a just as good of a candidate for a LV evaluation as a patient with 20/400 vision. The devices and services recommended are individualized for each patient’s personal degree of vision loss, physical and intellectual capabilities, motivation, and visual requirements. The objective of the LV examination is to rehabilitate the patient with the use of optical and non-optical devices. It is not a basic, dilated eye exam and should not be mistaken for an exam to diagnose, treat, or monitor any eye disease.

Basic Components of the Low Vision Exam

Prior to the LV evaluation, the low vision examiner will contact the referring eye care provider’s office for medical records to ensure the patient has had a recent full exam, the condition is relatively stable, the degree of vision/visual field loss is documented, and the patient has been compliant with recommended treatment and follow-up care. A typical LV evaluation is very detailed and time-intensive and can typically last up to two hours of one-to-one face time with the provider. In the course of the evaluation, the patients are exposed to and have the opportunity to try a wide range of LV devices that range from the simple to the complex. Patients who present to the LV clinic are often depressed, anxious, or angry about their vision loss. Most do not want to be labeled as “blind” and/or disabled. It is very helpful when patients have a supportive family member or primary caregiver accompany them, because the first encounter can be overwhelming. Addressing the psychosocial aspects of vision loss is just as critical as prescribing the appropriate optical devices. The “perfect” device may be available, but if the patient is unwilling to use it, or is intimidated by the technology, failure is inevitable. A good LV provider should not only address visual rehabilitation, but also the social and psychological issues associated with significant vision loss in our society by making the patient and/or his family aware of the various services and resources available in the community. It is often helpful to refer these patients to trained counselors and/or peer support groups who have also suffered vision loss and overcome disability. Patient History – The basic exam begins with a review of the systemic and ocular histories. The physical assessment is very important. For example, if a patient is suffering from Parkinson’s disease, a hand tremor may serve as a contraindication to a hand-held magnifier. A stand magnifier would be a more suitable option. The patient with a profound hearing deficit may not benefit from a talking device. The diabetic patient suffering from neuropathy may not benefit from learning Braille due to their sensory deficit. 38 Vol. 62, No. 2 2011 Northeast Florida Medicine

The patient’s visual goals are discussed. The individuals who benefit the most from the LV evaluation are those with clear goals of what visual tasks they want to master. Does the patient live alone or does he/she live with a spouse or adult child? Those who live alone usually take advantage of more of the devices and social services that are available because they are often more self-reliant. If a person is married and living with a healthy spouse, he/she is sometimes more dependent on that spouse for assistance with daily tasks such as cooking, grocery shopping, balancing the checkbook, and/or travel arrangements. Does the patient work on a computer or have a desire to learn? This question is important because the patient, who is currently using a computer, is usually less intimidated by the low vision electronic reading devices than the patient who has no computer experience. Does the patient have problems with glare, require a lot of light to see, or have eyeglasses and/or sunglasses that seem to help? Has the person used magnifiers purchased over the counter? Many patients have the preconceived notion that if an over the counter (OTC) magnifier does not work, then neither will prescribed devices. Most OTC magnifiers provide only 2X magnification; far too little for the average LV patient. Questions about difficulty with mobility are discussed, such as problems with navigating curbs or stairs or bumping into walls or furniture when walking. It is amazing how patients will answer “yes” to this question and then deny any problems with driving. The issue of driving has to be the most sensitive subject that is dealt with in any eye exam. It often falls to the LV specialist to be the one to “confront” the patient and “challenge” his/her ability and “right” to drive. Giving up driving represents a real loss of autonomy and independence. Some patients give up the activity willingly because they understand the dangers, but for most it is an intense emotional discussion. The minimum standards for driving in Florida require 20/70 vision in either eye, or both eyes together with or without corrective lenses. However, if one eye is blind or < 20/200, the other eye must be > 20/40. The driver must also have a minimum 1300 horizontal VF. If the VF is in question, The Florida Department of Highway Safety and Motor vehicles requires verification of the peripheral vision by the specified VF modalities. The use of telescopic lenses to meet visual standards is not allowed.12 If “any physician, person, or agency has knowledge of any licensed driver’s mental or physical disability to drive, they are authorized to report that driver to the Department of Highway and Safety and Motor Vehicles.” The report is confidential and no civil or criminal action may be brought against any physician, person or agency who provides information (HSMV Form 72190). It does require the reporting entity’s name, address, and phone number.13 The key words here are “authorized” and not “required”, thereby creating a potential dilemma for the physician. Continued on page 40 www . DCMS online . org

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Northeast Florida Medicine Vol. 62, No. 2 2011 39

Continued from page 38

Visual Assessment – The LV acuity determination starts at a distance of 10 feet (as opposed to the “standard” 20 feet viewing the Snellen chart projected on a screen across the room). Most LV patients cannot see this far away, so moveable charts are used. They can be repositioned as close as needed. They have more lines of vision that can be tested with more letters at each level of acuity represented. Each patient is checked for scotomas (blind spots) and metamorphopsias (distortions causing “bending” of straight lines). The LV fraction includes a trial spectacle frame and lenses worn by the patient. Although the frame is heavy and bulky, it allows a patient to move the head and turn the eyes allowing better functional vision. This is known as “eccentric” viewing and comes naturally to many low vision patients. The phoropter, the standard apparatus used for refraction, does not allow for head or eye movements necessary for eccentric viewing. Trial frame use allows the patient to experience the new eyeglass prescription before purchasing new glasses. This same process is repeated for near (reading) vision to determine what bifocal power is necessary and to let the patient know what size print he/she can realistically be expected to read. Low Vision Devices – The next step in the LV exam is to determine what LV devices might be best suited for the patient’s individual needs and visual goals. Depending on the level of vision, a hand-held or a stand-magnifier may be beneficial. Sometimes this same magnification can be used to create very high power eyeglasses. At other times, custom telescopes and microscopes are designed for the patient, either as hand-held or glasses-mounted devices. One should choose the least amount of magnification or power that will do the best job. Too much magnification requires that the patient either holds the material too close for comfort or decreases size of VF. In this case, the patient will only be able to read letter by letter, instead of viewing words and sentences as a whole. This adversely affects reading comprehension. Closed Circuit Televisions (CCTVs) provide a wider field of vision. CCTVs (also called video magnifiers or electronic magnifiers) are essential for those patients who still want to read for themselves and cannot use magnifiers. While they have been available for at least 20 years, they have changed drastically in the last 5 years. Reading materials are put under a camera and the text is magnified onto a screen. Most typed or written material (i.e. mail, books, magazines or newspapers) can be read with a larger field of view than with a regular magnifier. It gives the user the ability (with practice) to write checks, see photos, read pill bottles, etc. The vast majority of LV patients have problems with contrast. CCTVs (available in laptop and/or desktop models and hand-held portable devices) provide enhancement of text, background, color, and brightness and can work with screen enlargement software. Each type has different capabilities and can be used for tasks from seeing the front of the classroom to applying makeup. It is helpful for the patient to try the 40 Vol. 62, No. 2 2011 Northeast Florida Medicine

different expensive machines prior to purchasing because the camera, screen quality, print size, contrast enhancement and other features can vary tremendously. The “best” LV clinic is one that has a vast array of optical and non-optical devices available for hands-on use so that any devices prescribed have first been tried by the patient. It is very gratifying to see patients one step closer to achieving some of their visual goals. The LV exam also involves working with the certified low vision therapist (CLVT) who provides additional devicetraining, CCTV evaluations, lens tint, and optical filter selection. A demonstration of lighting requirements and an introduction to and discussion of non-optical aids and community resources is also undertaken.

Available Resources

There are many resources available for people with vision loss both at the local and national levels. In most states (FL and GA included), state funding provides rehabilitation for the blind. These services are available to patients with varying degrees of visual loss. They tend to focus on helping people maintain independence despite vision loss. Unfortunately, the amount of assistance is dependent on funding allocation. In Florida, the Division of Blind Services (DBS) provides counselors to assist children with accessibility to the school system. Vocational Rehabilitation can help people find or maintain work. DBS funding for devices is primarily available for pediatric patients, students, and adults in the preMedicare age group. 14

DBS teaches independent living skills for unemployed or retired persons and rehabilitation training through “Independent Living for the Adult Blind”(ILAB), a unique non-profit organization located at Florida State College of Jacksonville. ILAB has rehabilitation teachers who provide individual and group classes that teach necessary skills such as ways to identify money, cook meals, ambulate in the home and community and perform personal grooming skills. At least one ILAB staff member is visually-impaired and is available to help people overcome their disability suffered by vision loss and to provide counseling through that grieving process. Also on staff at ILAB are mobility instructors who teach safety and cane techniques and computer instructors that teach the screen enlargement software programs. There is also a transition program for teenagers to prepare them for the workforce, college, and/or life after high school. Many visually-impaired patients report missing the ability to read more than anything else. Several libraries in Duval County have a separate section for large print books. Large print books are also available for purchase at most bookstores and online. The new electronic book readers offer the ability to enlarge the font (not nearly as much as with the magnifiers mentioned above) and/or listen to books that are available to download and purchase. It is always best for the patient to try these readers prior to purchasing as they differ in contrast, font size, and voice. It is important to note that these e-readers are not LV devices. www . DCMS online . org

The talking book program is one of the many wonderful free services the National Library Service (NLS) provides. The patient’s optometrist, ophthalmologist, primary care provider, or therapist has to verify that the patient qualifies for services. Applicants are given the opportunity to select the subjects they would enjoy reading. The NLS will mail tapes or digital cartridges that read books within the chosen subject areas.15 The NLS will also provide the qualified applicant with a tape player or digital cartridge player. When the person is finished listening to the book, it is placed it in the original green package pre-marked “free matter for the blind” and put in the mailbox. The entire program is provided at no charge to the patient. The NLS also offers descriptive videos or DVDs through the same free mailing format. This allows visually-impaired people to listen to specific descriptions of activities happening throughout a movie that they would normally be unable to see. These descriptions do not interfere with the enjoyment of the movie for those who are sighted. Additionally, they also offer large print or Braille music in several categories and styles. The sheet music ranges from vocal to instruments such as the piano and organ. Many of the NLS music services are available as web pages or text files that can be downloaded to a computer.15 Veterans have top priority to book selections from NLS. They also have access to a host of other free services through the Veterans Administration Medical Center (VAMC). They provide LV exams, vocational rehabilitation, and some LV devices to honorably discharged, legally blind veterans regardless of whether vision loss occurred in the line of duty.16 For those patients that are unable to read the morning newspaper and/or those who prefer to use their auditory skills, the National Federation for the Blind offers a free telephone newspaper reading service which includes over 300 newspapers.17 The New York Times offers a weekly large print subscription to their newspaper, which includes a large print crossword puzzle and pictures.18 In Jacksonville, the WJCT (local NPR station) Radio Reading Service provides a special radio to the visually-impaired patient on which they can receive a daily schedule of the Florida Times Union. Portions of other newspapers and local literature are also read. These services are made possible by local donations.19 Some phone companies provide free directory assistance for individuals who provide a letter of verification of visual impairment by an eye doctor. By dialing “0” or “411” the operator verbally gives the visually-impaired person the requested phone number. The special needs department of the phone company can be contacted for more information.20 Cellular phones have become the primary phone for many people. There are quite a few styles that are easy and user friendly with large print and high contrast. Several companies offer free voice dialing services. Other companies offer software that can be downloaded to assist with cell phone use. www . DCMS online . org

Patients are advised to contact the individual companies to hear the full range of cell phone services available for people with visual impairments. 21 The computer presents numerous possibilities and challenges for people with vision loss. There are various screen magnifiers such as Zoomtext than can magnify as little as 1X-2X and as much as 36X.22 They also provide a bolder appearance with different color filtering schemes, as well as enhancements to help locate the cursor and pointer. There are also various applications that provide screen reading capabilities in several choices of voices and speeds.

Conclusion

The purpose of this article was to provide an overview of some of the options that are available to the visually-impaired patient. Despite all of the technology and resources reviewed, nothing replaces human interaction, encouragement, and positive re-enforcement. As physicians, our most important tasks may be to listen to our patients and try to see the world through their eyes and realize that while it may not be possible to rehabilitate the eyes, we can rehabilitate the lives of these patients.

References

Vision Problems in the U.S. Prevent Blindness America, National Eye Institute, 2002.

Massoff RW. A model of the prevalence and incidence of low vision and blindness among adults in the U.S. Optom and Vis Sci. 2002; 79 (1): 31-8.

The Eye Diseases Prevalence and Incidence Research Group, Causes and prevalence of visual impairment among adults in the United States. Arch Ophthalmology. 2004; 122: 477-85.

Vitale S, Cotch MF, Sperduto RD. Prevalence of visual impairment in the United States. JAMA. 2006; 295 (18): 2158-63.

United States Department of Commerce, Economics and Statistics Administration, Bureau of the Census. Statistical brief: 65+ in the United States. Washington, DC, December 2005.

American Foundation for the Blind website: http://www.afb. org/Section.asp? SectionID=3&TopicID=138&Document ID=3350. Accessed 2011.

National Advisory Eye Council. Vision research: a national plan 1999-2003. Report of the National Advisory Eye Council. DHHS publication no. (NIH) 98-4120. Washington, DC: U.S. Government Printing Office, 1998.

United States Department of Health and Human Services. The international classification of diseases, 9th revision, clinical modification (ICD-9-CM), 4th ed, vol 1. U.S. DHHS (PHSHCFA). Washington, DC, 1996.

West SK, Rubin GS, Broma AT, et al. How does visual impairment affect performance on tasks of everyday life? Arch Ophthalmol. 2002; 120: 774-80.

10. Fraser Freeman K, Cole RG, Faye, EE, et al. Optometric Clinical Practice Guideline Care of the Patient with Visual Impairment (Low Vision Rehabilitation) Reference Guide for Clinicians. American Optometric Association, St. Louis, MO, 2007; 1-8. 11. Social Security Act. United States Social Security Administration. Code of Federal Regulations, Title 20, Ch. III, Pt. 404, Subpt. P, App. 1. List of Impairments. U.S. DHHS (SSA). Washington, DC, 2006. Northeast Florida Medicine Vol. 62, No. 2 2011 41

12. State of Florida – Division of Blind Services website: http:www. flhsmv.gov/ddl/fagmed.html – HSMV form 72010. Accessed 2011. 13. National Library Service website: http:www.flhsmv.gov/ddl/ fagmed.html – HSMV form 72190. Accessed 2011. 14. Veterans Administration website: http://www.myflorida.com/ dbs/about-us/services.php. Accessed 2011. 15. National Foundation for the Blind website: http://www.loc. gov/nls/music/orderform.html. Accessed 2011. 16. New YorkTimes website: http://www1.va.gov/BLINDREHAB/ VIST.asp. Accessed 2011. 17. WJCT website: http://www.nfb.org/nfb/Newspapers_by_ Phone.asp. Accessed 2011. 18. AT & T phone company website: http://homedelivery. nytimes.com/HDS/ LargeTypeWeeklyHome.do?mode= ChooseCountry.LargeTypeWeekly Accessed 2011. 19. AT & T wireless: http://www.wjct.org/radio/reading. Accessed 2011. 20. Aisquared website: http://www.att.com/esupport/article. jsp?sid=KB403192. Accessed 2011. 21. Aisquared website: http://www.wireless.att.com/learn/ articles-resources/disability-resources/disability-resources. jsp. Accessed 2011. 22. Aisquared website: http://www.aisquared.com/zoomtext. Accessed 2011.

Meet the Doctor Dr. Jerry Maida has been setting the standard for laser vision correction for over 20 years. In 1989, Dr. Maida was one of the first in the U.S. to employ the excimer laser, which is now utilized for refractive laser surgery. He has performed over 30,000 surgeries and more than 18,000 Lasik procedures. He is one of the few in the southeast to utilize the next generation Intralase-ifs laser in combination with the advanced Eye-Q Allegretto Laser. This results in uniquely safe, precise, and predictable Lasik surgery. At Maida CustomVision, Dr. Maida and his exceptionally service oriented staff work diligently every day to do their utmost to improve the lives of patients, and to help them view their world with crisp, clear vision. Dr. Maida is one of Jacksonville’s most recommended Lasik surgeons based on his impeccable reputation. That is one of the many reasons why patients choose to place their vision in the hands of a trusted professional like Dr. Maida. It is this dedication to quality patient care and innovations in refractive technology that sets Maida CustomVision apart and has attracted patients from not only across the United States, but also from continents as far as Europe and Australia. Dr. Maida made a difference in so many lives. Call now for your evaluation to see if LASIK is right for you. You will be glad you did.

DCMS Hosts AMA President-Elect During Annual Leadership Visit The DCMS welcomed (above, L) Peter Carmel, MD, President-Elect of the American Medical Association to Jacksonville, May 8-9, 2011. A Pediatric Neurosurgeon, Dr. Carmel practices at the University Hospital of the New Jersey Medical School. Pictured with Dr. Carmel are (above, center) Malcolm Foster, Jr., MD, DCMS President and (above, R) Yank D. Coble, Jr., MD, a Past AMA President. While in Jacksonville, Dr. Carmel toured various medical institutions, met with local media and other area groups. He was the speaker at a DCMS Membership Dinner on May 9 at Epping Forest Yacht Club.

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LASIK

268-EYES

maidalaser.com

www . DCMS online . org

Knowledge about breast health empowers patients to partner with their physicians in order to receive the most effective healthcare possible.

www . DCMS online . org

Northeast Florida Medicine Vol. 62, No. 2 2011 43

DCMS Membership Applications These physicians’ applications for membership in the Duval County Medical Society are now being processed. Any information or opinions you may have concerning the eligibility of the applicants listed here may be directed to Ashley Booth Norse, MD, DCMS Membership Committee Chair (904-244-4106 or Barbara Braddock, Membership Director (904-355-6561 x107).

Larissa S. Buccolo, MD Family Medicine Jacksonville Family Practice Associates 1731 University Blvd. S. Medical Degree: Emory Univ. School of Medicine Residency: NHS JAX Nominated by: Robert Raspa, MD; Jack Giddings, MD; Neirouz Joseph, MD Kuo Yun Chen, MD Pediatrics/UF Pediatrics 655 W. 8th St. 3rd FL LRC Medical Degree: Medical College of Georgia School of Medicine Residency: Orlando Regional Medical Center Nominated by: UFJP Andrew P. Daigle, MD Palliative Medicine Community Palliative Consultants 4266 Sunbeam Rd. Medical Degree: LSU School of Medicine/New Orleans Residency: Greenville Hospital System Fellowship: UAB Birmingham School of Medicine Nominated by: Stephen Clark, MD; Jerry Sayre, MD; Reetu Grewal, MD Bryan A. Farford, DO Family Medicine/Mayo 4500 San Pablo Rd. Medical Degree: Nova Southeastern University College of Osteopathic Medicine Residency: Mayo Clinic Nominated by: John Presutti, MD; Paul Roberts, MD; Todd Brinker, MD Ashwani K. Gupta, MD Nephrology/UF Nephrology 655 W. 8th St. Clinical Center Basement Medical Degree: All India Institute of Medical Science Internship: Harvard School of Public Health Residency: Michigan State University Medical School Fellowship: Henry Ford Hospital Nominated by: UFJP Pratibha N. Gupta, MD Diagnostic Radiology/UF Radiology

655 W. 8th St. 2nd FL Clinical Center Medical Degree: Makerere Univ. School of Medicine Residency: New Jersey University of Medicine & Dentistry Fellowship: Stony Brook University Hospital & University of North Carolina Medical School Nominated by: UFJP Christopher Klassen, MD Radiology/UF Radiology 655 W. 8th St. 2nd FL Clinical Center Medical Degree: University of Minnesota Medical School Internship/Residency: Univ. of Texas Medical School Residency: University of Minnesota Medical School Fellowship: UFHSC/ Jacksonville & University of Texas SW Medical School Nominated by: UFJP Bettina A. Kohaut, MD OB-GYN Faben OB-GYN 836 Prudential Dr. #1506 Medical Degree: Michigan State University School of Medicine Residency: University of Florida College of MedicineJacksonville Nominated by: Mitzi Brock, MD; Todd Rasner, MD; Guy Benrubi, MD Susan H. Krieger, MD Pediatrics/Community Hospice PedsCare 4266 Sunbeam Road Medical Degree: Georgetown University School of Medicine Residency: Virginia Commonwealth University Medical School Nominated by: UFJP Naeem Latif, MD Hematology/Oncology UF Hematology/Oncology 655 W. 8th St. Pavilion 4th FL North Medical Degree: Ayub Medical College Residency: University of Pittsburgh College of Medicine Fellowship: UFHSC/ Jacksonville & Montefiore/ Einstein Medical Center Nominated by: UFJP Fatina E. Milfred, MD Neurology/Neuroscience Institute At Shands 580 W. 8th St. 9th FL Tower I Medical Degree: Universidad Nacional Pedro Hernandez Viena Internship: Woodhull Medical Center Residency: UFHSC/JAX Nominated by: UFJP

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Mark B. Phillips, MD Anesthesiology UF Anesthesiology 655 W. 8th St. 2nd FL Clinical Center Medical Degree: Univ. of Miami College of Medicine Residency: Jackson Memorial Hospital & UCLA Medical Center Nominated by: UFJP Jin Hee Ra, MD Trauma Surgery/Critical Care Medicine UF Trauma Surgery 655 W. 8th St. 8th FL Clinical Center Medical Degree: University of Louisville School of Medicine Residency/Fellowship: Hospital of the Univ. of Pennsylvania Nominated by: UFJP Luis Ramirez, MD Infectious Disease Rainbow Center 655 W. 8th St. 3rd FL Clinical Center Medical Degree: San Marcos University Residency: Bronx Lebanon Hospital Center Fellowship: SUNY Upstate Medical University Nominated by: UFJP Daniel K. Robie, MD Pediatric Surgery Nemours Children’s Clinic 807 Children’s Way Medical Degree: Hahnemann University School of Medicine Residency: Walter Reed Army Medical Center Fellowship: Baylor College of Medicine Nominated by: Albert Wilkinson, Jr., MD; Danielle Walsh, MD; Gary Josephson, MD Monali Sakhalkar, MD Ophthalmology/UF Ophthalmology/580 W. 8th St. 3rd FL Tower II Medical Degree: Baroda Medical College Internship: Staten Island University Hospital Residency: Interfaith Medical Center & LSU School of Medicine Fellowship: Dean McGee Eye Institute & University of Wisconsin Medical School Nominated by: UFJP Sukhwinder Sandhu, MD Radiology UF Radiology 655 W. 8th St. 2nd FL Clinical Center Medical Degree: The Johns Hopkins University School of Medicine Internship/Residency: Jackson Memorial Hospital Fellowship: MA General Nominated by: UFJP

Nipa R. Shah, MD Family Medicine UF Community Health Center 655 W. 8th St. 4th FL ACC Medical Degree: University of Illinois School of Medicine Internship: Metrohealth Hospital Residency: University of New Mexico Hospital Nominated by: UFJP Matthew B. Shannon, MD Emergency Medicine UF Emergency Medicine 655 W. 8th St. 1st FL Clinical Center Medical Degree: Creighton University School of Medicine Residency: University of Illinois College of Medicine-Peoria Nominated by: UFJP Stephanie V. Sims, MD Psychiatry/UF Psychiatry Cen. 580 W. 8th St. Tower II #6005 Medical Degree: Medical University of South Carolina Internship: Tulane University School of Medicine Residency: Baylor College of Medicine Fellowship: Medical University of South Carolina Nominated by: UFJP Phyliss N. Taylor, MD Psychiatry/UF Psychiatry Cen. 580 W. 8th St. Tower II #6005 Medical Degree: Meharry Medical College Residency: East Carolina University School of Medicine Nominated by: UFJP Paola F. Tumminello, MD Neurology/Neuroscience Institute At Shands 580 W. 8th St. 9th FL Tower I Medical Degree: Federico II School of Medicine Internship: St. Agnes Hospital Residency/Fellowship: Medical University of South Carolina Nominated by: UFJP Paul L. Wasserman, DO Radiology/UF Radiology 655 W. 8th St. 2nd FL Clinical Center Medical Degree: Kansas City Univ. of Medicine & Bioscience Internship: The Western Pennsylvania Hospital Residency: University of Pittsburgh Medical Center Fellowship: Wake Forest University Baptist Medical Center Nominated by: UFJP Richard Westenbarger, MD Emergency Medicine UF Emergency Medicine 655 W. 8th St. Medical Degree: University of Florida College of Medicine Residency: UFHSC/Jacksonville Nominated by: UFJP

www . DCMS online . org

A financial advisor dedicated to the medical industry can help you navigate changes in your practice’s finances. The business of medicine, much like your practice itself, is forever evolving. And with new financial opportunities and ongoing concerns — like protecting against fraud, managing risk and anticipating the impact of insurance and reimbursements on cash flow — you need the guidance of an advisor who uniquely understands your industry. At SunTrust, advisors with our Private Wealth Management Medical Specialty Group work solely with physicians and their practices to deliver solutions designed for the medical community. To schedule an appointment with an advisor, call 904.632.2854 or visit suntrust.com/medicine to learn more.

Treasury and Payment Solutions

Lending

Investments

Financial Planning

Deposit products and services are offered through SunTrust Bank, Member FDIC.

Securities and Insurance Products and Services: Are not FDIC or any other Government Agency Insured • Are not Bank Guaranteed • May Lose Value SunTrust Private Wealth Management Medical Specialty Group is a marketing name used by SunTrust Banks, Inc., and the following affiliates: Banking and trust products and services are provided by SunTrust Bank. Securities, insurance (including annuities and certain life insurance products) and other investment products and services are offered by SunTrust Investment Services, Inc., an SEC-registered investment adviser and broker/dealer and a member of FINRA and SIPC. Other insurance products and services are offered by SunTrust Insurance Services, Inc., a licensed insurance agency. ©2011 SunTrust Banks, Inc. SunTrust and Live Solid. Bank Solid. are federally registered service marks of SunTrust Banks, Inc.

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Northeast Florida Medicine Vol. 62, No. 2 2011 45

Introducing the

St Johns Vein Center

Dr. James St. George is proud to join the Jacksonville community, bringing more than 20 years experience in treating vascular disorders. The recent opening of the St Johns Vein Center provides you with a new option for patients suffering from lower extremity venous disease including: • Chronic venous insufficiency • Chronic distal skin changes including abnormal increased pigmentation, eczema, ulceration • Leg, ankle and foot swelling

• • • •

Leg pain, cramps, discomfort Restless legs Varicose veins Spider veins

Your patients no longer have to drive downtown for specialist vein care. Our state-of-the-art facility is conveniently located just off the Baymeadows road exit on 9A. We provide the following treatment options: • Radiofrequency ablation • Laser ablation • Ultrasound-guided chemical ablation

• Foam sclerotherapy • Liquid sclerotherapy • Ambulatory phlebectomy

We are a participating provider for Medicare, Tricare and most Commercial payers. Please visit www.stjohnsvein.com for more information or call (904) 402-VEIN (8346) to learn more about the care we can provide for your patients. James St. George, M.D. is a vascular specialist and a diplomat with the American Board of Radiology with a Certificate in Interventional Radiology. He completed his fellowship training at Harvard Medical School’s 9191 RG Skinner Parkway

•

Suite 303

w w w. s t j o h n sve i n . co m •

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Brigham and Women’s Hospital and served for 12 years as faculty at Harvard Medical School, Dartmouth Medical School and Drexal School of Medicine. He also held the position of Head of Special Procedures at Hahnemann Hospital in Philadelphia. Dr. St. George takes the time to know each patient and creates customized treatment programs to obtain the best possible results. •

Jacksonville, FL 32256

(904) 402-VEIN (8346) www . DCMS online . org

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helping families

it’s all about

live better For 30 years, family medicine physicians such as Dr. Stephen Clark have helped Northeast Florida residents and their loved ones have a better quality of life. For patients with advanced illness who need specialized care, these professionals call on Community Hospice of Northeast Florida. Community Hospice staff ensure that all patients’ care needs—body, mind and spirit—are met, wherever and whenever they are needed most. These multidisciplinary experts work alongside medical providers to help family caregivers know what to expect and make informed care choices. To learn more about how Community Hospice can help your patients and their family caregivers live better with advanced illness, call 904.407.6500 to schedule an in-office or in-hospital visit.

Stephen J. Clark, MD Jacksonville family medicine physician and practice owner for nearly 30 years Joined Community Hospice as Chief Medical Officer, June 2009

904.407.6500 referral line

Community Focused

Community Suppor ted

866.253.6681 toll-free

communityhospice.com

Ser ving Baker, Clay, Duval, Nassau and St. Johns counties since 1979