Ann Thorac Surg 2009;87:245-250. doi:10.1016/j.athoracsur.2008.10.013
© 2009 The Society of Thoracic Surgeons
Original Articles: General Thoracic
Mechanical Pleurodesis Aided by Peritoneal Drainage: Procedure for Hepatic Hydrothorax
Patrick G. Northup, MDa,*,
R. Christopher Harmon, MD, PhDa,
Timothy L. Pruett, MDb,
Worthington G. Schenk, III, MDb,
Thomas M. Daniel, MDb,
Carl L. Berg, MDa
a Division of Gastroenterology and Hepatology, University of Virginia Health System, Charlottesville, Virginia
b Department of Surgery, University of Virginia Health System, Charlottesville, Virginia
Accepted for publication October 8, 2008.
* Address correspondence to Dr Northup, Division of Gastroenterology and Hepatology, University of Virginia Health System, P.O. Box 800708, Charlottesville, VA 22908 (Email: pgn5qs{at}hscmail.mcc.virginia.edu).
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Abstract
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Background: Hepatic hydrothorax in the setting of decompensated cirrhosis is a challenging and common clinical problem. Traditional therapies such as diuretics and transjugular intrahepatic portosystemic shunts can be effective therapies in selected patients but in patients ineligible for, or intolerant of, these traditional therapies, few effective therapeutic options remain for the management of hepatic hydrothorax.
Methods: We present a series of 5 consecutive patients with refractory hepatic hydrothorax who underwent combined thorascopically guided mechanical and chemical pleurodesis aided by an intraperitoneal drain that prevented reaccumulation of the ascites while pleural inflammation and adhesion were progressing. We speculate that the prolonged contact between the parietal and visceral pleura allowed by prevention of reaccumulation of intraabdominal ascites and subsequent flux through the pleural space enhanced the efficacy of this procedure in comparison with those presented in the literature.
Results: Despite the fact that all of our patients presented with decompensated cirrhosis, the surgical procedure and subsequent hospitalization were tolerated well by our entire cohort. Colonization of the pleural and peritoneal drainage fluid was a common complication of this procedure but was not associated with prolonged morbidity or mortality.
Conclusions: We present a therapy for the difficult clinical problem of refractory hepatic hydrothorax that may allow selected patients an opportunity for prolonged symptomatic control.
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Introduction
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Hepatic hydrothorax, recurrent symptomatic transudative pleural effusions associated with portal hypertension, affects up to 25% of patients with cirrhosis [1, 2] and asymptomatic pleural effusions are common in this population. Dyspnea and other chest symptoms associated with large hydrothorax can be bothersome to the patient, and a source of considerable debility and morbidity. Unlike the peritoneal cavity, the thoracic cavity has limited compliance and large effusions can cause significant respiratory compromise through ventilation-perfusion mismatch and compressive atelectasis [3]. The pathophysiologic mechanisms underlying hepatic hydrothorax in most patients relate to diaphragmatic defects (either microscopic or macroscopic) allowing free flow of ascites from the relative high pressures of the peritoneal cavity to the lower pressure of the pleural space. These diaphragmatic defects can be demonstrated using radionuclide labeling of ascitic fluid [4], radiologic imaging [5], or in some cases, direct thoracoscopic visualization [6]. Right-sided pleural effusions occur more frequently (85% of hepatic hydrothoraces) and are believed to be due to microscopic defects in the membranous diaphragm near the bare area of the liver [7].
Diuretics alone do not frequently control a large symptomatic hepatic hydrothorax and their use is often limited by renal dysfunction and other side effects [8]. The transjugular intrahepatic portosystemic shunt (TIPS) can be effective in control of ascites and hydrothorax in patients without contraindication but shunt stenosis and the lack of a complete response in many patients limits its utility [9–11]. Selective closure of the diaphragmatic defects can be effective in controlling hepatic hydrothorax even without complete control of ascites. However, the defect cannot be definitively identified in 25% to 72% of patients [6, 12, 13]. Various pleurodesis techniques have been described [2, 13–15] but efficacy is uncertain, with reported long-term success rates between 22% and 89%, due to recurrence of pleural fluid before definitive adherence of the parietal and visceral pleura can be achieved.
We present a series of 5 patients with refractory hydrothorax, which resulted in severe pulmonary compromise despite maximization of diuretic therapy and fluid restriction. All 5 of these consecutive patients were either not candidates for TIPS due to poorly controlled encephalopathy and high model for end-stage liver disease (MELD) scores or had a persistent hydrothorax despite the presence of a mature, functioning TIPS. These patients subsequently underwent thoracoscopic guided mechanical pleurodesis followed by talc instillation combined with simultaneous extended percutaneous peritoneal drainage tube placement to allow complete adherence of the pleural surfaces (Fig 1).
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Fig 1. Diagrammatic representation of combined pleural and peritoneal drainage procedure. 1. Placement of peritoneal drainage catheter and chest tube. 2. Aspiration of ascites. 3. Simultaneous aspiration of ascites and pleural fluid to allow apposition of visceral and parietal pleura and thus closure of defect(s) in diaphragm.
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Patients and Methods
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Patient Population
Table 1
shows the baseline characteristics of the patients. All patients had refractory hepatic hydrothorax requiring multiple admissions and(or) procedures for hypoxia, respiratory distress, or recurrent empyema. All effusions were right sided, consistent with previously published literature showing a right-sided predominance. Prior to the procedure one patient had a chest tube placed at an outside hospital for respiratory distress associated with a large right pleural effusion with persistent high output of transudative pleural fluid, preventing removal of the chest tube. Another had refractory hydrothorax and failed TIPS due to extensive portal vein thrombosis. Two patients had refractory portosystemic encephalopathy and therefore could not undergo TIPS as a treatment for their hydrothorax. One patient had recurrent empyema with loculations and trapped lung, and another had a patent TIPS placed greater than 120 days prior to the procedure despite a trans-TIPS gradient of 6 mm Hg and still had a persistent hydrothorax. These latter 2 patients had a median of six hospitalizations and nine thoracenteses prior to their procedures. All patients had severe decompensated cirrhosis and significantly elevated MELD scores prior to the procedure. Because all patients were not eligible for, or had failed to respond, to standard of care, it was the clinical judgment of the physicians caring for the patients that this procedure was indicated. Informed consent was obtained from the patients for procedures. The University of Virginia Institutional Review Board approved the use of patient care data for research purposes and waived the need for patient consent for its use in this study.
Procedure Description
The patient undergoes general anesthesia with placement of a double-lumen endotracheal tube to allow ventilation of the left (contralateral) lung while the right lung is allowed to collapse and thus allow visualization of the visceral and parietal pleural surfaces. During the procedure one gram of cefazolin is administered intravenously for prophylaxis and 50 to 70 g of human albumin is given after removal of ascites in the operating room. The patient is positioned in the left lateral decubitus position. After sterile prepping of the chest wall a 30-degree 5-mm diameter thoracoscope is placed through a 5-mm trocar to confirm adequate lung collapse. A 1-cm additional incision is made in the right chest wall in the sixth or seventh interspace and a catheter is introduced to aspirate all pleural fluid. If visualized, defects in the diaphragmatic pleural surface are closed. Next, a cautery scratch pad is folded over on itself with the abrasive surface facing out and cut to the width of a Kaiser-Pilling thoracoscopic sponge forceps. The folded pad is then placed in the grasper so that the protruding end contains the abrasive surface. The instrument is introduced through the access incision and, under direct endoscopic vision, the entire right diaphragmatic pleural surface is abraded. This process needs to be thorough and takes at least 30 minutes. The pleural surfaces of the chest wall and mediastinum adjacent to the diaphragm are also abraded circumferentially for a distance of 2 cm.
Attention is then turned to the diaphragmatic surface of the right lower lobe. Partial inflation of the lobe by anesthesiology assists in this abrasion. A 5-mm grasper placed through a second 5-mm port can assist with stabilizing the lung while the abrasion is being carried out. Once the two pleural surfaces have been abraded, sterile talc is then applied through the 1-cm port and sprayed directly on the diaphragmatic and lung pleural surfaces that have been mechanically abraded. A 28-French right angled chest tube is inserted through the larger incision, the camera is removed, and the chest evacuation chamber set on 20-cm suction.
The patient is then turned to the supine position and an intraoperative ultrasound is performed to evaluate for varices in the right perihepatic space. If no vascular structures intervene and an adequate amount of ascites is present, an ultrasound guided abdominal drain is placed over a guidewire. If an open procedure is decided upon, a short transverse incision is made in the right upper quadrant. The anterior rectus muscle and the posterior rectus sheath are then visualized and opened. A single-cuffed, 10 French peritoneal dialysis catheter or a multihole Jackson-Pratt drain is directed up over the right lobe of the liver. Next, this is tunneled out through a counter incision approximately 2 inches inferior to the major incision. The cuff is kept in the subcutaneous position, approximately midway between the two incisions. The catheter is secured to the posterior rectus sheath using a 3-0 Prolene pursestring suture (Ethicon Inc, Somerville, NJ).
Postoperative management consists of continuous suction on the chest tube until a successful pleurodesis is achieved and the drainage is less than 150 cc per 8 hours. The peritoneal catheter is drained to gravity only and is left in place until after the chest tube is removed. Postoperatively, intravascular volume is replete with daily intravenous albumin to match ascites losses, on average 50 to 75 g/day.
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Results
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The clinical outcomes and procedural details are shown in Table 2. Four of 5 patients survived to liver transplantation and all 4 are alive at the present time. The one death occurred in a patient not eligible for liver transplantation at day 132 after the pleurodesis procedure. Death in this patient was due to complications of spontaneous bacterial peritonitis with resulting hepatorenal syndrome. Peritoneal drains and chest tubes were left in place for a mean of 12.6 days after the procedure and the only immediate procedural complication was intraoperative bleeding in the thoracic cavity requiring blood transfusion in one patient. This patient had a trapped lung and a complex empyema requiring complete decortication and drainage. His preoperative international normalized ratio was 3.1 and he had a platelet count of 38,000 /µL. The resuscitation related to the intraoperative bleeding resulted in the administration of 2 units of packed red blood cells, 3 units of fresh frozen plasma, 6 units of platelet concentrate, and a single dose of recombinant factor VII (40 µg/kg). Estimated blood loss during the procedure was 2,000 mL.
The procedure for patient No. 5 was initially unsuccessful. The pleurodesis and chest tube placement was uncomplicated; however, the peritoneal cavity could not be accessed due to adhesions from a prior surgery. There was, initially, a high output of transudative pleural fluid from the chest tube (approximately 4 L/24 hours). This was managed by clamping the chest tube and applying a continuous positive airway pressure (CPAP) to allow for reaccumulation of ascites fluid (Fig 2). Successful placement of an ultrasound guided peritoneal drain was then achieved. Subsequent, simultaneous drainage of pleural and peritoneal fluid allowed for a dramatic decrease in chest tube output to less than 250 cc in a 24-hour period within one day. Significant adhesions were noted at the time of his liver transplant and were felt to be due to the prior remote surgery. These adhesions may have been exacerbated by retrograde passage of talc across the diaphragmatic defect in the setting of CPAP use.
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Fig 2. Positive pressure causes reversal of pressure gradient for passage of ascites through the diaphragm. Arrows indicate pressure-flow. (CPAP = continuous positive airway pressure.)
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Four of 5 patients had culture positive infections of pleural or peritoneal fluid while drainage or chest tubes were in place, although it was notable that fluid cell counts did not support bacterial peritonitis at the time of positive cultures. These infections were all clinically suspected with fever or new onset portosystemic encephalopathy, although all fevers observed were limited to a single temperature elevation. It should be noted that all of these infections or colonizations responded clinically to antibiotic therapy combined with removal of the drains and none recurred after removal of the tubes. None of the infectious agents were detected in blood cultures drawn at the same time as the pleural and peritoneal cultures. Despite the inability to find a specific diaphragmatic defect amenable to closure during the thorascopic procedure in any of the patients, 4 patients had complete resolution of their hepatic hydrothorax while one patient with aggressively recurrent pleural effusions prior to the procedure had the need for only a single additional thoracentesis during the 92 days between chest surgery and the subsequent liver transplantation (Fig 3).
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Fig 3. Representative chest radiographs from one of the patients who underwent the procedure (patient 3). Image (A), taken preoperatively, shows a large right-sided hydrothorax occupying the entire right hemithorax. Image (B) was taken on postoperative day 1 and shows improvement in the hydrothorax and the chest tube and peritoneal drain in place (arrows). There is also some right-sided airspace disease on this image which was treated as pneumonia. Image (C), obtained on the day of discharge, shows near complete resolution of the hydrothorax and removal of the drains.
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None of the patients were readmitted to the hospital for hydrothorax after the procedure and all but one remained strictly outpatients until they were called for liver transplantation. The single patient who was readmitted was not eligible for transplantation and was readmitted for spontaneous bacterial peritonitis and hepatorenal syndrome more than 100 days after discharge from the procedural hospitalization. The patients spent variable times in the intensive care unit (ICU) after the procedure with 2 recovering in the postanesthesia care unit and not requiring ICU stays after the procedure. Patient 1 had significant portosystemic encephalopathy prior to the procedure and required ICU care postoperatively for encephalopathy. Due to the empyema and required decortication and resulting bleeding, patient 3 had a complicated operation and significant respiratory compromise after the procedure requiring ICU care for 6 days after the procedure. No adverse ventilatory effects were noted during or after liver transplantation in any of the patients who underwent the pleurodesis procedure and were later transplanted.
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Comment
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Transudative pleural effusions are notoriously difficult to pleurodese due to the absence of inflamed pleural surfaces that are the prerequisite for successful adhering of parietal and visceral surfaces together. The success of the technique described above appears to be based on meticulous mechanical abrasion of the entire diaphragmatic surface and the entire diaphragmatic surface of the right lower lobe. Focal placement of the sterile talc to these inflamed opposing pleural surfaces enhances the creation of the pleurodesis. In addition, it is felt that the addition of a catheter to decompress ascitic fluid decreases the hydrostatic pressure from the peritoneal cavity driving the fluid into the pleural space. This series describes only right-sided effusions; however, this may also be applicable to left-sided or bilateral effusions.
The common occurrence of infection in the pleural and peritoneal spaces after the procedures is of special concern and is probably related to contamination from external sources with migration into the body space through the catheters themselves. Although not employed in our series, prophylactic antibiotics could perhaps be warranted in patients undergoing these procedures in the future. Maintenance of caloric intake to support the inflammatory response is also felt to play a role in the multifactorial approach to this difficult clinical problem.
Some authors have recommended an aggressive visual search for diaphragmatic defects in the pleura during thoracoscopy and closure of these defects in combination with pleurodesis as the optimal therapy for hepatic hydrothorax [6, 14]. However, finding a macroscopic defect in the pleura is uncommon during thoracoscopy for hepatic hydrothorax [13]. Indeed, in the series by Ferrante and colleagues [14], no visual defect in the pleural surface was detected in any of the 15 consecutive patients undergoing thoracoscopy. Similarly, we were unable to localize a definitive pleural defect in any of our 5 patients with hepatic hydrothorax. We believe our technique of total diaphragmatic surface mechanical pleurodesis offers the optimal chance of successful closure of defects too small to directly visualize during thoracoscopy. We also believe that relief of the hydrostatic pressure exacted by the peritoneal ascites on the diaphragmatic surface during the healing process is a key component of the success of this procedure. We feel this is likely to be the most important factor in those patients without a clear pleural defect seen on thoracoscopy. Finally, a CPAP may be used as an adjunct to facilitate pleural apposition by creating a positive intrathoracic pressure gradient, which inhibits the flux of ascites into the pleural space.
Despite culture positive body fluid infections after the procedure, the patients tolerated the procedure reasonably well and the hydrothorax resolved or significantly improved. All of the patients had multiple admissions to the hospital and thoracenteses prior to the procedure for refractory hydrothorax. Patient 1 had two ICU admissions for respiratory compromise related to hydrothorax prior to the procedure. We feel, in selected candidates not eligible for TIPS or immediate transplantation, that the risk and expense of this procedure are more than balanced by the symptomatic benefit offered by the pleurodesis procedure. Although a formal cost analysis was not done, we expect that significant amounts of money were saved because of the prevention of hospitalizations and procedures. This procedure may be of the most benefit as a bridge to liver transplantation in patients with low MELD scores and severely symptomatic hydrothoraces.
In summary, we report a surgical approach to the management of refractory hepatic hydrothorax. The universal success of our procedure compares very favorably with surgical success rates previously published in the literature [2, 13–15]. We propose that the described procedure be considered as therapy in cirrhotic patients with hepatic hydrothorax refractory to TIPS or maximal medical management.
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References
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- Morrow CS, Kantor M, Armen RN. Hepatic hydrothorax Ann Intern Med 1958;49:193-203.[Abstract/Free Full Text]
- Mouroux J, Perrin C, Venissac N, Blaive B, Richelme H. Management of pleural effusion of cirrhotic origin Chest 1996;109:1093-1096.[Abstract/Free Full Text]
- Xiol X, Castellote J, Cortes-Beut R, Delgado M, Guardiola J, Sesé E. Usefulness and complications of thoracentesis in cirrhotic patients Am J Med 2001;111:67-69.[Medline]
- Rajnish A, Sudhakar P. Diagnosis of hepatic hydrothorax by Tc-99m sulfur colloid peritoneal scintigraphy Clin Nucl Med 2001;26:888.[Medline]
- Zenda T, Miyamoto S, Murata S, Mabuchi H. Detection of diaphragmatic defect as the cause of severe hepatic hydrothorax with magnetic resonance imaging Am J Gastroenterol 1998;93:2288-2289.[Medline]
- Huang PM, Chang YL, Yang CY, Lee YC. The morphology of diaphragmatic defects in hepatic hydrothorax: thoracoscopic finding J Thorac Cardiovasc Surg 2005;130:141-145.[Abstract/Free Full Text]
- Strauss RM, Boyer TD. Hepatic hydrothorax Semin Liver Dis 1997;17:227-232.[Medline]
- Garcia Jr N, Mihas AA. Hepatic hydrothorax: pathophysiology, diagnosis, and management J Clin Gastroenterol 2004;38:52-58.[Medline]
- Andrade RJ, Martin-Palanca A, Fraile JM, et al. Transjugular intrahepatic portosystemic shunt for the management of hepatic hydrothorax in the absence of ascites J Clin Gastroenterol 1996;22:305-307.[Medline]
- Gordon FD, Anastopoulos HT, Crenshaw W, et al. The successful treatment of symptomatic, refractory hepatic hydrothorax with transjugular intrahepatic portosystemic shunt Hepatology 1997;25:1366-1369.[Medline]
- Siegerstetter V, Deibert P, Ochs A, Olschewski M, Blum HE, Rössle M. Treatment of refractory hepatic hydrothorax with transjugular intrahepatic portosystemic shunt: long-term results in 40 patients Eur J Gastroenterol Hepatol 2001;13:529-534.[Medline]
- Temes RT, Davis MS, Follis FM, Pett Jr SB, Wernly JA. Videothoracoscopic treatment of hepatic hydrothorax Ann Thorac Surg 1997;64:1468-1469.[Abstract/Free Full Text]
- Milanez de Campos JR, Filho LO, de Campos Werebe E, et al. Thoracoscopy and talc poudrage in the management of hepatic hydrothorax Chest 2000;118:13-17.[Abstract/Free Full Text]
- Ferrante D, Arguedas MR, Cerfolio RJ, Collins BG, van Leeuwen DJ. Video-assisted thoracoscopic surgery with talc pleurodesis in the management of symptomatic hepatic hydrothorax Am J Gastroenterol 2002;97:3172-3175.[Medline]
- Takayama T, Kurokawa Y, Kaiwa Y, et al. A new technique of thoracoscopic pleurodesis for refractory hepatic hydrothorax Surg Endosc 2004;18:140-143.[Medline]
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Abstract
Introduction
