key: cord-021742-sdz6d1r5 authors: Karnik, Ankur A.; Karnik, Ashok M. title: Pneumothorax and Barotrauma date: 2009-05-15 journal: Critical Care Medicine DOI: 10.1016/b978-032304841-5.50050-9 sha: doc_id: 21742 cord_uid: sdz6d1r5 nan Weissberg and Refaely 6 reported on 1199 patients with pneumothorax. Of 865 male and 334 female patients, 60 .3% of the pneumothoraces were spontaneous, 33.6% were traumatic, and 6.1% were iatrogenic. Chen and col-leagues, 7 in their university-based teaching hospital ICU, found that of 60 patients who developed pneumothorax while in the ICU, 58% were related to procedures, most commonly thoracentesis. The reported recurrence rates of pneumothorax vary widely, depending on the type of pneumothorax and the duration of follow-up. A compilation of 11 studies showed that the recurrence rate in "primary" spontaneous pneumothorax (PSP) ranged from 16% to 52% with a mean recurrence rate of 30% in those without defi nitive preventive treatment. 8 Table 48 -1 categorizes episodes of pneumothorax seen at Nassau University Medical Center, a 530-bed hospital and trauma center in the suburbs of New York City. Conventionally, PSP has been defi ned as a pneumothorax that occurs spontaneously in a patient who has no underlying lung disease. However, a condition is unlikely to remain "primary" or "idiopathic" as we gain understanding about this disease process. Diagnoses labeled as "primary" then shift into the category of "secondary." Understanding the development of PTX in a patient who has known blebs and bullae is easy. However, computed tomography (CT) can detect abnormalities predisposing to PSP in patients with normal chest radiograph. CT has demonstrated emphysema-like changes (ELCs) in patients with PSP. Bense and others 9 reported on 27 nonsmoking cases of spontaneous pneumothorax (SP) who were not defi cient in alpha-1 antitrypsin. In 22 cases (81%), CT showed ELCs. These changes were found mainly in the upper and peripheral regions. No ELCs were detected in the control group. Other investigators 10, 11 have also reported similar fi ndings on CT in their cases of PSP. described a patient with recurrent PSP in whom inhalation of aerosolized fl uorescein followed by autofl uorescence thoracoscopy allowed in vivo localization of various areas of extensive subpleural fl uorescein accumulation, which were not visible with normal white thoracoscopy. This has led to the concept of "porous" pleura. 15 In a study on 138 Swedish patients, Bense and colleagues 16 found that smoking increased the risk of developing PSP 9-fold in women and 22-fold in men. Although cessation of smoking appears to reduce the risk of recurrence, 17 continued smoking increases the risk of recurrence. 18 Cottin and colleagues 19 found that in 79 smokers who underwent surgery for recurrence or persistence of PSP, 70 (88.6%) had evidence of respiratory bronchiolitis. Smit and colleagues 20 performed spirometrically controlled high-resolution CT density measurements in 41 patients with SP and found that the mean lung density was lower in patients with pneumothorax. They hypothesized that peripheral airway infl ammation leads to airway obstruction with a check valve phenomenon, causing air trapping and development of pneumothorax. No correlation was found between air trapping and smoking habit or ELCs. Although rare, familial inheritance of pneumothorax has been reported. 21, 22 The analyses suggest two possible models of inheritance: an autosomal dominant gene with incomplete penetrance and an X-linked recessive gene. The occurrence of recurrent SP in a Finnish brother and his sisters also raises the possibility of autosomal recessive inheritance. 23 As in SP, patients with Marfan syndrome are tall, and pneumothorax is a common pulmonary complication. Marfan syndrome is caused by the mutation in the FBN1 gene on chromosome 15. This gene is responsible for the formation of 10-to 12-nm microfi brils in the extracellular matrix of connective tissue. Cardy and colleagues 24 hypothesized that familial SP is caused by a connective tissue disorder that exhibits mendelian inheritance and postulated FBN1 as the causative gene. Another interesting syndrome in which patients develop SP has been described. Brit-Hogg-Dube (BHD) is an autosomal dominant cancer syndrome characterized by benign skin and renal tumors, pleuropulmonary blebs and cysts, and SP. The gene has been mapped to chromosome 17p11.2 and recently identifi ed, expressing a novel protein called folliculin. 25, 26 As a result of a breach in the visceral or parietal pleura, air enters the pleural space. When the amount of air is large and the increase in intrapleural pressure great, the mediastinum shifts to the opposite side and the diaphragm is depressed (Fig. 48-1) . A decrease in vital capacity, functional residual capacity, total lung capacity, and oxygen transfer occurs. 27 In a large pneumothorax, the arterial oxygen pressure (PaO 2 ) falls and the alveolar-arterial oxygen pressure difference [P(A-a)O 2 ] increases. The factors that lead to hypoxemia during a large pneumothorax are anatomic shunt, 28 hypoventilation, 29 and relative overperfusion of partially collapsed, underventilated lungs. 30 Anthonisen 31 reported that in patients with pneumothorax, airway closure occurs at low lung volumes and suggested that this was the main cause of ventilation maldistribution in such patients. Animal studies suggest that the progressive hypoxemia with increasing pneumothorax is primarily the result of increasing degrees of pulmonary vascular shunting associated with increasing parenchymal collapse. 32 The classifi cation given in Box 48-1 combines the circumstances of occurrence of pneumothorax, the etiologic factors, and the state of the underlying lung. When pneumothorax occurs without trauma and is not iatrogenically induced, it is called SP. SP occurring in an otherwise healthy person is called PSP, as mentioned earlier. Secondary SP (SSP) occurs in patients with a variety of underlying lung diseases. Other interesting categories of SP are catamenial pneumothorax, pneumothorax in drug addicts and acquired immunodefi ciency syndrome (AIDS) patients, and familial SP. Investigators have found subpleural blebs or bullae at apices on chest radiographs and at thoracotomy in patients with SP. 33 The pathogenesis of these blebs and the factors that lead to their rupture remain controversial. PSP is classically seen in previously healthy young men with an asthenic body habitus. Melton and colleagues 34 found that the incidence of PSP rose with increasing height among adults of both sexes, more so in males. It reached a fi gure of more than 200 per 100,000 personyears for those 76 inches or taller. It has been suggested that the greater prevalence of SP in tall, thin males is the result of a combination of circumstances. In an extremely long and narrow chest, the apical alveoli are underperfused; such alveoli are more readily torn by gravitational stress. Inherited weakness of connective tissue might also contribute to the pathogenesis, as suggested by the numerous reports of SP in families and concurrent occurrence of SP in twins. 35 Morrison and colleagues 36 have reported a family exhibiting spontaneous pneumothorax in a father and three offspring and suggested that isolated autosomal dominant pneumothorax may be a distinct entity. Most patients with SP are heavy smokers. In one series, 37 72% of all patients were smokers. An increase in cigarette consumption during a particular year was followed within 1 to 2 years by an increased incidence of SP; the reverse occurred with decreased cigarette consumption. 38 Smoking increases the relative risk of developing SP about 9-fold in women and 22-fold among men, and there is a statistically signifi cant dose-response relationship between smoking and SP. 39 Pneumothorax Secondary to Underlying Lung Disease In adults, SP has been reported to occur as a result of a large variety of diseases including asthma, staphylococcal septicemia, pulmonary infarction, sarcoidosis, idiopathic pulmonary hemorrhage, pulmonary alveolar proteinosis, familial fi brocystic pulmonary dysplasia, tuberous sclerosis, cryptogenic fi brosing alveolitis, eosinophilic granuloma, coccidioidomycosis, echinococcal disease, chronic obstructive pulmonary disease (COPD), Shaver's disease (bauxite pneumoconiosis), lymphangioleiomyomatosis, von Recklinghausen's disease, gastropleural and colopleural fi stulas through the diaphragm into the left pleural cavity, radiation therapy to the thorax, Wegener's granulomatosis, cystic fi brosis, acute bacterial pneumonia, and as a complication of the chemotherapy used in the treatment of malignancy and pulmonary metastases from a variety of malignancies. 40 The most common cause of secondary SP, however, is COPD. SP in COPD patients is a serious complication with excessive morbidity and mortality. 8, 41 The clinical presentation of pneumothorax in COPD patients is often atypical-pain may be absent, anxiety and breathlessness may predominate and be out of proportion to the collapsed lung, and the classic sign of hyperresonance may not be helpful because of the underlying emphysema. The air leak in these patients is usually large, and the tissues slow to heal, so it is weeks before the tubes can be taken out. 42 When the peripheral veins of chronic abusers of drugs become obliterated because of a sclerotic or infectious process, the individual may attempt to use larger veins in the groin or neck. Attempted subclavicular or supraclavicular injection ("pocket shoot") of drugs in the street setting has led to unilateral or bilateral pneumothoraces. [43] [44] [45] [46] [47] Douglas and Levison 47 found that the incidence of pneumothoraces is equal in both sexes and that it is less of a problem in teenagers (because they are unwilling to invade the clearly dangerous territory of neck veins or because they have not yet exhausted the peripheral veins) and in addicts older than 40 years of age (probably because either conservation alters their behavior or they do not survive to their fi fth decade). It was also noted that although most drug users describe using small (21-or 22-gauge) needles, a large, complete, or tension pneumothorax usually develops. Quite often the pneumothorax is bilateral. 43, 45 Pneumothorax in Acquired Immune Defi ciency Syndrome Patients Since the fi rst report of spontaneous pneumothorax in patients with AIDS in 1984 by Wollschlager and colleagues, 48 numerous other authors [49] [50] [51] [52] [53] [54] [55] [56] [57] [58] [59] [60] have reported on the occurrence of pneumothorax in these patients. SP is an uncommon event (0.06%) in the general population and occurs rarely in association with infectious pneumonia. 61 Spontaneous pneumothorax in patients with AIDS has become the leading cause of nontraumatic pneumothorax in this population. 62 With the diagnosis of AIDS, a patient's risk of sustaining a nontraumatic pneumothorax increases to 450 times that of general population. 63 A high incidence (2% to 9%) has been reported in patients with AIDS and Pneumocystis carinii pneumonia (PCP). 58, 59, 64 Pneumocystis carinii, which was thought to be a protozoan, has been renamed as Pneumocystis jerovici and is now classifi ed as an Archiascomycetous fungus. 65 Mechanical ventilation and bronchoscopy are quite often required in AIDS patients, and these two factors further increase the chance of pneumothorax occurring in these patients. 53, 66 In patients with AIDS, the pneumothorax is frequently bilateral, recurrent, and not responsive to conservative therapy. 67, 68 Most often it is related to the infection with P. jerovici, but other infections like Mycobacterium tuberculosis, M. avium intracellulare, pulmonary cytomegalovirus, Pneumococcus organisms, 53 or pulmonary toxoplasmosis 69 may be associated. In a study of 144 patients of AIDS with PCP, the overall mortality was reported to be 21.5%; pneumothorax was found to be one of the seven factors that predicted 90-day mortality. 70 The exact pathogenesis of the pneumothorax in these patients is not clear. In AIDS patients who have or have had active PCP, large confl uent areas of thin-walled blebs, distributed randomly on the surface of each lobe, have been reported. 53 It has been postulated that the cystic changes may result from a check-valve mechanism caused by airway infl ammation and resultant partial airway obstruction or may be the result of disordered parenchymal architecture secondary to chronic infection and infl ammation. 54, 55 Various investigators 51, 55, 58 have pointed out that the incidence of spontaneous pneumothorax is especially high in those patients who receive aerosolized pentamidine for PCP prophylaxis. This has been attributed to poor distribution of the aerosolized pentamidine at the periphery of the lung, which allows the development of a peripheral necrotizing pneumonitis, producing a bronchopleural fi stula with resultant pneumothorax. 58 Alternately, an ongoing acute infection in inadequately treated areas may eventually result in cystic dilation of distal airway. 55 Martinez and colleagues 51 have suggested that the sulfi te in the isethionate component of the aerosol may cause an irritant cough, resulting in a rupture of the cysts. It has been found that low diffusing capacity of lung for carbon monoxide before pentamidine therapy for secondary prophylaxis is associated with an increased risk of bilateral pneumothoraces and increased mortality in these patients. 60 A "catamenial pneumothorax" is defi ned as a spontaneous or recurrent pneumothorax occurring within 72 hours from the onset of menstruation. Alifano and colleagues 71 described 32 women with spontaneous pneumothorax who had been referred for surgical treatment. In eight cases (25%), the catamenial character of the pneumothorax was recognized by clinical history. In all eight cases, the pneumothorax was recurrent (one to four previous episodes) and right sided. A diaphragmatic abnormality was found in all eight cases. Two mechanisms have been described for pneumothorax related to endometriosis. The most common is the movement of endometrial implants to the diaphragm, preferentially to the right side because of the recognized peritoneal circulation up from the pelvis to the right side. These implants then create channels or "holes" through the diaphragm that allow the implants or air to move into the chest. The second and much less frequent cause of endometrial implants in the chest is through the venous implants that lodge in the lung itself. 72 Clinical manifestations of thoracic endometriosis include chest pain, dyspnea, and hemoptysis. Bilateral pneumothoraces and concurrent hemothorax, hemoptysis, chest pain, and pneumothorax have been described. 73 Traumatic pneumothorax most often occurs as a result of penetrating injury but may also occur with closed chest trauma consequent to alveolar rupture from thoracic compression, fracture of a bronchus, esophageal rupture, or rib fractures that lacerate the pleura. 74, 75 Traumatic pneu-mothorax can be subclassifi ed into open, closed, tension, or hemopneumothorax. A tension pneumothorax needs to be managed immediately by letting the air out with a large-bore needle. Open pneumothorax should have a moist sterile gauze pack placed over the open wound, followed by a chest tube. Hemopneumothorax requires insertion of a chest tube. 76 Increasing use of computed tomography (CT) scan to evaluate blunt abdominal trauma has revealed a new diagnostic entity that has been called occult pneumothorax. [77] [78] [79] [80] [81] [82] In the series of trauma patients reported by Hill and colleagues, 83 there were 67 patients (71 pneumothoraces) who were seen to have a pneumothorax on CT that was not seen on admission chest radiograph. The management of these pneumothoraces is controversial. Wolfman and colleagues, 84 reporting on 44 occult pneumothoraces, suggested that most small (minuscule) occult pneumothoraces can be managed by close observation. Moderatesized pneumothoraces can also be managed by observation if the patient is not on a ventilator, but most of the anterolateral pneumothoraces need chest tube placement. The leading causes of iatrogenic pneumothorax are transthoracic needle aspiration (24% to 36%), subclavian venipuncture (22% to 23%), and thoracentesis (20% to 31%). Positive pressure ventilation has been reported to be the causative factor in only 7% of all iatrogenic pneumothoraces. Most patients require treatment for 4 to 7 days, and hospitalization is prolonged in only a small number of patients because of this complication. 85, 86 An important complication of mechanical ventilation is barotrauma. In one of the series, 87 15 of 430 patients receiving ventilatory support for longer than 12 hours developed pneumothorax. More recently, Lassence and colleagues 88 reported that iatrogenic pneumothorax occurred in 3% of intensive care unit patients. Risk factors were AIDS, acute respiratory distress syndrome (ARDS), or cardiogenic pulmonary edema at admission, body weight less than 80 kg, central vein or pulmonary artery catheter insertion, and use of inotropic agents during the fi rst 24 hours. When the lungs are exposed to high volumes, tissue disruption may occur. Air passes along bronchovascular bundles to the lung hilum and then to other interstitial spaces and may enter pleural or pericardial cavities. 89 In a ventilated patient, a rise in peak and plateau pressures should alert the clinician to the possible complication of pneumothorax. 90 Petersen and Baier 91 reported a 43% incidence of barotrauma in patients who required a peak airway pressure above 70 cm H 2 O. An early radiologic feature and a harbinger of life-threatening barotrauma is the presence of pulmonary interstitial emphysema. Pulmonary interstitial emphysema manifests radiologically as small parenchymal cysts, circular cuffs around larger pulmonary vessels projected end-on (perivascular halos), small dots representing small peripheral vessels surrounded by areas of radiolucency, linear streaks of air radiating toward the hilum, and large cystic collections of air and subpleural air. 92, 93 The air, having entered the interstitium, then dissects proximally along bronchovascular sheaths toward the lung hilum and mediastinum. Once in the mediastinum, the accumulated air takes the path of least resistance and may produce subcutaneous emphysema, pneumopericardium, pneumoperitoneum, or retroperitoneum ( Fig. 48-2 ). If the mediastinal pressure rises abruptly or if decompression via these routes is not suffi cient, the mediastinal parietal pleura may rupture, resulting in pneumothorax. Entry of gas into the pulmonary circulation may produce systemic air embolism. 94 Even pneumoscrotum has been described as an unusual complication of barotrauma. 95 Pneumomediastinum can produce several interesting radiographic signs such as pneumopericardium, continuous diaphragm sign, continuous left hemidiaphragm sign, Naclerio's sign, V sign at confl uence of brachiocephalic veins, thymic spinnaker-sail sign, ring-round-the-artery sign, and extrapleural sign. 96 Previous studies had shown that the factors that predispose to barotrauma are high peak and mean airway pressures, positive end-expiratory pressure (PEEP), use of volume-cycled ventilators, intubation of the right bronchus, chronic airways obstruction, and aspiration pneumonia. [97] [98] [99] [100] However, some studies 101, 102 have shown that the incidence of barotrauma is independent of airway pressure. Experts now accept that pulmonary edema and lung injury during mechanical ventilation are the consequence of "volutrauma" rather than "barotrauma." 103 The best treatment for barotrauma is early recognition, and prevention-delayed treatment has a mortality of 31%. 97 The recommended preventive measures are to decrease peak airway pressure by decreasing tidal volume, peak fl ow, and ventilatory rate; to use the best PEEP; and to employ assist-control mode, independent lung ventilation, and high-frequency positive pressure ventilation. 100 In a study published by the Acute Respiratory Distress Syndrome Network, it was found that treatment with a ventilator strategy designed to protect the lungs from excessive stretch resulted in decreased mortality and increased the number of days without ventilator use in patients with acute lung injury and acute respiratory distress syndrome. 104 After a literature review of more than 9000 procedures of fi beroptic bronchoscopy (FOB) with transbronchial biopsy, Milam and colleagues 105 found that the rate of pneumothorax was 1.9%. After analyzing their series of patients who had undergone FOB with transbronchial biopsy, Milam and colleagues, 105 Frazier and colleagues, 106 and Blasco and colleagues 107 concluded that an immediate postbronchoscopic chest radiograph rarely provides clinically useful information and that in FOB without transbronchial biopsy, an immediate postbronchoscopy radiograph is not necessary. In a study published in June 2006, Izbicki and colleagues 108 also concluded that in asymptomatic patients, routine radiograph after transbronchial biopsy is not necessary. When biopsies are performed, the following groups of patients should be considered for postbronchoscopy radiograph: comatose or mentally retarded patients, patients receiving positivepressure ventilation, patients with severe respiratory compromise as a result of disease or surgery, patients with bullous disease, patients who complain of chest pain, and outpatients. Pneumothorax after bronchoalveolar lavage without biopsy is extremely rare. Similarly, the complication of pneumothorax after transbronchial needle aspiration is also low (1 of 152 patients). 109 The incidence of pneumothorax after percutaneous needle biopsy [110] [111] [112] [113] is much higher and ranges from 17% to 43%. Although some authors have found that a more central location of the lesion, COPD, and lung hyperinfl ation increase the risk of pneumothorax, [114] [115] others found no correlation between development of pneumothorax and spirometric parameters or the presence of obstructive airways disease. 111, 116 However, Kazerooni and others 117 found that in patients with emphysema, there is a high incidence of pneumothorax after transthoracic needle aspiration; there is rapid development of pneumothorax in these cases, requiring chest tube placement. Delayed pneumothorax after percutaneous fi ne needle aspiration, although extremely unusual, has been reported in two cases and patients should be warned of this possible complication. 118 More recently, Choi and colleagues 119 reported on their series of 458 patients who had undergone transthoracic needle biopsy (TTNB). A follow-up chest radiograph was obtained immediately and 3 hours, 8 hours, and 24 hours after the biopsy procedure. A pneumothorax that developed after 3 hours was defi ned as delayed pneumothorax. Pneumothorax developed in 100 of the 458 patients (21.8%), and delayed pneumothorax developed in 15 patients (3.3%). Female gender and absence of emphysematous changes correlated with an increased rate of delayed pneumothorax. The reported incidence of pneumothorax after thoracentesis ranges from 5.7% to 19.2%. [120] [121] [122] [123] [124] Various mechanisms may explain the pneumothoraces that occur after thoracentesis: the lung may be punctured at the time of needle entry or after the fl uid has been withdrawn or a small amount of air may be drawn into the chest during aspiration or along the needle track if high negative intrapleural pressures develop. 125 Raptopoulos and colleagues 126 found that ultrasonographically guided thoracentesis, use of the smallest possible needle, and aspiration of the smallest possible amount of fl uid are complicated by pneumothorax signifi cantly less often than thoracentesis done with conventional techniques. Age, sex, underlying lung condition, overall clinical condition, size of the effusion, and type of tap (diagnostic or therapeutic) had no signifi cant effect on the occurrence of pneumothorax after thoracentesis. In a recent review article, Feller-Kopman 127 concluded that the use of ultrasound for thoracentesis has been associated with improved yield and reduced complication rate and is quickly becoming the standard of care for procedural guidance. Colt and colleagues, 128 reporting on 255 thoracenteses performed in 205 adult patients, found that hospitalization status, critical illness, effusion size or type, presence of loculations, operator, needle type, amount of fl uid withdrawn, occurrence of dry tap, and type of thoracentesis were not associated with increased frequency of pneumothorax. The only predictor showing signifi cant correlation was repeated thoracentesis. After an analysis of 506 thoracenteses in 370 patients, Aleman and colleagues 129 concluded that, in asymptomatic patients, the risk of developing pneumothorax was so low that the practice of obtaining a routine chest radiograph may not be justifi ed. Chakrabarti and colleagues 130 reported the use of blind percutaneous pleural biopsy by Abrams needle in 75 patients; pneumothorax was seen in eight patients (11%), with only two patients requiring specifi c intervention. In 1978 James 131 fi rst reported pneumothorax as a complication of passing a narrow-bore nasogastric tube. Since that time numerous authors [132] [133] [134] [135] [136] [137] [138] [139] have reported this complication. Narrow-bore feeding tubes are particularly likely to give rise to pneumothorax because of the tube's small diameter (2.7 mm), self-lubricating properties, and wire stylet-all of which permit their undetected entry into the tracheobronchial tree, perforation of pulmonary tissue, and lodging in the pleural cavity. 134 Other factors associated with increased risk of a misplaced feeding tube include the presence of an endotracheal or tracheostomy tube (these may increase pulmonary passage of the tube by preventing glottis closure and perhaps by inhibiting swallowing), altered mental status, denervation of airways, esophageal stricture, enlargement of the heart, and neuromuscular weakness. 137 The clinical signs commonly used to ascertain correct placement of the feeding tube may be misleading. Normally, to confi rm the correct placement of a feeding tube in the stomach, a small amount of air is injected. This produces a characteristic gurgle in the left upper quadrant of the abdomen, but a "pseudoconfi rmatory gurgle" with a feeding tube in the chest has been reported. 133 Aspiration of large amounts of fl uid through the tube is also taken to be a test of correct placement into the stomach, but delayed aspiration of a large quantity of undigested enteral feeding solution from the pleural space, mistaken for gastric contents, has been reported. 132 Percutaneous tracheostomy was fi rst described in 1955. In 1985, Ciaglia and colleagues 140 described percutaneous dilational tracheostomy (PDT). Fikkers and colleagues 141 described cases of subcutaneous emphysema and pneumothorax after percutaneous tracheostomy in a series of 326 cases. They described 7 of their own cases which had developed complications to include subcutaneous emphysema, mediastinal emphysema, and pneumothorax. Their review of literature showed that the incidence of subcutaneous emphysema was 1.4% and that of pneumothorax 0.8%. Findings associated with PTX included diffi cult PDT and the use of a fenestrated cannula. Development of air in the pleural space after partial resolution of total bronchial obstruction, 142 as a complication of lobar collapse, 143 and after therapeutic thoracentesis for malignant effusions 144 has been described. Acute lobar collapse results in a sudden increase in negative pleural pressure surrounding the collapsed lobe. Although the parietal and visceral pleural surfaces remain intact, the gas originating from the ambient tissues and blood is drawn into the pleural space, producing a pneumothorax called pneumothorax ex vacuo. Recognition of this type of pneumothorax is crucial because managing it requires relieving the bronchial obstruction rather than inserting a chest tube. The diagnosis of trapped lung requires documentation of chronicity and absence of pleural infl ammation, pleural malignancy, or endobronchial lesion. The pathognomonic radiographic sign of a trapped lung is the pneumothorax ex vacuo, characterized as a small to moderate-sized air collection after evacuation of effusion. 145 Experts have recognized that sports-related air leaks and pneumothorax occur more frequently than the literature suggests. Levy and colleagues 146 and Patridge and colleagues 147 each described three cases of pneumothorax or pneumomediastinum caused by blunt trauma sustained during a contact sport. Kizer and colleagues 148 identifi ed 20 patients who had sustained a spontaneous or traumatic air leak while engaged in an outdoor sport. Although traditionally the term barotrauma has been used to describe development of extra alveolar air in a patient on mechanical ventilation, there are other situations in which, because of increased intraalveolar pressure, air leaks out of alveoli. Pulmonary barotrauma (PBT) of ascent is a well-known complication of compressed air diving. Tetzlaff and colleagues 149 found that preexisting small lung cysts or end-expiratory fl ow limitation may increase the risk of PBT, although Neuman and colleagues 150 contested these conclusions. Some experts have suggested that even minor forms of PBT should be considered a contraindication to further diving because the divers are prone to recurrences that can occur even at shallow depths. 151 Clinically signifi cant PBT has been reported from self-infl ating bag-valve devices, 152 after infl ation of party balloons, 153 as a result of blast injury, 154, 155 during submarine escape training, 156 after automobile air bag deployment, 157 and in a normal healthy volunteer after repeated measurements of maximal respiratory pressure. 158 The clinical features of pneumothorax depend on its size, the underlying lung condition, and whether the pneumothorax is tension in type. PSP usually develops in tall, thin males while the patients are at rest. Most often the onset of symptoms is not related to physical exertion. Surprisingly, many patients do not seek medical attention immediately after developing symptoms. In one series, 159 18% of patients waited for more than 1 week after developing symptoms. Chest pain and dyspnea are the two main symptoms associated with the development of pneumothorax. In one series of 39 patients, all patients had one of the two symptoms and 25 of 39 patients (64%) had both. 160 The chest pain is sudden in onset; pleuritic in nature initially; and then becomes a persistent dull ache, localized to the affected site. The degree of dyspnea depends on the size of the pneumothorax and the condition of the underlying lung. Cough, malaise, orthopnea, or hemoptysis may be the presenting symptoms. Small pneumothoraces (<25%) may not be detectable clinically, especially in a patient with emphysema. Larger pneumothorax may produce tachycardia and tachypnea. Decreased motion, vocal resonance, and breath sounds on the side of pneumothorax; hyperinfl ation; and hyperresonance usually exist. Pleural friction rub may be present. In a large pneumothorax, the trachea and apex beat may be shifted to the opposite side and liver dullness may be masked. The presentation in tension pneumothorax is more dramatic. Because of a ball-valve mechanism, air enters the pleural cavity but cannot escape, thereby building up positive pressure. As the tension continues to increase, the diaphragm is fl attened, the mediastinum is shifted to the opposite side, and ultimately cardiopulmonary collapse results. In left-sided pneumothorax and in pneumomediastinum, systolic clicks, crunching, and whooping sounds have been described. [161] [162] [163] Various unusual presentations and physical signs of pneumothorax have been described. Horner's syndrome may occur and is attributed to traction on sympathetic ganglion, secondary to mediastinal shift in tension pneumothorax. 164, 165 Unilateral periorbital emphysema resembling ptosis was reported by Widder in two obtunded, cachectic patients. 166 The presence of undue resonance obtained by digital percussion on the medial zone of the clavicle with the patient in the orthostatic position has been described as an early and sole sign of pneumothorax. 167 The clinical features of pneumothorax in certain situations may not be typical, and the diagnosis is made by having a high index of suspicion. During a transbronchial biopsy a patient may complain of pleuritic pain, followed by progressive dyspnea. After subclavian vein catheterization, progressive dyspnea or alteration in the vital signs should alert the clinician to this complication. In a mechanically ventilated patient, development of pneumothorax can be suspected by new-onset respiratory distress, hypotension, agitation, unilateral decrease in breath sounds, worsening oxygenation, and a decrease in static and dynamic compliance. 42, 168, 169 In sports-related pneumothorax, the presentation may be atypical, and pneumothorax may be diffi cult to recognize because an athlete's physical fi tness may mask the serious injury and athletes may be more inclined to downplay their symptoms. 148 Simultaneous bilateral pneumothoraces is a rare and interesting condition. In humans, the right and left pleural spaces are completely separated. Theoretically, any patient who has undergone a median sternotomy, mediastinal surgery, heart or heart-lung transplant surgery is at risk for having a persistent pleuro-pleural channel. Most pleural rents probably heal but rarely a pleuro-pleural channel persists. Schorlemmer and colleagues 170 have referred to this condition as "iatrogenic buffalo chest" because the North American buffalo is one of few mammals that have communicating pleural spaces. A unilateral thoracic procedure in this situation has been described to cause bilateral pneumothoraces 171, 172 and "shifting pneumothorax." 173 Johri and colleagues 174 reported a patient who had undergone a thymoma resection in the remote past and developed bilateral pneumothoraces after undergoing transthoracic needle biopsy of a right lung nodule. Sayar and colleagues 175 described 12 patients who presented with simultaneous bilateral spontaneous pneumothorax (SBSP). They represented 1% of all patients with pneumothorax. Of the 12 patients, 5 (42%) had no underlying lung disease. In seven patients, SBSP was secondary to pulmonary metastases, histiocytosis, undefi ned interstitial pulmonary disease, tuberculosis, pneumonia, and chronic obstructive pulmonary disease. The presence of pneumothorax may produce electrocardiographic changes suggesting myocardial ischemia or infarction. Poor R wave progression in the anterior precordial leads with a decrease in R-wave from V 4 to V 5 , rightward shift of frontal axis, diminution of precordial R voltage, decrease in QRS amplitude, and precordial Twave inversion have all been described. [176] [177] [178] The absence of ST-segment elevation and a signifi cant Q-wave and reversal of electrocardiographic changes in the sitting position suggest pneumothorax. Most of these changes have been described in left-sided pneumothorax. Alikhan and Biddison 179 have described a new ECG sign of right-sided pneumothorax: loss of S-wave in lead V 2 and prominent R-wave voltage, which may mimic posterior wall myocardial infarction. Strizik and Forman 180 found PR-segment elevation in inferior leads and reciprocal PRsegment depression in an aVR lead in a case of left tension pneumothorax and attributed these to atrial ischemia or injury. The chest radiograph confi rms the presence of pneumothorax in most cases. The air in the pleural space rises to the apex of the hemithorax and causes relaxation atelectasis of the upper portion of the lung. Classically, the clinician fi nds a visceral pleural line with absence of lung markings peripheral to this line. When the fi lm cartridge used for the portable chest fi lm is placed under the patient, the skin on the back can fold over on itself to produce a line that runs down the hemithorax, which can easily be mistaken for pneumothorax ( Fig. 48-3 ). This line, pro- duced by the redundant skinfold, can be differentiated from the line of pneumothorax by the following three features: (1) the lung markings are present peripheral to the skinfold; (2) the skinfold has a wavy appearance; and (3) in the skinfold, there is a gradual increase in radiodensity as the line is approached from the hilum. However, in the presence of a consolidated lung, a pneumothorax presents as an edge instead of a line. 181 When pneumothorax is strongly suspected clinically but a pleural line is not clearly seen, possibly because of an overlying rib, gas in the pleural space can be detected by either of two procedures: (1) radiography in the erect posture (potentially more diagnostic with full expiration) or (2) radiography in the lateral decubitus position with a horizontal x-ray beam. Some authors, 182-184 however, have suggested that the expiratory fi lm does not increase diagnostic capability. The diagnosis of pneumothorax in the critically ill patient is more diffi cult to establish. The following four variables occur statistically more often in patients with initial failure to diagnose pneumothorax: mechanical ventilation, atypical radiographic location of pneumothorax, altered mental status, and development of pneumothorax after peak physician staffi ng hours. 185 In the ICU setting, radiographs are typically obtained in the supine position, making pneumothorax diagnosis more diffi cult. In the supine position the gas within the pleural space rises to the highest point in the hemithorax, which, in this position, is the anterior costophrenic sulcus. Various authors have described the depression and clear visualization of the diaphragm anteriorly, creating a "double" appearance to the diaphragm, a deep lateral costophrenic angle on the involved side ("the deep sulcus sign") ( Fig. 48-4) , an unusually distinct cardiac apex and pericardial fat tags, and increased hyperlucency of the upper abdominal quadrants. [186] [187] [188] [189] [190] A sharp line outlining the descending aorta may be produced by air trapped behind the inferior pulmonary ligament. Any of these fi ndings should lead to a prompt cross-table lateral or decubitus study or a CT scan to establish the diagnosis of pneumothorax. Although not done commonly for the diagnosis of pneumothorax, CT of the chest may detect an unsuspected pneumothorax in a critically ill patient (Fig. 48-5) . 191 In view of the diffi culty of clinically diagnosing pneumothorax in critically ill patients, Hall and colleagues 192 have recommended daily chest radiographs for this group of patients. In those patients who are treated with PEEP, interstitial gas may be seen as an early sign of barotrauma: More than 50% of these go on to develop features of barotrauma. 92 The interstitial gas is manifested radiographically by cystic changes, linear streaks along the bronchi and vessels, halos of gas around vessels, and subpleural gas. CT scan may also be useful to detect pneumothorax in complex cystic lung diseases. 193 Ultrasound examination is not used in the routine diagnosis of pneumothorax but may be of diagnostic utility. During the ultrasound examination, a kind of back-andforth movement of lung ("lung sliding"), synchronized with respiration, is normally seen. Lichtenstein and Menu 194 found that absence of lung sliding was suggestive of pneumothorax. In a normal subject, in vertical orientation, the ultrasound screen shows artifacts rising from the pleural line and spreading to the edge of the screen ("comet-tail" artifacts). Lichtenstein and colleagues, 195 in a more recent report, concluded that ultrasound detection of "comet-tail" artifact at the anterior wall allows complete pneumothorax to be excluded. The goals of management of pneumothorax are (1) to rid the pleural space of air and allow re-expansion of the lung with the least possible morbidity and (2) to decrease the likelihood of recurrence. Approaches for the management of the initial episode include observation, supplemental oxygen, simple aspiration of the pneumothorax, or tube thoracostomy. The choice of therapy in a given patient depends on various factors such as the size of pneumothorax, whether the pneumothorax is primary or secondary, the condition of the lungs, the clinical stability of the patient, the occupation of the patient, and whether the pneumothorax has occurred in a special setting. For prevention of recurrence, chest tube placement with pleurodesis or various surgical interventions including thoracotomy or video-assisted thoracic surgery (VATS) may be necessary. However, as a postal survey of 3000 American College of Chest Physicians (ACCP) members showed, there exists marked practice variation in the clinicians' approaches to the management of spontaneous pneumothorax and bronchopleural fi stula. This was partially explained by differences between pulmonologists and thoracic surgeons. 196 Many new recommendations that suggest a shift from the previous practices have been made and are discussed later. 197 A number of methods have been described to measure the size of pneumothorax. [198] [199] [200] Engdahl and colleagues 201 found that the size of pneumothorax measured from a chest radiograph did not correlate with CT, whereas the size of pneumothorax as estimated by CT correlated well with the amount of air aspirated in 12 of 16 patients treated with drainage. They suggested that the decision to treat should be based on clinical status and, if it is considered important to determine the size, CT should be used. Various approaches to the management of pneumothorax are discussed in subsequent sections. An estimated 1.25% of the volume of pneumothorax is absorbed each 24 hours. Therefore if a patient has a 20% pneumothorax, it will take 16 days for the air to be absorbed spontaneously. Different authors have used different sizes of pneumothorax in recommending expectant management: less than 15%, 199 less than 25%, 56, 76 or an apical collapse of less than 4 cm and lateral collapse of less than 1 cm. 202 The absorption of gas from the pleural space depends, besides other factors, on the gradient between the partial pressure in the capillaries and in the pleural space. On room air, the net gradient is only 54 mm Hg, whereas it exceeds 550 mm Hg when the patient is on 100% oxygen. 199 Studies 203, 204 have shown that administering 100% oxygen increases absorption of air fourfold to sixfold. Hospitalized patients with any type of pneumothorax, who are not subjected to aspiration of air or tube thoracostomy, should be treated with supplemental oxygen at high concentrations. 199 In those patients whose pneumothorax is large (more than 20% to 25%), progressive, or tension type; who are symptomatic; have an underlying chronic lung disease; are on a ventilator; or who have a recurrent pneumothorax, the pleural space air needs to be removed by various therapeutic means rather than be allowed to be absorbed spontaneously. The following methods have been used for the removal of air. Inserting an intercostal tube is a traumatic, painful procedure associated with a risk of hemorrhage. If connected to an underwater seal, the tube confi nes the patient to bed, thereby increasing the risk of thromboembolism and prolonging the duration of hospitalization. In view of these disadvantages, some investigators have treated pneumothorax by simple aspiration. [205] [206] [207] [208] Simple aspiration is usually performed in the second intercostal space in the midclavicular line. The catheter is connected to a three-way tap with the exit tube placed under water to ensure correct direction of airfl ow. Resistance is felt as the reexpanded lung impinges on the cannula. A confi rmatory chest radiograph is performed. A large tension pneumothorax needs to be evacuated immediately. Thoracocentesis using a catheter (e.g., Seldinger technique) that is advanced into the pleural cavity by means of a metal needle, a butterfl y needle, or a regular disposable needle is fraught with danger because the lung may be punctured. Wung and colleagues 209 have described the use of a spring-loaded Veress needle (American Cystoscope Makers, Inc., Stamford, Conn.) for emergency thoracentesis. This needle consists of a slender spring-loaded inner tube, which is blunt tipped and has a side aperture, enclosed in a 16-gauge sharp needle. The spring action allows the inner needle to retract while the outer needle is puncturing the chest wall but lets it spring out as soon as the pleural cavity is punctured. Simple aspiration is a technique with low morbidity that is well tolerated and allows the patient to be mobile and return to work rapidly. It may be used as the initial procedure in the absence of signs of tension. 210 Unfortunately, simple aspiration leaves the patient with a 10% to 50% chance of recurrence. 159, [204] [205] [206] However, in a recent randomized, prospective, multicenter pilot study involving 60 patients with the fi rst episode of PSP, Noppen and colleagues 211 reported that manual aspiration seemed equally effective as chest tube drainage and was safe, well tolerated, and feasible as an outpatient procedure in the majority of patients. Devanand and colleagues, 212 after a meta-analysis of three randomized controlled trials (RCTs) with a combined total of 194 patients, concluded that simple aspiration is advantageous in the initial management of PSP because of shorter hospitalization. No significant difference in recurrence was reported at 1 year using either modality, but the effi cacy data were inconclusive. Modern chest tubes are made of clear plastic with varying internal diameters, multiple holes and distance markers, and radiopaque stripes that outline the proximal drainage hole. They are pliable but not supple enough to kink. The second intercostal space in the midclavicular line is generally chosen for insertion of the tube because the area is wide and avascular. The tube is inserted using the trocar or blunt dissection method. Most institutions now prefer the latter. After insertion the tube is directed anteroapically and secured to prevent accidental removal. The tube is then connected to a water-seal drainage or a drainage system. 213 To avoid the risk of reexpansion pulmonary edema, it is recommended that negative suction not be applied in the absence of a bronchopleural fi stula. 214 Bell and colleagues, 215 in 102 chest tube removals in 69 trauma patients, found that the post-chest tube removal pneumothoraces rates did not differ whether the chest tube was removed at end-expiration or end-inspiration. In the absence of trauma and with good aseptic technique, prophylactic antibiotics are not recommended. The complications associated with thoracostomy that have been reported in the literature include laceration of the lung, spleen, liver, and stomach; intercostal artery bleeding; infarction of a peripheral segment of the lung aspirated into the drainage part of the chest tube; and delayed pulmonary perforation and subcutaneous emphysema. 213, 216 A blocked tube may result in a residual pleural space with the development of empyema. 217 A number of authors 218,219 have described the use of small lumen catheters for treating a simple pneumothorax. In view of the ease of insertion, good response, and low incidence of complications, it has been suggested that a small lumen catheter may be a useful alternative to tube thoracotomy. Although catheter failure included kinking, malposition, inadvertent removal by the patient, occlusion of the tube or valve by pleural fl uid, and large air leak, no complication attributable to tube placement occurred. 218 Liu and colleagues 220 reported their experience with the use of pigtail catheters in 50 patients versus traditional chest tube in 52 patients and found that the pigtail drainage was no less effective than the traditional chest tube. The questions pertaining to chest tubes such as smallbore tube versus large-bore tube, whether to apply suction or not, and whether the tube should be taken out at the end of inspiration or expiration have been discussed nicely by Baumann should be 15 in a review article in 2006. These points are summarized in the management algorithms given later. Samelson and colleagues 221 and Martin and colleagues 222 have described their experiences with the thoracic vent (one-way valve feature) in managing simple pneumothorax. The thoracic vent is inserted in the second intercostal space in the midclavicular line. The authors point out that this device has the advantage of a urethane tube that does not kink, a self-contained one-way valve, and a unique signal diaphragm that refl ects pleural pressure; however, the device is not suitable for use in patients who are expected to have large-volume or protracted air leaks. As mentioned earlier, the initial episode of spontaneous pneumothorax may be managed by simple observation or drainage. Once the initial episode of pneumothorax has resolved, the decision as to the need for measures to prevent recurrence must be made. In the following groups of patients, further management needs to be planned after the resolution of pneumothorax: recurrent pneumothorax, patients with chronic air leak, patients with demonstrable large bullae, and patients who live in remote areas or pursue an occupation in which a recurrence could be a hazard (e.g., airline personnel or divers). Different recurrence rates have been reported by various authors and range from 20% to 52%. 1, 202, 223, 224 The following are established risk factors for recurrence: more than one previous episode, COPD, air leak for more than 48 hours during the fi rst episode, and large cysts seen on radiograph. The following are possible risk factors for recurrence: nonoperative management of fi rst episode (versus tube drainage) and tube drainage for only 24 hours during fi rst episode (versus 3 to 4 days). Further management in these high-risk groups is aimed at preventing recurrence. The following approaches have been used. Chemical pleurodesis via chest tube, at thoracotomy, or VATS can be used to institute preventive measures. Pleurodesis (adhesion of visceral and parietal pleura) can be done by introducing the sclerotic agent via a chest tube, or it can be done in the operating room with open thoracotomy or thorascopy. However, there is no consensus about the timing or method of pleurodesis. 225 A practical approach is outlined later in the management algorithm. Because sterile tetracycline is no longer available, intrapleural instillation of doxycycline has been used as an alternative for pleurodesis. 226 Talc, fi nely powdered magnesium silicate, is another effective pleural irritant, producing fi brosis and adhesions. Numerous complications and side effects such as fever, pain, infection, and respiratory failure have been reported with its use, 227 but Lange and colleagues 228 found that although talc may result in mild restrictive respiratory impairment in long-term follow-up, it was not clinically signifi cant and there were no recorded cases of mesothelioma. In the past, patients with failed pleurodesis underwent surgical intervention. Thoracic surgery in such patients is complicated by partial pleural symphysis. Also, previous chemical pleurodesis makes lung transplantation more diffi cult technically. In view of these concerns, Kirby and Ginsberg 76 recommend that chemical pleurodesis be used only in selected patients who are too ill for surgery. The objectives of surgical treatment are to obtain full reexpansion of the affected lung, control complications, tackle the underlying lung problem, and prevent recurrence through pleural sclerosis by mechanical abrasion or pleurectomy. Surgical management during the fi rst episode of SP is indicated under the following circumstances: 3% to 4% of patients have a persistent leak resulting from a large fi stula that needs to be closed surgically; about 5% of patients have frank hemothorax, and surgical intervention is required in these patients to control the bleeding; a trapped lung may fail to reexpand, and decortication is required in such cases. If the patient is a diver, airline pilot, or lives in a remote area, surgery should be considered after the fi rst episode to prevent a recurrence. Apical bullous disease can be surgically approached by a transaxillary approach 76, 229 or through the auscultation triangle. 230 In a young female, a cosmetically acceptable scar is produced by a submammary anterolateral incision. 210 In an older individual with diffi cult pneumothorax complicated by other problems, a formal posterolateral thoracotomy is recommended. 76, 210, 229 If bilateral pleurectomy is required, a midline sternotomy is preferred. This permits access to both pleural cavities with minimum interference with respiratory function and causes minimal postoperative pain. 210 Sites of air leaks and obvious bullae are oversewn. 229 With modern stapling instruments, blebs and bullae can be excised easily with an airtight seal, without sacrifi cing a great amount of normal underlying lung tissue. 76 If one large cyst is fed by a major bronchial branch, then control of the feeding bronchus and marsupialization or plication of the bulla is performed. Segmentectomy and lobectomy to deal with underlying pathology are rarely necessary. 210 Obliteration of pleural space can be achieved by abrasion of the pleura with a dry gauze sponge, apical pleurectomy, 210 or an extensive pleurectomy. 231 When bilateral pleurectomy is advisable, it should be done in stages, 10 to 30 days apart. In most of the cases, blebectomy and pleural abrasion are suffi cient. In their study, Murray and colleagues 232 suggested an entirely different approach to the problem of recurrent pneumothorax. They used a limited axillary thoracotomy as primary treatment for recurrent pneumothorax, without a preoperative chest tube. Modern thoracoscopy allows minimally invasive access to the chest cavity. It allows full visualization of the lung and pleura and, when combined with resection of blebs and pleurodesis or pleurectomy, results in a low recurrence rate, minimal patient discomfort, and rapid recovery. Identifi ed bullae can be treated with a variety of modalities. [233] [234] [235] Chemical or mechanical pleurodesis can be performed during VATS. [236] [237] [238] Thoracoscopic identifi cation and treatment of bronchopleural fi stulas are also possible in patients with prolonged air leaks despite chest tube drainage. 239 Bilateral VATS has been found to be a safe and effi cacious procedure for patients with bilateral bullous disease and patients presenting with simultaneous or nonsimultaneous bilateral SP. 240, 241 Pneumocystis jerovici pneumonia-related pneumothorax is complicated by a virulent form of necrotizing subpleural lesions, which result in diffuse air leaks that are refractory to the standard treatment. 52, 57 Asymptomatic patients can be observed. An aggressive stepped-care management with large-bore intercostal tube drainage, chemical pleurodesis, and early video-assisted thoracic talc poudrage has been recommended for symptomatic patients. 242 In patients with an air leak persisting for more than 7 days, thoracotomy with stapling of blebs and mechanical pleurodesis has been recommended. When chemical pleurodesis is unsuccessful and open surgical pleurectomy is not desirable because of the patient's underlying disease, morbidity, and poor prognosis, thoracoscopic pleural ablation offers a therapeutic alternative. 239 Pleurodesis as an initial step in the management of pneumothorax in cystic fi brosis is considered contraindicated because it results in extensive pleural adhesions that jeopardize subsequent lung transplantation. 243 Therefore Noyes and Orenstein 244 have recommended a stepwise management of pneumothorax in cystic fi brosis. If initial tube thoracostomy does not bring resolution of air leak within 5 days, blebectomy should be performed. If blebectomy proves unsuccessful, with either continuing air leak or recurrence, a defi nitive pleural ablative procedure should be undertaken. The initial episode of catamenial pneumothorax is managed in the usual manner. Recurrences, which occur 72 hours before or after menstrual fl ow, are managed by pleurodesis or hormonal treatment. 245 Therapeutic options include oral contraceptive pills, danazol, progestational agents, and gonadotropin-releasing hormone (GnRH) analogues. 72 Thoracotomy should be considered if the patient is unable to take ovulation-suppressing drugs, has a recurrent pneumothorax while on drugs, or wants to become pregnant. At thoracotomy, any diaphragmatic defects should be closed, any subpleural blebs should be oversewn, and pleural abrasion should be performed to effect a pleurodesis. 246, 247 A patient who has a previous or current catamenial pneumothorax is at increased risk for barotrauma with positive pressure ventilation and represents a unique challenge to the anesthetist. Postoperative hormonal therapy is often required to prevent recurrences. Hysterectomy or tubal ligation may benefi t selected patients. 72 Pneumothorax complicating pregnancy is managed in the usual way, but in view of the high rate of recurrence of pneumothorax during parturition, thoracotomy with resection of apical blebs (if present) should be considered. 248 Air or gas trapped in body cavities expands in direct proportion to the decrease in atmospheric pressure. At an altitude of 10,000 feet, a pneumothorax will increase 1.5 times in size. 249 If a patient with pneumothorax, especially secondary to COPD, has to be transported, the following precautions should be taken: (a) the ability of the patient to take supplemental oxygen without causing alveolar hypoventilation must be established before the fl ight and supplemental oxygen administered during the fl ight; (b) a chest tube with a Heimlich fl utter valve should be in place; and (c) the patient should travel with a medically knowledgeable companion. 250 The 2002 epidemic of the severe acute respiratory syndrome (SARS) brought several ethical issues associated with new, severe epidemic diseases into sharp focus. Of the six cases described by Sihoe, 251 pneumothoraces were bilateral in three patients, mechanical ventilation was indicated in three patients, and two patients died. Air leaks or recurrences occurred in all four patients who accepted chest tubes. These air leaks took 14 to 31 days to resolve. Peripheral leukocytes and serum lactate dehydrogenase were higher in SARS patients with pneumothorax. These complications refl ected severe pathologic changes in lung tissues and the strong pulmonary and systemic infl ammatory responses that accompany SARS. During the SARS epidemic, health care providers were at risk, with substantial risk for those who performed bronchoscopy. By the end of the epidemic, approximately 30% of reported cases were in health care workers and some died. Felice 252 concluded that if multiple management options are available and they can be expected to result in equivalent, optimal patient outcomes, options that pose lesser risks to health care providers should be selected. Lymphangioleiomyomatosis (LAM) is a rare and frequently fatal disease that exclusively affects women of childbearing age. Thin-walled cyst formation occurs in the pulmonary parenchyma, and lung function declines progressively. The LAM Pleural Disease Consensus Group reviewed the responses to a questionnaire by 395 patients. Of these, 260 patients (incidence, 66%) reported at least one spontaneous pneumothorax during their lifetime and 200 out of 260 (77%) indicated that they had subsequent pneumothoraces. 253 Because of the morbidity and cost associated with multiple recurrences, the authors recommended early, defi nitive intervention, preferably at the time of the initial pneumothorax. Although pleurodesis may be associated with an increased risk of perioperative bleeding with lung transplantation, their data suggested that the complications are manageable and do not preclude successful transplantation. A persistent pulmonary air leak, which may occur as a result of pneumothorax or after pulmonary resection, is a diffi cult and frustrating problem to manage. Convention-ally, the air leak persisting for more than 7 days is called bronchopleural fi stula and it is not an uncommon problem. In the series reported by Chee and colleagues, 254 the overall incidence of bronchopleural fi stula was 34.6%. In pulmonary resection cases, Cerfolio and colleagues, 255 on univariate analysis, found that the increased age and the following fi ndings on pulmonary function testing predicted air leak on postoperative day one: low forced expiratory volume in 1 second/forced vital capacity ratio (FEV 1 /FVC), increased residual volume/total lung capacity ratio (RV/TLC), increased RV, and increased functional residual capacity (FRC). In the patients with air leaks who are managed by tube thoracostomy, Cerfolio and colleagues 255 found that conversion from suction to a water seal is an effective way of sealing an expiratory air leak. If the leak persists beyond 7 days, tube thoracostomy is deemed to have failed and a more defi nitive treatment is planned. Such cases are usually managed surgically, but patients who are unfi t or unwilling for surgery pose a management dilemma. Chemical pleurodesis may be tried but does not succeed if the lung has failed to expand. In such a situation, autologous "blood patch" pleurodesis has been found useful. 256, 257 Kinoshita and colleagues 258 have described a technique for such cases. They used a large amount of diluted fi brin glue for pleurodesis in patients with intractable pneumothorax or intrapleural dead space and found it useful. If pleurodesis also fails, the leak is localized during fi ber-optic bronchoscopy and the fi stula is sealed by using a sealant. 259 Pectoral myoplasty, in which the right pectoralis major muscle was transferred into the thorax and draped over the area of lung with multiple leaks, has been used when other interventions fail. 260 Murata and colleagues 261 have described a closure with intravenous administration of a coagulation factor XIII concentrate. Ferguson and colleagues 262 reported closure of a persistent distal bronchopleural fi stula using a one-way endobronchial valve designed for the treatment of emphysema. Ziskind and colleagues, 263 in 1965, described a case of pneumothorax in which accidental application of high, negative intrapleural pressure led to acute pulmonary edema. Since that time, unilateral expansion pulmonary edema has been recognized as a complication that can occur during the management of pneumothorax (Fig. 48-6 ). Re-expansion pulmonary edema tends to occur with greater frequency in patients 20 to 39 years of age, when there is complete collapse of the lung, when the pneumothorax has remained untreated for more than 72 hours, and when rapid re-expansion occurs secondary to the application of negative pressure; age-related changes in the older patients seem to afford some protection. 214, 264 The exact pathogenesis of re-expansion pulmonary edema is not known, but various factors such as bronchial obstruction, 265 decrease in surfactant, 266 and increased capillary permeability 267, 268 have been implicated. The development of bilateral re-expansion pulmonary edema after unilateral pleurodesis in a young male without heart disease might suggest that forces leading to ipsilateral reexpansion pulmonary edema also affect the contralateral lung. 269 Pavlin and colleagues 270 have described three cases of re-expansion hypotension that followed rapid evacuation of persistent unilateral pneumothorax. Besides the presence of pulmonary collapse for more than 3 days, the other risk factors were signifi cant arterial hypoxemia during pneumothorax, an elevated or rising hemoglobin and hematocrit level, and development of respiratory distress after insertion of a pleural drain. The mechanism of hypotension and shock after pulmonary re-expansion is not clear, but volume depletion and myocardial depression possibly play a role. Slow expansion by intermittent clamping of the chest tube, especially in high-risk patients, may prevent both reexpansion edema and reexpansion hypotension. 214, 270 Paradoxically, vigorous fl uid therapy may be advantageous in preserving circulation dynamics despite coexisting pulmonary edema. Myocardial stimulants may be useful if myocardial depression is suspected. 270 Diuretics have been used to manage re-expansion pulmonary edema 214 but may prove dangerous in the presence of hypovolemia and shock. 271 It has been recommended that a more logical approach in patients with shock and hypoxemia may be to use mechanical ventilation with PEEP, which would reduce further fl uid shift into the re-expanded lung. Plasma expanders, fl uid replacement, and vasopressor therapy can be used as needed. 270, 272 Development of tension pneumothorax has been reported after inadvertent, improper attachment of a Heimlich valve. 273, 274 A more aggressive approach to managing pneumothorax has been advocated recently. 275 Guidelines for managing pneumothorax have been published. 276, 277 Pneumothorax size: American College of Chest Physician (ACCP) guidelines defi ne a small pneumothorax as less than 3 cm in apex-to-cupola distance; British Thoracic Society (BTS) guidelines defi ne a small pneumothorax as a visible rim of less than 2 cm between the lung margin and chest wall. Stable patient: The ACCP defi nes a stable patient as one who has all of the following: respiratory rate less than 24 breaths per minute; heart rate greater than 60 beats per minute or less than 120 beats per minute; normal blood pressure; room air saturation of greater than 90%; and ability to speak in whole sentences. may need to be replaced by a larger tube if leaking persists and creates management diffi culty. The clinician fi nds it most practical to use a "roadmap" in different clinical scenarios. The difference between didactic medicine and bedside medicine is that the former is taught in a classroom and begins with a "diagnosis"; the latter starts at the bedside with a clinical scenario as the starting point. Figure 48 -7 represents an algorithmic approach to management that is based on the ACCP and BTS guidelines and practical experience. It can be applied to most patients with pneumothoraces. ■ PSP occurs primarily in tall, thin, previously healthy young men, most of whom are smokers. Chest radiograph often shows apical subpleural blebs or bullae. Rupture of these bullae is not related to physical activity but may be related to changes in atmospheric pressure. COPD is the most common cause of secondary pneumothorax. Presentation of pneumothorax in COPD is often atypical and causes excessive morbidity and mortality. ■ A high incidence of pneumothorax occurs in AIDS patients, related to PCP and the mechanical ventilation and bronchoscopy that are commonly required in these patients. In this group of patients, pneumothorax is frequently bilateral, recurrent, and unresponsive to conservative therapy. ■ Traumatic pneumothorax, which occurs as a result of a penetrating injury, may occur with closed chest trauma. ■ PTX is a common complication of mechanical ventilation. Interstitial emphysema is a harbinger of this complication. High peak and mean airway pressures, PEEP, use of volume-cycled ventilators, intubation of right mainstem bronchus, chronic airways obstruction, and aspiration pneumonia increase the incidence. ■ Pneumothorax ex vacuo, sports-related pneumothorax, and barotrauma unrelated to mechanical ventilation are interesting conditions that are not common, but they are important to be aware of. ■ Simultaneous bilateral pneumothoraces and "shifting pneumothoraces" are rare but interesting conditions and may develop because of persistent pleuro-pleural communication called iatrogenic buffalo chest. ■ An immediate postbronchoscopy chest radiograph is rarely useful but should be done in certain groups of patients (e.g., comatose, mentally retarded, ventilated, or with respiratory compromise). ■ PTX induced by a misplaced small-bore feeding tube is not uncommon. Clinical signs may be misleading. ■ A visceral pleural line with absence of lung markings peripherally is the classic radiographic sign of PTX. When the chest radiograph is obtained in the supine position, the signs are very different. ■ The approach to management of a PTX is dictated by the clinical condition rather than merely the size of the PTX, which is best estimated by CT scan of the chest. Expectant therapy is recommended for a small PSP in a stable patient. Reabsorption of air is hastened by 100% oxygen. ■ Air can be removed by simple aspiration, a small lumen catheter, or tube thoracostomy. Unstable patients with large secondary PTXs must be managed with tube thoracostomy. ■ A staged approach is recommended for chest tube removal. In PSP cases, the tube can be removed 6 to 12 hours after evidence of air leak was last seen; this waiting period is 12 to 24 hours in secondary PTX. ■ Defi nitive management of recurrent pneumothorax or persistent leak can be done by open thoracotomy or video-assisted thoracoscopy associated with pleurodesis, pleural abrasion, parietal pleurectomy, or bullectomy. In patients unsuitable or unwilling for surgery, chemical pleurodesis via a chest tube may be done. ■ PTX tends to recur in patients with cystic fi brosis. Blebectomy, without stripping the pleura, is recommended in these patients so that they may remain transplant candidates. Pleurodesis should not be done in these cases because adhesion development jeopardizes subsequent lung transplantation. ■ PTX in pregnancy is managed in the usual manner initially. In view of the high recurrence rates during parturition, thoracotomy with resection of blebs should be considered. ■ Re-expansion pulmonary edema is an important complication and can be prevented by slow expansion in high-risk patients. Spontaneous pneumothorax Cited by Ransdell HT, McPherson: Management of spontaneous pneumothorax Spontaneous pneumothorax )1:159. Cited by Kirby TJ, Ginsberg RJ: Management of the pneumothorax and barotrauma Thoracentesis: The plan of continuous aspiration Experience with 1,199 patients Pneumothorax in the ICU. Patient outcomes and prognostic factors Current aspects of spontaneous pneumothorax Nonsmoking, non-alpha 1-antitrypsin defi ciency-induced emphysema in nonsmokers with healed spontaneous pneumothorax identifi ed by computed tomography of the lungs Computed tomography in the etiologic assessment of idiopathic spontaneous pneumothorax Value of computed tomography in the detection of bullae and blebs in patients with primary spontaneous pneumothorax Do bullae indicate a predisposition to recurrent pneumothorax? Management of primary spontaneous pneumothorax Fluorescein-enhanced autofl uorescence thoracoscopy in primary spontaneous pneumothorax Management of spontaneous pneumothorax Smoking and the increased risk of contracting spontaneous pneumothorax Recurrence of pneumothorax The impact of spontaneous pneumothorax, and its treatment, on the smoking behavior of young adult smokers Respiratory bronchiolitis in smokers with spontaneous pneumothorax Lung density measurements in spontaneous pneumothorax demonstrate air trapping Familial primary spontaneous pneumothorax consistent with true autosomal dominant inheritance Familial primary spontaneous pneumothorax consistent with true autosomal dominant inheritance Primary spontaneous pneumothorax in two siblings suggests autosomal recessive inheritance Familial spontaneous pneumothorax and FBN1 mutations Clinical and genetic studies of Brit-Hogg-Dube syndrome Pleuropulmonary pathology of Birt-Hogg-Dube syndrome Fishman's Pulmonary Diseases and Disorders Respiratory gas exchange in patients with spontaneous pneumothorax Spontaneous pneumothorax in emphysema Regional pulmonary function during experimental unilateral pneumothorax in the awake state Regional lung function in spontaneous pneumothorax The pathophysiology of progressive tension pneumothorax Pathogenesis of spontaneous pneumothorax with special reference to the ultrastructure of emphysematous bullae Infl uence of height on the risk of spontaneous pneumothorax Familial spontaneous pneumothorax Familial primary spontaneous pneumothorax consistent with true autosomal dominant inheritance Spontaneous pneumothorax in Norfolk Time relation between sale of cigarettes and the incidence of spontaneous pneumothorax Smoking and the increased risk of contracting spontaneous pneumothorax Fraser and Paré's Diagnosis of Diseases of the Chest Spontaneous pneumothorax in chronic obstructive pulmonary disease: Complications, treatment and recurrences Diseases of the pleural space Complications of attempted central venous injection performed by drug abusers Man's worst enemy-himself Spontaneous bilateral pneumothorax in drug addicts Alternate therapy for traumatic pneumothorax in "pocketshooters Pneumothorax in drug abusers: An urban epidemic? Pulmonary manifestations of acquired immunodefi ciency syndrome (AIDS) Pneumocystis carinii pneumonia with spontaneous pneumothorax: A report of three cases Spontaneous pneumothorax with Pneumocystis carinii infection: Occurrence in patients with acquired immuno-defi ciency syndrome Spontaneous pneumothoraces in AIDS patients receiving aerosolized pentamidine (letter) Pneumocystis carinii pneumonia complicated by lymphadenopathy and pneumothorax Pneumothorax in patients with immunodefi ciency syndrome Cystic parenchymal changes associated with spontaneous pneumothorax in an HIV-positive patient Spontaneous pneumothorax in patients with acquired immunodefi ciency syndrome treated with prophylactic aerosolized pentamidine Pneumothorax with Pneumocystis carinii pneumonia in AIDS: Incidence and clinical characteristics Spontaneous pneumothorax in AIDS patients with recurrent Pneumocystis carinii pneumonia despite aerosolized pentamidine prophylaxis Pneumothorax in AIDS Safi rstein BH: Spontaneous pneumothorax in Pneumocystis carinii pneumonia: Common or uncommon? Bilateral pneumothoraces hasten mortality in AIDS patients receiving secondary prophylaxis with aerosolized pentamidine: Association with a lower DCO prior to receiving aerosolized pentamidine Spontaneous pneumothorax complicating pneumonia Spontaneous pneumothorax in the AIDS population Treatment of pneumothorax in the patients with AIDS Surgical management of spontaneous pneumothorax in patients with acquired immunodefi ciency syndrome Pneumocystis carinii: An update Value of bronchoalveolar lavage in the diagnosis of pulmonary infection in acquired immunedefi ciency syndrome Pneumothorax in AIDS: Case reviews and proposed clinical management Simultaneous bilateral pneumothorax in an HIV-infected patient Pneumothorax during pulmonary toxoplasmosis in an AIDS patient (letter) AIDS-related Pneumocystis carinii pneumonia in the era of adjunctive steroids Catamenial pneumothorax. A prospective study Secondary spontaneous pneumothorax. Catamenial pneumothorax Catamenial pneumothorax and other thoracic manifestations of endometriosis Major airway injury in closed chest trauma Injuries to the tracheobronchial tree in closed trauma Management of the pneumothorax and barotrauma An objective method to measure and manage occult pneumothorax Occult traumatic pneumothorax: Immediate tube thoracostomy versus expectant management Occult pneumothorax in patients with abnormal trauma: CT studies CT detection of occult pneumothorax in multiple trauma patients Tube thoracostomy for occult pneumothorax: A prospective randomized study of its use Failure of chest x-rays to diagnose pneumothoraces after blunt trauma The occult pneumothorax: An increasing diagnostic entity in trauma Validity of CT classifi cation on management of occult pneumothorax: A prospective study Iatrogenic pneumothorax: Etiology and morbidity. Results of a Department of Veterans Affairs cooperative study Signifi cance of iatrogenic pneumothoraces Management of subcutaneous emphysema, pneumomediastinum, and pneumothorax during respirator therapy Pneumothorax in the intensive care unit: Incidence, risk factors and outcome Barotrauma in human research (editorial) The ICU Book Incidence of pulmonary barotrauma in a medical ICU Pulmonary interstitial gas: First sign of barotrauma due to PEEP therapy Pulmonary interstitial emphysema in the adult respiratory distress syndrome Pneumothorax and barotrauma Another complication of barotrauma (letter) Pneumomediastinum: Old signs and new signs Pneumothorax complicating continuous ventilatory support Pulmonary barotrauma complicating positive end expiratory pressure (abstract) Incidence of pneumothorax and pneumomediastinum in patients with aspiration pneumonia requiring ventilatory support Barotrauma: Pathophysiology, risk factors and prevention The relation of pneumothorax and other air leaks to mortality in the acute respiratory distress syndrome Evaluation of a ventilator strategy to prevent barotrauma in patients at high risk for acute respiratory distress syndrome The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome Immediate chest roentgenography following fi beroptic bronchoscopy Pneumothorax following transbronchial biopsy: Low diagnostic yield with routine chest roentgenograms Safety of the transbronchial biopsy in outpatients Is routine chest radiography after transbronchial biopsy necessary? A prospective study of 350 cases The value of transbronchial needle aspiration in the diagnosis of peripheral pulmonary lesions Predicting risk of pneumothorax in needle biopsy of the lung Pneumothorax with fi ne-needle aspiration of thoracic lesions. Is spirometry a predictor? Transthoracic needle aspiration in the study of pulmonary infections in patients with HIV Percutaneous transthoracic needle aspiration biopsy: A comprehensive review of its current role in the diagnosis and treatment of lung tumors Prediction of pneumothorax rate in percutaneous aspiration of the lung Postbiopsy pneumothorax: Estimating the risk by chest radiography and pulmonary function tests Risk of pneumothorax not increased by obstructive lung disease in percutaneous needle biopsy Traill ZC, Gleeson FV: Delayed pneumothorax after CT-guided percutaneous fi ne needle aspiration lung biopsy Incidence and risk factors of delayed pneumothorax after transthoracic needle biopsy of the lung Thoracentesis: a safer needle Thoracentesis: complications, patient experience and diagnostic value Value of chest ultrasonography versus decubitus roentgenography for thoracentesis Complications associated with thoracentesis Complications associated with thoracentesis: A prospective, randomized study comparing three different methods Pneumothorax after thoracentesis (letter) Factors affecting the development of pneumothorax associated with thoracentesis Ultrasound-guided thoracentesis Evaluation of patient-related and procedure-related factors contributing to pneumothorax following thoracentesis The value of chest roentgenography in the diagnosis of pneumothorax after thoracentesis The role of Abrams percutaneous pleural biopsy in the investigation of exudative pleural effusion An unusual complication of passing a narrow bore nasogastric tube Pneumothorax attributable to nasogastric tube Fatal hydrothorax and empyema complicating a malpositioned nasogastric tube Inadvertent transbronchial insertion of narrow-bore feeding tubes into the pleural space Pneumothorax from nasogastric feeding tube insertion: A report of fi ve cases Pneumothorax complicating smallbore feeding tube placement Incorrect positioning of nasogastric feeding tubes and the development of pneumothorax Entrifl ex feeding tube: Need for care in using it Patient safety: Effect of institutional protocols on adverse events related to feeding tube placement in the critically ill Elective percutaneous dilational tracheostomy: A new simple bedside procedure; preliminary report Emphysema and pneumothorax after percutaneous tracheostomy. Case reports and an anatomic study Spontaneous pneumothorax following partial resolution of total bronchial obstruction Pneumothorax ex vacuo Asymptomatic hydropneumothorax after therapeutic thoracentesis for malignant pleural effusion Pleural fi brosis Pulmonary barotrauma: Diagnosis in American football players. Three cases in three years Sports-related pneumothorax Pulmonary air leaks resulting from outdoor sports. A clinical series and literature review Risk factors for pulmonary barotrauma in divers Recommend caution in defi ning risk factors for barotrauma in divers (letter) Pulmonary barotrauma and related events in divers Sudden severe barotrauma from self-infl ating bag-valve devices Clinically signifi cant pulmonary barotrauma after infl ation of party balloons Tension pneumoperitoneum after blast injury: Dramatic improvement in ventilatory and hemodynamic parameters after surgical decompression Blast lung injury from an explosion on a civilian bus Pulmonary barotrauma in submarine escape training Bilateral pneumothorax following airbag deployment Pneumomediastinum, pneumothorax and subcutaneous emphysema following the measurement of maximal expiratory pressure in a normal subject The management of spontaneous pneumothorax Spontaneous pneumothorax Systolic clicks due to left sided pneumothorax Clicks and sounds (whoops) in left sided pneumothorax: Clinical and phonocardiographic study Clicks secondary to pneumothorax confounding the diagnosis of mitral valve prolapse Horner's syndrome occurring with spontaneous pneumothorax Horner's syndrome occurring with spontaneous pneumothorax Ptosis associated with iatrogenic pneumothorax: A false lateralizing sign Orriols R: A new physical sign in pneumothorax Cardiovascular-pulmonary monitoring in the intensive care unit Worsening oxygenation in the mechanically ventilated patient: causes, mechanisms, and early detection Bilateral pneumothoraces secondary to iatrogenic buffalo chest; an unusual complication of median sternotomy and subclavian catheterization Frequency and management of pneumothoraces in heart-lung transplant recipients Communication between the two pleural cavities after major cardiothoracic surgery: Relevance to percutaneous intervention Shifting pneumothorax after heartlung transplantation Bilateral pneumothoraces after unilateral transthoracic needle biopsy of a lung nodule Simultaneous bilateral spontaneous pneumothorax report of 12 cases and review of literature Electrocardiogram changes suggestive of coronary artery disease in pneumothorax: Their reversibility with upright posture The electrocardiographic manifestations of spontaneous left pneumothorax Left tension pneumothorax mimicking myocardial ischemia after percutaneous central venous cannulation Electrocardiographic changes with right-sided pneumothorax New ECG changes associated with a tension pneumothorax The radiology of abnormal intrathoracic air The value of routine expiratory chest fi lms in the diagnosis of pneumothorax Comparison of upright inspiratory and expiratory chest radiographs for detecting pneumothoraces Expiratory chest radiographs do not improve visibility of small apical pneumothoraces by enhanced contrast Risk factors for the misdiagnosis of pneumothorax in the intensive care unit Basilar pneumothorax in the supine adult The deep sulcus sign Supine subpulmonary pneumothorax Radiographic recognition of pneumothorax in the intensive care unit Radiology in the intensive care unit Thoracic computed tomography in the critically ill patient Effi cacy of daily routine chest radiographs in intubated, mechanically ventilated patients Role of CT in management of pneumothorax in patients with complex cystic lung disease A bedside ultrasound sign ruling out pneumothorax in the critically ill A comet-tail artefact: An ultrasound sign ruling out pneumothorax The clinician's perspective on pneumothorax management Spontaneous pneumothorax management guidelines previewed Determining the size of pneumothorax in the upright patient Textbook of Respiratory Medicine Pneumothorax size: Correlation of supine anteroposterior with erect posteroanterior chest radiographs Chest radiograph-a poor method for determining the size of a pneumothorax Pneumothorax: A therapeutic update Spontaneous alveolar rupture at birth Northfi eld TC: Oxygen therapy for spontaneous pneumothorax Treatment of pneumothorax by simple aspiration A place for aspiration in the treatment of spontaneous pneumothorax Results of simple aspiration of pneumothoraces Spontaneous pneumothorax (SP): Comparison of simple aspiration and tube thoracostomy A spring-loaded needle for emergency evacuation of pneumothorax The diffi cult pneumothorax Manual aspiration versus chest tube drainage in fi rst episodes of primary spontaneous pneumothorax. A multicenter, prospective, randomized pilot study Simple aspiration versus chest-tube insertion in the management of primary spontaneous pneumothorax: A systematic review Chest tubes: indications, techniques, management and complications Recurrent re-expansion pulmonary edema Chest tube removal: End-inspiration or end-expiration? Delayed pulmonary perforation: A rare complication of the tube thoracostomy Complications of percutaneous dart therapy in management of pneumothorax Treatment of pneumothoraces utilizing small caliber chest tubes Role of small caliber chest tube drainage for iatrogenic pneumothorax Pigtail tube drainage in the treatment of spontaneous pneumothorax The thoracic vent: Clinical experience with a new device for treating simple pneumothorax Use of a pleural catheter for the management of simple pneumothorax Spontaneous pneumothorax Spontaneous pneumothorax in Norfolk Management of secondary spontaneous pneumothorax. There is confusion in the air Tetracycline pleurodesis: adios, farewell, adieu Talc pleurodesis for the treatment of pneumothorax and pleural effusion Lung function 22-35 years after treatment of idiopathic spontaneous pneumothorax with talc poudrage or simple drainage Surgical experience in the management of spontaneous pneumothorax Pleurectomy through the triangle of auscultation Pleurectomy for recurrent pneumothorax (letter) A limited axillary thoracotomy as primary treatment for recurrent spontaneous pneumothorax Thoracoscopic ablation of blebs in the treatment of recurrent or persistent spontaneous pneumothorax Nd:YAG laser pleurodesis through thoracoscopy: New curative therapy in spontaneous pneumothorax Videothoracoscopic ligation of bulla and pleurectomy for spontaneous pneumothorax Talc pleurodesis during videothoracoscopy for Pneumocystis carinii pneumonia-related pneumothorax. A new technique Treatment of complicated spontaneous pneumothorax by simple talc pleurodesis under thoracoscopy and local anesthesia Pleural abrasion: A new method of pleurodesis Colt HG: Thoracoscopy: New frontiers Bilateral video-assisted thoracoscopic surgery for bilateral spontaneous pneumothorax Bilateral videoassisted thoracoscopic surgery in the supine position for primary spontaneous pneumothorax Treatment of AIDS-related spontaneous pneumothorax. A decade of experience Heart-lung transplantation: Lessons learned and future hopes Treatment of pneumothorax in cystic fi brosis in the era of lung transplantation (editorial) Recurring catamenial pneumothorax treated with a Gn-RH analogue Catamenial pneumothorax Catamenial pneumothorax Spontaneous pneumothorax complicating pregnancy-case report and review of the literature AMA Commission on Emergency Medical Services: Medical aspects of transportation board commercial aircraft Commercial air transportation of a patient recovering from pneumothorax Severe acute respiratory distress syndrome complicated by spontaneous pneumothorax SARS, pneumothorax and our response to epidemics Lymphangioleiomyomatosis. Management of pneumothorax in lymphangioleiomyomatosis. Effects on recurrence and lung transplantation complications Persistent air leak in spontaneous pneumothorax-clinical course and outcome A prospective algorithm for the management of air leaks after pulmonary resection Autologous "blood patch" pleurodesis for persistent pulmonary air leak Autologous blood patch pleurodesis for secondary spontaneous pneumothorax with persistent air leak Intrapleural administration of a large amount of diluted fi brin glue for intractable pneumothorax Medical management and therapy of bronchopleural fi stulas in the mechanically ventilated patient Pectoral myoplasty for recurrent pneumothorax: An extrathoracic solution to an intrathoracic problem The treatment of refractory pneumothorax in diffuse panbronchiolitis by intravenous administration of coagulation factor XIII concentrate Closure of a bronchopleural fi stula using bronchoscopic placement of an endobronchial valve designed for the treatment of emphysema Acute pulmonary edema following treatment of spontaneous pneumothorax with excessive negative intrapleural pressure Clinical analysis of reexpansion pulmonary edema Unilateral pulmonary edema resulting from treatment of spontaneous pneumothorax Experimental pulmonary edema following re-expansion of pneumothorax Evidence for increased permeability in reexpansion pulmonary edema Changes in pulmonary microvascular permeability accompanying re-expansion oedema: Evidence from dual isotope scintigraphy Bilateral reexpansion pulmonary edema following unilateral pleurocentesis Reexpansion hypotension: A complication of rapid evacuation of prolonged pneumothorax Re-expansion pulmonary edema: A potentially serious complication of delayed diagnosis of pneumothorax PEEP ventilation-the treatment for life-threatening re-expansion pulmonary edema Tension pneumothorax complicating smallcaliber chest tube insertion Baumann MH, Strange C: Treatment of spontaneous pneumothorax. A more aggressive approach? Management of spontaneous pneumothorax on behalf of the BTS Pleural Disease Group, a subgroup of the BTS Standards of Care Committee: BTS guidelines for the management of spontaneous pneumothorax The authors thank Faroque Khan, MB, MACP, for valuable advice and for contributing most of the radiographs; Dvorah Balsam, MD, for Fig. 48-2; and Leonard Octavius Barrett, MD, FACS, Chief of Thoracic Surgery at NUMC, for his comments regarding the surgical therapy.