report on haemopty

View with images Report on Haemopty INTRODUCTION Haemoptysis is defined as the expectoration of blood from the respiratory tract that varies from blood- streaking of sputum to coughing up large amounts of pure blood. Blood may be coughed up alone or sputum may be blood stained. Haemoptysis is a common medical problem and may present as an acute life-threatening emergency, which requires immediate attention and intervention. The most common site of bleeding is the airway i.e. trachea , bronchial tree which can be affected by inflammation (acute or chronic bronchitis, bronchiectasis) or, neoplasm (bronchogenic carcinoma, endobrochial metastiatic carcinoma or bronchial carcinoid tumour). Blood originating from the pulmonary parenchyma can be either from a localized source, such as an infection (pneumonia, lung abscess, tuberculosis) or from a process diffusely affecting the parenchyma i.e. coagulopathy. Disorders primarily affecting the pulmonary vasculature include pulmonary embolic disease and those conditions associated with elevation of pulmonary venous and capillary pressure e.g. mitral stenosis or left ventricular failure.

Infectious diseases occur most frequently in Bangladesh due to various sociodemographic factors e.g. socio-economic status, education, nutrition, environmental pollution and sharing of bedroom etc.

Environmental pollution has emerged as a major health hazard in our country, which is likely to increase respiratory diseases and alter the aeitiological pattern of haemoptysis in our country over the years. It is very much fortunate that the patient seeks medical advice as soon as he or she develops haemoptysis, because this symptom is due frequently to serious disease and in many instances is the early sign, which can lead to an early diagnosis if proper investigations are carried out promptly.

Haemoptysis is the common presenting feature of various diseases responsible for major morbidity and mortality. Aetiological pattern in our country is different from that of developed countries. Sophisticated investigation facilities such as CT scan, bronchoscopy, etc. are only available in limited centres and we have to diagnose and treat cases within our limited resources. So a study on haemoptysis will be helpful for prompt diagnosis and management of our patients within limited resources.

Structure of Respiratory System The main role of the respiratory system is to work closely with the heart and blood to extract oxygen from the external environment and dispose of waste gases, principally carbon dioxide. This requires the lungs to function as an efficient bellows, expelling used air, bringing fresh air in and mixing it efficiently with the air remaining in the lungs. The lungs have to provide a large surface area for gas exchange and the alveolar walls have to present minimal resistance to gas diffusion. This means the lungs have to damage by dusts, gases and infective agents. Host defense is therefore a key priority for the lung and is achieved by a combination of structural and immunological defenses.

The Nose

The anterior one-third of the nasal cavity is divided into right and left halves by the nasal septum. The nasal vestibule leads to the internal ostium which is the narrowest part of the nasal cavity. This causes a 50% increased resistance to airflow when breathing through the nose rather than through the mouth. The respiratory region is divided by three folds arising from the lateral wall, termed the superior, middle and inferior turbinate. Behind these turbinates are situated the openings of the nasolacrimal duct and the frontal, ethomoidal and maxillary sinuses. The olfactory region for smell is found above the superior turbinate. The nasal cavities communicate with the nasopharynx via the posterior nasal apertures (the choanae) and the Eustachian tube opens into this area just above the soft palate.

The Pharynx and Larynx The pharynx is divided by the soft palate into an upper nasopharyngeal and lower oropharyngeal region. There are numerous collections of lymphoid tissue arranged in a circular fashion around the nasopharynx , these include the adenoids. The tonsils lie between the anterior and posterior fauces, separating the mouth from the oropharynx.

The larynx consists of a number of articulated cartilages, vocal cords, muscles and ligaments, all of which serve to keep the airway open during breathing and occlude it during swallowing.

The main motor nerve to the larynx is the recurrent laryngeal nerve. The left recurrent laryngeal nerve leaves the vagus at the level of the aortic arch, hooking round it to run upwards through the mediastinum between the trachea and the oesophagus; it can be affected by disease in these areas. The principal tensor of the vocal cords is the external branch of the superior laryngeal nerve, which can be injured during thyroidectomy.

Anatomy of The Lungs Air Passage After passing through the nasal passages and pharynx, where it is warmed and takes up water vapor, the inspired air passes down the trachea and through the bronchioles, respiratory bronchioles, and alveolar ducts to the alveoli.

Between the trachea and the alveolar sacs, the airways divide 23 times. The first 16 generations of passages form the conducting zone of the airways that transports gas from and to the exterior. They are made up of bronchi, bronchioles, and terminal bronchioles. The remaining seven generations form the transitional and respiratory zones where gas exchange occurs and are made up of respiratory bronchioles, alveolar ducts, and alveoli. These multiple divisions greatly increase the total cross-sectional area of the airways, from 2.5 cm in the trachea to 11,800 cm in the alveoli.

Consequently, the velocity of air flow in the small airways declines to very low values.

The alveoli are surrounded by pulmonary capillaries. In most areas, air and blood are separated only by the alveolar epithelium and the capillary endothelium, so they are about 0.5 Âľm apart. Humans have 300 million alveoli, and the total area of the alveolar walls in contact with capillaries in both lungs is about 70 m.

The alveoli are lined by two types of epithelial cells. Type I cells are flat cells with large cytoplasmic extensions are the primary lining cells. Type II cells (granular

pneumocytes) are thicker and contain numerous lemellar inclusion bodies. These cells secrete surfactant. Other special types of epithelial cells may be present, and the lungs also contain pulmonary alveolar macrophages (PAMs), lymphocytes, plasma cells, APUD cells and mast cells. The mast cells contain heparin, various lipids, histamine, and various proteases that participate in allergic reactions.

The Trachea, Bronchi and Bronchioles The trachea is 10-12 cm in length. It lies slightly to the right to the midline and divides at the carina into right and left main bronchi. The carina lies under the junction of the manubrium sternum and the second right costal cartilage. The right main bronchus is more vertical than the left and, hence, inhaled material is more likely to pass into it.

The right main bronchus divides into the upper lobe brochus and the intermediate bronchus, which further subdivides into the middle and lower lobe bronchi. On the left the main bronchus divides into upper and lower lobe bronchi only. Each lobar bronchus further divides into segmental and sub segmental bronchi. There are about 25 divisions in all between the trachea and the alveoli.

Of the first seven divisions, the bronchi have: • Walls consisting of cartilage and smooth muscle • Epithelial lining with cilia and goblet cells • Submucosal mucus-secreting glands • Endocrine cells- Kulchitsky or APUD (amine precursor and uptake decarboxylation) containing 4-hydroxytryptamine.

In the next 16-18 divisons the bronchioles have.

• No cartillage and muscular layer that progressively becomes thinner • A single layer of ciliated cells but very few goblet cells • Granulated Clara cells that produce a surfactant-like substance.

The ciliated epithelium is an important defence mechanism. Each cell contains approximately 200 cilia beating at 1000 beats per minute in organized waves of contraction. Each cilium consists of nine peripheral parts and two inner longitudinal fibrils in a cytoplasmic matrix.

Nexin links join the peripheral pairs. Dynein arms consisting of ATPase protein project towards the adjacent pairs. Bending of the cilia results from a sliding movement between adjacent fibrils powered by an ATP-dependent shearing force developed by the dynein arms.

Absence of dynein arms leads to immotile cilia. Mucus, which contains macrophages, cell debris, inhaled particles and bacteria, is moved by the cilia towards the larynx at about 1.5 cm/min.

The bronchioles finally divide within the acinus into smaller respiratory bronchioles that have alveoli arising from the surface. Each respiratory bronchiole supplies approximately 200 alveoli via alveolar ducts. The term small airways refers to bronchioles of less than 2 mm; there are 30000 of these in the average lung.

The Bronchi & their Innervation The trachea and bronchi have cartilage in their walls but relatively little smooth muscle. They are lined by ciliated epithelium that contains mucous and serous glands. Cilia are present as far as the respiratory bronchioles, but glands are absent from the epithelium of the bronchioles and terminal bronchioles, and their walls do not contain cartilage. However, their walls contain more smooth muscle, of which the largest amount relative to the thickness of the walls is present in the terminal bronchioles.

The walls of the bronchi and bronchioles are innervated by the autonomic nervous system.

Muscarinic receptors are abundant, and cholinergic discharge causes bronchoconstriction.

The bronchial epithelium and smooth muscle contain β2-adrenergic receptors. Many of these are not innervated. Some may be located on cholinergic endings, where they inhibit acetylcholine release. The β2 receptors mediate bronchodilation. They increase bronchial secretion, while ι1 adrenergic receptors inhibit secretion. There is in addition a noncholinergic, nonadrenergic innervation of the bronchioles that produces bronchodilation, and evidence suggests that VIP is the mediator responsible for the dilation.

The Alveoli: There approximately 300 million alveoli in each lung. Their total surface area is 40-80 m 2.

The epithelial lining consists largely of type I pneumocytes. These cells have an extremely attenuated cytoplasm, and thus provide only a thin barrier to gas exchange. They are derived from type II pneumocytes. Type I cells are connected to each other by tight junctions that limit the fluid movements in and out of the alveoli. Type II pneumocytes are slightly more numerous that type I cells but cover less or the epithelial lining. They are found generally in the borders of the alveolus and contain distinctive lamellar vacuoles, which are the source of surfactant. Macrophages are also present in the alveoli and are involved in the defence mechanisms of the lung.

The pores of Kohn are holes in the alveolar wall allowing communication between alveoli of adjoining lobules.

The Lungs: The lungs are separated into lobes by invaginations of the pleura, which are often incomplete.

The right lung has three lobes, whereas the left lung has two lobes. The upper lobe lies mainly in front of the lower lobe and therefore signs on the right side in the front of the chest found on physical examination are due to lesions mainly of the upper lobe or part of the middle lobe.

Each lobe is further subdivided into bronchopulmonary segments by fibrous septa that extend inwards from the pleural surface. Each segment receives its own segmental bronchus.

The bronchopulmonary segment is further divided into individual lobules approximately 1 cm in diameter and generally pyramidal in shape, the apex lying towards the bronchioles supplying them. Within each lobule a terminal bronchus supplies an acinus and within this structure further divisions of the bronchioles eventually give rise to the alveoli.

Broncho Pulmonary Segments: Primary branches of the right and4 left lobar bronchi are termed segmental bronchi because each ramifies in a structurally separate, functionally independent unit of lung tissue called a broncho pulmonary segment. There are typically 10 broncho pulmonary segment in each lung and therefore 10 segmental bronchi. Each lung segment is roughly pyramidal in shape, with its apex towards the hilum and base towards the surface of the lung. The main segments are named and numbered as follows: Right Lung: Superior Lobe

:

(i) Apical, (ii) Posterior, (iii) Anterior

Middle lobe

: (iv) Lateral (v) Medial.

Inferior Lobe

: (v) Superior (apical) (vii) Medial basal (viii) Anterior basal (ix) Lateral basal (x) Posterior basal.

Left lung: Superior Lobe Inferior Lobe

: (i) Apical (ii) Posterior (iii) Anterior (iv) Superior lingual (v) Inferior lingual. :

(vi) Superior (apical) (vii) Medial basal (viii) Anterior basal (ix) Lateral basal (x) Posterior basal.

The Pleura The pleura is a layer of connective tissue covered by a simple squamous epithelium. The visceral pleura covers the surface of the lung, lines the interlobar fissures, and is continuous at the hilum with the parietal pleura, which lines the inside of the hemithorax. At the hilum the visceral pleura continues alongside the branching bronchial tree for some distance before reflecting back to join the parietal pleura. In health, the pleurae are in apposition apart from a small quantity of lubricating fluid, so the pleural cavity is only a potential space.

The Diaphragm: The diaphragm is lined by parietal pleura and peritoneum. Its muscle fibres arise from the lower ribs and insert into the central tendon. Motor and sensory nerve fibres go separately to each half of the diaphragm via the phrenic nerves. Fifty percent of the muscle fibres are of the slow-twitch type with a low glycolytic capacity; they are relatively resistant to fatigue.

Lung Volumes: The amount of air that moves into the lungs with each inspiration (or the amount that moves out with each expriation) is called the tidal volume. The air inspired with a maximal inspiratory effort in excess of the tidal volume is the inspiratory reserve volume. The volume expelled by an active expiratory effort after passive expiration is the expiratory reserve volume, and the air left in the lungs after a maximal expiratory effort is the residual volume.

The space in the conducting zone of the airways occupied by gas that does not exchange with blood in the pulmonary vessels is the respiratory dead space. The vital capacity, the largest amount of air that can be expired after a maximal inspiratory effort, is frequently measured clinically as an index of pulmonary function. It gives useful information about the strength of the respiratory muscles and other aspects of pulmonary function. The fraction of the vital capacity expired during, the first second of a forced expiration (FEF, timed vital capacity) gives additional information; the vital capacity may be normal but the FEV, reduced in diseases such as asthma, in which airway resistance is increased because of bronchial constriction. The amount of air inspired per minute (pulmonary ventilation, respiratory minute volume) is normally about 6L (500 mL/breath Ă—12 breaths/min). The maximal voluntary ventilation (MVV), or as it was formerly called, the maximal breathing capacity, is the largest volume of gas that can be moved into and out of the lungs of 1 minute by voluntary effort. The normal MVV is 125-170 L/min.

Differences in Ventilation & Blood Flow in Different Parts of the Lung:

In the upright position, ventilation per unit lung volume is greater at the base of the lung than at the apex. The reason for this is that at the start of inspiration, intrapleural pressure is less negative at the base than at the apex, and since the intrapulmonaryintrapleural pressure difference is less than at the apex, the lung is less expanded. Conversely, at the apex, the lung is more expanded; ie, the percentage of maximum lung volume is greater. Because of the stiffness of the lung, the increase in lung volume per unit increase in pressure is smaller when the lung is initially more expanded, and ventilation is consequently greater at the base. Blood flow is also greater at the base than the apex. The relative change in blood flow form the apex to the base is greater than the relative change in ventilation, so the ventilation/perfusion ratio is low at the base and high at the apex.

The ventilation and perfusion differences from the apex to the base of the lung have usually been attributed to gravity, they tend to disappear in the supine position , and the weight of the lung would be expected to make the intrapleural pressure lower at the base in the upright position. However, the inequalities of ventilation and blood flow in humans were found to persist to a remarkable degree in the weightlessness of space. Therefore, other as yet unknown factors apparently also play a role in producing the inequalities.

It should be noted that at very low lung volumes such as those after forced expiration, intrapleural pressure at the bases of the lungs can actually exceed the atmospheric pressure in the airways, and the small airways such as respiratory bronchioles collapse (Airway closure).

In older people and in those with chronic lung disease, some of the elastic recoil is lost, with a resulting decrease in intrapleural pressure. Consequently, airway closure may occur in the bases of the lungs in the upright position without forced expiration, at volumes as high as the functional residual capacity.

Dead Space & Uneven Ventilation: Since gaseous exchange in the respiratory system occurs only in the terminal portions of the airways, the gas that occupies the rest of the respiratory system is not available for gas exchange with pulmonary capillary blood. Normally, the volume of this anatomic dead space is approximately equal to the body weight in pounds. Thus, in a man who weighs 150 Ib (68 kg), only the first 350 mL of the 500 mL inspired with each breath at rest mixes with the air in the alveoli. Conversely, with each expiration, the first 150 mL expired is gas that occupied the dead space, and only the last 350 mL is gas from the alveoli. Consequently, the alveolar ventilation, ie, the amount of air reaching the alveoli per minute, is less than the respiratory minute volume. Note in addition that because of the dead space, rapid shallow breathing produces much less alveolar ventilation than slow deep breathing at the same respiratory minute volume.

It is important to distinguish between the anatomic dead space (respiratory system volume exclusive of alveoli) and the total (physiologic) dead space (volume of gas not equilibrating with blood, ie, wasted ventilation). In healthy individuals, the two dead spaces are identical; but in disease states, no exchange may take place between the gas in some of the alveoli and the blood, and some of the alveoli may be over ventilated. The volume of gas in nonperfused alveoli and any volume of air in the alveoli in excess of that necessary to arterialize the blood in the alveolar capillaries is part of the dead space (no equilibrating) gas volume.

Composition of Alveolar Air:

Oxygen continuously diffuses out of the gas in the alveoli into the bloodstream, and CO 2 continuously diffuses into the alveoli from the blood. In the steady state, inspired air mixes with the alveolar gas, replacing the O2 that has entered the blood and diluting the CO 2 that has entered the alveoli. Part of this mixture is expired. The O 2 content of the alveolar gas then falls and its CO2 content rises until the next inspiration. Since the volume of gas in the alveoli is about 2 L at the end of expiration (functional residual capacity); each 350-mL increment of inspired and expired air has relatively little effect on PO2 and PCO2. Indeed, the composition of alveolar gas remains remarkably constant, not only at rest but also under a variety of other conditions.

Alveolar stability The alveoli of the lung are essentially hollow spheres. Surface tension acting at the curved internal surface tends to cause the sphere to decrease in size. The surface tension within the alveoli would make the lungs extremely difficult to distend were it not for the presence of surfactant. The type II cells within the alveolus secrete an insoluble lipoprotein largely consisting of dipalmitoyl lecithin, which forms a thin monomolecular layer at the air-fluid interface. Surfactant reduces surface tension so that alveoli remain stable.

Fluid surfaces covered with surfactant exhibit a phenomenon known as hysteresis, that is, the surface tension lowering effect of the surfactant can be improved by a transient increase in the size of the surface area of the alveoli. During quiet breathing, small areas of the lung undergo collapse, but it is possible to re-expand these rapidly by a deep breath; hence the important of sighs or deep breaths as a feature of normal breathing. Failure of such a mechanism-which can occur, for example, in patients with fractured ribs-gives rise to patchy basal lung collapse. Surfactant levels may be reduced in a number of diseases that cause damage to the lung (e.g. pneumonia). Lack of surfactant plays a central role in the respiratory distress syndrome of the new-born. Severe reduction in perfusion of the lung causes impairment of surfactant activity and may well account for the characteristic areas of collapse associated with pulmonary embolism.

Pulmonary Circulation Pulmonary Blood Vessels The pulmonary vascular bed7 resembles the systemic, except that the walls of the pulmonary artery and its large branches are about 30% as thick as the wall of the aorta, and the small arterial vessels, unlike the systemic arterioles, are endothelial tubes with relatively little muscle in their walls. The walls of the post capillary vessels also contain some smooth muscle. The pulmonary capillaries are large, and there are multiple anastomoses, so that each alveolus sits in a capillary basket.

Pressure, Volume, & Flow With two quantitatively minor exceptions, the blood put out by the left ventricle returns to the right atrium and is ejected by the right ventricle, making the pulmonary vasculature unique in that it accommodates a blood flow that is almost equal to that of all the other organs in the body. One of the exceptions is part of the bronchial blood flow. As noted above, there are anastomoses between the bronchial capillaries and the pulmonary capillaries and veins, and although some of the bronchial blood enters the bronchial veins, some enters the pulmonary capillaries and veins, bypassing the right ventricle. The other exception is blood that flows

from the coronary arteries into the chambers of the left side of the heart. Because of the small physiologic shunt created by those two exceptions, the blood in systemic arteries has a PO 2 about 2 mm Hg lower than that of blood that has equilibrated with alveolar air, and the saturation of hemoglobin is 0.5% less.

The pressure gradient in the pulmonary system is about 7 mm Hg, compared with a gradient of about 90 mm Hg in the systemic circulation.

The volume of blood in the pulmonary vessels at any one time is about 1 L, of which less than 100 mL is in the capillaries. The mean velocity of the blood in the root of the pulmonary artery is the same as that in the aorta (about 40 cm/s). It falls off rapidly, then rises slightly again in the larger pulmonary veins. It takes a red cell about 0.75 s to traverse the pulmonary capillaries at rest and 0.3s or less during exercise.

Capillary Pressure Pulmonary capillary pressure is about 10 mm Hg, whereas the oncotic pressure is 25 mm Hg, so that an inward-directed pressure gradient of about 15 mm Hg keeps the alveoli free of all but a thin film of fluid. When the pulmonary capillary pressure is more than 25 mm Hg-as it may be, for example, in “backward failure” of the left ventricle- pulmonary congestion and edema result. Patients with mitral stenosis also have a chronic, progressive rise in pulmonary capillary pressure and extensive fibrotic changes in the pulmonary vessels.

Effect of Gravity: Gravity has a relatively marked effect on the pulmonary circulation. In the upright position, the upper portions of the lungs are well above the level of the heart, and the bases are at or below it. Consequently, in the upper part of the lungs, the blood flow is less, the alveoli are larger, and ventilation is less than at the base. The pressure in the capillaries at the top of the lungs is close to the atmospheric pressure in the alveoli. Pulmonary arterial pressure is normally just sufficient to maintain perfusion, but if it is reduced or if alveolar pressure is increased, some of the capillaries collapse. Under these circumstances, no gas exchange takes place in the affected alveoli and they become part of the physiologic dead space.

In the middle portions of the lungs, the pulmonary arterial and capillary pressure exceeds alveolar pressure, but the pressure in the pulmonary venules may be lower than alveolar pressure during normal expiration, so they are collapsed. Under these circumstances, blood flow is determined by the pulmonary artery-alveolar pressure difference rather than the pulmonary artery pulmonary vein difference. Beyond the constriction, blood “falls” into the pulmonary veins, which are compliant and take whatever amount of blood the constriction lets flow into them. This has been called the waterfall effect. Obviously, the compression of vessels produced by alveolar pressure decreases and pulmonary blood flow increases as the arterial pressure increases toward the base of the lung.

In the lower portions of the lungs, alveolar pressure is lower than the pressure in all parts of the pulmonary circulation and blood flow is determined by the arterial-venous pressure difference.

Ventilation and Perfusion Relationships For efficient gas exchange it is important that there is a match between ventilation of the alveoli (VA) and their perfusion (Q). There is a wide variation in the V A/Q ratio throughout

both normal and diseased lung. In the normal lung the extreme relationships between alveolar ventilation and perfusion are: • Ventilation with reduced perfusion (physiological dead space) • Perfusion with reduced ventilation (physiological shunting).

In normal lungs there is a tendency for ventilation not to be matched by perfusion towards the apices, with the reverse occurring at the bases.

An increased physiological shunt results in arterial hypoxaemia. The effects of an increased physiological deadspace can usually be overcome by a compensatory increase in the ventilation of normally perfused alveoli. In advanced disease this compensation cannot occur, leading to increased alveolar and arterial PCO2 , together with hypoxaemia which cannot be compensated by increasing ventilation.

Hypoxaemia occurs more readily that hypercapnia because of the different ways in which oxygen and carbondioxide are carried in the blood. Carbondioxide can be considered to be in simple solution in the plasma, the volume carried being proportional to the partial pressure.

Oxygen is carried in chemical combination with haemoglobin in the red blood cells, and the relationship between the volume carried and the partial pressure is not linear. Alveolar hyperventilation reduces the alveolar PCO2 and diffusion leads to a proportional fall in the carbondioxide content of the blood. However, as the haemoglobin is already saturated with oxygen, there is no significant increase in the blood oxygen content as a result of increasing the alveolar Po2 through hyperventilation. The hypoxaemia of even a small amount of physiological shunting cannot therefore be compensated for by hyperventilation.

The Pao2 and PaCO2 of some individuals who have mild disease of the lung causing slight VA/Q mismatch may still be normal. Increasing the requirements for gas exchange by exercise will widen the VA/Q mismatch and the Pao2 will fall. VA/Q mismatch is by far the most common cause of arterial hypoxaemia.

Plumonary Reservoir: Because of their distensibility, the pulmonary veins are an important blood reservoir. When a normal individual lies down, the pulmonary blood volume increases by up to 400 mL, and when the person stands up this blood is discharged into the general circulation. This shift is the cause of the decrease in vital capacity in the supine position and is responsible for the occurrence of orthopnea in heart failure.

Regulation of Pulmonary Blood Flow: It is unsettled whether pulmonary veins and pulmonary arteries are regulated separately, although constriction of the veins increases pulmonary capillary pressure and constriction of pulmonary arteries increases the load on the right side of the heart.

Plumonary blood flow is affected by both active and passive factors. There is an extensive autonomic innervation of the pulmonary vessels, and stimulation of the cervical sympathetic ganglia reduces pulmonary blood flow by as much as 30%. The vessels also respond to circulating humoral agents. Many of the dialator responses are endothelium dependent and presumably operate via release of NO (Nitric Oxide).

Passive factors such as cardiac output and gravitational forces also have significant effects on pulmonary blood flow. Local adjustments of perfusion to ventilation are determined by local effects of O2 or its lack. With exercise, cardiac output increases and pulmonary arterial pressure rises proportionately with little or no vasodilation. More red cells move through the lungs without any reduction in the O2 saturation of the hemoglobin in them, and consequently, the total amount of O2 delivered to the systemic circulation is increased.

Capillaries dilate, and previously underperfused capillaries are “recruited” to carry blood.

The net effect is a market increase in pulmonary blood flow with few if any alterations in autonomic outflow to the pulmonary vessels.

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Xe can used to survey local pulmonary blood flow by injecting a saline solution of the gas intravenously while monitoring the chest. The gas rapidly enters the alveoli that are perfused normally but fails to enter those that are not perfused. Another technique for locating poorly perfused areas is injection of macroaggregates of albumin labeled with radioactive iodine.

These aggregates are large enough to block capillaries and small arterioles, and they lodge only in vessels in which blood was flowing when they reached the lungs. Although it seems paradoxic to study patients with defective pulmonary blood flow by producing vascular obstruction, the technique is safe because relatively few particles are injected. The particles block only small number of pulmonary vessels and are rapidly removed by the body.

When a bronchus or a bronchiole is obstructed, hypoxia develops in the underventilated alveoli beyond the obstruction. The O2 deficiency apparently acts directly on vascular smooth muscle in the area to produce constriction, shunting blood away from the hypoxic area.

Accumulation of CO2 leads to a drop in pH in the area, and a decline in pH also produces vasoconstriction in the lungs, as opposed to the vasodilation it produces in other tissues.

Conversely, reduction of the blood flow to a portion of the lung lowers the alveolar PCO 2 in that area, and this leads to constriction of bronchi supplying it, shifting ventilation away from the poorly perfused area.

Systemic hypoxia also causes the pulmonary arterioles to constrict, with a resultant increase in pulmonary arterial pressure.

Functions of the Respiratory System Lung Defense Mechanisms The respiratory passage that lead from the exterior to the alveoli do more than serve as gas conduits. They humidify and cool or warm the inspired air so that even very hot or very cold air is at or near body temperature by the time it reaches the alveoli. Bronchial secretions contain secretory immunolobulins and substances that help resist infections and maintain the intergrity of the mucosa. In addition, the epithelium of the paranasal sinuses appears to produce NO, which is bacteriostatic and helps prevent infections.

The pulmonary epithelium contains an interesting group of protease-activated receptors (PARs) that when activated trigger release of PGE 2, which in turn protects the epithelial cells.

These receptors, which are also present in the gastrointestinal tract, are activated when thrombin or trypsin partially digests ligands tethered to them. The PAR2 is form is the form of the receptor in the respiratory tract.

The pulmonary alveolar macrophages (PAMs, “dust cells”) are another important component of the pulmonary defense mechanisms. Like other macrophages, these cells come orginally

from the bone marrow. They are actively phagocytic and ingest inhaled bacteria and small particles. They also help process inhaled antigens for immunologic attack, and they secrete substances that attract granulocytes to the lungs as well as substances to stimulate granulocyte and monocyte formation in the bone marrow. When the macrophages ingest large amounts of the substances in cigarette smoke, they may also release lysosomal products into the extracellular space. This causes inflammation. Silica and asbestos particles also cause extracellular release of lysosomal enzymes.

Various mechanisms operate to prevent foreign matter form reaching the alveoli. The hairs in the nostrils strain out many particles larger than 10 µm in diameter. Most of the remaining particles of this size settle on mucous membranes in the nose and pharynx; because of their momentum, they do not follow the airstream as it curves downward into the lungs, and they impact on or near the tonsils and adenoids, large collections of immunologically active lymphoid tissue in the back of the pharynx. Particles 2-10µm in diameter generally fall on the walls of the bronchi as the air flow slows in the smaller passages. There they initiate reflex bronchial constriction and coughing. They are also moved away from the lungs by the “ciliary escalator.” The epithelium of the respiratory passages from the anterior third of the nose to the beginning of the respiratory bronchioles is ciliated, and the cilia, which are covered with mucus, beat in a coordinated fashion at a frequency of 1000-1500 cycles per minute. The ciliary mechanism is capable of moving particles away form the lungs at a rate of at least 16 mm/min. Particles less than 2 µm in diameter generally reach the alveoli, where they are ingested by the macrophages. The importance of these defense mechanisms is evident when one remembers that in modern cities, each liter of air may contain several million particles of dust and irritants.

When ciliary motility is defective, mucus transport is virtually absent. This leads to chronic sinusitis, recurrent lung infections, and bronchiectasis. Ciliary immotility may be produced by various air pollutants, or it may be congenital. One congenital form is Kartagener’s syndrome, in which the axonemal dynein, the ATPase molecular motor that produces ciliary beating, is absent. Patients with this condition also are infertile because they lack motile sperm, and they often have situs inversus, presumably because the cilia necessary for rotating the viscera are nonfunctional during embryonic development.

Metabolic & Endocrine Functions of the Lungs In addition to their functions in gas exchange, the lungs have a number of metabolic functions. They manufacture surfactant for local use as noted above. They also contain a fibrinolytic system that lyses clots in the pulmonary vessels. They release a variety of substances that enter the systemic arterial blood, and they remove other substances form the systemic venous blood that reach them via the pulmonary artery. Prostaglandins are removed from the circulation, but they are also synthesized in the lungs and released into the blood when lung tissue is stretched.

The lungs also activate one hormone; the physiologically inactive decapeptide angiotensin I is converted to the pressor, aldosterone-stimulating octapeptide angiotension II in the pulmonary circulation. The reaction occurs in other tissues as well, but it is particularly prominent in the lungs. Large amounts of the angiotensin-converting enzyme responsible for this activation are located on the surface of the endothelial cells of the pulmonary capillaries.

The converting

enzyme also inactivates bradykinin. About 70% of the angiotensin I reaching the lungs , is converted to angiotensin II in a single trip through the capillaries.

Removal of serotonin and norepinephrine reduces the amounts of these vasoactive substances reaching the systemic circulation. However, many other vasoactive hormones pass through the lungs without being metabolized. These include epinephrine, dopamine, oxytocin, vasopressin, and angiotensin II. In addition, as noted in various amines and polypeptides are secreted by neuroendocrine cells in the lungs.

Defence mechanisms of the respiratory tract: Pulmonary disease often results form a failure of the many defence mechanisms that usually protect the lung in a healthy individual. These can be divided into :  Physical and Physiological Mechanisms 

Humoral and Cellular Mechanisms.

Physical and Physiological mechanisms Humidification This prevents dehydration of the epithelium.

Particle Removal: Over 90% of particles greater than 10 Âľm diameter are removed in the nostril or nasophrynx.

This includes most pollen grains which are typically > 20 microns in diameter. Particles between 5-10 microns become impacted in the carina. Particles smaller than 1 micron tend to remain airborne, thus the particles capable of reaching the deep lung are confined to the 1-5 micron range.

Particle Expulsion This is affected by coughing, sneezing or gagging.

Respiratory Tract Secretions The mucus of the respiratory8 tract is a gelatinous sub-stance consisting chiefly of acid and neutral polysaccharides. The mucus consists of 5 mm thick get that is relatively impermeable to water. This floats on a liquid or sol layer that is present around the cilia of the epithelial cells. The gel layer is secreted form goblet cells and mucous glands as distinct globules that coalesce increasingly in the central airways to form a more or less continuous mucus blanket.

Under normal conditions the tips of the cilia are in contact with the under surface of the gel phase and coordinate their movement to push the mucus blanket upwards. Whilst it may only take 30-60 minutes for mucus to be cleared from the large bronchi, there may be a delay of several days before clearance is achieved from respiratory bronchioles. One of the major long-term effects of cigarette smoking is a reduction in mucociliary transport. This contributes to recurrent infection and in the larger airways it prolongs contact with carcinogens. Air pollutants, local and general anesthetics and bacterial and viral infections also reduce mucociliary clearance.

Congenital defects in mucociliary transport occur. In the immotile cilia syndrome there is an absence of the dynein arms in the cilia themselves, and in cystic fibrosis an abnormal mucus is associated with ciliary dyskinesia. Both diseases are characterized by recurrent infections and eventually with the development of bronchiectasis.

Humoral and cellular mechanisms Non- Specific soluble factors • • • • • • •

α1 Antitrypsin is present in lung secretions derived from plasma. It inhibits chymotrypsin and trypsin and neutralizes proteases and elastase.

Lysozyme is an enzyme found in granulocytes that has bactericidal properties.

Lactoferrin is synthesized from epithelial cells and neutrophil granulocytes and has bactericidal properties.

Interferon is produced by most cells in response to viral infection. It is a potent modulator of lymphocyte function. It renders other cells resistant to infection by a other virus.

Complement is present in secretions and is derived by diffusion from plasma. In association with antibodies, it plays an importnt cytotoxic role.

Surfactant protein A (SPA) is one of four species of surfactant proteins which opsonizes bacteria/ particles, enhancing phagocytosis by macrophages.

Defensins are bactericidal peptides present in the azurophil granules of neutrophils.

Pulmonary Alveolar Macrophages These are derived from precursors in the bone marrow and migrate to the lungs via the bloodstream. They phagocytose particles, including bacteria, and are removed by the mucociliary escalator, lymphatics and bloodstream. They are the dominant cell in the airways at the level of the alveoli and comprise 90% of all cells obtained by bronchoalveolar lavage.

Alveolar macrophages work principally as scavengers and are not particularly good at presenting antigens to the immune system. Dendritic cells form a network throughout the airways and are thought to be the key antigen-presenting cell in the airway.

Lymphoid Tissue The lung contains large numbers of lymphocytes which are scattered throughout the airways.

In animals, aggregates of bronchus-associated lymphoid tissue (BALT) can be identified but these are not normally found in humans. Sensitized lymphocytes contribute to local immunity through differentiation into IgA-secreting plasma cells. IgG and IgE are found in low concentrations in airway secretions from a combination of local and systemic production.

In addition to these resident cells, the lung has the usual range of acute inflammatory responses and can mobilize neutrophils promptly in response to injury or infection and play a major part in inflammatory conditions such as asthma.

Haemoptysis Haemoptysis is defined as the expectoration of blood from the respiratory tract, a spectrum that varies from blood-streaking of sputum to coughing up large amounts of pure blood.

Massive haemoptysis is variably defined as the expectoration of >100 to > 600 mL of blood over a 24-h period, although the patient’s estimation of the amount of blood is notoriously unreliable. Expectoration of even relatively small

amounts of blood is a frightening symptom and can be a marker for potentially serious disease, such as bronchogenic carcinoma. Massive haemoptysis, on the other hand, can represent an acutely life-threatening problem. Large amounts of blood can fill the airways and the alveolar spaces, not only seriously disturbing gas exchange but potentially causing the patient to suffocate.

Aetiology: Because blood originating from the nasopharynx or the gastrointestinal tract can mimic blood coming from the lower respiratory tract, it is important to determine initially that the blood is not coming from one of these alternative sites. Clues that the blood is originating from the gastrointestinal tract include a dark red appearance and an acidic pH, in contrast to the typical bright red appearance and alkaline pH of true haemoptysis.

The bronchial arteries, which are part of the high-pressure systemic circulation, originate either from the aorta or from intercostal arteries and are the source of bleeding in bronchitis or bronchiectasis or with endobronchial tumours.

The most common site of bleeding is the airways, i.e., the tracheobronchial tree, which can be affected by inflammation (acute or chronic bronchitis, bronchiectasis) or by neoplasm (bronchogenic carcinoma, endobronchial metastatic carcinoma, or bronchial carcinoid tumor). Blood orginating from the pulmonary parenchyma can be either from a localized source, such as an infection (pneumonia, lung abscess, tuberculosis, or from a process diffusely affecting the parenchyma (as with a coagulopathy or with an autoimmune process such as Goodpasture’s syndrome). Disorders primarily affecting the pulmonary vasculature include pulmonary embolic disease and those conditions associated with elevated pulmonary venous and capillary pressures, such as mitral stenosis or left ventricular failure.

Although the relative frequency of the different etiologies of hemoptysis varies, most recent studies indicate that bronchitis and bronchogenic carcinoma are the two most common causes. Tuberculosis and bronchiectasis are the most common causes of massive haemoptysis. Even after extensive evaluation, a sizable proportion of patients (up to 30%) have no identifiable aetiology for their haemoptysis. These patients are classified as having idiopathic or cryptogenic haemoptysis, and subtle airway or paranchymal disease is presumably responsible for the bleeding.

Aetiology of Haemoptysis 1.

Diseases of the respiratory system

A.

Infective and inflammatory conditions i.

Pulmonary tuberculosis

ii.

Bronchiectasis

iii.

Lung abscess

iv.

Chronic bronchitis.

v.

Pulmonary infarction

vi.

Pneumonia

vii.

Primary pulmonary hypertension

viii.

Acute bronchitis

ix.

Mycotic infection of the lung

x.

Parasitic diseases of the lunga. Pulmonary amoebiasis. b. Hydatid cyst c. Lung fluke ix.

B.

Viral infection: Small pox, chicken pox, measles

Neoplastic conditions I.

Bronchial carcinoma

II.

Bronchial adenoma

III.

Metastatic tumours.

IV.

Cavernous haemangioma.

V.

Alveolar cell carcinoma.

VI.

Mediastinal turnours.

VII.

Carcinoma of the trachea.

2.

Diseases of the cardiovascular system:

I.

Mitral stenosis

II.

Left heart failure

III.

Aortic aneurysm

IV.

Hypertension

V.

Hereditary telangiectasia

VI.

Left atrial tumours.

VII.

Congenital heart disease.

VIII. 3.

Infective endocarditis.

Connective tissue diseases: i) Systemic lupus erythematosus. ii) Poly arteritis nodosa. iii) Wegener’s granulomatosis.

4.

Haemorrhagic diseases: i) Idiopathic thrombocytopenic purpura. ii) Leukaemia iii) Aplastic anaemia. iv) Anticoagulants v) DIC vi) Scurvy

5.

Miscellaneous: I. Traumatic II.

Foreign body

III.

Idiopathic pulmonary haemosiderosis

IV.

Good Pasteur’s syndrome

V. VI. VII. VIII. IX. X.

Sarcoidosis Cystic fibrosis Pulmonary alveolar microlithiasis.

Middle lobe syndrome Pulmonary eosinophilia Pulmonary endometriosis

Haemoptysis in Different Diseases: Pulmonary tuberculosis Haemoptysis is a classical symptom of pulmonary tuberculosis and may vary from mere blood staining of the sputum to the rarer occurrence of sudden eruption of half a litre or more of blood, occasionally immediately fatal. The mechanism of bleeding depends upon the site, type and the stage of lesion.

In exudative lesion small pulmonary vessels are necrosed due to softening of the lung parenchyma.

In tuberculosis, abscess formation and cavitations may occur. The blood vessels that traverse through the wall of the cavity or through the cavity

undergo aneurysmal dilation which rupture on straining and may result in profuse haemoptysis. A healed and calcified tuberculous lymph node may impinge into the bronchial wall. Erosion and later ulceration occurs due to pressure of the hard lymph node resulting in haemoptysis. The haemoptysis usually proceed the coughing out of a broncholith or accompany it. If the lymph node contains tubercle bacilli, there may result in bronchial spread of tuberculosis. Tuberculous ulceration of the trachea or bronchi may be the result of primary infection or a part of wide spread parenchymal infection.

This ulceration of the mucosa erodes the smaller bronchial vessels and cause haemoptysis. Occasionally severe and repeated haemoptysis may be due to quite localized apical fibrosis associated with healed tuberculosis.

Radiologically calcified spots may be found. Sometimes bronchiectatic changes are found in these area where bleeding occurs from the granulation tissue on the wall of the dilated bronchi that may or may not be tubercolous.

Brochiectasis: Bronchiectasis is the term used to describe abnormal dilatation of the bronchi. It is usually acquired but may result from an underlying genetic or congenital defect of airway defences.Bronchiectasis is usually caused by chronic inflammation and infection in the airways.

Localized bronchiectasis may be due to bronchial distension resulting from the accumulation of pus beyond an obstructing bronchial lesion, such as enlarged tuberculous hilar lymph nodes, a bronchial tumour or an inhaled foreign body (e.g. an aspirated peanut.)

The bronchiectatic cavities are lined by granulation tissue, squamous epithelium or normal ciliated epithelium.

There may be also inflammatory changes in the deeper layers of the bronchial wall and hypertrophy of the bronchial arteries. Chronic inflammatory and fibrotic changes are usually found in the surrounding lung tissue.

SYMPTOMS OF BRONCHIECTASIS: 1). Due to accumulation of pus in dilated bronchi: Chronic productive cough is usually worse in morning and often brought on by changes of posture. Sputum is often copious and persistently purulent in advanced disease. Halitosis is a common accompanying feature.

Due to inflammatory changes in lung and pleura surrounding dilated bronchi: Fever, malaise, and increased cough and sputum production and when spread of infection causes pneumonia, which may be associated with pleurisy. Recurrent pleurisy in the same site often occurs in bronchiectasis.

Haemoptysis: Can be slight or massive and is often recurrent. Usually associated with purulent sputum or an increase in sputum production, which can be the only symptom in dry bronchiectasis.

General health: When disease is extensive and sputum persistently purulent a decline in general health occurs with weight loss, anorexia, lassitude, low-grade fever, and failure to thrive in children. In these patients digital clubbing is common.

In bronchiectasis there are three varieties of dilations. These are cylindrical, fusiform and saccular. Haemoptysis is more common in saccular variety.

Bleeding may occur from highly vascular granulation tissue that appears in the wall of dilated bronchi. There is anatomical communication between the pulmonary and bronchial arteries. In the wall of the dilated bronchi these vessels get wide aneurysmal dilatation. The walls become thin. Severe haemoptysis may result from the rupture of these anastomosing aneurysms.

The dilated and deformed bronchi are the site of chronic infection which causes mucosal ulceration and erosion of blood vessels causing bleeding.

LUNG ABSCESS: Suppurative pneumonia is the term used to describe a form of penumonic consolidation in which there is destruction of the lung parenchyma by the inflammatory process. Although microabscess formation is a characteristic histological feature of suppurative pneumonia, it is usual to restrict the term pulmonary abscess to lesions in which there is a large localized collection of pus or a cavity lined by chronic inflammatory issue, from which pus has escaped by rupture into a bronchus.

Suppurative pneumonia and pulmonary abscess may be produced by infection of previously healthy lung tissue with Staphylococcus aureus or Klebsiella pneumoniae. These are, in effect, primary bacterial pneumonias associated with pulmonary suppuration. More frequently, suppurative pneumonia10 and pulmonary abscess develop after the inhalation of septic material during operations on the nose, mouth or throat under general anaesthesia, or of vomitus during anaesthesia or coma. In such circumstances gross oral sepsis may be a predisposing factor. Additional risk factors for aspiration pneumonia include vocal cord palsy, achalasia or oesophageal reflux and alcoholism. Aspiration into the lungs of acid gastric contents can give rise to a severe haemorrhagic pneumonia often complicated by the acute respiratory distress syndrome. Intravenous drugusers are at particular risk of developing haematogenous lung abscess, often in association with endocarditis affecting the pulmonary and tricuspid valves.

Bacterial infection of a pulmonary infarct or of a collapsed lobe may also produce a suppurative pneumonia or a lung abscess. The organism isolated from the sputum include Strep. pneumoniae, staph. aureus, strep. pyogenes, H. influenzae and in some cases, anaerobic bacteria. In many cases, however, no pathogen can be isolated, particularly when antibiotics have been given.

The

clinical

features

of

suppurative

pneumonia

are

:

1) Symptoms:

• Cough productive of large amounts of sputum which is sometimes fetid and blood stained.

• Pleural pain common.

• Sudden expectoration of copious amounts of foul smelling sputum occurs if abscess ruptures into a bronchus.

2) Clinical signs:

• High remittent pyrexia.

• Profound systemic upset.

• Digital clubbing may develop quickly (10-14 days).

• Chest examination usually reveals signs of consolidation or sings of cavitation may found.

• Pleural rub is common.

• Rapid deterioration in general health with marked weight loss can occur if disease not adequately treated.

Acute Bronchitis and Tracheitis: Initially irritating unproductive cough accompanied by retrosternal discomfort present in tracheitis. Chest tightness, wheeze and breathlessness when bronchi become involved. Tracheitis causes pain on coughing. Sputum is initially scanty or mucoid. After a day or so sputum becomes mucopurulent, more copious and, in tracheitis, often blood-stained. Acute bronchial infection may be associated with a pyrexia of 38-39 0C and a neutrophil leucocytosis. Spontaneous recovery occurs over a few days.

Complication:

a) Bronchopneumonia b) Exacerbation of chronic bronchitis which often results in type II Respiratory failure in patients with severe COPD. c) Acute exacerbation of bronchial asthma.

PNEUMONIA: Pneumonia is defined as an acute respiratory illness associated with recently developed radiological pulmonary shadowing which may be segmental, lobar or multilobar. The clinical context in which a pneumonia develops is highly suggestive of the likely organism involved and hence the immediate choice of antibiotics; pneumonias are therefore usually classified as community acquired, hospital acquired (nosocomial), or those occurring in immunocompromised hosts or patients with underlying damaged lung (including suppurative and aspirational pneumonias). Lobar pneumonia is a radiological and pathological term referering to homogeneous consolidation of one or more lung lobes, often with associated pleural inflammation; bronchopneumonia refers to more patchy alveolar consolidation associated with bronchial and bronchiolar inflammation often affecting both lower lobes.

Community-Acquired pneumonia (CAP) The incidence varies with age, being much higher in the very young and the elderly. Pneumonia accounts for almost one-fifth of childhood deaths worldwide, with approximately 2 million children under 5 dying each year. Most patients may be safely managed at home, but hospital admission is necessary in 20-40% of patients (5-10% of whom require intensive care). The mortality rate of adults managed at home is very low (< 1%); hospital death rates are typically between 5 and 10% and may be as high as 50% in severe illness.

Community acquired pneumonia is usually spread by droplet infection and most cases occur in previously healthy individuals. Several factors can impair the effectiveness of local defenses and predispose to community acquired pneumonia. Once the organism settles in the alveoli, an inflammatory response ensures. The classical pathological response evolves through the phases of congestion, red and then grey hepatisation, and finally resolution with little or no scarring.

Clinical features: Pneumonia typically presents as an acute illness in which systemic features such as fever, rigors, shivering and vomiting often predominate. The appetite is usually lost and headache frequently reported. Pulmonary symptoms include cough, which at first is characteristically short, painful and dry, but later accompanied by the expectoration of mucopurulent sputum. Rustcoloured sputum may be seen in patients with Streptococcus pneumoniae, and the occasional patient may report haemoptysis. Pleuritic chest pain may be a presenting feature and on occasion may be referred to the shoulder or

anterior abdominal wall. Upper abdominal tenderness is sometimes apparent in patients with lower lobe pneumonia or if there is associated hepatitis. Less typical presentations may be seen in the very young and the elderly.

The majority of cases of community acquired pneumonia are due to infection with Strep. Pneumoniae. Thereafter the most likely alternatives depend on the age of the patient and the clinical circumstances. For example, Mycoplasma pneumoniae and Chlamydia pneumoniae are common in young adults but seldom reported in the elderly, whereas Haemophilus influenzae should be considered in elderly patients but is rarely reported in young adults.

Hospital-Acquired Pneumonia: Hospital-acquired or nosocomial pneumonia refers to a new episode of pneumonia occurring at least 2 days after admission to hospital. The term includes post-operative and certain forms of aspiration pneumonia, and pneumonia or bronchopneumonia developing in patients with chronic lung disease, general debility or those receiving assisted ventilation.

The elderly are particularly at risk and this condition now occurs in 2.5% of all hospital admissions.

The most important distinction between hospital and community-acquired pneumonia is the difference in the spectrum of pathogenic organisms, with the majority of hospital acquired infections caused by Gram-negative bacteria. These include Escherichia, Pseudomonas and Klebsiella species.

Infections caused by Staph. aureus (including multidrug-resistant â&#x20AC;&#x201C; MRSAforms) are also common in hospital, and anaerobic organisms are much more likely than in pneumonia acquired in the community. This profile of organisms in part reflects the high rate of colonisation of the nasopharynx of hospital patients with Gram-negative bacteria together with poor host defenses and general inability of the severely ill or semiconscious patient to clear upper airway and respiratory tract secretion.

In the elderly or debilitated patient who develops acute bronchopneumonia symptoms of acute bronchitis are followed after 2 or 3 days by increased cough and sputum purulence associated with a rise in temperature.

Breathlessness and central cyanosis may then appear, but pleural pain is uncommon. In the early stages the physical signs are those of acute bronchitis followed by the development of crackles. There is a neutrophil leucocytosis and the chest X-ray shows mottled opacities in both lung fields, chiefly in the lower zones.

Respiratory diseases caused by fungi: The majority of fungi encountered by humans are harmless saprophytes but in certain circumstances some species may cause disease by infecting human tissue, promoting damaging allergic reactions or producing toxins. â&#x20AC;&#x2DC;Mycosisâ&#x20AC;&#x2122; is the term applied to disease caused by fungal infection.

Aspergillosis: Most cases of bronchopulmonary aspergillosis are caused by Aspergillus fumigatus, but other members of the genus (A. clavatus, A. flavus, A. niger and A. terreus) occasionally cause disease.

Allergic Bronchopulmonary aspergillosis (ABPA) ABPA is caused by a hypersensitivity reaction to A. fumigatus involving the bronchial wall and peripheral parts of the lung. It is more common in the autumn and winter and is usually associated with asthma. ABPA can occur in non-asthmatic patients and is a recognised complication of cystic fibrosis.

It is one of the causes of pulmonary eosinophilia.

Radiographic features include transient diffuse pulmonary infiltrates and lobar or segmental pulmonary collapse. Permanent radiographic changes of bronchiectasis (tramline, ring and gloved-finger shadows) are seen predominantly in the upper lobes in patients with advanced disease.

Features of Allergic bronchopulmonary aspergillosis: • Asthma (in the majority of cases) • Proximal bronchiectasis • Positive skin test to an extract of Aspergillus fumigatus • Elevated total serum IgE>417 KU/I or 1000 ng/ml.

• Elevated serum IgE-A fumigatus or IgG-A fumigatus • Peripheral blood eosinophilia > 0.5 × 109/litre • Presence or history of chest X-ray abnormalities.

• Fungal hyphae of Aspergillus fumigatus on microscopic examination of sputum Intracavitary mycetoma Inhaled air-borne spores of fungi may lodge and germinate in areas of damaged lung tissue forming a fungal ball (mycetoma). These may form in any area of damaged lung but the upper lobes are most frequently involved, reflecting the fact that mycetomas readily form in tuberculous cavities. Less common causes include damage from a lung abscess cavity, a bronchiectatic space, pulmonary infarct, sarcoidosis, ankylosing spondylitis or even a cavitated tumour. As Aspergillus fumigatus is the most common organism identified, the term aspergilloma is often used, but other fungi may be implicated.

The range of presentation is varied. Mycetomas are often asymptomatic, being identified on chest X-ray as a dense rounded shadow in the upper lobe.

However, in some patients they may be responsible for recurrent

haemoptysis, which may be severe and life-threatening. Non-specific systemic features such as lethargy and weight loss may also reported.

Treatment is often disappointing. Selected patients with good respiratory reserve may benefit from surgery, particularly those who experience massive haemoptysis25. However, surgical resection may be accompanied by significant morbidity and mortality. Bronchial artery embolisation provides a palliative approach to haemoptysis.

Invasive pulmonary aspergillosis: Invasion of previously healthy lung tissue by Aspergillus fumigatus is uncommon but can produce a serious and often fatal condition, which usually occurs in patients who are immunocompromised by either drugs or disease.

Spread of the disease to the lungs is usually rapid, with the production of consolidation, necrosis and cavitation. There is grave systemic disturbance.

The formation of multiple abscesses is associated with the production of copious amounts of purulent sputum which is often blood-stained.

Hydatid Cyst: A hydatid cyst is typically acquired in childhood and it may, after growing for some years, causes pressure symptoms. These symptoms vary, depending on the organ or tissue involved. In nearly 75% of patients with hydatid disease the right lobe of the liver is invaded and contains a single cyst. In others a cyst may be found in lung, bone, brain or elsewhere.

The diagnosis depends on the clinical, radiological and ultrasound findings in a patient who has lived in close contact with dogs in an endemic area.

Complement fixation and ELISA are positive in 70-90% of patients.

Hydatid cysts should be excised wherever possible. Great care is taken to avoid spillage and cavities are sterilised with 0.5% silver nitrate or 2.7% sodium chloride. Albendazole (400 mg 12-hourly for 3 months) is used for inoperable disease, and to reduce the infectivity of cysts pre-operatively.

Praziquantel 20 mg/kg 12 hourly for 14 days kills protoscolices perioperatively.

Bronchogenic Carcinoma: Bronchial carcinomas arise from the bronchial epithelium or mucous glands.

When the tumour arises in a large brochus, symptoms arise early, but tumours originating in a peripheral bronchus can attain a very large size without producing symptoms. Peripheral squamous tumours may undergo central necrosis and cavitation, and may have similar radiographic features to a lung abscess. Bronchial carcinoma may involve the pleura either directly or by lymphatic spread and may extend into the chest wall, invading the intercostal nerves or the brachial plexus and causing severe pain. The primary tumour, or tumour within lymph node metastases, may spread into the mediastinum and invade or compress the pericardium, oesophagus, superior vena cava, trachea, phrenic or left recurrent laryngeal nerves.

Lymphatic spread to supraclavicular and mediastinal lymph nodes is also

frequently observed. Blood-borne metastases occur most commonly in liver, bone, brain, adrenals and skin. Even a small primary tumour may cause widespread metastatic deposits and this is a particular characteristic of small cell type lung cancers.

Non-metastatic extrapulmonary manifestations of bronchial carcinoma: Endocrine: • Inappropriate antiduretic hyponatraemia.

hormone

(ADH)

secretion

causing

• Ectopic adrenocorticotrophic homone (ACTH) secretion.

• Hypercalcaemia due to secretion of parathyroid hormone (PTH).

• Carcinoid syndrome.

• Gynaecomastia Neurological • Polymeuropathy.

• Myelopathy • Cerebellar degeneration.

• Myasthenia Gravis Others: • Digital clubbing • Hypertrophic pulmonary osteoarthropathy • Nephrotic syndrome • Polymyositis and dermatomyositis.

• Eosinophilia.

Lung cancer presents in many different ways. Most commonly, symptoms reflect local involvement of the bronchus, but may also arise from spread to the chest wall or mediastinum, from distant blood-borne spread or, less commonly as a result of a variety of non-metastatic paraneoplastic syndromes.

Cough is the most common early symptom; it is often dry but sputum may be purulent if there is secondary infection. A change in the character of the regular cough of a smoker, particularly if it is associated with other new respiratory symptoms, should always alert the clinician to the possibility of bronchial carcinoma.

Heamoptysis is a common symptom, especially in tumours arising in central bronchi. Occasionally, central tumours invade large vessels, causing massive haemoptysis which may be fatal. Repeated episodes of scanty haemoptysis or blood-streaking of sputum in a smoker are highly suggestive of bronchial carcinoma and should always be investigated.

The patient may also present with symptoms due to blood-borne metastases, such as focal neurological defects, epileptic seizures, personality change, jaundice, bone pain or skin nodules. Lassitude, anorexia and weight loss usually indicate the presence of metastasis spread. Finally, the patient may present with symptoms referable to the presence of a number of nonmetastasis extra pulmonary manifestations. The most frequently encountered endocrine syndromes (inappropriate anti diuretic hormone (ADH) secretion and ectopic adrenocorticotrophic hormone (ACTH) secretion are usually associated with small-cell lung cancer. Hypercalcaemia due to secretion of parathyroid hormone (PTH)-like peptides is usually caused by squamous cell carcinoma. Associated neurological syndromes may occur with any type of bronchial carcinoma.

Secondary Tumours of the Lung : Metastasis occurs in the lungs through haematogenous dissemination from other organs like intestine, testes, liver, kidney, thyroid etc. and haemoptysis occurs in some cases due to invasion of bronchial mucosa or erosion of blood vessels or due to secondary infection.

The secondary deposits are usually multiple and bilateral. Often there are no respiratory symptoms and the diagnosis is made by radiological examination. Breathlessness may occur if a considerable amount of lung tissue has been replaced by metastatic tumour. Endobronchial deposits are uncommon but can cause haemoptysis and lobar collapse. Haemoptysis occurs in some cases due to invasion of bronchial mucosa or erosion of blood vessels or due to secondary infection.

Lymphangitic spread of carcinoma in the lung: Lymphatic infiltration may develop in patients with carcinoma of the breast, stomach, intestine, pancreas or bronchus. This grave condition causes severe and rapidly progressive breathlessness associate with marked hypoxaemia.

The chest X-ray shows diffuse pulmonary shadowing radiating from the hilar regions, often associated with septal lines, and CT scan shows characteristic polygonal thickened interlobular septa.

Mitral Stenosis: Mitral Stenosis is mostly rheumatic in origin and very rarely, it is congenital.

Pure or predominant occurs in approximately 40% of all patients with rheumatic heart disease. In others, lesser degrees of Mitral Stenosis may accompany mitral regurgitation (MR) and aortic valve lesions. In rheumatic stenosis the valve leaflets are diffusely thickened by fibrous tissue and/or calcific deposits. The mitral commissures fuse, the chordae tendineae fuse

and shorten, the valvular cusps become rigid, and these changes, in turn lead to narrowing at the apex of the funnel-shaped valve.

Thrombus formation and arterial embolization may arise from the calcified valve itself, but more frequently arise from the dilated left atrium (LA) in patients with atrial fibrillation.

In normal adults the mitral valve orifice is 4 to 6 cm 2. In the presence of significant obstruction, when the orifice is less than approximately 2 cm 2, blood can flow from the left atium to left ventricle only, if propelled by an abnormally elevated left atrioventricular pressure gradient, and that is the hemodynamic hallmark of mitral stenosis. When the mitral valve opening is reduced to 1cm2, then pressure of approximately 25 mm of Hg is required to maintain a normal cardiac output. The elevated pulmonary venous and pulmonary arterial wedge pressures reduce pulmonary compliance, contributing to exertional dyspnoea.

The clinical and hemodynamic features of MS are influenced importantly by the level of the Pulmonary arterial pressure. Pulmonary hypertension results from : (1) passive backward transmission of the elevated pressure; (2) pulmonary arteriolar constriction, which presumably is triggered by left atrium and pulmonary venous hypertension (reactive pulmonary hypertension); (3) interstitial edema in the walls of the small pulmonary vessels; and (4) organic obliterative change in the pulmonary vascular bed.

Severe pulmonary hypertension results in tricuspid regurgitation and pulmonary incompetence as well as right-sided heart failure.

As mitral stenosis progresses, lesser stresses precipitate dyspnoea, and patient becomes limited in daily activities. The redistribution of blood from the dependent portions of the body to the lungs, which occurs when the recumbent position is assumed, leads to orthopnoea and paroxysmal nocturnal dyspnoea. Pulmonary oedema develops when there is a sudden surge in flow across a markedly narrowed mitral orifice.

Haemoptysis results from rupture of pulmonary bronchial venous connections secondary to pulmonary venous hepertension. It occurs most frequently in patients who have elevated left atrial pressures without markedly elevated pulmonary vascular resistances.

As the severity of mitral stenosis progresses and the pulmonary vascular resistance rises or when tricuspid stenosis or tricuspid regurgitation develop, symptoms secondary to pulmonary congestion sometimes diminish, and the episodes of acute pulmonary oedema and hamoptysis may become reduced in frequency and severity. The elevation of pulmonary vascular resistance further increases RV systolic pressure leading to RV failure, fatigue, abdominal discomfort due to hepatic congestion and oedema.

Recurrent pulmonary emboli sometimes with infarction are an important cause of morbidity and mortality late in the course of mitral stenosis.

Pulmonary infection, like bronchitis, bronchopneumonia, and lobar

pneumonia, commonly complicate untreated mitral stenosis . Infective endocarditis is less common in mitral stenosis but more common in patients with combined mitral stenosis and mitral regurgitation. Chest pain occurs in about 10% of patients with severe mitral stenosis and it may be due to pulmonary hypertension or myocardial ischemia secondary to accompanying coronary atherosclerosis.

Pulmonary Thromboembolism When venous thrombi become dislodged from their site of formation, they embolize to the pulmonary arterial circulation or, paradoxically to the arterial circulation, through a patent foramen ovale or atrial septal defect.

About half of patients with pelvic vein thrombosis or proximal leg deep venous thrombosis (DVT) have pulmonary thromboembolism which is usually asymptomatic. Isolated calf vein or upper extremity venous thrombosis also poses a risk of pulmonary thromboembolism. Isolated calf vein thrombi are the most common source of paradoxical embolism.

Pulmonary embolism can have the following effects: 1.

Increased pulmonary vascular resistance due to vascular obstruction or neurohumoral agents including serotonin.

2.

Impaired gas exchange due to increased alveolar dead space from vascular obstruction and hypoxaemia from alveolar hypoventilation in the nonobstructed lung, right-to-left shunting, and impaired carbon monoxide transfer due to loss of gas exchange surface.

3.

Alveolar hyperventilation due to reflex stimulation of irritant receptors.

4.

Increased airway resistance due to bronchoconstriction.

5.

Decreased pulmonary compliance due to pulmonary oedema, haermorrhage, or loss of surfactant.

Progressive right heart failure is the usual cause of death from pulmonary thromboembolism. As pulmonary vascular resistance increases, right ventricular wall tension rises and perpetuates further right ventricular dilatation and dysfunction. Consequently, the interventricular septum bulges into and compresses an intrinsically normal left ventricle. Increased right ventricular wall tension also compresses the right coronary artery and may precipitate myocardial ischemia and right ventricular infarction. Underfilling of the left ventricle may lead to a fall in left ventricular output and systemic arterial pressure, thereby provoking myocardial ischemia due to compromised coronary artery perfusion. Eventually, circulartory collapse and death may ensue.

Patients with massive pulmonary thromboembolism present with systemic arterial hypotension. Primary therapy with thrombolysis or embolectomy offers the greatest chance of survival.

Those with moderate to large pulmonary thromboembolism have right ventricular hypokinesis on echocardiography but normal systemic arterial pressure. Patients with small to moderate pulmonary thromboembolism have both normal right heart function and normal systemic arterial pressure. They have a good prognosis with either adequate anticoagulation or an inferior vena caval filter.

Dyspnoea is the most frequent symptom of pulmonary thromboembolism , and tachypnoea is its most frequent sign. Whereas dyspnea, syncope, hypotension, or cyanosis indicate a massive pulmonary thromboembolism and pleuritic pain, cough, or hemoptysis often suggest a small embolism located distally near the pleura.

PULMONARY HYPERTENSION: Pulmonary hypertension is defined as a mean pulmonary artery pressure >25 mmHg at rest or 30 mmHg with exercise.

Although respiratory failure due to intrinsic pulmonary disease is the most common cause of pulmonary hypertension, servere pulmonary hypertension may occur as a primary disorder or as a result of chronic repeated thromboembolic events.

Pathological features include hypertrophy of both the media and intima of the vessel wall, and a clonal expansion of endothelial cells which take the appearance of plexiform lesions. There is marked narrowing of the vessel lumen and this, together with the frequently observed in situ thrombosis, leads to an increase in pulmonary vascular resistance and pulmonary hypertension.

Congenital Heart Disease: Congenital heart disease usually manifests in childhood but may pass unrecognised and not present until adult life. Defects which are well tolerated, e.g. atrial septal defect, may cause no symptoms until adult life or may be detected incidentally on routine examination or chest X-ray.

Congenital defects that were previously fatal in childhood can now be corrected, or at least partially corrected. Such patients may remain well for many years and subsequently re-present in later life with related problems such as arrhythmia or ventricular dysfunction.

Presentation of congenital Heart Diseases in Different Stages of life: 1) Birth and neonatal period: • Cyanosis • Heart failure.

2) Infancy and childhood: • Cyanosis

• Heart failure • Arrythmia • Murmur • Failure to thrive.

3) Adolescence and adulthood: • Heart failure.

• Murmur • Arrythmia • Cyanosis due to shunt revesal (Eisenmenger’s syndrome) • Hypertension (coarctation of aorta) • Late consequences of previous cardiac surgery e.g., arrythmia, heart failure, etc.

Symptoms may be absent, or the child may be breathless or fail to attain normal growth and development. Murmur, thrill or signs of cardiomegaly may be present. In coarctation of the aorta, radio-femoral delay may be noted. Tall stature with long limbs and lens dislocation may be obvious in Marfan’s syndrome. Features of other congenital conditions such as Down’s syndrome, may also be apparent. Cerebrovascular accidents and cerebral abscesses are complications of severe cyanotic congenital disease.

Early diagnosis is important because many type of congenital heart disease are amenable to surgical treatment, but this opportunity may be lost if secondary changes such as pulmonary vascular damage occur.Central cyanosis of cardiac origin occurs when desaturated blood enters the systemic circulation without passing through the lungs (i.e. a right-to-left shunt).

Persistently raised pulmonary flow (e.g. with left-to-right shunt) leads to increased pulmonary resistance followed by pulmonary hypertension.

Progressive changes, including obliteration of distal vessels, take place in the pulmonary vasculature and once established, the increased pulmonary resistance is irreversible. Central cyanosis appears and digital clubbing develops. The chest X-ray shows enlarged central pulmonary arteries and peripheral pruning of the pulmonary vessels. The ECG shows right ventricular hypertrophy. If severe pulmonary hypertension develops, a leftto-right shunt may reverse, resulting in right-to-left shunting and marked cyanosis (Eisenmenger’s syndrome). This is more common with large ventricular septal defects or persistent ductus arteriosus than with atrial sepal defects. Patients with Eisenmenger’s syndrome are at particular risk from abrupt changes in afterload that exacerbate right-to-left shunting, e.g. vasodilatation, anaesthesia, pregnancy.

Patients with congenital heart disease may develop haemoptysis due to development of left heart failure, subacute bacterial endocarditis, pulmonary hypertensionion etc. The commonest anomalies which cause left heart failure are, hypoplasia of the left ventricular out flow tract with aortic atresia, coarctation of the aorta, ventricular septal defect and patent ductus arteriosus. Fallotâ&#x20AC;&#x2122;s tetralogy with pulmonary artery atresia is a special situation in which the patient can survive up to middle-age. In these cases some complications such as haemoptysis can appear which can endangers the life of the patient.

Infective Endocarditis: Infective endocarditis is due to microbial infection of a heart valve (native or prosthetic), the lining of a cardiac chamber or blood vessel, or a congenital anomaly (e.g. septal defect). The causative organism is usually bacteria, but may be a rickettsia, chlamydia or fungus also.

Infective endocanditis typically occurs at sites of pre-existing endocardial damage. However, infection with particularly virulent or aggressive organisms (e.g. Staphylococcus aureus) can cause endocarditis in a previously normal heart, for example, staphylococcal endocarditis of the tricuspid valve is a common complication of intravenous drug misuse. Many acquired and congenital cardiac lesions are vulnerable to endocarditis, particularly areas of endocardial damage caused by a high-pressure jet of blood, such as ventricular septal defect, mitral regurgitation and aortic regurgitation. Infection tends to occur at sites of endothelial damage because these areas attract deposits of platelets and fibrin, which are vulnerable to colonization by blood-borne organisms. The avascular valve tissue and presence of fibrin aggregates help to protect proliferating organisms from host defense mechanisms. When the infection is established, vegetations composed of organisms, fibrin and platelets grow and many become large enough to cause obstruction; they may also break away as emboli. Adjacent tissues are destroyed and abscesses may form, valve regurgitation may develop or increase if the affected valve is damaged by tissue distortion, cusp perforation or disruption of chordae. Extracardiac manifestations such as vasculitis and skin lesions are due to emboli or immune complex deposition. Mycotic aneurysms may develop in arteries at the site of infected emboli.

Staphylococcus aureus is a common cause of acute endocartitis, orginating from skin infections, abscesses or vascular access sites (e.g. intravenous and central lines), or from intravenous drug misuse. It is a highly virulent and invasive organism, usually producing florid vegetations, rapid valve destruction and abscess formation.

Post-operative endocarditis after cardiac surgery may affect native or prosthetic heart valves or other prosthetic materials. The most common organism is a coagulase negative staphylococcus (staph. epidermidis), which is a normal skin commensal.

Staph. epidermidis occasionally causes endocarditis in patients who have not had cardiac surgery and its presence in

blood cultures may be erroneously dismissed as contamination. Another coagulase negative staphylococcus, Staph. lugdenensis, has recently been recognised as a cause of rapidly destructive acute endocarditis that is frequently associated with multiple emboli and often affects previously normal valves.

Yeasts and fungi (Candida, Aspergillus) may attack previously normal or prosthetic valves, particularly in immunocompromised patients or those with indwelling intravenous lines. Abscesses and emboli are common, and the mortality is high. Concomitant bacterial infection may be present.

Systemic Lupus Erythematosus (SLE): Acute alveolitis may be associated with diffuse alveolar haemorrhage. This condition is life-threatening and requires immunosuppression.

Pleuropulmonary involvement is more common in lupus than in any other connective tissue disorder and may be a presenting problem when it is sometimes attributed incorrectly to infection or pulmonary embolism. Up to two-thirds of patients have repeated episodes of pleurisy, with or without effusions. Effusions may be bilateral and may also involve the pericardium.

Some patients with SLE present with exertional dyspnoea and orthopnoea but without overt signs of pulmonary fibrosis. The chest X-ray reveals elevated diaphragms, and pulmonary function testing shows reduced lung volumes. This condition has been described as shrinking lungs and has been attributed to diaphragmatic myopathy.

Antiphospholipid sydrome is associated with an increased risk of venous and pulmoary thromboembolism and these patients require life-long anticoagulation.

Polyarteritis Nodosa (PAN) Polyarteritis nodusa is a necrotising vasculitis characterised by transmural inflammation of medium 26 sized to small arteries. All age groups can be affected, with a peak incidence in the fourth and fifth decades, and male female ratio is 2:1. Hepatitis B is a risk factor.

The basic pathological lesion affects the media of smaller blood vessels where there is fibrinoid necrosis with infiltration of neutrophil, plasma cells and giant cells. Weakening of the pulmonary vessels may result in small aneurysms which may rupture giving rise of haemoptysis. In the lungs there may be necrosis and cavity formation which may bleed. The bronchial vessels may also be involved and resulting ulceration of the trachea and bronchi which may be the source of bleeding. Sometimes there may be secondary infection and abscess formation which may also cause haemoptysis.

Clinical presentation is with myalgia, arthralgia, fever and weight loss in combination with manifestations of multisystem disease. The most common

skin lesions are palpable purpura, ulceration, infarction and livedo reticularis. In 70% of patients arteritis of the vasa nervorum leads to neuropathy which is typically symmetrical and affects both sensory and motor function. Severe hypertension and renal impairment may occur due to multiple renal infarctions.

Diagnosis is confirmed by finding multiple aneurysms and smooth narrowing of either the mesenteric, hepatic or renal arterial systems on angiography. Tissue biopsy may be definitive (muscle or sural nerve), even in the absence of angiographic abnormality.

Wegenerâ&#x20AC;&#x2122;s Granulomatosis: This granulomatous disease is one of the primary systemic vasculitides in which the small arteries are predominantly affected. It is characterized by lesions involving the upper respiratory tract, the lungs and the kidneys.

Often the disease starts with nasal mucosal ulceration followed by cough, haemoptysis and pleuritic pain. There may be involvement of skin and nervous system. The most remarkable radiographic feature is the migratory pattern, with large lesions clearing in one area and new lesions appearing in another area. The typical histological changes are usually best seen in the kidney where there is necrotizing microvascular glomerulonephritis.

Haemorrhagic diathesis: Haemoptysis may occur in any type of haemorrhagic diathesis. It occur with thrombocytopenia, haemophilia, aplastic anemia and leukaemia. It can also occur in scurvy.Diffuse alveolar haemorrhage may also occur due to thrombolytic therapy for acute myocardial infarction.

Traumatic: Different types of chest injury or damage of tissue by any chemicals, irritants cause haemoptysis in various ways. Lung tissue may be punctured by a fractured rib, stab injury, gunshot injury etc. which may lead to haemoptysis. Lungs may be contused by severe blunt trauma to the chest wall. The trachea, bronchial tree may be damaged by blunt trauma or automobile accidents.

Foreign Bodies: Foreign bodies in the respiratory tract cause direct trauma leading to laceration and ulceration causing haemoptysis. Removal of the foreign body is immediately required if it obstructed the respiratory tract. But removal of the foreign body must be carefully done so the it can not cause any injury which leads to bleeding.

Goodpastureâ&#x20AC;&#x2122;s Syndrome:

Rapidly progressive glomerulonephrtis is an inflammatory nephritis which causes rapid loss of renal function over days to weeks. This RPGN is typically seen in Good pasture’s syndrome. Renal biopsy shows crescentic lesions often associated with haemorrhage in the lung which may cause heamoptysis.

Sarcoidosis: Sarcoidosis is a multisystem27 granulomatous disorder. The aetiology remains uncertain. Links with atypical mycobacteria and viruses remain speculative; there is some evidence of familial clustering and genetic factor are undoubtedly important. Sarcoidosis appears less commonly in smokers.

The mediastinal and superficial lymph glands, lungs, liver, spleen, skin, eyes, parotid glands and phalangeal bones are most frequently affected, but all tissues may be involved. The characteristic histological feature is a noncaseating epithelioid granuloma ; fibrosis is seen in up to 20% of cases of pulmonary sarcoidosis. Disturbances in calcium metabolism reflect increased formation of calcitrol by alveolar macrophages and may lead to hypercalciuria, hypercalcaemia and rarely nephrocalcinosis.

Sarcoidosis is considered under the diagnostic term of Diffuse Paranchymal Lung Disease is over 90% of cases affect the lungs, but the presentation can be quite variable which mentioned below – • Asymptomatic – abnormal routine chest X-ray or abnormal liver function tests.

• Respiratory and constitutional symptoms (20-30%) • Erythema nodosum and arthralgia (20-30%) • Ocular symptoms (5-10%) • Skin sarcoid (including lupus pernio) (5%) • Superficial lymphadenopathy (5%) • Other (1%), e.g. hypercalcaemia, arrhythmias, nephrocalcinosis.

diabetes

insipidus,

cardiac

Lofgren’s syndrome: Lofgren’s syndrome an acute illness characterised by erythema nodosum, peripheral arthopathy, uveitis, bilateral hilar lymphadenopathy (BHL), lethargy and occasionally fever – is often seen in young women.

Alternatively, BHL may be detected in an otherwise asymptomatic individual undergoing a chest X-ray for other purposes. Pulmonary disease may also present in a more insidious manner with cough, exertional breathlessness and radiographic infiltrates; chest auscultation is often unremarkable. Fibrosis occurs in some patients and may cause a silent loss of lung function. Complications such as bronchiectasis, aspergilloma, pneumothorax, pulmonary hypertension have been reported , but these are fortunately rare.

CYSTIC FIBROSIS: Cystic Fibrosis is the result of mutations affecting a gene (on the long arm of chromosome 7) coding for a chloride channel known as cystic fibrosis transmembrane conductance regulator , which controls salt and water movement across epithelial cell membranes.

The genetic defect causes increased sodium chloride content in sweat and increased resorption of sodium and water from respiratory epithelium.

Relative dehydration of the airway epithelium is thought to predispose to chronic bacterial infection and ciliary dysfunction. The gene defect also causes disorders in the gut epithelium, pancrease, liver and reproductive tract.

The lungs are macroscopically normal at birth, however bronchiolar inflammation and infections usually lead to bronchiectasis in childhood. At this stage, the lungs are most commonly infected with Staphylococcus aureus; however, the majority of patients have Pseudomonas aeruginosa infection by the time they reach adolescence. Recurrent exacerbations of bronchiectasis, initially in the upper lobes but subsequently throughout both lungs, cause progressive lung damage resulting ultimately in death from respiratory failure. Other clinical manifestations of the gene defect include intestinal obstruction, exocrine pancreatic failure with malabsorption, diabetes and hepatic cirrhosis. Most men with Cystic Fibrosis are infertile due to failure of development of the vas deferens, but microsurgical sperm aspiration and in vitro fertilization are now possible. Genotype is a poor predictor of severity of disease in most individuals; even siblings with matching genotypes may have quite different phenotypes. This suggests that other modifier genes (as yet unidentified) influence clinical outcome.

The abnormality in the lung is bronchial obstruction by unusually viscid secretion of the mucus glands leading to secondary infection and later on purulent bronchitis and bronchiectasis which may cause haemoptysis.

Pulmonary Eosinophilia and Vasculitides: In pulmonary Eosinophilia lesions in the lungs produce a chest X-ray abnormality associated with pulmonary eosinophilia, with or without a peripheral blood eosinophilia.

Some causes of extrinsic pulmonary eosinophilia are described below: A. Extrinsic:

i) Helminths Ascaris , Toxocara, Filaria. ii) Drugs Nitrofurantion, para-aminosalicytic acid (PAS), sulfasalazine, imipramine, chlorpropamide, phynylbutazone. iii) Fungi Asperpillus fumigatus causing allergic bronchopulmonary aspergillosis.

B. Intrinsic:

i) Cryptogenic eosinophilic pneumonia. ii) Churg-Strauss syndrome (diagnossed on the basis of four or more of the following features : asthma, peripheral blood eosinophilia >1.5Ă&#x2014;109/l (or > 10% of a total white cell count), mononeuropathy or polyneuropathy, pulmonary infiltrates, paranasal sinus desease or eosinophilic vasculitis on biopsy of an affected site). ii) Hypereosinophilic syndrome. iii) Polyarteritis nodosa.

DIAGNOSIS OF HAEMOPTYSIS When a patient presents with haemoptysis ,underlying cause of the haemoptysis has to be find out . In order to find the underlying cause we should proceed in following ways : I) History of the patient should be taken properly II) Thorough physical examination of the patient III) Investigation I. History Age of the patient: Certain respiratory illness is more common in certain age group . Thus when a young patient comes with history of haemoptysis ,it is likely that he has got pulmonary tuberculosis or mitral stenosis. Congenital bronchiectasis can occur in children and it is also common in older age. Pneumonia occurs at all ages but commonly occur in early age and at mid adult life.Young women are more prone to systemic lupus erythomatosus .Bronchogenic carcinoma occurs most frequently between the age 50 â&#x20AC;&#x201C; 70 years.The incidence of hypertension increases with age .

Sexes: Certain diseases has predilection for sex. Thus bronchial carcinoma is five times more common in male than female while bronchial adenoma is equal on both sexes.

Tuberculosis is predominant in male population. Above two thirds of the patients with mitral stenosis are female. Hypertension is more common in male than female.

Mode of Onset of the Disease: Mode of onset is of great importance. In pneumonia the onset is very sudden with fever, chest pain, cough, breathing difficulty etc. On the other hand the onset may be chronic, as in pulmonary tuberculosis where there is chronic cough, irregular fever, sometimes haemoptysis with deterioration of health. In pulmonary embolism and infarction the onset is very sudden with sensation of oppression in the chest, dyspnoea followed by cyanosis and shock. There is usually a history of postoperative immobilization, trauma or heart disease. The onset of lung abscess may be cough with purulent sputum, usually large in amount, very much foul smelling and occasionally blood stained is present from an early stage.

The onset of chronic bronchitis is more chronic and usually starts with repeated attack of winter cough which shows a steady increase in severity and duration with successive years until the cough is present all the year round. Bronchiectasis is usually manifestation of other etiological factors like infection, collapse, fibrosis etc.

Onset is usually insidious in bronchial carcinoma with cough, chest pain or repeated small haemoptysis etc. Illiteracy, ignorance and lack of knowledge about health and nutrition, poverty, etc. may all predispose to the disease process.

Occupation besides â&#x20AC;&#x153;occupational lung diseasesâ&#x20AC;? like pneumoconiosis or silicosis, other diseases like pulmonary tuberculosis may also have some occupational background. Thus, the doctors, nurses or other personals who work in tuberculosis hospital or comes in contact with open cases of tuberculosis are more liable to develop tuberculosis. Incidence of chronic bronchitis is directly related to dust exposure and occupation such as coal mining predisposes to the condition .

Smoking: Smoking has definite role in various lung diseases . A number of ciliotoxic substances enter in the body by cigarette smoking , which inhibit the bronchial ciliary action and encourage bacterial infection. It also inhibits the alveolar macrophage. In vitro it has been shown that smoking inhibits the action of surfactants which allows greater distension of the alveoli. In addition the changes in the loss of cilia, there is basal hyperplasia, appearance of atypical cells with irregular panchromatic nuclei.

All the available evidence incriminates the smoking of tobacco, specially of cigarettes as the main cause of the great rise in mortality from bronchial carcinoma.

The risk of cancers rapidly decreases in those who stopped smoking. It was halved in those who stopped smoking for 1-5 years and down to twice that of nonsmokers in those who had stopped for 15 years. Smoking appeared to be associated with squamous bronchial carcinoma and with the anaplastic type (including oat cell variety).

Tuberculosis is more common in smokers. In both sexes above the age 30 years suffering from tuberculosis, the incidence of smoking is much higher. Death rate from chronic bronchitis was significantly higher in cigarette smokers . The incidence of death from chronic bronchitis also reduced after stopped smoking.

Cough: Cough is the most frequent symptom of respiratory disease. It is caused by stimulation of sensory nerves in the mucosa of the pharynx, larynx, trachea and bronchi. Acute sensitisation of the normal cough reflex occurs in a number of conditions and the patient typically reports cough induced by changes in air temperature or exposure to cigarette smoke or perfumes.

The explosive quality of a normal cough is lost in patients with respiratory muscle paralysis or vocal cord palsy. Paralysis of a single vocal cord gives rise to a prolonged, low-pitched, inefficient bovine cough accompanied by

hoarseness. Coexistence of an inspiratory noise (stridor) indicates partial obstruction of a major airway (e.g. laryngeal oedema, tracheal tumour, scarring or compression or an inhaled foreign body) and requires urgent investigation and treatement. Sputum poduction is common in patients with acute or chronic cough, and its nature and appearance can provide valuable clues as to the aetiology.

Acute or transient cough most commonly relates to viral lower respiratory tract infection, post-nasal drip resulting from rhinitis or sinusitis, aspiration of a foreign body or throatclearing secondary to laryngitis or pharyngitis. Acute cough occurring in the contest of more serious diseases such as pneumonia, aspiration, congestive heart failure or pulmonary embolisim is usally easy to diagnose due to the presence of other clinical features. Cough may also arise following stimulation of the parietal pleura; for example, during the aspiration of a pleural effusion.

Patients with chronic cough present more of a diagnostic challenge, especially those individuals with a normal examinaion, chest X-ray and lung function studies. In this context, most cough can be explained by post-nasal drip secondary to nasal or sinus disease; cough variant asthma (where cough may be the principal or exclusive clinical manifestation) or gastro-oesophageal reflux with aspiration. The latter cause may require ambulatory pH monitoring or a prolonged trial of anti-reflux therapy to diagnose. Ten to fifteen per cent of patients (paricularly women) taking angiotensin converting enzyme (ACE) inhibitors develop drug induced chronic cough. Bordetella pertussis infection in adults can also result in protracted cough and should always be suspected in those in close contact with children.

While most patients with a bronchogenic carcinoma have an abnormal chest Xâ&#x20AC;&#x201D;ray on presentation fibreoptic bronchoscopy or spiral CT scan of the airways is advisable in most adults with otherwise unexplained cough of recent onset (especially in smokers) as this may reveal a small endobronchial tumour or unexpected foreign body.

Dyspnoea: Breathlessness or dyspnoea can be defined as the feeling of an uncomfortable need to breathe. It is unusual among sensations in having no defined receptors, no localised representation in the brain, and multiple causes both in health (e.g. exercise) and in diseases of the lungs, heart or muscles.

Respiratory diseases can stimulate breathing and dyspnoea by stimulating intrapulmonary sensory nerves (e.g. pneumothorax, interstitial inflammation and pulmonary embolus), by increasing the mechanical load on the respiratory muscles (e.g. airflow obstruction or pulmonary fibrosis) or by causing hypoxia, hypercapnia or acidosis, stimulating chemoreceptors. In cardiac failure, pulmonary congestion reduces lung compliance and can obstruct the small airways. In addition, reduced cardiac output limits oxygen supply to the skeletal muscles during exercise causing early lactic acidaemia, further stimulating breathing via the central chemoreceptors. Dyspnoea and the effects of treatment can be quantified using a symptom scale. Patients tend to report dyspnoea in proportion to the sum of the above stimuli to breathe. Individual patients differ greately in the intensity of breathlessness reported for a given set of circumstances, but breathlessness scores during

exercise within individuals are reproducible, and can be used to monitor the effects of theraphy.

Chest Pain: Chest pain is a frequent complaint for which a person seeks medical advice.

Careful attention to the details of complaints of thoracic pain may provide the physician the clues that will direct appropriate examination. Severe inflammatory, neoplastic or other diseases may invade lung parenchyma without causing pain. On the other hand there may be referred pain in the chest when there is no lesion in the lungs. Pain occurs when there is involvement of parietal pleura, chest wall, the diaphragm or mediastinal structures. Thoracic pain like abdominal pain may be referred to the areas of the skin supplied by the same segment of nerves.

Pleuritic pain, associated with dry pleurisy which may be due to many conditions like pneumonia, pulmonary embolism, tuberculosis, malignant disease etc. Pain of pleural origin is localized rather than diffuse . Other features of the disease that cause pleurisy will be there. The pain of intercostal fibrosis occurs mainly on coughing rather than breathing and local tenderness is found. The pain of costochondritis is localised to one or more cartilages with tenderness and sometimes palpable enlargement of the cartilaginous bridge between the ribs and the sternum. Most common site is 2nd, 3rd and 4th cartilage. The pain is usually dull with little or no relationship to respiration and movement. It is growing or aching pain, most often noticable at night when the patient is lying in bed. The pain of coronary insuffficiency is sometimes very much characteristic. The pain is localized beneath the sternum or to the left which radiate to shoulder, arm or neck. It may be caused by physical exertion or anxiety and is relieved by rest.

The character of the coronary pain may be otherwise like retrosternal discomfort of tightness of the chest related to physical effort or excitement.

Pericardial pain is retrosternal and to the left and is usually related to exertion and also respiration. Pain of aortic aneurysm is usually deep seated, agonizing type of distress. It may be related to exertion. The location of pain may be interscapular when aneurysm presses the thoracic spine.

Chest pain may also be rarely associated with rheumatism like ankylosing spondylitis affecting the thoracic spine. Sometimes there may be referred pain from abdominal organ such as gallbladder, hiatus hernia or from a lesion in the spine.

Palpitation: Palpatation is very much common symptom in disease of the chest. It is common in various heart diseases like mitral stenosis, paroxysmal tachycardia, extrasystole, corpulmonale etc. Other common causes of palpitation are anxiety, thyrotoxicosis, anaemia, hypertension, tabesdorsalis, tobacco, tea, coffee, alcohol or drugs like digitalis, morphine, atropine etc.

Systemic Manifestation of Thoracic Disease: Several disease of the respiratory system like pulmonary tuberculosis, pneumonia, bronchial carcinoma, bronchiectasis, lung abscess are associated with systemic manifestation like fever with or without rigor, night sweats, anorexia, malaise, weight loss etc. Bronchial carcinoma may metastasize in other organs or it may produce other several manifestation like Cushing syndrome, acromegaly etc. Carcinomatous neuropathy is not an uncommon feature. Pulmonary tuberculosis may have a haematogenous dissemination and result in extra pulmonary tuberculosis. A chronically ill patient may come with pain in the bones near joints due to pulmonary osteoarthropathy without any symptom in the thorax and a physician should always be careful about the extra pulmonary manifestations of pulmonary diseases.

Family history: Family history should emphasize diseases with a genetic component and those pulmonary diseases which are considered contagious. In the first category the disease to be considered are cystic disease of the lung, bronchiectasis, asthma, hamartoma, congenital heart disease, sickle cell disease, telangiectasia and Kartagenerâ&#x20AC;&#x2122;s syndrome. The most frequently encountered contagious disease that give a positive family history is still tuberculosis. All family members of a tuberculous patient should be investigated throughly.

Past history: Past history of illness should carefully be taken. Past history of pleural effusion suggests pulmonary tuberculosis. Previous X-ray chest should be preserved. There may be reactivation of pulmonary tuberculosis without further infection after many years. History of operative removal of a cancer even in a remote past may suggest metastatic infiltration of the lung.

II. Physical examination Physical examination includes 1. General examination and 2. Systemic examination 1.General examination General appearance of the patient is to be noted. State of nutrition is usually poor in pulmonary tuberculosis or malignancy. Cyanosis may be present in severe pulmonary disorder and certain congenital heart diseases. Dyspnoea is an important symptom in many respiratory and cardiac diseases. Hoarseness of voice indicate laryngeal paralysis as occur in bronchial carcinoma. Patients breathing when becomes foul smelling indicate lung abscess, bronchiectasis or other infective process in the lung. Venous engorgement is present in heart failure. Neck and face my be engorged in superior mediastinal syndrome.

Clubbing of the fingers and toes may be present in suppurative lung diseases, chronic lung disease, bronchial carcinoma or some congenital heart disease. Cigarette smokers have their fingers and nails stained. There may be evidences of pulmonary osteoarthroapathy. Lymph node enlargement may be due to metastasis of bronchial carcinoma or other disease like lymphomas, leukaemias, mycotic diseases, sarcoidosis or tubercular lymphadenopathy.

There may be metastatic cutaneous nodules. Skin rashes, echymoses may be present in coagulation disorders. Dependent oedema is a feature of congestive cardiac failure. Rate of respiration is increased in pneumonia, pulmonary infarction, pleural effusion, superior vena caval obstruction or pulmonary oedema. Temperature is raised in tuberculosis, pneumonia, bronchial carcinoma and other malignancy, lung abscess or any other infective conditions.

Pulse is a good guide for different heart diseases. Thus it is irregular in atrial fibrillation as occurs in mitral stenosis. Blood pressure has to be chequed in each and every patient carefully and repeatedly who is suffering from hypertension or other cardiorespiratory disorders.

Systemic examination Examination of the chestExamination of the chest is undertaken very carefully to elicit any physical sign. This is done under inspection, palpation, percussion and auscultation. In many cases no physical sign can be elicited while in others the underlying pathology can easily be understood. There may be signs suggestive of consolidation, collapse, cavity, pleurisy, pleural effusion, pneumothorax, mediastinal displacement or growth, pulmonary oedema etc. Other diseases like chronic bronchitis, bronchiectasis, pulmonary infarction can also be detected. Various cardiac diseases like pericardial effusion, valvular disease of the heart, arrhythmias can also be detected.

Inspection of the chest may show engorged superficial vein indicating obstruction to venous flow or in coarctation of the aorta there may be engorgment of arterial collateral circulation with pulsation. Chest deformity may be present as in pulmonary fibrosis of tuberculosis or barrel shaped chest in emphysema. Precordium may be bulged in cardiac enlargement during early age of life.

Palpation may detect tenderness over right upper abdomen as occurs in liver abscess, a shift of the trachea as in collapse, fibrosis, pleural effusion.

Dullness on percussion indicates consolidation, collapse, growth or fluid. Crepitation is present in accumulation of fluid in the airways and alveoli. Narrowing of the bronchi will produce rhonchi in asthma or a bronchial tumour obstructing a bronchus.

Bronchial breath sound may be audible over a consolidation or cavitation or just above the level of pleural effusion.

Abdomen-

Examination of the abdomen may reveals ascites or a growth on the abdominal structure which might be a primary source. Liver may be enlarged and tender in amoebic liver abscess . Testes should always be examined for testicular tumours which may be a primary site for pulmonary metastasis.

Examination of the pelvis may reveal genital tuberculosis or carcinoma in female, which may be primary source.

Per rectal examination may reveal a tubercular fistula or carcinoma of the rectum or prostate.

Examination of female breast is important to exclude breast cancers, which may metastasize in the lungs.

Examination of nervous system may reveal involvement of brachial plexus or carcinomatous neuropathy in bronchial carcinoma.

All other system are to be carefully examined for a primary source of tuberculosis or malignancy or secondary tubercular dissemination.

III. Investigations: Blood examination: Each and every patient with history of haemoptysis should have their blood examined for Hb%, total and differential count of white cell, erythrocyte sedimentation rate, platelet count, bleeding time and coagulation time routinely. Other biochemical test and special test are to be done when required.

High neutrophil count is present in pneumonia, lung abscess, liver abscess, pulmonary infarction, bronchiectasis or any other infection. In pulmonary tuberculosis the neutrophil count is usually normal and a raised neutrophil count should suspect a secondary infection .

Lymphocyte count increased in tuberculosis. A very high leukocyte count with immature cells indicates leukaemia.

A high eosinophil count is present in tropical pulmonary eosinophilia, parasitic infection, lymphoma, polyarteritis nodosa etc. Patient treated with streptomycin and INH may develop eosinophilia. It may also be high in Good Pastureâ&#x20AC;&#x2122;s syndrome and idiopathic pulmonary haemosiderosis. In haemorrahgic dyscrasias, platelet count, bleeding time and clotting time is usually abnormal. Hb% generally low in leukemia, pulmonary tuberculosis, malignancy including lymphomas.

Erythrocyte sadimentation rate though not a diagnostic criteria should be done to see the prognosis of the disease . It is generally high in malignancy, tuberculosis, lung abscess, collagen disease, pulmonary infarction and leukaemias.

Tuberculin Test :

Tuberculin test should be done in a case of suspected tuberculosis.

Reading of the Mantoux test or tuberculin test should be taken after 24 days. The result is positive when induration is more than 10 mm. In following condition false negative result may found â&#x20AC;&#x201C; 1.

Severe TB (25% of negative cases) 2.

Newborn and elderly.

3.

HIV (if CD4 count <200 cells/ml) 4.

Recent Infection (ex: measles) or immunization.

5.

Malnutrition.

6.

Immunosuppressive drugs.

7.

Malignancy., Techniques for obtaining biologic specimens: Collection of sputum: Sputum can be collected either be spontaneous expectoration or after inhalation of an irritating aerosol, such as hypertonic saline. The later method, called sputum induction, is commonly used to obtain sputum for diagnostic studies. Sputum consists mainly of secretions from the tracheobronchial tree rather than the upper airway, the finding of alveolar macrophanges and other inflammatory cells is consistent with a lower respiratory tract origin of the sample, whereas the presence of squamous epithelial cells in a sputum sample indicates contamination by secretions from the upper airways.

Besides processing for routine bacterial pathogens by Gramâ&#x20AC;&#x2122;s staining and culture, sputum can be processed for a variety of other pathogens including staining and culture for fungi, culture for viruses, and staining for viruses, and staining for Pneumocystis carinii. In the specific case of sputum obtained for evaluation of Pneumocystis carinii pneumonia in a patient infected with HIV, for example, sputum should be collected by induction, rather than spontaneous expectoration, and an immunofluorescent stain should be used to detect the organisms. Cytologic staining of sputum for malignant cells, using the traditional Papanicolaou method allows noninvasive evaluation for suspected lung cancer. Traditional stains and cultures are now also being supplemented in some by immunologic techniques and by molecular biologic methods, including the use of polymerase chain reaction amplification and DNA probes.

PERCUTANEOUS NEEDLE ASPIRATION: A needle can be inserted through the chest wall into a pulmonary lesion for the purpose of aspirating material for analysis by cytologic or microbiologic techniques. The procedure is usually carried out under CT guidance, which assists in the positioning of the needle and assures that it is localized in the lesion. Although the potential risks of this procedure include intrapulmonary bleeding and creation of a pneumothorax with collapse of the underlying lung, the low risk of complication in experienced hands is usually worth the information obtained. However, a limitation of the

technique is sampling error due to the small amount of material obtained.

Thus, findings other than a specific cytologic or microbiologic diagnosis are of limited clinical value.

THORACENTESIS: Sampling of pleural liquid by thoracentesis is commonly performed for diagnostic purposes or, in the case of a large effusion, for palliation of dyspnoea. Diagnostic sampling, either by blind needle aspiration or after localization by ultrasound allows the collection of liquid for microbiologic and cytologic studies. Analysis of the fluid obtained for its cellular composition and chemical constituents, including glucose, protein, and lactate dehydrogenase, allows the effusion to be classified as either exudative or transudative. In some cases, particularly in the setting of possible tuberculous involvement of the pleura (tuberculous pleuritis), closed biopsy of a the parietal pleura is also performed, using a cutting needle (either an Abrams or a Cope biopsy needle) to sample tissue for histopathologic examination and culture.

Bronchoscopy Bronchoscopy is the process of direct visualization of the tracheobronchial tree. Bronchoscopy with a rigid-bronchoscope is generally performed in an operating room on a patient under general anesthesia. The development of a flexible fiberoptic has revolutionized the diagnostic use of bronchoscopy.

Although bronchoscopy is now performed almost exclusively with fiberoptic instruments, rigid bronchoscopes still have a role in selected circumstances, primarily because of their larger suction channel and the fact patient can be ventilated through the bronchoscope channel. These situations include the retrieval of a foreign body and the suctioning of a massive hemorrhage, for which the small suction channel of the bronchoscope may be insufficient.

Flexible Fiberoptic Bronchoscopy This is an outpatient procedure that is usually performed in an awake but sedated patient. The bronchoscope is passed through either the mouth or the nose, between the vocal cords, and into the trachea. The ability to flex the scope makes it possible to visualize virtually all airways to the level of subsegmental bronchi. The bronchoscopes is able to identify various pathology in bronchus, including tumors, granulomas, bronchitis, foreign bodies, and sites of bleeding. Samples from airway lesions can he taken by several methods, including washing, brushing, and biopsy. Washing involves instillation of sterile saline through a channel of the bronchoscope and onto the surface of a lesion. A portion of the liquid is collected by suctioning through the bronchoscope, and the recovered material can be analyzed for cells (cytology) or organisms (by standard stains and cultures). Brushing or biopsy of the surface of the lesion, using a small brush or biopsy forceps at the end of a long cable inserted through a channel of the bronchoscope, allows recovery of cellular material or tissue for analysis by standard cytologic and histopathologic methods.

The bronchoscope can be used to sample material not only from the regions that can be directly visualized (i.e., the airways) but also from the more distal pulmonary parenchyma. With the bronchoscope wedged into a subsegmental airway, aliquots of sterile saline can be instilled through the scope, allowing sampling of cells and organisms even from alveolar spaces.

This procedure, called bronchoalveolar lavage, has been particularly useful for the recovery of organisms such as Pneumocystis carinii in patients with HIV infection.

Brushing and biopsy of the distal lung parenchyma can also be performed with the same instruments that are used for end bronchial sampling. These instruments can be passed through the scope into small airways, where they penetrate the airway wall, allowing biopsy of peribronchial alveolar tissue.

This procedure, called transbronchial biopsy, is used when there is either relatively diffuse disease or a localized lesion of adequate size. With the aid of fluoroscopic imaging, the bronchoscopist is able to determine not only whether and when the instrument is in the area of abnormality, but also the proximity of the instrument to the pleural surface. If the forcep are too close to the pleural surface, there is a risk of violating the visceral pleura and creating a pneumothorax; the other potential complication of transbronchial biopsy is pulmonary hemorrhage. The incidence of these complications is less than several percent.

Another procedure involves use of a hollow-bore needle passed through the bronchoscope for sampling of tissue adjacent to the trachea or a large bronchus. The needle is passed through the airway wall, and cellular material can be aspirated from mass lesions or enlarged lymph nodes, generally in a search for malignant cells. This procedure can facilitate the staging of lung cancer by identifying mediastinal lymph node involvement and in some cases obviates the need for a more invasive procedure.

The bronchoscope may provide the opportunity for treatment as well as diagnosis. For example, an aspirated foreign body may be retrieved with an instrument passed through the scope, and bleeding may be controlled with a balloon catheter similarly introduced. Newer interventional techniques performed through a bronchoscope include methods for achieving and maintaining patency of airways that are partially or completely occluded, especially by tumors. These techniques include laser therapy, cryotherapy, electrocautery, and stent placement.

VIDEO-ASSISTED THORACIC SURGERY Recent advances in video technology have allowed the development of thoracoscopy, or video-assisted thoracic surgery (VATS), for the diagnosis and management of pleural as well as parenchymal lung disease. This procedure done under general anesthesia, involves the passage of a rigid scope with a distal lens through a trocar inserted into the pleura. A highquality image is shown on a monitor screen, allowing the operator to manipulate instruments passed into the pleural space through separate small intercostal incisions. With these instruments, the operator can take biopsy

from the lesions of the pleura under direct vision, which provides an obvious advantage over closed pleural biopsy. In addition, this procedure is now used commonly to biopsy peripheral lung tissue or to remove peripheral nodules, for both diagnostic and therapeutic purposes. Because this procedure is much less invasive than the traditional thoracotomy performed for lung biopsy, it has largely supplanted open lung biopsy.

THORACOTOMY Although frequently replaced by video-assisted thoracic surgery , thoracotomy remains an option for the diagnostic sampling of lung tissue. It provides the largest amount of material, and it can be used to biopsy and/or excise lesions that are too deep or too close to vital structures for removal by video-assisted thoracic surgery . The choice between video-assisted thoracic surgery and thoracotomy needs to be made on a case-by-case basis, and the relative indications for each are still evolving as more experience is being gained with video-assisted thoracic surgery .

MEDIASTINOSCOPY AND MEDIASTINOTOMY Tissue biopsy is often critical for the diagnosis of mediastinal masses or enlarged mediastinal lymph nodes. Although CT scan is useful for determining the size of mediastinal lymph nodes as part of the staging of lung cancer, confirmation that enlarged lymph nodes are actually involved with tumor generally requires biopsy and histopathologic examination. The two major procedures used to obtain specimens from masses or nodes in the mediastinum are mediastinoscopy (via a suprasternal approach) and mediastinotomy (via a parasternal approach). Both procedures are performed under general anesthesia by a thoracic surgeon. In the case of suprasternal mediastinoscopy, a rigid mediastinoscope is inserted at the suprasternal notch and passed into the mediastinum along a pathway just anterior to the trachea. Tissue can be obtained with biopsy forceps passed through the scope, sampling masses or nodes that are in a paratracheal or pretracheal position. Left paratracheal and aortopulmonary lymph nodes are not accessible by this route and thus are commonly sampled by parasternal mediastinotomy (the Chamberlain procedure). This approach involves either a right or left parasternal incision and dissection directly down to a mass or node that requires biopsy.

Pleural Aspiration and Biopsy: Pleural aspiration and biopsy using an Abramâ&#x20AC;&#x2122;s needle is a blind procedure but often provides histological evidence of the cause of a pleural effusion. In difficult cases, video assisted thoracoscopy may be used to obtain pleural or lung biopsies.

Pleural fluid should always be examined when present. If the fluid is serous it is examined for AFB and if purulent both AFB stain and gram stain is done. If malignancy is suspected cytology for malignant cell is done. Pleural fluid is also tested biochemically to determine its glucose, protein and electrolyte content.

Imaging: Chest Radiogaraphy: Chest radiography is often the initial diagnostic study performed to evaluate patients with respiratory symptoms, but it can also provide the initial evidence of disease in patients who are free of symptoms. Perhaps the most common example of the latter situation is the finding of one or more nodules or masses when the radiograph is performed for a reason other than evaluation of respiratory symptoms.

A number of diagnostic possibilities are often suggested by the radiographic pattern. A localized region of opacification involving the pulmonary parenchyma can be described as a nodule (usually <6 cm in diameter), a mass (usually > 6 cm in diameter), or an infiltrate. Diffuse disease with increased opacification is usually characterized as having an alveolar, an interstitial, or a nodular pattern. In contrast, increased radiolucency can be localized, as seen with a cyst or bulla, or generalized, as occurs with emphysema. The chest radiograph is also particularly useful for the detection of pleural disease, especially if manifested by the presence of air or liquid in the pleural space. An abnormal appearance of the hilar region and/or the mediastinum can suggest a mass or enlargement of lymph nodes.

Major Respiratory Diagnosis with Common Pattern

Chest Radiographic

Solitary circumscribed density – nodule (<6 cm) or mass (>6 cm) • Primary or metastatic neoplasm • Localized infection (Bacterial abscess, mycobacterial or fungal infection) • Wegener’s gramulomatosis (one or several nodules) • Rheumatoid nodule (one or several nodules) • Vascular malformation • Bronchogenic cyst.

Localized opacification (infiltrate) • Pneumonia (bacterial, atypical, mycobacterial, or fungal infection) • Neoplasm • Radiation pneumonitis • Bronchiolitis obliterans with organizing pneumonia • Bronchocentric granulomatosis • Pulmonary infarction.

Diffuse interstitial disease

• Idiopathic pulmonary fibrosis • Pulmonary fibrosis with systemic rheumatic disease • Sarcoidosis • Drug-induced lung disease • Pneumoconiosis • Hypersensitivity pneumonitis • Infection (Pneumocystic, Viral, pneumonia) • Eosinophilic granuloma Diffuse alveolar disease • Cardiogenic pulmonary edema • Acute respiratory distrress syndrome • Diffuse alveolar hemorrhage • Infection (Pneumocystic, viral or bacterial pneumonia) • Sarcoidosis Diffuse nodular disease • Metastatic neoplasm • Hematogenous spread of infection (bacterial, mycobacterial, fungal) • pneumoconiosis • Eosinophilic granuloma Routine Radiography: Lateral decubitus views are often useful for determining whether pleural abnormalities, represent freely flowing fluid, whereas apical lordotic views can often visualize disease at the lung apices better than the standard posteroanterior view. Portable equipment, which is often used for acutely ill patients who either cannot be transported to a radiology suite or cannot stand up for posteroanterior and lateral views, generally yields just a single radiograph taken in the anteroposterior direction.

Computed tomography: Computed tomography (CT) scan offers several advantages over routine chest radiography. First the use of cross-sectional images often makes it possible to distinguish between densities that would be superimposed on

plain radiographs. Second, CT scan is far better than routine radiographic studies at characterizing tissue density distinguishing subtle differences in density between adjacent structures, and providing accurate size assessment of lesions. As a result CT scan is particularly valuable in assessing hilar and mediastinal disease (which is often poorly characterized by plain radiography), in identifying and characterizing disease adjacent to the chest wall or spine (including pleural disease), and in identifying areas of fat density or calcification in pulmonary nodules. Its utility in the assessment of mediastinal disease has made CT scan an important tool in the staging of lung cancer, as an assessment of tumor involvement of mediastinal lymph nodes is critical to proper staging. With the additional use of contrast material , CT scan also makes it possible to distinguish vascular from nonvascular structures, which is particularly important in distinguishing lymph nodes and masses from vascular structures.

Helical CT scanning allows the collection of continuous data over a larger volume of lung during a single breath-holding maneuver than is possible with conventional CT scan. With CT angiography, in which intravenous contrast is administered and images are acquired rapidly by helical scanning, pulmonary emboli can be detected in segmental and larger pulmonary arteries. With high-resolution CT scan (HRCT), the thickness of individual cross-sectional images is approximately 1 to 2 mm, rather than the usual 10 mm and the images are reconstructed with high-spatial-resolution algorithms. The detail that can be seen on HRCT scans allows better recognition of subtle parenchymal and air way disease, such a bronchiectasis, emphysema, and diffuse parenchymal disease. Certain nearly pathognomonic patterns have now been recognized for many of the interstitial lung diseases, such as lymphangitic carcinomatosis, idiopathic pulmonary fibrosis, sarcoidosis, and eosinophilic granuloma; at present it is not yet clear in what settings these patterns will obviate the need for obtaining lung tissue.

MAGNETIC RESONANCE IMAGING The role of magnetic resonance imaging (MRI) in the evaluation of respiratory system disease is less well defined than that of CT scan. Because MRI generally provides a less detailed view of the pulmonary parenchyma as well as poorer spatial resolution, its usefulness in the evaluation of parenchymal lung disease is limited at present. However MRI has advantages over CT scan in certain clinical settings. Because its images can be reconstructed in sagittal and coronal as well as transverse planes, MRI is better for imaging abnormalities near the lung apex, the spine , and the thoracoabdoniinal junction. In addition, vascular structures can be distinguished from nonvascular structures without the need for contrast.

Flowing blood does not produce a signal on MRI, so vessels appear as hollow tubular structures. This feature can be useful in determining whether abnormal hilar or mediastinal densities are vascular in origin and in defining aortic lesions such as aneurysms or dissection.

Scintigraphic Imaging

Radioactive isotopes, administered by either intravenous or inhaled routes, allow the lungs to be imaged with a gamma camera. The most common use of such imaging is ventilation-perfusion lung scanning performed for evaluation of pulmonary embolism. When injected intravenously, albumin macroaggregates labeled with technetium become lodged in pulmonary capillaries; therefore, the distribution of the trapped radioisotope follows the distribution of blood flow. When inhaled, radiolabeled xenon gas can be used to demonstrate the distribution of ventilation. For example, pulmonary thromboembolism usually produces one or more regions of ventilationperfusion mismatch—that is, regions in which there is a defect in perfusion that follows the distribution of a vessel and that is not accompanied by a corresponding defect in ventilation.

Another common use of such radioisotope scans is in a patient with impaired lung function who is being considered for lung resection. The distribution of the isotope can be used to assess the regional distribution of blood flow and ventilation, allowing the physician to estimate the level of postoperative lung function.

Another scintigraphic imaging technique, gallium imaging, has been of diagnostic value in patients with Pneumocystis carinii pneumonia and other opportunistic infections. Use of gallium imaging may provide clues to sort out the differential diagnosis of pulmonary infiltrates in immunosuppressed patients, especially patients with AIDS. PULMONARY ANGIOGRAPHY The pulmonary arterial stem can be visualized by pulmonary angiography, in which radiopaque contrast medium is injected through a catheter previously threaded into the pulmonary artery. When performed in cases of pulmonary embolism, pulmonary angiography demonstrates the consequences of an intravascular clot—either a defect in the lumen of a vessel (a “filling defect”) or an abrupt termination (“cutoff”) of the vessel. Other, less common indications for pulmonary angiography include visualization of a suspected pulmonary arteriovenous malformation and assessment of pulmonary arterial invasion by a neoplasm.

ULTRASOUND Because ultrasound energy is rapidly dissipated in air, ultrasound imaging is not useful for evaluation of the pulmonary parenchyma. However, it is helpful in the detection and localization of pleural abnormalities. Ultrasound is sensitive at detecting pleural fluid and may also be used to direct and improve the diagnostic yield from pleural biopsy. Information may also be provided on the anatomy of an empyema cavity and facilitate directed drainage.

POSITRON EMISSION TOMOGRAPHY (PET)

PET scanners exploit the avid ability of malignant tissue to absorb and metabolise glucose. The radiotracer F-fluorodeoxyglucose (FDG) is administered and rapidly taken up by malignant tissue. It is then phosphorylated but cannot be metabolised further, becoming trapped in the cell. PET scanning is useful in the investigation of pulmonary nodules, and in staging mediastinal lymph nodes and distal metastatic disease in patients with lung cancer. The negative predictive value is high; however, the positive predictive value is poor. Co-registration of PET and CT scan (PETCT) enhances localization and characterization of the metabolic abnormalities.

Immunological and Serological Tests: The presence of pneumococcal antigen(revealed by counterimmunoelectrophoresis) in sputum, blood or urine may be of diagnostic importance. Exfoliated cells colonised by influenza A virus can be detected by fluorescent antibody techniques. In blood, high or rising antibody titres to specific organisms such as legionella, Mycoplasma, Chlamydia or viruses may eventually clinch a diagnosis suspected on clinical grounds. Precipitating antibodies may be found as a reaction to fungi such as Aspergillus or to antigens involved in hypersensitivity pneumonitis.

Microbiological Investigations: Sputum, pleural fluid, throat swabs, blood and bronchial washings and aspirates can be examined for bacteria, fungi and viruses. In some cases, as when mycobacterium tuberculosis is isolated, the information is diagnostically conclusive but in other circumstances the findings must be interpreted in conjunction with the results of clinical and radiological examination.

Histopathological and Cytological Examination: Histopathological examination of biopsy material (obtained from pleura, lymph node or lung) often allows a tissue diagnosis to be made. This is of particular importance in suspected malignancy or in elucidating the pathological changes in interstitial lung disease. Important causative organisms, such as Mycobacterium tuberculosis, Pneumocystis carinii (now jirovecii) or fungi, may be identified in bronchial washing, brushings or transbronchial biopsies.

Cytological examination of exfoliated cells in sputum, pleural fluid or bronchial brushings and washings or of fine-needle aspirates from lymph nodes or pulmonary lesions can support a diagnosis of malignancy but if this is indeterminate a tissue biopsy is necessary to confirm the diagnosis.

Cellular patterns in bronchial lavage fluid may help to distinguish pulmonary changes due to sarcoidosis from those caused by idiopathic pulmonary fibrosis or hypersensitivity pneumonitis.

Respiratory Function Testing:

Respiratory function tests are used to aid diagnosis, assess functional impairment and monitor treatment or progression of disease. In diseases characterised by airway narrowing (ex: asthma, bronchitis and emphysyma) maximum expiratory flow is limited by dynamic compression of small intrathoracic airways, some of which close completely during expiration, limiting the volume which can be expired. Hyperinflation of the chest results, and can become extreme if elastic recoil is also lost due to parenchymal destruction, if elastic recoil is also lost due to parenchymal destruction, as in emphysema. In contrast, diseases which cause lung inflammation and/or scarring and fibrosis are characterised by progressive loss of lung volume with normal expiratory flow rates. Gas exchange is impaired by both parenchymal destruction (emphysema) and by interstitial disease, which disrupts the local matching of ventilation and perfusion.

In respiratory function testing, airway narrowing, lung volume and gas exchange capacity are quantified and compared with normal values adjusted for age, gender, height and ethnic origin.

Airway narrowing is assessed by forced expiration into a peak flow meter or a spirometer. Peak flow meters are cheap and convenient for home monitoring (e.g. detection and monitoring of asthma) but values are effortdependent. The forced expiratory volume in I second (FEV 1) and vital capacity (VC) are obtained from maximal forced and relaxed expirations into a spirometer. FEV1 is disproportionately reduced in airflow obstruction resulting in FEV1/VC ratios of less than 70%. When airflow obstruction is seen, spirometry should be repeated following inhaled short-acting β2adrenoceptor agonists (e.g. salbutamol); reversibility to normal is suggestive of asthma . To distinguish large airway narrowing (e.g. tracheal stenosis or compression) from small airway narrowing, flow-volume loops are recorded during maximum expiratory and inspiratory efforts.

Lung volume can be measured by dilution of an inhaled inert gas (usually helium) or by determining the pressure/volume relationship of the thorax by body plethysmography. The former method measures the volume of intrathoracic gas which mixes quickly with tidal breaths, while the latter measures total intrathoracic gas volume, including poorly ventilated areas such as bullae.

To measure the capacity of the lungs to exchange gas, patients inhale a test mixture of 0.3% carbon monoxide, which is avidly bound to haemoglobin in pulmonary capillaries. After a short breath-hold, the rate of disappearance of CO into the circulation is calculated from a sample of expirate and expressed as the TLco or carbon monoxide transfer factor. Helium is also included in the test breath to allow calculation of the volume of lung examined by the test breath.

Arterial blood gases and Oximetry: The measurement of hydrogen ion concentration, P aO2 and PaCO2, and derived bicarbonate concentration of arterial blood is essential in assessing the degree and type of respiratory failure and for measuring acid-base status.

Interpretation of results is made easier by blood gas diagrams which indicate

whether any acidosis or alkalosis is due to acute or chronic respiratory derangements of PaCO2, or to metabolic causes. Pulse oximeters allow noninvasive continuous assessment of oxygen saturation in patients who require monitoring in order to assess hypoxaemia and its response to therapy.

Exercise tests: Resting measurements are sometimes unhelpful in early disease or in patients complaining only of exercise-induced symptoms. Exercise testing with spirometry before and after can be helpful in demonstrating exertiseinduced asthma. Walk tests include the self-paced 6 minute walk and the externally paced incremental â&#x20AC;&#x2DC;shuttleâ&#x20AC;&#x2122; test. These can provide simple, repeatable assessments of disability and response to treatment. Finally, cardiopulmonary exercise testing using cycle or treadmill exercise with measurement of metabolic gas exchange, ventilation and cardiac responses is useful in distinguishing cardiac limitation from respiratory limitation in the breathless patient.

Examination for tuberculi bacilli: Mycobacterial infection is usually confirmed by direct microscopy (Ziehl-Neelsen or auramine staining) and culture of samples. It has been estimated that 5000-10,000 acid-fast bacilli must be present in sputum for a patient to be smear-positive, whereas only 10-100 viable organisms are required for sputum to be culture-positive. A stain-positive sputum sample requres confirmation by the use of standard culture methods (growth characteristics, pigment production and biochemical tests) or molecular DNA technology (hybridisation probes, polymerase chain reaction.

Following decontamination, samples should be cultured on a solid medium (Lowenstein-Jensen or Middlebrook). However, as the organism grows slowly, simultaneous culture in liquid culture media (BACTEC or MGIT) should be performed to expedite the testing of drug sensitivities (typically within 7-21 days). Where multiple drug-resistant TB (MDRTB) is suspected, molecular tools may be employed to test for the presence of the rpo gene, currently associated with around 95% of rifampicin-resistant cases. Rapid tests for other forms of drug resistance are under development. If a cluster of cases suggests a common source, fingerprinting of isolates with restrictionfragment length polymorphism (RFLP) or DNA amplification can help confirm this.

Culture of Tuberculi bacilli: Culture of tubercle bacillus is done in special media like Lowenstein Jensen media or Dorsettâ&#x20AC;&#x2122;s egg media. Bacteria grows very slowly and 4-6 weeks may be necessary before obtaining a positive result.

Examination for other bacteria:

Sputum is examined by staining the smear in Gramâ&#x20AC;&#x2122;s method. There may be one type or more causative organism in the sputum. More than one type of organism is generally present in tracheobronchitis or lung abscess. Culture and sensitivity should also be done in each case. Culture should be made both aerobically and anaerobically.

Examination for Fungi Radiographic features include transient diffuse pulmonary infiltrates and lobar or segmental pulmonary collapse. Permanent radiographic changes of bronchiectasis (tram line, ring and gloved-finger shadows) are seen predominantly in the upper lobes in patients with advanced disease.

Intracavitary Mycetoma: The development of a mycetoma produces a tumour-like opacity on X-ray, but can usually be distinguished from a peripheral bronchial carcinoma by the presence of a crescent of air between the fungal ball and the upper wall of the cavity . HRCT provides greater clarity and often demonstrates the presence of multiple mycetomas. Serum precipitins to Aspergillus fumigatus can be demonstrated in virtually all patients. Sputum microscopy typically demonstrates scanty hyphal fragments and is usually positive on culture.

Less than 50% of patients exhibit skin hypersensitivity to extracts of Aspergillus fumigatus.

Invasive Pulmonary Aspergillosis: Invasive pulmonary aspergillosis should be suspected in any patient thought to have severe suppurative pneumonia that has not responded to antibiotic therapy. The diagnosis can be established by the demonstration of abundant fungal elements in stained smears of sputum. Serum precipitins can be demonstrated in some, but not all, patients.

Aims and Objectives: Haemoptysis is a common medical problem and may present as an acute life threatening emergency which requires immediate attention and intervention.

Determining the causes, sometimes becomes difficult creating diagnostic enigma. So approach to the patients therefore has to be rational. To establish the causes of haemoptysis, maximum emphasis was given to history, clinical examination and interpretation of vailable investigations. The objectives of this study are : A. General Objectives:

To find out the demographic profile, common presentation in cases of haemoptysis.

B. Specific Objectives:

aetiologies, clinical

1. To determine what investigation procedures help maximum in diagnosis in our situation and to give a specific management plan.

2. To compare the study with those of the others in the relevant field Materials and Methods: So consecutive cases of haemoptysis admitted in the medicine unit of a teaching Hospital (combined Military Hospital, Dhaka) during July 2009 to December 2009 were prospectively studied.

After ascertaining was supplemented by routine blood, sputum, stool, urine examinations and chest x-ray postero-anterior view. Other special investigations were done in selected cases to establish the diagnosis.

Sophisticated investigations like CT, Bronchoscopy were not done routinely.

Maximum emphasis was given on history, clinical examination, chest x-ray, sputum examination and other supportive investigations.

Table describes the record sheet which were duly filled in for each individual cases. The patients left hospital with incomplete investigations, were not included in the study. Patients were informed and the purpose of the study was duly explained.

Aeitiological Diagnosis of Haemoptysis in the Medical Unit of a Teaching Hospital QUESTIONNAIRE & DATA COLLECTION SHEET No. Name: Age: Sex: Date of Admission: Date of Discharge: Hospital stay in days: Weight in kg: Height: Address: Local Permanent â&#x20AC;&#x201C; Number of Siblings: Family members/Co workers living in one room: Contact with T.B patients H/O pneumonia: Within/outside the family: H/O Smoking: H/O FB inhalation: H/O Rheumatic fever: H/O malignancy: Occupation: Socio-economic status: H/O Tubercolosis :- 1. On treatment: 2. Completed treatment: 3. Treatment failure/interrupted:

Presenting complaints: Duration of illness (in days): Haemoptysis………….days Attacks (Mild/Moderate/Massive)…

Fever…………….days

Chest pain…………days Respiratory distress…………days Purulent sputum…….....days Loss of appetite……………..days Weight loss…………….days Similar attacks or other types of chest pain …………………………………………………….

Treatment History: General Examination: Appearance: Nutrition: Polycythaemia: Jaundice: Clubbing: Leuconychia:

Body built: Pulse: Anaemia: BP: Nicotine stains: Respiratory rate: Oedema: Temperature (degree): Lymphadenopathy: Koilonychia:

Respiratory System: Movement of the chest wall: Scar Mark: Apex beat: Vocal resonance: Breath sound: Ronchi: Pleural rub: CVS: Visible cardiac impulse: Right parasternal heave: Heart sound: S1 S2 Pericardial rub:

Position of the trachea: Intercostal/Subcostal recession: Deformity: Percussion note: Vocal fremitus: Crepitation:

Palpable P2: Thrill: S3 S4

Abdomen : Size: Engorged: Kidneys: Investigations: Complete blood count with ESR:

Shape: Liver: Bowel sound:

Murmur:

Ascites: Spleen:

Date

Hb(gm/dl) TLC/cm m

Sputum for

N%

L%

E%

M%

ESR (mm hour)

in

- AFB Stain - Gram stain: ……………………

-

C/S -

Malignant cell

MT: Chest X-ray findings: Serial no

1st

Costophrenic Cardiophreni Angle c Angle

Mediastinal Shifting

Pulmonary lesion

Others

Blood culture …………………..

Pleural fluid for : - R/M/E …………………..

- AFB stain -

Gram stain: ……………………………

-

C/S

-

Malignant cell

Pleural Biopsy: Bronchosopy: CT scan of the chest: Others: Diagnosis: …………………………………………………………………

Name of the doctor who filled the questionnaire ……………………………..

Signature …………………….

Date…………………………..

RESULTS OF THE STUDY

Table I: Distribution of haemoptysis among the 50 cases.

Name of the Disease Pulmonary tuberculosios Mitral valvular disease Bronchiectasis Pneumonia Bronchogenic Carinoma Lung abscess Idiopathic thrombocytopenic pupura Acute myeloid leukaemia Acute bronchitis Non-specific respiratory tract infection Total

No. of the Patients 12 2 6 8 11 3 2 2 3 1 50

Percentage 24 4 12 16 22 6 4 4 6 2 100

Pulmonary tuberculosis is the most common cause of haemoptysis comprising 12(24%)(Table-I)of the total cases. In this study number of the patients with Mitral valvualr heart disease were 02(4%)(Table-I), Bronchiectasis 6(12%)(Table-I), Pneumonia 8(16%)(Table-I), Brochogenic carcinoma 11(22%)(Table-I), and Lung abscess 3(6%)(Table-I), Idiopathic Thrombocytopenic purpura 2(4%)(Table-I), Acute Myeloid leukaemia 2 (4%)(Table-I), Acute Bronchitis 3(6%)(Table-I), Non-specific respiratory tract infection comprising 1 (2%)(Table-I) in total 50 patients.

Table II: Describes the distribution of age under various aetiology. (n=50) Name of the Disease

21-30 yrs

31-40 yrs

41-50 yrs

51-60 yrs

No.

%

No.

%

No.

%

No.

%

Pulmonary Tuberculosios

02

4

02

4

06

12

02

4

Mitral Valvular Disease

02

4

-

-

-

-

-

-

Bronchiectasis

00

00

-

-

02

4

4

8

Pneumonia Bronchogenic Carinoma

2 -

4 -

6 -

12 -

2

4

9

18

01

2

2

4

Lung Abscess

IdiopathicThrombocytopeni c Pupura

2

4

-

-

-

-

-

-

Acute Myeloid Leukaemia

2

4

-

-

-

-

-

Acute Bronchitis

0

0

-

-

02

4

01

2

Non-specific Respiratory Tract Infection

-

-

-

-

01

2

-

-

Total

10

20

08

16

14

28

18

36

The mean age of the patient with standard deviation in the series was 21.49Âą32.84 years, a range from twenty one to sixty. The age of the patients in the study were a range from 21 to 60years. Out of 50 patients, 10 patients(20%) (Table-II) belong to the age group 21-30 years, 08 patients(16%)(Table-II) belong to the age group 31-40 years,14 patients(28%)(Table-II) belong to the age group 41-50 years and 18 patients(36%) were between 51-60 years age group(Table-II). The mean age for pulmonary tuberculosis was 35.52+10.68 years of age.

Table III: Shows the smoking habit in different causes of haemoptysis among the patients Name of the Disease

Smoker

Non smoker

No

%

No.

%

Pulmonary Tuberculosios

10

20

02

6

Mitral Valvular Disease

-

-

02

4

Bronchiectasis

05

10

01

2

Pneumonia Bronchogenic Carinoma

6 11

12 22

02 -

4 -

Lung Abscess

03

06

-

-

Idiopathic Thrombocytopenic Pupura

-

-

2

4

Acute Myeloid Leukaemia

-

-

2

4

Acute Bronchitis

3

6

-

-

Non-specific Respiratory Tract Infection

1

2

-

-

Total

39

78

11

22

Among the 50 patients , 39 (78%)(Table III) were smoker and 11 (22%)(Table III) were non-smoker. Out of 12(24%)(Table III) patients with tuberculosis 10(20%)(Table III) were smoker and 2(4%)(Table III) were non-smoker. None of the patients of mitral valvular heart disease were smoker which were 2(4%)(Table III) in number. In this study among the patients with Bronchiectasis, 5(10%)(Table III) of them were smoker and 1(2%)(Table III) of them was nonsmoker. Among the patients suffered from pneumonia 6(12%)(Table III) of them were smoker and 2(4%)(Table III) of them were nonsmoker.

All patients, of bronchogenic carcinoma that was 11(22%)(Table III) in number were smoker. All the 3(6%)(Table III) patients with lung abscess were smoker. 2(4%)(Table III) patients suffered from acute myeloid leukaemia and other 2(4%)(Table III) patents suffered from idiopathic thrombocytopenic pupura were nonsmoker. All the 3(6%) (Table III) patients who were suffering from acute bronchitis and also one patient who was suffering from non specific respiratory tract infection were smoker.

Table IV: Shows the number of male and female patients haemoptysis Name of the Disease

Male

with different causes of Female

No

%

No.

%

Pulmonary Tuberculosios

10

20

02

4

Mitral Valvular Disease

02

4

Bronchiectasis

05

10

01

2

Pneumonia Bronchogenic Carinoma

06 09

12 18

02 2

4 4

Lung Abscess

03

06

-

-

Idiopathic Thrombocytopenic Pupura

02

4

Acute Myeloid Leukaemia

02

4

Acute Bronchitis Non-specific Respiratory Tract Infection

02 01

4 2

1 -

2-

Total

42

84

08

16

Among the 50 patients , 42 (84%)(Table-IV) were male and 8 (16%)(Table-IV) were female . Out of 12(24%)(Table-IV) patients with tuberculosis 10(20%)(Table-IV) were male and 02(4%)(Table-IV) were female. 2(4%)(Table-IV) patients of mitral valvular heart disease were male.In this study among the patients with Bronchiectasis, 5(10%)(Table-IV) of them were male and 1(2%)(Table-IV) of them was female.

Among the patients suffered from pneumonia, 6(12%)(Table-IV) of them were male and 2(4%)(Table-IV) of them were female.

Among of the patients of bronchogenic carcinoma, 9(18%)(Table-IV) of them were male and 2(4%)(Table-IV) of them were female. The 2(4%)(Table-IV) patients suffered from acute myeloid leukaemia were male and other 2(4%)(Table-IV) patients suffered from idiopathic thrombocytopenic pupura were also male. Among of the 03(6%)(Table-IV) patients who were suffering from acute bronchitis 2(4%)(TableIV) of them were male and 1(2%)(Table-IV) of them was female. Another 1(2%) (Table-IV) patient who was suffering from non specific respiratory tract infection was male.

Table V: Shows the extent of haemoptysis in different patients of this study Name of the Disease

Streaks

Mild (loss of blood <150 ml/day)

Pulmonary Tuberculosios

No 6

% 12

Mitral valvular disease

2

4

Bronchiectasis

4

Pneumonia Bronchogenic Carinoma

Moderate (loss of blood from 150ml/day to 400ml/day) No. % 1 2

Massive (loss of blood > 400ml/day) No. 1

% 2

No. 04

% 8

08

02

4

6 9

12 18

2 2

4 4

-

-

-

-

Lung abscess

2

04

01

2

-

-

-

-

Idiopathic thrombocytopenic Pupura

2

4

-

-

-

-

Acute myeloid Leukaemia

1

2

1

2

-

-

-

-

Acute bronchitis

3

6

-

-

-

-

-

-

Non-specific respiratory tract infection

1

2

Total

36

72

12

24

-

-

01

02

01

02

The haemoptysis pattern varies from Streaking of blood, followed by Mild (loss of blood <150 ml/day), Moderate (loss of blood from 150ml/day to 400ml/day) and Massive (loss of blood>400ml/day) haemoptysis. Among the 50 patients, 36 (72%) (Table-V) patients were presented with streaks . In this study 12 (24%)(Table-V) patients had with mild haemoptysis . Among the all patients, 1(2%)(Table-V) patient had moderate haemoptysis and another 1(2%)(Table-V) patient had massive haemoptysis .

Discussion The causes of haemoptysis has been studied in different countries including our country. In a prospectively studies on 52 patients, the aetiologies were bronchiectasis (24.2%), pulmonary tuberculosis (23.3%), bronchogenic carcinoma (19.5%), bronchitis (11%), reheumatic heart disease (6.9%). Aetiology could not be identified in 15% of patients.31 In another study aetiology of haemoptysis was found to be active pulmonary tuberculosis (38%), bronchiectasis (30%), pneumonia (9%), lung abscess (4.87%), bronchogenic carcinoma (4.87%), bronchovascular fistula (4%), primary pulmonary fungal infection (3.45%) and miscellaneous (5.69%). 32 In a study33, 324 cases were reviewed. The causes were like upper respiratory tract infection 26.77%, bronchitis 19.3% bronchiectasis 13.3%, pulmonary tuberculosis 11.73%, pneumonia 6.2%, mitral valvular disease 2.16%, bronchogenic carcinoma 4.3% and others like acute myeloid leukaemia and immune thrombocyto penic purpura 1.23% each. No diagnosis could be achieved in 11% cases.

In Bangladesh, in a study of 30 patients 34, the causes of haemoptysis that found are, pulmonary tuberculosis 36.6%, bronchiectasis 20%, broncial carcinoma 10%, mitral stenosis 10%, bacterial peumonia 6.7%, lung abscess, chronic bronchitis, and tropical eoslnophilia 3.3% each and 5.3% of cases were undiagnosed.

There were 50 cases in this study to determine the aetiological diagnosis of haemoptysis. In this study among the patients presented with haemoptysis, there were pulmonary tuberculosis 6(12%) (Table-I) , mitral stenosis 2(4%)(Table-I), bronchiectasis 6(12%)(Table-I), pneumonia 8(16%)(Table-I), bronchial carcinoma 11(22%)(Table-I), lung abscess 3(6%)(Table-I) and others like idiopathic thrombocytopenic purpura (ITP), acute myeloid leukaemia (AML) comprises 2(4%) (Table-I) each and non-specific respiratory tract infection 1(2%)(Table-I) and acute bronchitis 3(6%)(Table-I).

There were 12(24%)(Table-I) patients found in this study, who suffered from pulmonary tuberculosis and age of all the patients were between 21-60 years (TableII). 10 (20%)(Table-III) patients of them were smoker and all of them were male(Table-IV) and rest of the 2(4%)(Table-III) patients were nonsmoker who were female(Table-IV). Among all the patients of pulmonary tuberculosis 6(12%)(TableV) of them presented with streaks. 4(8%)(Table-V) patients had mild haemoptysis.

1(2%)(Table-V) patient had mild haemoptysis and massive haemoptysis.

1(2%)(Table-V) patient had

The incidence of pulmonary tuberculosis is higher than other diseases causes haemoptysis . It indicates the fact that pulmonary tuberculosis is still prevalent in this part of the world. Moreover massive haemoptysis in TB patients may be due to delay and inadequate treatment of the patients leading to extensive parenchymal damage, which bleeds easily. Factors responsible for the high incidence of tuberculosis in this country including low socioeconomic condition , over crowding , poor hygiene condition, malnutrition and lack of knowledge etc.

In this study , there were 2(4%)(Table-I) patients had mitral stenosis and belongs to 21- 30 years (Table-II) of age group and both of them were nonsmoker(Table-III) .

2(4%)(Table-IV) patients of mitral stenosis were male and both of them had streaks(Table-V).

Poor environmental and socio-economic conditions leads to increased incidence of rheumatic fever in our country and inadequate treatment of rheumatic fever, sore throat leads to higher incidence of rheumatic heart disease.

There were 6(12%)(Table-I) cases of bronchiectasis in this study. All of the patients were more than 40 years (Table-II) and found that all of them were smoker (Table-III) and one of them was non-smoker (Table-III) and 5(10%)(Table-IV) patients of them were male and 1(2%)(Table-IV) of them was female and 4(8%)(Table-V) patients had streaks and 2(4%)(Table-V) patients had mild haemoptysis.

There were 8 (16%)(Table-I) cases of pneumonia in this study and 2(4%)(Table-II) of them were between 21-30 years and 6(12%)(Table-II) of them were between 31-40 years. Among the 8(16%)(Table-I) cases of pneumonia, 6(12%)(Table-III) of them were smoker who were male (Table-IV) and 2(4%)(Table-III) of them were nonsmoker who were female (Table-IV). 6(12%)(Table-V) patients had streaks and 2(4%)(Table-V) patients had mild haemoptysis.

In this study, total number of patients suffering from Bronchogenic carcinoma were 11(22%)(Table-I). In this study it was found that age of the patient suffering from Bronchogenic carcinoma were between 40 to 60 years (Table-II). All of the patients suffering from Bronchogenic carinoma were smoker (Table-III) and among them 9(18%)(Table-IV) of them were male and 2(4%)(Table-IV) of them were female.

9(18%)(Table-V) patients had streaks and 2(4%)(Table-V) patients had mild haemoptysis.

In this study, 3(6%)(Table-I) patients were found suffering from lung abscess. All of them had very foul smelling sputum. The age of the patients were between 40 to 60 (Table-II) and all of them were smoker (Table-III) and male (Table-IV). 2(4%)(TableV) patients had streaks and 1(2%)(Table-V) patient had mild haemoptysis. The incidence of lung abscess is higher in our country than developed countries, which is due to poor nutrition, unhealthy environment and inadequate treatment of the infection in the respiratory system.

Other diseases causing haemoptysis , which had been found in this study were idiopathic thrombocytopenic purpura , acute myeloid leukaemia , non-specific respiratory tract infection and acute bronchitis .

There were 2(4%)(Table-I) patients had Idiopathic thrombocytopenic purpura (ITP) and they were belongs to the age group 21 – 30 years (Table-I) and both of the patients were nonsmoker (Table-III) and male (Table-IV) and both of the patients had streaks(Table-V). 2(4%)(Table-I) patients suffered from acute myeloid leukaemia (AML) and belongs to the age group 21 – 30 years (Table-II) and both of the patients were nonsmoker (Table-III) and male (Table-IV) and both of them had streaks(Table-V).

In this study there were 3(6%)(Table-I) patients of acute bronchitis and belongs to the age group between 41 – 60 years (Table-II) and all of them were smoker(Table-III) .

2(4%)(Table-IV) patients were male and 1(2%)(Table-IV) patient was female.All the 3(6%)(Table-V) patients of acute bronchitis had streaks.

1(2%)(Table-I) patient suffered from non-specific respiratory tract infection who was smoker (Table-III) and belongs to the age group between 41- 60 years (Table-II) and who was male (Table-IV) and presented with streaks (Table-V).

All the 50 cases in this study, diagnosed within limited investigation facilities.

Relevant investigation including Complete blood picture, Chest-Xray , sputum for AFB stain , MT , Bronchoscopy , CT scan of the chest etc. had been done in order to make the diagnosis.

SUMMARY It was a prospective study which was carried out at Combind Military Hospital, Dhaka, on 50 patients admitted in the medicine unit with the complaints of haemoptysis during July 2009 to December 2009. In this study we have tried to identify the various aetiologies of haemoptysis. In order to diagnose the under lying disease of the patient presented with haemoptysis, initially history of the patient had been taken very carefully and then thorough clinical examination of the patient had been carried out. Simultaneously necessary investigation had also been done.

Subsequently on the basis of history, clinical examination and investigation diagnosis had been made.

Pulmonary tuberculosis is the most common cause of haemoptysis comprising 12(24%)(Table-I)of the total cases. In this study, the number of patients with Mitral valvular heart disease were 2(4%)(Table-I), Bronchiectasis 6(12%)(Table-I), Pneumonia 8(16%)(Table-I), Brochogenic carcinoma 11(22%)(Table-I), and Lung abscess 3(6%)(Table-I), Idiopathic Thrombocytopenic purpura 2(4%)(Table-I), Acute Myeloid leukaemia 2 (4%)(Table-I), Acute Bronchitis 3(6%)(Table-I), Non-specific respiratory tract infection comprising 1 (2%)(Table-I) in total 50 patients.

The age of the patients in the study were a range from 21 to 60years. Out of 50 patients, 10 patients(20%) (Table-II) belong to the age group 21-30 years, 08 patients(16%)(Table-II) belong to the age group 31-40 years,14 patients(28%)(TableII) belong to the age group 41-50 years and 18 patients(36%) were between 51-60 years age group(Table-II).

Among the 50 patients, 39 (78%)(Table-III) were smoker and 11 (22%)(Table-III) were non-smoker. Out of 12(24%)(Table-III) patients with tuberculosis 10(20%)

(Table-III) were smoker and 02(4%)(Table-III) were non-smoker. None of the patients of mitral valvular heart disease were smoker which were 2(4%)(Table-III) in number. In this study among the patients with Bronchiectasis, 5(10%)(Table-III) of them were smoker and 1(2%)(Table-III) of them was nonsmoker. Among the patients suffered from pneumonia 6(12%)(Table-III) of them were smoker and 2(4%)(TableIII) of them were nonsmoker.

All of the patients, of bronchogenic carcinoma that was 11(22%)(Table-III) in number were smoker All of the 3(6%)(Table-III) patients with lung abscess were smoker. The 2(4%)(Table-III) patients suffered from acute myeloid leukaemia and other 2(4%)(Table-III) patents suffered from idiopathic thrombocytopenic pupura were nonsmoker. All of the 03(6%)(Table-III) patients who were suffering from acute bronchitis and also one patient who was suffering from non specific respiratory tract infection were smoker.

Among the 50 patients , 42 (84%)(Table-IV) were male and 8 (16%)(Table-IV) were female. Out of 12(24%)(Table-IV) patients with tuberculosis 10(20%)(Table-IV) were male and 02(4%)(Table-IV) were female. 2(4%)(Table-IV) patients of mitral valvular heart disease were male.In this study among the patients with Bronchiectasis, 5(10%)(Table-IV) of them were male and 1(2%)(Table-IV) of them was female.

Among the patients suffered from pneumonia, 6(12%)(Table-IV) of them were male and 2(4%)(Table-IV) of them were female.

Among of the patients of bronchogenic carcinoma, 9(18%)(Table-IV) of them were male and 2(4%)(Table-IV) of them were female. The 2(4%)(Table-IV) patients suffered from acute myeloid leukaemia were male and other 2(4%)(Table-IV) patients suffered from idiopathic thrombocytopenic pupura were also male. Among of the 03(6%)(Table-IV) patients who were suffering from acute bronchitis 2(4%)(TableIV) of them were male and 1(2%)(Table-IV) of them was female. Another 1(2%) (Table-IV) patient who was suffering from non specific respiratory tract infection was male.

The extent of haemoptysis starts with Streaks, which is followed by Mild(loss of blood <150 ml/day) ,Moderate(loss of blood from 150ml/day to 400ml/day ) and Massive(loss of blood >400ml/day) haemoptysis. Among the 50 patients, 36 (72%) (Table-V) patients were presented with streaks . In this study 12 (24%)(Table-V) patients had with mild haemoptysis . Among the all patients, 1(2%)(Table-V) patient had moderate haemoptysis and another 1(2%)(Table-V) patient had massive haemoptysis.

CONCLUSION In our country many patient presented with cough and haemoptysis and the underlying diseases which may involve respiratory system, cardiovascular system, haematological malignancy etc. The diseases of respiratory system that causes haemoptysis and which has been found in this study are : Pulmonary Tuberculosis, Bronchogenic carcinoma , Acute Bronchitis , Lung abscess , Pneumonia . Patient presented with haemoptysis may suffer from the diseases like Mitral valvular disease , Idiopathic Thrombocytopenic purpura , Acute Myeloid leukaemia which has also been found in this study .

Patient presented with haemoptysis must be thoroughly examined and necessary investigation should carried out in order to make the diagnosis earlier . Subsecuently appropriate treatment can be started as soon as possible so that fatal complication of the disease can be prevented.

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