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Thoracoscopy and Talc Poudrage in the Management of Hepatic Hydrothorax^*

^* Divisions of Thoracic Surgery (Drs. de Campos, Filho, Andrade, Werebe, Fernandez, Filomeno, and Jatene) and Hepatology (Dr. Sette), Hospital Israelita Albert Einstein and Hospital das Clínicas of the University of São Paulo Medical School, São Paulo, Brazil.

Correspondence to: Jose Ribas Milanez de Campos, MD, Thoracic Division, University of São Paulo, Rua Almirante Soares Dutra n. 520, São Paulo, Brazil 05654.000; e-mail: jribas{at}usp.br

	Abstract

TOP Abstract Introduction Materials and Methods Results Discussion References

 
Study objective: To determine indications, limitations, morbidity and mortality of surgical thoracoscopy for management of hepatic hydrothorax, a rare, but often recurrent, complication in cirrhotic patients.

Patients and methods: From May 1985 through May 1999, 10 men and 8 women, with a mean age of 57.6 years (range, 26 to 76 years), underwent 21 therapeutic thoracoscopies to achieve pleurodesis by application of talc.

Results: The procedure was effective in 10 of 21 procedures. There were four recurrences (19.1%) that were retreated, with only one being successful. In this specific group, we detected high morbidity (57.1%) and mortality (38.9%) during the follow-up period of 3 months. Diaphragmatic defects were localized and closed five times (23.8%). Hospital stay was approximately 15 days (range, 5 to 41 days).

Conclusion: The procedure appears to be indicated for these fragile patients, especially when medical therapy fails. Immediate efficacy was 47.6%, increasing to 60% with videothoracoscopy and suture of the diaphragmatic defect. However, morbidity and mortality were high.

Key Words: hepatic hydrothorax • pleurodesis • talc poudrage • thoracoscopy

	Introduction

TOP Abstract Introduction Materials and Methods Results Discussion References

 
Hepatic hydrothorax (HH) is a complication of cirrhosis in patients with ascites. Prevalence varies with the patient population studied and criteria applied. A reasonable estimate is that it ranges from 4 to 6%, and even up to 10% with advanced disease.¹ Usually, it is found in the right hemithorax, but can also be seen on the left side, bilaterally,² and even in the absence of ascites.^{3 4 5}

The exact mechanism of pleural effusion remains unknown, and a number of different mechanisms have been proposed to explain it.^{1 6} However, demonstration by a number of investigators that ascites fluid moves directly from the abdominal cavity to the pleural space via defects in the diaphragm is an argument against these theories.^{7 8 9}

Traditional treatment in a patient who fails to respond to aggressive medical management of ascites remains problematic and controversial. Review of the literature has revealed that, to date, no method is ideal. This report describes our experience in treating patients with cirrhosis and ascites by thoracoscopy and talc poudrage. A special attempt was made to evaluate morbidity and mortality.

	Materials and Methods

TOP Abstract Introduction Materials and Methods Results Discussion References

 
A retrospective study is presented of 18 consecutive patients with clinical, laboratory, and radiologic evidence of liver disease, portal hypertension, and persistent right-sided symptomatic HH who were admitted to the Hospital Israelita Albert Einstein and Hospital das Clínicas, from May 1985 through May 1999. They underwent 21 procedures to control the pleural effusions. All patients had undergone multiple medical management and thoracenteses before transfer to our hospitals.

The series consists of 10 men (55.6%) and 8 women (44.4%), ranging in age from 26 to 76 years (mean, 57.5 years), who underwent therapeutic thoracoscopy with talc poudrage pleurodesis. Analysis of peritoneal as well as pleural fluid was always performed on admission, with samples being sent for bacterial cultures, smears for tuberculosis, and cytologic examinations. All tests yielded negative results. The chief characteristics of the composition of the HH fluid were a serous transudate, low cell count, mostly mononuclear cells, pH < 7.40, glucose concentration similar to serum, low amylase concentration, and rarely sanguineous. The protein concentration of the pleural fluid was slightly higher than that of the ascites fluid, as reported by Giacobbe et al.¹⁰ Radionuclide imaging demonstrated an abnormal communication between the peritoneum to the right pleural cavity in three of the five patients when the examination was performed.

The patients were positioned in the lateral decubitus position, under general anesthesia. Seven conventional thoracoscopies (CTH) were performed using a Carlen’s mediastinoscope (fifth intercostal space) with single-lung ventilation. Fourteen video-assisted thoracic surgery (VATS) procedures with three ports (two in the fifth and one in the eighth intercostal space) were performed using selective bronchial intubation that allowed ventilatory exclusion of the lung on the side of the operation.

After complete evacuation of the pleural fluid, the diaphragm was explored in search of defects. An x-shaped suture was used to close any defects found. The pleural cavity was then covered with 2 g of aerosolized talc and drained by placing one or two chest tubes in the cavity. Postoperatively, medical therapy was maintained, suction (20 cm H₂O) was inserted, and the chest tubes were removed when the volume collected remained < 100 mL, or at least 2 to 3 days after sealing the air leaks.

A broad-spectrum antibiotic (cephalothin) was started before the procedure and was continued until the chest tubes were removed. Analgesics were administered if necessary. Chest radiographs were performed shortly after the patient was admitted to the ICU and were repeated on the second postoperative day and at subsequent follow-up visits. For statistical analysis, the success of talc pleurodesis was defined as the absence of pleural fluid on the follow-up chest radiographs; any reaccumulation was regarded as a recurrence.

	Results

TOP Abstract Introduction Materials and Methods Results Discussion References

 
Thoracoscopy and talc insufflation were well tolerated by the patients in the present series (Table 1 ). Aerosolized talc was effective in the treatment of HH in 10 of 21 procedures (47.6%). Four recurrences (19.1%) occurred and were retreated. However, only one remained without recurrence during the next 3 months. The follow-up period was at least 3 months in all the surviving patients. During the study period, 7 of 18 patients (38.9%) died of hemorrhage secondary to esophageal varices (n = 2) and hepatocellular insufficiency (n = 5), during (mean ± SD) 21.43 ± 14.56 days (range, 5 to 40 days).

In five of the VATS procedures, the defects were located on the tendinous area of the diaphragm and were closed by sutures. Nine procedures failed to detect any defect, despite intraoperative maneuvers and injection of methylene blue into the peritoneal cavity. We noticed that the pleural fluid accumulated slowly and progressively, as though it filtered across the diaphragm through numerous small orifices that were impossible to identify singly. Additionally, no defect was found in the CTH group; perhaps, these results can be partly attributed to the technical difficulties associated with the use of this type of apparatus.

The following should be emphasized regarding the rate of recurrence between the two groups (with and without diaphragmatic suture): among the five patients in whom the defects were found and sutured, three did not present recurrence or morbidity, one evolved with high and prolonged drainage for > 30 days, which converted into empyema, and one died on the 18th postoperative day secondary to pneumonia and liver failure. Therefore, we obtained a 60% rate of success in this specific group of patients. Talc application alone, by CTH or VATS, was effective in 43.7%.

A total of 27 chest tubes were inserted: one tube (posterior, 36F) in 15 patients (71.4%); and two tubes (anterior, 28F; posterior, 36F) in 6 patients (28.6%). The average time to remove these tubes was 12.8 ± 9.5 days (range, 4 to 38 days). Seven tubes (33.4%) were associated with significant complications (hyponatremia and hypoalbuminemia) caused by the large volumes of fluid loss (600 mL/d), for > 25.57 ± 10.52 days (range, 10 to 38 days). All of our patients were maintained in the ICU for at least 24 h after the procedure. Patients continued to be monitored closely for fluid depletion or electrolyte disturbance.

No episodes of respiratory distress syndrome or pneumonitis were observed after talc pleurodesis in this group. There was no statistical difference in patient demographics between the CTH and VATS groups in terms of age, sex, chest drainage duration time, hospital stay, or procedure-related morbidity and mortality. Postprocedure hospital stay was 15.05 ± 10.68 days (range, 5 to 41 days).

	Discussion

TOP Abstract Introduction Materials and Methods Results Discussion References

 
Since the article in 1958 by Morrow et al¹¹ describing HH as a rapid accumulation of massive right pleural effusion, after a diagnosis of cirrhosis of the liver, various studies have been published. Although a wealth of literature on the treatment of symptomatic HH exists, the optimal or standard therapy remains unclear. Once the diagnosis of HH is established, medical therapy with salt restriction and diuretics is initiated. The term refractory HH is used when these measures are ineffective. However, prolonged diuretic treatment may result in depletion of the intravascular volume and impaired renal function. Medical therapy has proved to be effective in just one third of the reported patients, but the effect has been chiefly temporary.⁴ Many authors also consider that clinical management of HH is usually difficult and ineffective and can result in deterioration of the clinical status.^{1 12 13}

Although the exact mechanism is somewhat controversial, it appears that the ascites fluid is transported directly into the pleural space. A number of different mechanisms have been proposed to explain the development of HH,^{1 5} including hypoalbuminemia and a decrease in colloid osmotic pressure; leakage of plasma from hypertensive azygos veins; lymphatic leakage from the thoracic duct; passage of ascites fluid from the peritoneal cavity to the pleural space via lymphatic channels in the diaphragm; and passage of peritoneal fluid into the pleural space directly via defects in the diaphragm.

These defects probably result from anatomic thinning and separation of the taut collagenous fibers of the tendinous portion of the diaphragm.¹ Congenital factors, high intra-abdominal pressure, or prolonged bed rest may contribute to the diaphragmatic thinning.⁶ Another possible explanation for the formation of transdiaphragmatic holes that allow the peritoneum to rupture into the pleural space may be caused by an increase of pressure caused by Valsalva maneuvers (cough, defecation, parturition) and trauma.⁸ These defects are rarer on the left side because the left diaphragm is thicker and more muscular.¹⁰ A rapid and simple method for establishing whether there is any communication between the two cavities is to inject a radiotracer into the peritoneal cavity. Diagnostic modalities of diaphragmatic fenestration have included intraperitoneal instillation of air or contrast agents,⁹ nuclear scintigraphy,^{10 14} MRI,¹⁵ and surgical exploration by thoracoscopy.⁸

Mild symptoms are usually not present in most patients until the ascites becomes massive (< 10 L). In contrast, relatively small volumes of fluid (< 1 L) within the chest cavity cause significant symptoms and occasionally urgent need for rapid removal. Because of the severity of symptoms, HH is considered a major clinical problem in the management of portal hypertension. According to Strauss and Boyer,¹⁶ 85.4% of HHs are located on the right side, 12.5% are on the left, and 2.0% are bilateral. Dyspnea secondary to massive pleural effusion may call for repeated thoracentesis, which in turn can lead to substantial protein depletion without preventing fluid reaccumulation. In addition, our immediate concern regarding repetition of this procedure is the risk of bleeding. Thoracentesis is the most effective method for rapid relief of symptoms associated with HH. The goal is to remove as much of the pleural fluid as possible. In patients with both HH and massive ascites, the ascites is removed first. Hence, the patient’s symptoms improve and the thoracentesis is simplified.

It is important to bear in mind that tube thoracostomy can be very dangerous in patients with massive ascites and pleural effusion. It is imperative to resist the temptation, for in addition to being ineffective, it can cause life-threatening fluid and electrolyte imbalance. Runyon et al¹⁷ reported two deaths resulting from massive protein and electrolyte depletion. Pleural drainage by chest tube thoracostomy, followed by intrapleural introduction of a drug capable of inducing pleural symphysis, was attempted since 1977 by Falchuk et al¹⁸ using tetracycline. According to Yim et al,¹⁹ "of all sclerosants available, talc is generally considered the agent of choice because of its good track record (> 90% success rate), wide availability and low cost." In 1992, Colombo et al²⁰ reported a new treatment for HH, using pleurodesis with talc, as simple, with no major complications and without recurrences at 6-month check-up. However, on the basis of the present series and a previously published report,²¹ aerosolized talc appears to be the agent of choice.

Videothoracoscopy is an excellent method for diagnosis and therapy of HH, allowing identification and closure of tiny flaws in the diaphragm.⁷ It is one of the best ways to insufflate talc in the pleural cavity²² and the safest technique to handle pleural affections, even in debilitated patients, and is associated with a mortality rate of 3%.²³ In the present series, videothoracoscopy was particularly suitable for treatment of HH. It permitted an excellent location of the diaphragmatic defects in 5 of 14 procedures (35.7%) so that it was possible to close them by direct suture. When no defect was identified, recurrence was more frequent (25%). Talc application alone, applied by CTH or VATS, was sufficient in this series in 43.7% to permit creation of a total or partial symphysis that limited recurrence. In addition, if the defect cannot be identified, the patient is at risk for an extensive period of drainage via chest tube (33.4%), and associated complications may occur in patients with end-stage liver disease. We were unable to reproduce the results obtained by Haitjema and Maat,⁴ who state that holes in the diaphragm were found in six of seven patients undergoing either surgery or autopsy. In our series, we failed to find any defect in 9 of 14 procedures in the VATS group. Additionally, none were found in the seven patients in the CTH group.

Transjugular intrahepatic portosystemic shunts (TIPS), have been used in the treatment of refractory ascites and HH. TIPS was initially reported in 1994 by Strauss et al ⁶ and also in 1997 by Gordon et al,¹² who mentioned that 58.3% of patients had complete relief of symptoms. A transjugular approach is used to create a decompressive channel between a hepatic vein and portal vein. Although from a limited number of patients, TIPS may be the best initial procedure for those patients with HH who require frequent thoracentesis to control their symptoms.²⁴ Although the shunt is placed with the patient under local anesthesia and in a nonoperative fashion, we must remember that it functions as a highly effective side-to-side shunt with attendant complications, including hepatic encephalopathy and occasional liver failure. According to Rossle et al,²⁵ "with respect to the technique, the TIPS procedure is probably one of the most difficult interventions and, therefore, technical success and complications clearly depend on the skills of the operator." Jeffries et al²⁶ conclude also that "TIPS may be a safe and effective temporizing treatment for carefully selected patients with refractory hepatic hydrothorax. However, patient survival is limited after TIPS and is primarily determined by availability of liver transplantation."

Finally, we agree with Mouroux et al¹³ that "it is clear that no one method is totally effective, and that certain techniques have a morbidity and a mortality directly attributable to the procedure. Aggressive treatment of hydrothorax and ascites can lead easily to hepatic encephalopathy. However, utilization of videothoracoscopy after failure of medical therapy appears suitable for these particularly fragile patients." Despite the role of VATS in relieving symptomatic HH, patient survival remains poor. The subsequent deaths of these seven patients in our series do not seem to be directly attributable to the thoracoscopic procedure. For definitive treatment of HH associated with end-stage cirrhosis, liver transplantation should be considered. The majority of deaths in this series are attributable to the course of the disease or are linked or correlated to the difficulty of manipulation and reposition of ascites and pleural fluids. We should emphasize that a high rate of morbidity and mortality exists in the management of HH.

	Footnotes

 
Abbreviations: CTH = conventional thoracoscopies; HH = hepatic hydrothorax; TIPS = transjugular intrahepatic portosystemic shunt; VATS = video-assisted thoracic surgery

Received for publication August 13, 1999. Accepted for publication December 7, 1999.

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