ࡱ> q`%bjbjqPqP.::8Nd %%%%Lf%D P2%%%%%% \/ 2dsOuOuOuOuOuOuO$>QhSdO-5%%55O%%Oi?i?i?5%%sOi?5sOi?i?_MN%% 0řcU%;=rNsOO0 PN T> T NN TN|3h3Ji?64<r4?333OO_? 333 P5555v$v$djJ   THE KURSK STATE MEDICAL UNIVERSITY Department of surgical diseases ! 1 Pleuritis Information for self-training of English-speaking students The chair of surgical diseases N 1 (Chair-head - prof. S.V.Ivanov) By ass. professor I.S. IVANOV KURSK-2010 Pleuritis (pleurisy) 1.Pleural Effusion Excess fluid in the pleural space. Normally, 10 to 20 mL of fluid is spread thinly over the visceral and parietal pleurae. The fluid is similar in composition to plasma except that it is lower in protein (< 1.5 g/dL). Pleural fluid enters from the pleural capillaries and exits via parietal pleural stomas and the lymphatics. Pleural effusions are classified as transudates or exudates. Transudates are due to elevations in microvascular pressure or to decreases in oncotic pressure; exudates are due to pleural inflammation (pleurisy), with an increased permeability of the pleural surface to proteinaceous fluid. Lymphatic obstruction may also contribute to accumulation of pleural fluid. Many conditions can produce either transudates or exudates. Hemothorax (blood in the pleural space) occurs most often from trauma and rarely after rupture of a vessel in a parietopleural adhesion associated with spontaneous pneumothorax. Spontaneous hemothorax occurs rarely as a complication of a coagulation defect. Rarely, an aortic aneurysm ruptures into the pleural space. Pleural blood often does not clot and may be easily withdrawn via a needle or a water-sealed tube thoracostomy. Chylothorax (a milky or chylous pleural effusion) is caused by traumatic or neoplastic (most often lymphomatous) injury to the thoracic duct. The lipid content (neutral fat and fatty acids) of pleural fluid is high; sudanophilic fat droplets are often seen microscopically. Cholesterol content is low. The diagnosis is confirmed by a triglyceride level >= 110 mg/dL (1.24 mmol/L) in the effusion. Conditions Causing Transudates Heart failure, which increases systemic venous and pulmonary capillary pressures, is the most common cause of transudative pleural effusions. Usually bilateral, such effusions tend to be larger on the right side and, if unilateral, are generally right-sided. Hypoalbuminemia may cause pleural effusions, which are usually bilateral and associated with fluid accumulation elsewhere in the body. Ascites may be associated with pleural effusion because fluid can move from the peritoneal space into the pleural space through diaphragmatic defects or lymphatic channels; 70% of para-ascitic effusions are right-sided, 15% left-sided, and 15% bilateral. They occur in about 5% of patients with cirrhosis and ascites. Meigs' syndrome (pleural effusion and ascites associated with ovarian fibromas and other ovarian tumors) has a similar mechanism, but the pleural fluid associated with ovarian tumors is generally an exudate. The mechanism is also similar for pleural effusion associated with peritoneal dialysis or acute pancreatitis. In myxedema, pleural effusions are usually transudates but may be exudates. After parturition, small effusions, which clear rapidly, may be seen during the first 24 h. Iatrogenic pleural effusions result when fluid infused through a catheter meant for a subclavian vein enters the pleural space. Misplaced small feeding tubes can sometimes perforate a main bronchus and enter the pleural space. The resulting pleural fluid is identical to the infusate. Conditions Causing Exudates Mycotic pleurisy produces an exudate, and pleural biopsy may show granulomas. Organisms can be cultured from pleural fluid and tissue. The geographic history, skin and serologic tests, microbiologic examination of airway secretions, and histology of other tissues are useful in establishing a diagnosis. About 10% of patients with blastomycosis have pleural effusions, usually with extensive underlying parenchymal disease. Pleural effusion, usually large and unilateral, occurs in about 7% of patients with primary coccidioidomycosis. About 1/2 of them have an associated parenchymal lesion; erythema multiforme or erythema nodosum is common. Pleural effusion also occurs at a later stage of coccidioidomycosis when a coccidioidal cavity ruptures into the pleural space--a serious complication. Pleural effusion is rare in primary histoplasmosis and in cryptococcosis, occurring usually as part of disseminated disease or with massive parenchymal involvement. In parapneumonic effusions, the visceral pleura overlying a pneumonia becomes inflamed; often, an outpouring of serous exudative fluid accompanies acute pleurisy. The fluid contains many neutrophils and may contain bacteria. Parapneumonic effusions are usually caused by bacteria, but small effusions may occur with viral or mycoplasmal pneumonia. Viral pleural effusions may also occur without evident pneumonia. Pulmonary embolism produces pleural effusions in 30 to 50% of patients. About 80% of the effusions are exudates, which are often blood-tinged. The main mechanism of pleural fluid formation is increased permeability of the visceral pleura over the infarcted lung, although about 1/3 of such effusions occur without evidence of infarction on x-ray. However, a transudate may occur when heart failure is present. Atelectasis due to pulmonary embolism can also cause a transudate. Metastatic neoplasms are the most common cause of exudates in persons > 60 yr. The most common primary site is the lung, followed by the breast, but carcinomas from any site can metastasize to the pleura. Lymphatic obstruction by pleural implants of tumor is the major mechanism of fluid formation. The effusions are often large and cause dyspnea on exertion. Blood-tinged or grossly bloody exudates are the rule. Most carcinomatous pleural effusions can be diagnosed by cytologic fluid examination, but up to three fluid samples may be needed. Pleural biopsy is less sensitive than pleural fluid cytology but is sometimes positive when cytology is negative; in difficult cases, both procedures may be needed. In Hodgkin's disease and non-Hodgkin's lymphoma, pleural effusion is common; it may be a presenting sign in non-Hodgkin's lymphoma. The mechanism is varied, with lymphatic obstruction predominating in Hodgkin's disease and pleural infiltration predominating in non-Hodgkin's lymphoma. Establishing the neoplastic nature of the process is rarely necessary in Hodgkin's disease, and pleural biopsy results are rarely positive. The diagnosis of lymphomatous pleural effusion can occasionally be made by pleural fluid cytology and needle biopsy of the pleura. Malignant mesothelioma (a malignant tumor arising from the pleural mesothelium) is strongly linked to asbestos exposure. Incidence in the USA is about 2000 cases/yr. Insidious nonpleuritic chest pain and dyspnea are the most common presenting symptoms. The tumor, which gradually encases the lungs and invades the chest wall, produces pleural effusion in about 75% of patients. CT reveals irregular thickening of the pleura. The pleural fluid is a serous or blood-tinged exudate, with glucose < 50 mg/dL (< 2.78 mmol/L) and pH < 7.2 in about 1/3 of patients. Pleural fluid cytology may reveal malignant cells not easily differentiated from adenocarcinoma. Because needle pleural biopsies are also difficult to interpret, open biopsy or biopsy visually directed through a thoracoscope (video-assisted thoracic surgery [VATS]) is often needed to establish the diagnosis. Immunohistochemistry and electron microscopy can differentiate this tumor from adenocarcinoma. The prognosis is dismal, with poor response to radical surgery, chemotherapy, radiation therapy, or combination therapy. Benign fibrous mesothelioma is a rare solid tumor of the pleura that produces chest pain, dyspnea, fever, and hypertrophic osteoarthropathy in 50% of patients. The fluid is an exudate that may be viscid due to the presence of hyaluronate. Diagnosis and cure are by thoracotomy and excision of the tumor. SLE or drug-induced lupuslike syndromes (most often with hydralazine, procainamide, isoniazid, phenytoin, and chlorpromazine) produce pleural effusions in up to 40% of patients. The drugs have usually been given for long periods, and the symptoms usually abate within 10 days of stopping the drug. Fever, pleuritic pain, and some systemic manifestations of lupus are usual; rarely, isolated pleural disease occurs. A parenchymal lesion is usually but not always present. The pleural fluid is exudative, with neutrophils predominating early and monocytes late. Pleural fluid glucose is usually > 80 mg/dL (> 4.44 mmol/L), pH is > 7.35, and LDH is < 500 IU/L; pleural fluid complement is low, and pleural fluid antinuclear antibody (ANA) titers tend to be high. An ANA titer > 1:320 with a homogeneous pattern or a pleural fluid/serum ANA ratio >= 1 is highly suggestive. In drug-induced lupus, unlike in standard SLE, antibodies to histones and single-stranded DNA often occur in the blood. LE cells may be found and are thought to be diagnostic, but the test is labor-intensive and should not be ordered because the diagnosis is usually evident from the clinical features and pleural fluid serology. Drug-induced pleural effusions are uncommon. Nitrofurantoin is occasionally associated with an acute febrile illness with pulmonary infiltrates, pleural effusion, and peripheral blood eosinophilia. Chronic interstitial pneumonia with fibrosis occurs less often and produces pleural effusions less often. It occurs in persons who have taken the drug for many years. The muscle relaxant dantrolene occasionally causes unilateral pleural effusion with blood and pleural fluid eosinophilia but without parenchymal infiltration. Bromocriptine and other dopamine agonists, amiodarone, and interleukin-2 infrequently cause pleural effusions, usually with pulmonary infiltrates. Rheumatoid disease causes pleural effusion more often in males even though the disease is more common in females. Pleural effusions are small to moderate and typically occur in older men who have had rheumatoid disease for several years and who have subcutaneous rheumatoid nodules. The fluid is an exudate with low glucose (< 40 mg/dL [< 2.22 mmol/L]), high LDH (> 700 IU/L), low pH (< 7.2), low complement, and a high rheumatoid factor titer (>= 1:320). Cholesterol crystals are common. Subdiaphragmatic abscess most often produces a sympathetic pleural effusion, a sterile exudate with neutrophils predominating. Rarely does such an effusion become infected; 3/4 of subdiaphragmatic abscesses occur weeks to months after abdominal surgery. The diagnosis is established by ultrasonography or abdominal CT. Acute pancreatitis is complicated by para-ascitic pleural effusion in about 10% of cases. The pleural exudate is rich in neutrophils, containing much more amylase than the serum does. The effusions are usually small; about 60% are left-sided, 30% right-sided, and 10% bilateral. Pancreatic pseudocysts may burrow into the mediastinum through the aortic or esophageal hiatus and rupture into one or both pleural spaces. Amylase levels in the pleural fluid are very high (up to 100,000 IU/L), even though serum amylase may be normal. Abdominal ultrasound and CT scans help diagnose pancreatic pseudocyst. Because fluid reaccumulates rapidly after thoracentesis, the pseudocyst must be drained. Postcardiac injury syndrome is characterized by fever, pleuropericarditis, and parenchymal infiltrates beginning weeks after injury to the pericardium or myocardium. It occurs in about 1% of patients who have had MI, cardiac surgery, blunt chest trauma, pacemaker implantation, or angioplasty. Pleural effusions are generally small, are bilateral in about 1/2 the cases, and are often a bloody exudate with normal glucose and pH. The syndrome responds to NSAIDs and corticosteroids. Uremia is often complicated by a generalized serositis, and an exudative pleural effusion may occur with fibrinous pleurisy. The fluid may be grossly bloody and usually contains few cells, which are mainly mononuclear. The creatinine level is elevated but lower than that of the serum, distinguishing it from pleural effusion due to urinary tract obstruction and retroperitoneal accumulation of urine. Asbestos exposure produces benign pleural effusion in about 3% of asbestos workers after a latent period ranging from 5 yr to > 30 yr. Patients may be asymptomatic or have chest pain. Effusions are usually unilateral and small to moderate. Pleural plaques, generally without calcification, are common, and about half the patients have evidence of parenchymal disease. The effusion is an exudate, which may be blood-tinged. The WBC count may be as high as 25,000/L, with a variable differential count and many eosinophils. The diagnosis is one of exclusion, particularly of mesothelioma and metastatic carcinoma. AIDS causes pleural effusion (usually an exudate) in < 2% of patients. Effusion may be due to parapneumonic effusion, empyema, TB, Pneumocystis carinii pneumonia, or Kaposi's sarcoma. Management principles are similar to those for persons with normal immune systems. Symptoms, Signs, and Diagnosis Pleuritic pain and dyspnea are the most common symptoms, but many pleural effusions are asymptomatic and are discovered during physical examination or on chest x-ray. Physical examination may disclose percussion dullness, decreased motion of the hemithorax, absent tactile fremitus, and decreased or absent breath sounds. Despite extensive diagnostic evaluation, the etiology of an effusion is not established in about 20% of cases. Chest x-rays are the most precise way to confirm physical findings and demonstrate the presence of pleural fluid. When there are no adhesions between the visceral and parietal pleurae, fluid collects in the most dependent portion of the thorax. Because of lung recoil, the upper border of the fluid is meniscus-shaped. With the patient upright, the minimum amount of detectable fluid ranges from 200 to 500 mL. However, in the lateral decubitus view, < 100 mL of fluid is easily detectable. Large pleural effusions may result in complete opacification of the hemithorax and in mediastinal shift to the contralateral side. Adhesions between visceral and parietal pleurae may result in atypical loculated collections. Loculations in the horizontal or oblique fissure may be confused with an intrapulmonary tumor and are called "vanishing tumors." Obliteration of the costophrenic angle usually denotes a fibrosing and healing reaction and may remain after healing is complete. Pleural plaques due to asbestos exposure present as localized areas of pleural thickening, are sometimes calcified, and are usually in the lower 2/3 of the thorax. CT scan is valuable in evaluating the underlying lung parenchyma in patients with extensive pleural disease. A lung abscess, pneumonia, or a shadow due to a bronchogenic carcinoma may be revealed beneath a loculated pleural effusion. A lung abscess may be differentiated from an empyema with a bronchopleural fistula and an air-fluid level. Pleural plaques are easily differentiated from parenchymal lesions, and the pleural densities of mesothelioma are readily identified. Loculated pleural effusions are clearly seen with CT. MRI is not indicated. Ultrasonography can also identify and localize a loculated pleural effusion, which is echo-free in contrast to the lung and chest wall. In difficult cases, the chest wall can be marked or thoracentesis performed in the ultrasonography suite. Thoracentesis should almost always be performed to confirm the presence of fluid and to determine its characteristics. Fluid may be clear yellow (serous), milky (chylous), blood-tinged (serosanguineous), grossly bloody (sanguineous), or translucent or opaque and thick (purulent). Specimens should be taken for chemical, bacteriologic, and cytologic examination (the last uses tubes with heparin, 3 U/mL fluid, added). After thoracentesis, a sample of Gram-stained pleural fluid sediment should be examined microscopically for bacteria and fungi. Cultures for anaerobes should be sent to the laboratory in special transport media or in a capped syringe. Exudates have at least one of the following features: (1) pleural fluid/serum protein ratio > 0.5, with pleural fluid protein usually > 3.0 g/dL; (2) pleural fluid/serum LDH ratio > 0.6; and (3) pleural fluid LDH > 2/3 of the upper normal limit for serum. Transudates meet none of these criteria; they are usually clear and straw-colored but may be blood-tinged, with an RBC count > 10,000/L. WBC count is usually < 1000/L but is between 1,000 and 10,000/L in about 20% of transudates. The glucose level is similar to that in serum. Blood-tinged pleural fluid has little diagnostic significance. More than 15% of pleural transudates and > 40% of exudates are blood-tinged with RBC counts between 5,000 and 100,000/L. Only 5,000 to 10,000 RBCs/L need be present to make pleural fluid red, and only 1 mL of blood is needed to make 500 mL of pleural fluid look blood-tinged. Grossly bloody fluids have > 100,000 RBCs/L; bloody pleural fluids suggest trauma, malignancy, or pulmonary infarction. A hematocrit of > 50% in a bloody pleural fluid indicates hemothorax. If the body's defenses do not control infection in a patient with pneumonia and parapneumonic effusion, the number of neutrophils and bacteria increases, and the fluid takes on the gross appearance of pus. The result is empyema of the thorax (purulent exudate in the pleural space). Fluids with > 100,000 neutrophils/L, bacteria seen on Gram stain, and pH < 7.2 may be presumed to be empyema even if the fluid is not grossly purulent. Most empyemas are caused by anaerobic bacteria. Empyema can result from contamination of the pleural space by rupture of a lung abscess; a bronchopleural fistula complicates the process. A bronchopleural fistula can result from internal drainage of an empyema. Empyema may be a sequela of a penetrating wound, a thoracotomy, infection from a hepatic or subdiaphragmatic abscess, or a ruptured viscus (eg, esophagus). Total cell counts should be obtained routinely for clear or turbid fluids. A predominance of polymorphonuclear leukocytes (PMNs) suggests an underlying pneumonia and a parapneumonic effusion that is usually sterile even in bacterial pneumonia. In the early stages of bacterial infection, fluid is not visibly purulent, many PMNs are present, and bacteria may be seen in a Gram stain. The presence of many small mature lymphocytes, particularly with few mesothelial cells, strongly suggests TB. In pulmonary infarction, there is usually a mixture of lymphocytes, PMNs, and mesothelial cells; RBCs may be numerous. Eosinophils in the pleural fluid have little diagnostic significance but are rarely present in a tuberculous or malignant effusion. A glucose concentration of < 60 mg/dL (< 3.33 mmol/L) in an exudative pleural effusion indicates TB, malignancy, parapneumonic effusion, or rheumatoid disease. In most rheumatoid pleural effusions, glucose is < 30 mg/dL (< 1.67 mmol/L). Very high amylase levels occur in pleural effusions associated with acute pancreatitis, chronic pancreaticopleural fistulas, and esophageal rupture. The amylase in pleural effusions due to esophageal rupture is of salivary origin, is evident within hours of the rupture, and may be the key to early diagnosis and lifesaving surgery. In about 10% of malignant pleural effusions, amylase is slightly to moderately elevated. The pH of loculated pleural effusions that complicate pneumonia tends to be < 7.2. These laboratory tests are most useful when integrated with all of the clinical data and other appropriate tests, eg, a tuberculin skin test when pleural effusion from TB is suspected. Whenever the diagnosis of an exudative pleural effusion is not clear, a needle biopsy of the parietal pleura should be performed with a Cope's or Abrams' side-hook needle. Several pieces of tissue can be sent for histologic and bacteriologic examinations. The combination of microscopic examination and culture of pleural tissue yields a diagnosis in 90% of patients with pleural effusion from TB. However, repeat cytologic examination of pleural fluid is preferable to pleural biopsy for establishing pleural carcinomatosis. In obscure cases, larger amounts of pleural tissue can be obtained through a small thoracotomy incision (open pleural biopsy). For example, the diagnosis of pleural mesothelioma often is impossible from a needle biopsy and requires the larger amount of tissue obtained in an open pleural biopsy. Replacing fluid with air and performing a VATS biopsy is a comparable procedure. However, even with these more invasive procedures, the etiology of the pleural effusion may remain unknown. Pleural effusion complicates many pulmonary conditions. A clinician must judge whether to focus diagnostic studies on the lung, the pleural space, or both. If clinical and x-ray findings suggest the presence of important pulmonary disease, the initial focus should be on the lungs, and fiberoptic bronchoscopy should be performed early in the assessment. Unless pulmonary disease is evident, bronchoscopy is unlikely to reveal the etiology of the pleural process. However, bronchoscopy should be performed before the etiology is declared unknown. Treatment Thoracentesis often dramatically relieves dyspnea due to a large pleural effusion. Because cardiovascular collapse occurs (rarely) if too much fluid is removed too quickly, removal should be limited to 1200 to 1500 mL at one time. Pneumothorax may complicate thoracentesis if the visceral pleura is punctured or if air leaks into the pleural space (which is at subatmospheric pressure) as a result of a break in the continuity of the thoracentesis system. Indolent infection in the pleural space must be treated by a long course of antibiotic therapy. Pleural fluid is usually reabsorbed spontaneously. Empyema is treated with high doses of parenteral antibiotics and drainage. One or two needle aspirations daily may be adequate for small collections of thin pus, but water-sealed tube thoracostomy is usually preferable. When the empyema cavity is lined by a thick, organizing, fibrinous exudate or cortex, open drainage over weeks or months through a rib resection or intercostal tube may be necessary. If the lung is partially collapsed by a thick cortex or if the empyema is loculated, surgical decortication by thoracotomy or VATS is the best way to expand the lung and obliterate the space. Decortication for a loculated empyema is best performed within the first 3 to 6 wk of the illness. Surgery may also be necessary when a bronchopleural fistula complicates empyema. Treatment of pleural effusion due to malignant pleural implants is often difficult. Pleural fluid often reaccumulates after the thorax has been drained, especially if systemic antitumor therapy has not yet been adequate. When fluid reaccumulates, the treatment of choice is pleurodesis: The lung is reexpanded by tube thoracostomy, followed by instillation of a sclerosing agent, such as asbestos-free talc, given in a slurry, or doxycycline, a tetracycline derivative. The result is an intense pleuritis that obliterates the pleural space so that fluid cannot reaccumulate. For hemothorax, water-sealed tube drainage is generally sufficient, provided the bleeding has stopped. Fibrinolytic enzymes (streptokinase-streptodornase or urokinase) may be instilled through an intercostal drainage tube to lyse fibrinous adhesions if the effusion becomes loculated, but thoracotomy and decortication may be necessary to expand the lung and obliterate the pleural space. Pneumothorax Free air between the visceral and parietal pleurae. Etiology and Pathophysiology Traumatic pneumothorax: Normally, pressure in the pleural space is less than atmospheric pressure because of lung recoil. After trauma, air may enter the pleural space in several ways. Open pneumothorax occurs when a penetrating chest wound produces a persistent communication between the outside and the pleural space that allows outside air to enter the pleural space, causing the lung to collapse. In closed pneumothorax, the chest wall becomes airtight after penetration (eg, by a thoracentesis needle, central vein percutaneous catheter via the subclavian veins, fractured rib, or knife), or air may continue to enter the pleural space (eg, from a lung punctured by a fractured rib). Air may also leak from a ruptured bronchus or perforated esophagus into the mediastinum and then into the pleural space. Active TB or other infectious granulomas may (rarely) cause pneumothorax when a cavity perforates into the pleural space. Pulmonary barotrauma is an important cause of pneumomediastinum and pneumothorax in patients on mechanical ventilators. It occurs most often in the adult respiratory distress syndrome, particularly among patients requiring high peak inspiratory pressure or positive end-expiratory pressure. Spontaneous pneumothorax: Air enters the pleural space without antecedent trauma. Most spontaneous pneumothoraces occur without exertion. Some occur during diving or high-altitude flying, apparently related to ambient pressure changes unequally transmitted to different portions of the lung. Spontaneous pneumothorax is called simple when it occurs in a previously healthy person. It is usually caused by rupture of a small, localized, usually apical bulla. It may occur as a complication of an interstitial pulmonary air leak and pneumomediastinum, which may be spontaneous. Incidence is greatest in tall men < 40 yr, and the prognosis is excellent. Spontaneous pneumothorax is called complicated when it occurs in a person with extensive underlying pulmonary disease. It most often results from rupture of a bulla in a person with severe generalized emphysema and is thus predominantly a disease of middle-aged and older persons. It may also occur in persons with other chronic pulmonary diseases, such as asthma, eosinophilic granuloma, lung abscess with bronchopleural fistula and empyema, and cystic fibrosis. Because of the underlying pulmonary disease, physiologic derangements are much greater and the prognosis is much worse than those in simple spontaneous pneumothorax. Tension (positive pressure) pneumothorax: A check-valve mechanism in a bronchopleural fistula allows air to enter but not leave the pleural space, causing pressure in the space to rise above atmospheric pressure. The result is lung collapse and mediastinal shift to the opposite side, which may severely compromise pulmonary and cardiac function. Induced pneumothorax: Air may be used to replace fluid as a prelude to thoracoscopy or, rarely, for better x-ray visualization of masses or of intrathoracic structures. Symptoms, Signs, and Diagnosis Symptoms range from minimal disturbance to severe dyspnea, shock, and life-threatening respiratory failure and circulatory collapse. Sudden sharp chest pain, dyspnea, and, occasionally, a dry, hacking cough occur at onset. The pain may be referred to the corresponding shoulder, across the chest, or over the abdomen; it may simulate an acute MI or an acute abdomen. Symptoms tend to be less severe in a slowly developing pneumothorax and usually subside as accommodation to the altered physiologic state occurs. A small collection of air may produce no detectable physical signs or only diminution of voice and breath sounds. A large or tension pneumothorax produces diminished chest wall motion on the affected side, tympany on percussion, and diminished or absent tactile fremitus. Mediastinal shift may be detectable as displacement of cardiac dullness and apex beat away from the affected side. Breath sounds are markedly depressed or absent. Hypoxemia is minimal or absent in simple spontaneous pneumothorax but may be severe and associated with hypercapnia in complicated pneumothorax. The chest x-ray usually shows air without peripheral lung markings laterally, limited by a sharp visceral-pleural margin, with lung markings medially, indicating the position of the collapsed lung. A small pneumothorax may be overlooked on a routine inspiratory x-ray but is obvious on an expiratory x-ray because the size and density of the lung (but not of the pleural airspace) change during expiration. The mediastinum shifts to the contralateral side, especially with a large pneumothorax. Differential diagnosis includes emphysematous bullae, large lung abscess, and herniation of the stomach, colon, or, much less commonly, small bowel through the diaphragm. In patients on mechanical ventilators for the adult respiratory distress syndrome, pneumothorax may develop subtly in loculated form in a subpulmonic or paracardiac location. Interstitial air within the lung and pneumomediastinum may precede the development of pneumothorax. Prognosis and Treatment A small spontaneous pneumothorax requires no special treatment; the air is reabsorbed in a few days. Full absorption of a larger airspace may take 2 to 4 wk, during which time it is uncertain whether the pleural leak is closed and whether pleural effusion and epipleural fibrinous exudate will develop. The course can be shortened by simple aspiration of air through a small-bore catheter. If aspiration is unsuccessful, a chest tube should be introduced with water-sealed drainage or with a one-way valve. In both traumatic and spontaneous pneumothorax, the air leak usually closes and heals quickly as the lung initially collapses. Reexpansion of the lung can also promote sealing of the air leak because of symphysis of the visceral and parietal pleurae. If air continues to leak, chest tube drainage with suction may be used in the hope of expanding the lung rapidly. Reexpansion pulmonary edema is a risk after application of suction, particularly if the pneumothorax is large and if long-standing and high suction pressures are used. If a large, persistent fistula is present or if the pneumothorax becomes loculated, repair of the fistula or excision of the affected lung segment may be required. A sclerosing agent, such as intrapleural doxycycline or talc, may be used for persistent or recurrent pneumothorax in patients who are poor risks for thoracotomy (eg, those with cystic fibrosis or emphysema). In tension pneumothorax, quick removal of air may be lifesaving. Air may be removed simply by inserting into the chest a 19-gauge or larger needle attached through a three-way stopcock to a large syringe. The needle may be inserted anteriorly or laterally over a site with absent breath sounds and enhanced percussion note. When there is time for a chest x-ray, sites where the lung is held to the chest wall by adhesions should be avoided. Air is alternately withdrawn from the pleural space and expelled from the syringe into the room until a tube thoracostomy has been performed and water-sealed drainage of the hemithorax has been established. A check valve fitted to a catheter inserted into the pleural space may also be used to withdraw air. Recurrent pneumothorax may cause considerable disability. Surgical intervention is generally indicated after two spontaneous pneumothoraces on the same side. The preferred procedures are thoracotomy--in which bullae are oversewn or excised and the pleura roughened by rubbing with gauze--or, when bullous disease is extensive, parietal pleurectomy. The procedures may be performed using video assistance via a thoracoscope. Pleuritis Inflammation of the pleura, usually producing an exudative pleural effusion and stabbing chest pain worsened by respiration and cough. Etiology Pleurisy may result from an underlying lung process (eg, pneumonia, infarction, TB); direct entry of an infectious agent or irritating substance into the pleural space (eg, with a ruptured esophagus, amebic empyema, or pancreatitic pleurisy); transport of an infectious or noxious agent or neoplastic cells to the pleura via the bloodstream or lymphatics; parietal pleural injury (eg, trauma, especially rib fracture, or epidemic pleurodynia [due to coxsackievirus B]); asbestos-related pleural disease in which asbestos particles reach the pleura by traversing the conducting airways and respiratory tissues; or, rarely, pleural effusion related to drug ingestion. If the period of disease more than 8 weeks chronic empyema of pleura. Pathology The pleura usually first becomes edematous and congested. Cellular infiltration follows, and fibrinous exudate develops on the pleural surface. The exudate may be reabsorbed or organized into fibrous tissue resulting in pleural adhesions. In some diseases (eg, epidemic pleurodynia), the pleurisy remains dry or fibrinous, with no significant exudation of fluid from the inflamed pleura. More often, pleural exudate develops from an outpouring of fluid rich in plasma proteins from damaged capillaries. Occasionally, marked fibrous or even calcific thickening of pleura (eg, asbestos pleural plaques, idiopathic pleural calcification) develops without an antecedent acute pleurisy. Exudate Purulent Putrefactive Microflora Nonspecific (a staphylococcus, diplococcus) Specific (tubercular, fungoid) Mixed Prevalence of process Free (total, subtotal, small) Circumscribed (parietal, intralobal, basal, apical, mediastinal, multichamber) Symptoms and Signs Sudden pain is the dominant symptom of pleurisy. Typically, pleuritic pain is a stabbing sensation aggravated by breathing and coughing, but it can vary. It may be only a vague discomfort, or it may occur only when the patient breathes deeply or coughs. The visceral pleura is insensitive; pain results from inflammation of the parietal pleura, which is mainly innervated by intercostal nerves. Pain is usually felt over the pleuritic site but may be referred to distant regions. Irritation of posterior and peripheral portions of the diaphragmatic pleura, which are supplied by the lower six intercostal nerves, may cause pain referred to the lower chest wall or abdomen and may simulate intra-abdominal disease. Irritation of the central portion of the diaphragmatic pleura, innervated by the phrenic nerves, causes pain referred to the neck and shoulder. Respiration is usually rapid and shallow. Motion of the affected side may be limited. Breath sounds may be diminished. A pleural friction rub, although infrequent, is the characteristic physical sign. It need not be accompanied by pleuritic pain, but it usually is. The friction rub varies from a few intermittent sounds that may simulate crackles to a fully developed harsh grating, creaking, or leathery sound synchronous with respiration, heard on inspiration and expiration. Friction sounds due to pleuritis adjacent to the heart (pleuropericardial rub) may vary with the heartbeat as well. When pleural effusion develops, pleuritic pain usually subsides. Percussion dullness, absent tactile fremitus, decreased or absent breath sounds, and egophony at the upper border of the fluid are then noticeable. The larger the effusion, the more obvious the above signs. A large effusion may produce or contribute to dyspnea through diminished lung volume, especially if there is underlying pulmonary disease, mediastinal shift to the contralateral side, and diminished function and recruitment of inspiratory muscles due to an expanded thoracic cage. Diagnosis Pleurisy is readily diagnosed when characteristic pleuritic pain occurs. A pleural friction rub is pathognomonic. Pleurisy that produces referred abdominal pain is usually differentiated from acute inflammatory abdominal disease by x-ray and clinical evidence of a respiratory process; absence of nausea, vomiting, and disturbed bowel function; marked aggravation of pain by deep breathing or coughing; shallow rapid breathing; and a tendency toward relief of pain by pressure on the chest wall or abdomen. Intercostal neuritis may be confused with pleurisy, but the pain is rarely related to respiration and there is no friction rub. With herpetic neuritis, development of the characteristic skin eruption is diagnostic. MI, spontaneous pneumothorax, pericarditis, and chest wall lesions may simulate pleurisy. A pleural friction rub may be confused with the friction rub of pericarditis (pericardial rub), which is heard best over the left border of the sternum in the third and fourth interspaces, is characteristically a to-and-fro sound synchronous with the heartbeat, and is not influenced significantly by respiration. Chest x-rays are of limited value in diagnosing fibrinous pleurisy. The pleural lesion causes no shadow, but an associated pulmonary or chest wall lesion may. The presence of a pleural effusion, generally small, confirms the presence of acute pleurisy. Treatment Treatment of the underlying disease is essential. Acetaminophen 0.65 g qid or an NSAID is often effective. Oral narcotics may be necessary, but cough suppression may not be desired. Adequate bronchial drainage must be provided to prevent pneumonia. A patient receiving narcotics should be urged to breathe deeply and cough when pain relief from the drug is maximal. Antibiotics and bronchodilators should be considered for treatment of associated bronchitis. Surgical treatment acute empyema of the pleura. Thoracoscopy must be distinguished from video-assisted thoracic surgery (VATS). Thoracoscopy is primarily used for surgical treatment of pleural disease, pleurodesis and drainage. It is most often performed by surgeons but may be performed by other trained physicians. In contrast, VATS is used exclusively by surgeons to perform minimally invasive thoracic surgery. Thoracoscopy may be performed using a local, regional, or general anesthetic. A general anesthetic is preferred for patients with complex pleural disease, such as loculated fluid collection, and for those who might not tolerate unilateral pneumothorax without mechanical ventilation. After draining (2 drain- first in 7 intercostal space, second in 2 intercostal space) the pleural cavity irrigation solutions of antiseptics and antibiotics is necessary. Thoracotomy is most helpful in patients with undiagnosed focal or diffuse pulmonary problems, in which definitive diagnosis is likely to improve the management plan. It is used in patients with pulmonary problems of unknown etiology when less invasive procedures have not yielded a diagnosis or when other procedures are more dangerous or unlikely to yield a diagnosis. Main surgical methods of treatment at thoracotomy: Wide thoracotomy with the resection of lung Early decortication mild (erasion of pleural solderings and adhesion) Surgical treatment chronic empyema of the pleura. During 3-4 months make drainage of pleural cavity (with active aspiration and respiratory gymnastics). If the drainage is noneffective - operative treatment is necessary. Surgical treatment 1.pleuroectomy 2.thoracoplasty (a resection of several ribs, a tamponade of a cavity muscles and soft tissues) Sometimes apply scalene thoracoplasties . In the case of bronchopleural fistula the tamponade of a bronchi or a pleurectomy is necessary. Pleural Fibrosis And Calcification Fibrosis of the pleura can occur when inflammatory reactions heal. Even with long-standing or severe inflammation, often only a slight amount of scar tissue remains after complete healing, although the lung occasionally becomes encased in a thick fibrous layer that limits chest wall motion, retracts the mediastinum toward the side of disease, and impairs pulmonary function. Differentiating localized pleural thickening from loculated pleural fluid may be impossible except by thoracentesis, although characteristic differences may be present on ultrasound and CT scans. Pleural fibrosis should be minimized by early treatment of underlying pleural disease. 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