Reexpansion Pulmonary Edema

Transcription

1 CURRENT REVEW Reexpansion Pulmonary Edema Saade Mahfood, M.D., William R. Hix, M.D., Benjamin L. Aaron, M.D., Peter Blaes, M.D., and Donald C. Watson, M.D. ABSTRACT Unilateral reexpansion pulmonary edema (RPE) is a rare complication of the treatment of lung collapse secondary to pneumothorax, pleural effusion, or atelectasis. Although RPE generally is believed to occur only when a chronically collapsed lung is rapidly reexpanded by evacuation of large amounts of air or fluid, in this review 5 of 47 cases of RPE available for assessment occurred when the pulmonary collapse was of short duration or when the lung was reexpanded without suction. The pathogenesis of RPE is unknown and is probably multifactorial. mplicated in the etiological process of RPE are chronicity of collapse, technique of reexpansion, increased pulmonary vascular permeability, airway obstntction, loss of surfactant, and pulmonary artery pressure changes. Since the outcome of RPE was fatal in of 53 cases reviewed (0%), physicians treating lung collapse must be aware of the possible causes and endeavor to prevent the occurrence of this complication. Although there are numerous noncardiac causes of pulmonary edema [l], unilateral pulmonary edema following reexpansion of a collapsed lung is a rare complication [,3]. We report a case of reexpansion pulmonary edema (RPE) following pleural abrasion for spontaneous pneumothorax and present a literature review on unilateral pulmonary edema that occurs as a complication of lung reexpansion following pneumothorax, pleural effusion, and pulmonary atelectasis. Case Report A 4-year-old man suddenly experienced left-sided chest pain and dyspnea on exertion. There was clinical and roentgenographic evidence of complete pneumothorax. A chest tube and 0 cm H,O underwater-seal suction completely expanded the affected lung. Three days later, the tube was removed and he was discharged. Although the same complaints recurred the following day, he did not seek medical attention until one week later. There was again clinical and roentgenographic evidence of complete left pneumothorax (Fig ). Direct admission, lateral thoracotomy, inflation of the lung by hand ventilation, and pleural abrasion were performed. Two chest tubes were inserted and attached to 0 cm H,O underwater-seal suction. The patient was extubated and transferred to the recovery room breath- From the Divisions of Cardiothoracic Surgery, The University of Tennessee College of Medicine, Memphis, TN, and the George Washington University Medical Center, Washington, DC. Address reprint requests to Dr. Hix, The George Washington University Medical Center, 50 Pennsylvania Ave, NW, Washington, DC ing 40% 0, administered by high-humidity face mask. Five minutes later his clinical status deteriorated rapidly, with severe coughing, foamy sputum, agitation, cyanosis, tachypnea (50/min), tachycardia (44/min), and hypotension (systolic blood pressure, 84 mm Hg). Rales could be heard over the entire left side of the chest. Chest roentgenogram revealed unilateral pulmonary edema of the left lung (Fig ). Arterial blood gas analysis revealed hypoxemia with hypercapnic respiratory acidosis. Following immediate reintubation and mechanical ventilation with 0-cm positive end-expiratory pressure, the hypoxemia abated. Over the next two hours his hemodynamic and respiratory status stabilized. He was extubated the following day. The remainder of his hospital course was uneventful, and he was discharged on the ninth postoperative day. Reexpansion Pulmonary Edema following Pneumothorax RPE following pneumothorax was first reported in 958 by Carlson and colleagues [4] and was comprehensively reviewed by Ziskind and colleagues [5] in 965. A search of the literature disclosed 5 additional cases of unilateral pulmonary edema following lung reexpansion in pneumothorax. Clinical details were available for analysis in 47 patients, including the present patient (Table ) [-36. Of these patients, 38 were men and 9 were women; average age was 4 years (age range, 8-84 years); 57% were under 50 years old. Pneumothorax was present 3 days or longer in 39 of the 47 patients, or 83% (average, 9 days; range, 0-8 days). Methods of lung reexpansion included high negative suction with needle aspiration, pump suction, chest tube with undenvaterseal and suction, underwater-seal chest tube drainage without suction, Heimlich valves, and reinflation by positive-pressure ventilation. The onset of RPE was immediate or within hour in 30 of the 47 patients (64%), and within 4 hours in the remainder. Almost all cases of RPE were ipsilateral to the side of the pneumothorax; contralateral pulmonary edema occurred in 3 patients, of whom died. One patient had ipsilateral and contralateral pulmonary edema sequentially and recovered. The overall mortality was 9% (9 of 47 patients). n the cases reviewed the clinical manifestations of RPE varied from roentgenographic findings alone to mild or severe cardiorespiratory insufficiency, shock, coma, and death. Some patients received no specific therapy; others were treated with a variety of modalities and drugs, including oxygen, inotropic agents, digitalis, steroids, diuretics, bronchodilators, and sedatives. n severe cases, endotracheal intubation or tracheostomy 340 Ann Thorac Surg 45:34@345, Mar 988. Copyright by The Society of Thoracic Surgeons

2 34 Current Review: Mahfood et al: Reexpansion Pulmonary Edema Fig. Spontaneous pneumothorax with complete collapse of left lung. 4 cases of "albuminous expectoration" following thoracentesis. An analysis of these cases revealed a male-tofemale ratio of 30 :, with the condition mainly affecting young patients (8% were 0-50 years old). Pleurisy with serofibrinous effusion was the main indication for thoracentesis (8 patients). Three patients had empyema, 7 had hydrothorax due to heart failure or chronic renal disease, and 3 had malignant pleural effusion. Pulmonary edema seldom occurred unless at least L (range, 30-5,500 ml) of effusion was rapidly aspirated. Symptoms occurred several minutes to a few hours following reexpansion. n most instances improvement occurred rapidly, usually within 4 to 48 hours; however, 7 patients (6%) died. Recent reports of reexpansion pulmonary edema related to drainage of pleural effusion describe 7 patients, 6 in detail (Table ) [6, 3,34, Four were women, were men; age ranged from to 59 years; duration of symptoms was 4 to 0 days; and an average of,600 ml was removed (range,,000-4,500 ml). The onset of pulmonary edema was immediate in 3 patients and "a few hours" in one instance. Four patients recovered, and died. Reexpansion Pulmona y Edema following Atelectasis Two instances of unilateral pulmonary edema following rapid reexpansion of an atelectatic lung have been reported [8]. n the case reported by Ravin and Dahmash [49], total left lung atelectasis occurred during anesthesia for abdominal surgery due to right bronchial intubation. The malpositioned endotracheal tube was discovered in the recovery room. Unilateral left pulmonary edema followed rapid reexpansion of the lung after the endotracheal tube was repositioned. There was no pleural drainage in this patient. Fig. Unilateral reexpansion pulmonary edema of the left lung. and mechanical ventilation with positive end-expiratory pressure were required. Most patients who recovered did so within a week. Reexpansion Pulmona y Edema following Pleural Effusion n 853, Pinault [37] described RPE following pleural effusion in a patient who had a large volume of pleural fluid rapidly removed by thoracentesis. RPE was not unfamiliar in the late nineteenth and early twentieth centuries when thoracentesis with high negative pressure was often recommended for the aspiration of pleural effusions [38]. n 905, Hartley [39] reviewed in detail Comment RPE is generally considered a rare complication that occurs when a chronically collapsed lung is rapidly reexpanded by evacuation of large amounts of air or fluid, usually with application of high negative intrapleural pressure. Although this is most often the case, from this review it is clear that RPE can occur when the pulmonary collapse has been of short duration or when the lung is reexpanded without suction (5 of 47 patients). That RPE is an unusual event is substantiated by two large reviews in which 400 and 375 cases of spontaneous pneumothorax (duration greater than one week in 0%) were treated by tube thoracostomy and pleural suction without this complication developing [44, 45. Some observers believe that the true incidence of WE is unknown because at times it is only a roentgenographic phenomenon, without clinical manifestations [, 8. However, in most instances the onset of RPE is dramatic, and in our review the outcome was fatal in of 53 recently reported cases (0%). The exact cause of RPE is not known. Factors that have been implicated in the pathogenesis of this com-

3 34 The Annals of Thoracic Surgery Vol45 No 3 March 988 Table. Recently Reported Cases of Reexpansion Pulmonary Edema Related to Pneurnothorax No. of Age (yr)l Length of Reexpansion Onset of Affected Reference, Year Patients Sex Collapse Method RPE Side Outcome Carlson et a [4], 958 Ziskind et a [5], 965 Trapnell and Thurston [6], 970 Humphreys and Berne [q, 970 Sautter et a [8], 97 Childress et a [9], 97 Ratiff et a [lo], 973 Steckell [ll], 973 Schwander et a [], 973 Martinez et a (3, 973 Lopez et a [4], 973 Poulias and Prombonas (5, 974 Grant [6], 97 Jaeschock [lq, 974 Saini [M, 974 Rogaly and Memtz [9], 975 Shanahan et a [0], 975 Waqaruddin and Bernstein [], 975 Schaer and Roth [], 977 Body et a [3], 977 Mutz and Benzer [4], 977 Sewell et a [El, 978 Gurman et a [6], 978 Brennan and Fitzgerald [7], 979 Mahajan et a [8], 979 Peatfield et a [9], 979 Miller [30], 979 Sherman and Ravikrishna [3], 980 Kassis et a [3], 98 Sprung et a [3], 98 Karen et a [33], 983 Smith and Andersen (34, 983 Murphy and Tomlanovich [], 983 Shaw and Caterine [35], 984 Kernodle et a [36], 984 Present report, ()* 3lM 4 9/F 55M 8lM 67/F 53M 69lM #M 0M 8OlM 69M 45lM 3M 5M 58lM 5M 69M 63/M 53M lm WM 0lM 8M 3M 84/M M #M 45lM 7lF 9M 8lM 5m 3OlF 8F 9/F 65M 79M 63lM 7lM 36M 58/M 4A4 3lF 5/F 50M 58lM 4/M 3 9d 4d Few hours 4d hr 74d 4d d 0d 3 4d hr hr Od Od Long d UWS; no sxn C.T.; hi-vol sxn C.T.; rapid C.T.; 5 cm sxn C.T.; rapid C.T.; rapid C.T.; 5 cm sxn C.T. C.T.; 5 cm sxn PPV C.T.; 0 cm sxn No sxn C.T. C.T.; 0 cm sxn C.T.; sxn C.T.; 0 cm sxn C.T.; C.T.; 5 cm sxn C.T.; 0 cm sxn C.T.; 5 cm sxn C.T.; sxn C.T.; 0 cm sxn C.T.; 0 cm sxn C.T.; 0 cm sxn PPV h mmediate mmediate 4 hr 45 min hr hr mmediate mmediate mmediate mmediate mmediate mmediate mmediate 4 hr 4 hr mmediate 4 hr 5 hr mmediate hr mmediate mmediate mmediate hr Few minutes 3 hr 5 hr hr 3 hr mmediate mmediate Few minutes 30 min mmediate mmediate mmediate Few hours mmediate mmediate 3 min 3 hr hr 0 min 3 min 5 min C C C.. W E = reexpansion pulmonary edema; M = male; F = female; hi-vol pump sxn = high-volume pump suction; sxn = suction; UWS = underwater seal; C.T. = chest tube; PPV = positive-pressure ventilation; = Heimlich valve; = ipsilateral; C = contralateral. *Details only provided for patient

4 343 Current Review: Mahfood et al: Reexpansion Pulmonary Edema Table. Recently Reported Cases of Reexpansion Pulmonary Edema Caused by Drainage of Pleural Effusion Reference, Year Duration of Volume No. of Age (yr)/ Symptoms Aspirated Onset of Patients Sex (days) (mu RPE Outcome Trapnell and Thurston [6], /M 90 3,000 Few hours 58/M,000 mmediate Buczko et a [40], 98 59/F 4 3,000 5 min Sprung et a [3], 98 if 4,300 hr Marland and Glauser [4], 98 49/F 0,000 hr Smith and Andersen [34], 983 3,500 Milne et a [4], 983 /F 4,500 mmediate RPE = reexpansion pulmonary edema; M = male; F = female. plication include chronicity of collapse, technique of reexpansion, increased pulmonary vascular permeability, airway obstruction, loss of surfactant, and pulmonary artery pressure changes. Most authorities cite as major contributing factors in the development of RPE the chronicity of collapse (usually more than 3 days) and the rapidity of reexpansion (using negative intrapleural pressure) [5, 6, 9,, 5, 8, 30, 36, 46, 47. This clinical impression has been confirmed by animal experimental studies [45, 46, 48, 49. Therefore, it has been suggested that slow evacuation of air or fluid from the pleural space by underwaterseal drainage alone [48] or by repeated aspirations of less than,000 ml of fluid or air [50] may aid in preventing; RPE as well as the reexpansion hypotension that sometimes occurs concomitantly [5]. However, as noted in this review and in the literature, RPE can develop regardless of the duration of lung collapse [7,,5,6,3,33,49]. The rate of expansion appears to be more critical than the method of lung inflation or the level of negative pressure applied [7,5]. WE has occurred without suction and after reinflation of the lung by positive-pressure ventilation, as in the present case report. Recent evidence from clinical and experimental observations supports increased pulmonary vascular permeability as a major etiological factor in the development of RPE [3, 36, 40, 4, 43, 47, 5-54]. The cause of the increased permeability is unknown. Factors implicated include hypoxic injury to the capillary and alveolar membranes, increased pulmonary capillary pressure and blood flow, decreased surfactant, and mechanical damage. Rapid reexpansion of a collapsed lung or sudden increase in negative intrapleural pressure causes a rapid increase in pulmonary capillary pressure and blood flow [5]. This increase can lead to fluid transudation across the capillary and alveolar membranes, especially in the presence of hypoxic injury, and result in an increase in pulmonary extravascular water [5]. Pulmonary blood flow is reduced by atelectasis [7, 54, 55, and the resulting hypoxia may cause vascular damage directly [56], or such damage may be due in part to oxygen-derived free radicals generated by restoration of perfusion and ventilation to previously hypoxic areas of lung [57]. Mechanical stress to blood vessels during reexpansion may contribute to increased vascular permeability. Airway obstruction, with or without negative intrapleural pressure, increases the gradient between the capillaries and the alveolar membranes, resulting in transudation of fluid into the interstitial tissues and alveoli [9, 7. However, in experimental RPE studies, although microatelectasis was observed, bronchial obstruction was not demonstrated grossly or histologically [4, 5, 48. Major bronchial occlusion has not been demonstrated in RPE by bronchoscopic examination or autopsy [5]; therefore, this is probably not a major etiological factor. Loss of tissue surfactant has been documented in atelectatic lungs after 4 hours of induced pneumothorax [5, 58. Although decreased surfactant is not the cause of RPE, it probably contributes to the atelectasis that accompanies pulmonary edema [4, 0, 5. Although RPE is almost always ipsilateral to the side of collapse, 3 instances of contralateral RPE have been reported. Contralateral RPE occurred in patients with pneumothoraces following resuscitation from cardiac arrest. Both patients were in severe left ventricular failure. t was postulated that increased vascular resistance and hypoperfusion in the collapsed lung prevented development of pulmonary edema and that, by the time the collapsed lung was reexpanded, measures to treat pulmonary edema already had been instituted. Both patients died [ll]. The third reported case of contralateral RPE occurred in a patient who was cyanotic from a left pneumothorax secondary to insertion of a subclavian catheter. nitial roentgenograms showed right-sided pulmonary edema. There was no evidence of left ventricular failure, documented by low filling pressures. However, there was marked increase in pulmonary vascular resistance, associated with right-sided heart failure, leading to reduced flow through the lungs and a low-output state. t was believed that the causes of contralateral pulmonary edema in this patient were the acute, severe pulmonary hypertension and the associated capillary damage that was induced by systemic hypotension and hypoxemia [33].

5 344 The Annals of Thoracic Surgery Vol 45 No 3 March 988 t is not within the scope of this review to detail the clinical management of RPE. Since RPE is generally self-limited, the aim of treatment is to ensure that adequate oxygenation and circulation are provided until it resolves. The response of the lung to injury is edema and alveolar collapse. The degree of resulting hypoxemia depends on the extent of ventilation/perfusion mismatch and the resultant intrapulmonary shunting. Decreased pulmonary compliance and intraalveolar fluid accumulation are additional factors contributing to hypoxemia [59]. f sufficient fluid volume is sequestered in the lung, hypovolemia and hypotension occur. Roentgenographic appearance and physical findings (in the absence of frothy sputum and cyanosis) may not predict the degree of physiological disturbance. The patient must be closely monitored by arterial blood gas values and, if necessary, with Swan-Ganz catheterization to follow filling pressures and cardiac output. n the patient with only roentgenographic evidence of pulmonary edema and no hypoxemia, no specific treatment is necessary. Mild hypoxemia often is corrected by supplemental nasally administered oxygen. When severe hypoxemia is present, often accompanied by expectoration of large amounts of frothy sputum, intubation and mechanical ventilation with positive end-expiratory pressure is required. Positive end-expiratory pressure decreases intrapulmonary shunting and recruits collapsed alveoli as it increases functional residual capacity. Hypotension and low cardiac output must be managed by volume replacement and inotropic agents, with careful hemodynamic monitoring. Physicians who are called on to treat hydrothorax or pneumothorax must be aware of RPE. t usually occurs unexpectedly and dramatically. 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