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Dr. Kirsch is Chief, Division of Respiratory and Critical Care Medicine, Santa Clara Valley Medical Center, San Jose; and Clinical Professor of Medicine, Stanford University School of Medicine, Stanford, CA.
Correspondence to: Carl M. Kirsch, MD, FCCP, Division of Respiratory and Critical Care Medicine, Santa Clara Valley Medical Center, 751 S. Bascom Ave, San Jose, CA 95128
Humans are evolutionary "works in progress," who possess certain anatomic and physiologic features that may be considered disadvantages when compared with other animal species. The visceral and parietal pleural membranes along with the space that they surround have advantages and distinct disadvantages. The pleural surface seems to provide the optimal mechanism for smooth and frictionless movement of the lungs. The visceral and parietal pleural membranes and the minimal fluid lubricant between them allow the lung to expand and collapse uniformly and with minimal friction as it glides across the diaphragmatic and costal surfaces.1 Although sclerosis of the pleural space in humans can be shown to restrict diaphragmatic movement,2 the clinical consequences of this are thought to be small.3 Unfortunately, along with the theoretic advantages of a pleural space, come the "unintended consequences" of pneumothorax, hydrothorax, and hemothorax. Humans seem to be in the middle of the "pleural space spectrum," with the elephant at one end and the horse (and possibly the buffalo) at the other end. The elephant has a pleural space that is partially or totally restricted by fibrous tissue connecting visceral to parietal pleura that may not allow clinically significant collections of liquid or air,4 5 although this has been challenged.6 The horse has fenestrations (termed incomplete mediastinum by veterinarians) connecting both pleural spaces that can produce bilateral pneumothorax or hydrothorax simultaneously.7 Humans rarely have an incomplete mediastinum, but may acquire fenestrations similar to those of the horse and buffalo after cardiac bypass surgery.8
One result of a human-type pleural space is the potential to develop a transudative hydrothorax due to pathophysiology outside of the chest. Cirrhotic hydrothorax (CH) is noted in about 5% of patients with cirrhosis,9 and is occasionally not accompanied by demonstrable ascites.10 The pathophysiology of CH has been debated for years.9 The most likely mechanism attributes the passive collection of pleural fluid to movement of ascites along a pressure gradient through small fenestrations (similar to those between the pleural spaces of the horse) connecting the peritoneal and pleural spaces.9 11 Even in the absence of demonstrable ascites, peritoneal fluid is thought to preferentially move into the negatively pressurized pleural space before appreciable peritoneal fluid can collect.9 Any way one looks at it, these connections do not seem to be helpful. Although patients may tolerate large volumes of ascitic fluid with minimal symptoms, even small to moderate collections of pleural fluid often result in dyspnea.9 12
Once CH is diagnosed, and its pathophysiology understood, the initial therapeutic approach to the symptomatic patient is logically based on the standard medical management of ascites.9 12 The therapeutic options for patients who have persistent CH despite aggressive medical therapy constitute a group of variably successful maneuvers. Patients with CH usually have advanced liver disease with portal hypertension, intravascular hypovolemia, and an attendant high mortality. Repeated therapeutic thoracenteses and chest tube drainage are relatively contraindicated, since the continued pleural fluid loss often results in further hypovolemia, electrolyte and protein loss, and infection.13 Currently, the most favored therapy for refractory CH is transjugular intrahepatic portosystemic shunting (TIPS),14 15 which is designed to decrease hepatic sinusoidal pressure and the formation of ascites. This procedure does not usually require operating room facilities but does require interventional radiology and, occasionally, anesthesiology expertise.15 Strauss et al15 and Gordon et al14 have reported a total of 29 patients who were treated with TIPS for refractory CH. Complete relief of CH symptoms may be achieved in 58%,14 but 38% may develop worsening hepatic encephalopathy.14 Some shunts become occluded and clinical results may be improved when shunt patency is restored or another successful TIPS is done.15 Unfortunately, mortality rates after TIPS for refractory CH may be 25%14 to 40%,15 and death is usually due to the complications of end-stage liver disease.
Other approaches designed to either divert ascitic fluid and/or block the flow of ascitic fluid into the pleural space have usually been described in case-report format. One exception is a report of 22 patients who had CH treated with peritoneovenous shunts and tetracycline pleural sclerosis.11 This report does not tabulate data, but indicates that 18 of the 22 patients (82%) derived significant clinical benefit from the procedure.11 Peritoneovenous shunting (LeVeen or Denver shunt) with11 or without16 17 concomitant pleural sclerosis may be successful, but its efficacy is unreliable.18 The type of peritoneovenous shunt and valve mechanism may be an important factor in successful therapy of refractory CH. The valve in a LeVeen shunt requires a 3- to 4-cm H2O pressure difference for opening, compared with a 1-cm H2O pressure difference for the Denver shunt.17 Any increased pressure in the peritoneal space may facilitate ascitic fluid movement into the pleural space. Peritoneal shunts that require lower pressures for valve opening may facilitate more fluid movement into the venous vasculature rather than into the pleural space. Unfortunately, such valvular shunts develop occlusions and are associated with attendant clotting and infectious complications.19 In addition to diversion of ascites into the venous vasculature, there are case reports of patients who were successfully treated with drainage of pleural fluid into the central veins.20 Although there are reports of success,21 most experts are pessimistic about the efficacy of attempted chemical pleural symphysis alone, because the rapid reaccumulation of pleural fluid prevents pleural membranes from successfully adhering.9 12 Attempts at chemical pleural sclerosis combined with prevention of reaccumulation of pleural fluid may be more successful. The use of positive airway pressure to increase intrathoracic and pleural pressures in order to reverse the peritoneal-pleural pressure gradient and encourage the backward flow of fluid from the pleural to peritoneal space has been reported. The beneficial results of an increase in pleural pressure by means of continuous positive airway pressure (CPAP), combined with chemical pleural sclerosis has been described in abstract form.22 In addition, one patient had resolution of CH with the combined use of pleuroperitoneal and peritoneovenous shunts and CPAP to reverse the peritoneal-pleural pressure gradient and facilitate pleural drainage.23
Closure of transdiaphragmatic fenestrations by video-assisted thoracoscopy (VATS) with concomitant talc pleurodesis has been previously reported in a small retrospective series.24 In this issue of CHEST (see page 13), de Campos and colleagues have retrospectively reviewed their experience with the closure of transdiaphragmatic fenestrations and obliteration of the pleural space in a series of patients who had refractory CH. The authors studied the outcomes of 18 patients with medically refractory CH who had VATS (n = 13) or thoracoscopy with a Carlens mediastinoscope (n = 5) for suture closure of transdiaphragmatic fenestrations followed by intrapleural instillation of aerosolized talc. Seven of the 18 patients (39%) died of the consequences of cirrhosis within 40 days of the procedure, which reinforces the dire condition of patients with refractory CH. Five patients had demonstrable diaphragmatic fenestrations (all by VATS) that were closed before attempted pleural sclerosis with an attendant success of 60% (three of five patients), compared with a success of 44% in patients who had attempted pleural sclerosis without demonstrable diaphragmatic fenestrations. All patients had chest tubes in place postoperatively that were discontinued only when pleural fluid drainage dropped to < 100 mL/d, or when pleural drainage of air stopped for 2 to 3 days. Chest tubes were used for an average of 13 days (longer for patients without demonstrable diaphragmatic fenestrations), but duration ranged from 4 to 38 days and the postoperative hospitalization lasted an average of 15 days (range, 5 to 41 days). Two patients developed empyema (10%), and 33% developed hyponatremia and hypoalbuminemia due to prolonged and voluminous pleural fluid drainage. These results may be compared to those reported by Mouroux et al,24 who described eight patients with refractory CH treated with talc pleurodesis and VATS to seal demonstrable diaphragmatic fenestrations. Mouroux et al24 found demonstrable diaphragmatic fenestrations in 6 of 8 patients (75%), compared to 5 of 13 patients (38%) who had VATS in the study by de Campos and colleagues. Both groups used methylene blue labeling of ascites to enhance detection of fenestrations. The mean duration of chest tube drainage was 7.6 days for the patients of Mouroux et al,24 who had demonstrable diaphragmatic fenestrations, compared with an average of 16.5 days in the two patients without demonstrable fenestrations. None of the patients of Mouroux et al24 who had demonstrable fenestrations had recurrent CH after VATS and fenestration closure, but both patients without demonstrable fenestrations had recurrent CH after surgery. Four of eight patients (50%) of Mouroux et al24 died an average of 11.5 months (range, 1 to 36 months) after VATS and attempted pleural sclerosis.
The points to remember from the studies by de Campos and colleagues and Mouroux et al24 are as follows: (1) medically refractory CH is a highly mortal condition; (2) VATS for refractory CH is successful in 40 to 75% of patients, but may result in prolonged hospitalization and pleural space intubation with attendant complications of fluid/electrolyte imbalance and empyema; and (3) patients who have closure of demonstrable diaphragmatic fenestrations before attempted talc pleural symphysis have a better result than those without demonstrable fenestrations.
In view of the high mortality from underlying liver failure, the most definitive long-term therapeutic approach for refractory CH may be liver transplantation.12 However, many patients are not transplant candidates, and successful transplant may not be possible for months or years. Therefore, a more expeditious but effective approach to therapy for refractory CH is needed. The remaining approaches are either designed to reduce the formation of ascites (TIPS), divert ascites from movement into the pleural space (peritoneovenous shunts), facilitate drainage of pleural fluid from the pleural space (pleurovenous shunts), or prevent ascites from movement into the pleural space (closure of diaphragmatic fenestrations and pleurodesis). Compared with other procedures for refractory CH described in the literature and in view of published algorithms, TIPS is probably the first choice,9 12 when and where available. TIPS is the only procedure designed to ameliorate or reverse the pathophysiology causing ascites and CH. If TIPS is not available, refused by the patient, or is unsuccessful, the remaining procedures designed to divert and/or block movement of ascites into the pleural space are probably equivalent in efficacy. The significant problems of peritoneovenous and pleurovenous shunting may make VATS a more attractive alternative, but the choice among these remaining procedures depends on available equipment and technical expertise. Humans may continue to evolve a better mechanism of coupling the lung to the chest wall in order to avoid the unintended consequences of the pleural space. In the meantime, we will need to deal with our hydrothoraces and pneumothoraces as best we can.
References
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