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PubMed1992

Liquid volume, Na+ and mannitol concentration in a hypertonic mannitol-Ringer hydrothorax.

In anesthetised rabbits with a 2 ml hypertonic mannitol-Ringer hydrothorax in the right space 30 mM/L mannitol were required for an unchanged volume of the hydrothorax after 60 min. [Na+] in the pleural liquid 10, 30 and 60 min after this hydrothorax was 8, 7 and 5 mEq/L, respectively, lower (P less than 0.01) than the initial one and that in a Ringer-hydrothorax. This seems due to the active transport of Na+ out of the pleural space followed by little water because of the osmotic pressure exerted by mannitol. This finding provides further evidence for an active transport without using inhibitors, and implies that the mesothelium offers an appreciable resistance to small solute diffusion. Mannitol concentration, measured at corresponding times from the activity of labeled mannitol, was 76, 68 and 56%, respectively, of the initial one (24.5 mM/L). From 30 to 60 min 6.5 microM of mannitol left the right space mainly by diffusion. The diffusional permeability of the mesothelium was indirectly assessed from the diffusional outflux of mannitol, the surface of the pleural space, and an estimate of mannitol concentration in the interstitium next to the mesothelium: it is smaller than that found in vitro.

Animals↗

PubMed2003

Management of massive and persistent ascites and/or hydrothorax after liver transplantation.

PURPOSE: To describe the results of the treatment of eight liver transplantation (LT) patients subsequently developing large volumes of long-lasting ascites. PATIENTS AND METHODS: Between August 1996 and February 2003, 405 LTs were performed in 375 patients, eight (1.97%) of whom (six men and two women of mean age of 55.4 +/- 5.2 years) subsequently developed massive (> 500 mL/d) and persistent ascites and/or hydrothorax. All patients were HCV positive. The mean age of the liver donors was 66.8 +/- 21.9 years. All LTs were performed by replacement of the recipient retrohepatic vena cava. RESULTS: The eight patients displayed sinusoidal portal hypertension related to biopsy-proven recurrence of HCV infection. Mean wedged hepatic venous pressure was 14.9 +/- 5.1 mm Hg and mean portal vein/right atrial pressure gradient (PAPG) was 17.3 +/- 4.8 mm Hg. In two patients, the ascites appeared the day after LT; in the remaining six, ascites and/or hydrothorax appeared after 342.3 +/- 167.7 days. Seven patients with a mean PAPG of 18.4 +/- 3.9 mm Hg and a mean plasma/ascites albumin concentration gradient of 2.8 +/- 0.3 g/L were treated by means of a trans-jugular intrahepatic portosystemic shunt TIPS, and one (with a PAPG of 9 mm Hg and a plasma/ascites albumin concentration gradient of 1.38 g/L) by means of spleen arterial embolisation. After a mean follow-up of 558 +/- 147.2 days, the ascites and/or hydrothorax have resolved in five patients (62.5%), one (12.5%) has stable ascites not requiring paracentesis, and two (25%) have died of multiorgan failure. CONCLUSIONS: These data suggest the efficacy of the aggressive treatment of massive and persistent ascites and/or hydrothorax.

Ascites↗

PubMed1995

Resolution of unilateral fetal hydrothorax with associated non-immune hydrops after intrauterine thoracentesis.

Congenital hydrothorax has been successfully managed in utero by two different treatment modalities: thoracentesis and pleuroamniotic shunting. Unfortunately, there is a paucity of data as to which method is better for the management of this problem. This case report supports the use of thoracentesis as the initial procedure for primary fetal hydrothorax. We report a pregnancy complicated by primary fetal hydrothorax with non-immune hydrops that completely resolved after two thoracenteses in the early third trimester. Complete resolution was maintained throughout pregnancy without the need for further antenatal or neonatal intervention, i.e. further thoracentesis, pleuroamniotic shunt placement, intubation, or chest and/or abdominal tube placement. The child was delivered at 42 weeks and is doing well without problems at 1 year of age. We believe that intrauterine thoracentesis should be the initial procedure of choice for the treatment of primary fetal hydrothorax with mediastinal shift, and pleuroamniotic shunting should be reserved for cases that require repetitive thoracenteses.

Adult↗

PubMed2006

Thoracoscopic diaphragmatic repair for refractory hepatic hydrothorax: application of pleural flap and mesh onlay reinforcement.

BACKGROUND: Management of hepatic hydrothorax is difficult, and no radical treatment has been established. Based on accumulating evidence that diaphragmatic defects contribute to hepatic hydrothorax, we developed a diaphragmatic repair method for the management of this complex condition. METHODS: From October 2003 to March 2005, 10 patients (age, 32 - 83 years; 6 men and 4 women) with refractory hepatic hydrothorax (Child-Pugh class B-C) underwent thoracoscopic pleura (n = 7) or mesh (n = 3) onlay reinforcement to repair the diaphragmatic defects on which this study focuses, and all patients have since been under follow-up in a prospective observation study. RESULTS: After a mean of 7.7 months of follow-up examinations, no local recurrence occurred in all patients. Two patients died of hemorrhage from esophageal varices two months postoperatively. All patients had a better postoperative pulmonary function. CONCLUSION: The use of pleura and mesh onlay reinforcement of the diaphragm is an encouraging treatment for refractory hepatic hydrothorax.

Adult↗

PubMed1997

[Refractory hydrothorax in primary biliary cirrhosis: successful treatment with transjugular intrahepatic portosystemic stent shunt].

HISTORY AND CLINICAL FINDINGS: A 55-year-old woman with known primary biliary cirrhosis (PBC) was hospitalized because of increasing dyspnoea. A year before she had for the first time experienced a right-sided pleural effusion which had to be drained every 4 weeks. Physical examination revealed dullness on percussion and greatly decreased breath sounds on auscultation over the entire right thorax. In addition there were signs of moderate ascites and leg oedema. INVESTIGATIONS: Chest radiograph showed a homogeneous shadowing of the right thorax without mediastinal shift. Diagnostic thoracocentesis produced a serous effusion, a transudate on chemical analysis, comparable to the composition of the ascitic fluid. Bacteriological and cytological tests on both fluids were unremarkable. TREATMENT AND COURSE: The right pleural effusion was presumed to be due to a hydrothorax from the ascites caused by portal hypertension associated with the PBC. Despite continuous diuretic treatment and thoracocentesis with albumin substitution every 3 days there was no improvement and implantation of a transjugular intrahepatic portosystemic stent shunt (TIPSS) was performed. This effectively lowered portal pressure and markedly improved the patient's condition so that further thoracocentesis were no longer necessary. 3 weeks after TIPSS implantation she was discharged in good condition. Radiography 3 weeks later demonstrated continued reduction in the hydrothorax. CONCLUSION: Hydrothorax is a rare complication of liver cirrhosis. TIPSS implantation can provide lasting resolution and corresponding clinical improvement of a hydrothorax, especially in those conditions which are refractory to diuretic treatment and thoracocentesis.

Diuretics↗

PubMed2003

Video-assisted thoracoscopic talc pleurodesis is effective for maintenance of peritoneal dialysis in acute hydrothorax complicating peritoneal dialysis.

BACKGROUND: Acute, massive, unilateral hydrothorax is an uncommon but well-recognized complication of peritoneal dialysis. Its clinical course and treatment outcome after a recently advocated technique of video-assisted thoracoscopic (VATS) talc pleurodesis remains unclear. METHODS AND RESULTS: Between July 1998 and March 2002, among 475 CAPD patients in two regional hospitals in Hong Kong, nine patients (three men, six women, mean age 53+/-12 years) developed acute hydrothorax due to pleuroperitoneal communication (R=8, L=1) within 5.8+/-4.2 months (median, 5.2 m; range, 2 days to 11.6 months) of commencing peritoneal dialysis. Analysis of simultaneously obtained peritoneal and pleural fluid in all subjects only showed concordance in protein content (consistently<4 g/l), while fluid glucose and lactate dehydrogenase levels were not comparable. The methylene blue test was negative (n=4). Radionuclide scan (n=6) and contrast CT peritoneography (CTP, n=3) detected pleuroperitoneal communication in half and one-third of the patients, respectively. All patients underwent pleurodesis achieved by talc insufflation into the pleural cavity under VATS guidance. All patients were successfully returned to peritoneal dialysis. After a mean follow-up of 18.8+/-12.5 months, hydrothorax recurred in one patient (at 7 months after pleurodesis), who was successfully treated by repeating the procedure. CONCLUSIONS: Hydrothorax complicating CAPD is more commonly right-sided, and tends to occur within the first year of starting peritoneal dialysis. Isotope scan and CTP are insensitive in diagnosing pleuroperitoneal communication. A low pleural fluid protein content is the most consistent biochemical finding. VATS talc pleurodesis is a safe and reliable treatment of choice that allows sustained continuation of CAPD with low recurrence rate.

Acute Disease↗

PubMed1986

Hydrothorax, ascites, and right diaphragmatic hernia.

Hydrothorax and/or ascites may be the most striking finding in children with right diaphragmatic hernia. The clinical, radiographic, and pathologic findings of five children with right diaphragmatic defects through which the liver had herniated are described. Three presented with a right hydrothorax, one with a right hydrothorax and ascites, and another with ascites. All four children with large right hydrothoraxes were found to have an incarcerated peritoneal sac filled with fluid in the right side of the chest at surgery or autopsy. Lymphatic congestion and obstruction was the probable cause for the fluid collection, which tended to enlarge with time. This condition may be life threatening, and two of the four patients died soon after birth because of hypoplasia of the lungs. Fetal ultrasonography in both had disclosed right intrathoracic cystic masses, and in one, intrauterine aspiration to decompress the lungs had been attempted. The other two patients are alive and well following surgical repair at 1 week and 7 months of age. Ascites was present in two patients and was believed to be due to hepatic venous obstruction, a mechanism similar to that responsible for the Budd-Chiari syndrome.

Ascites↗

PubMedDate not supplied

Hepatic hydrothorax -- how would you manage it?

A 53-year-old woman with a history of chronic alcoholism presented with symptomatic large right-sided pleural effusion with no evidence of ascites. After a diagnosis of hepatic hydrothorax was established, her symptoms improved with therapeutic thoracentesis. She required multiple emergency department visits for recurrent right-sided pleural effusion treated with urgent therapeutic taps. Hepatic hydrothorax is a relatively infrequent but potentially serious complication of liver cirrhosis. The management of hepatic hydrothorax, usually required in symptomatic patients, is controversial and contradictory. The case summary is followed by a question regarding available management options. The pathophysiology of hepatic hydrothorax, the role of various therapeutic options and the current favoured therapy for this not so uncommon disorder are reviewed.

Drainage↗

PubMed2000

Resolution of refractory hepatic hydrothorax after chemical pleurodesis with minocycline.

Management of refractory hepatic hydrothorax is a challenge to physicians in clinical practice. We reported two patients with hepatic hydrothorax, non-alcoholic cirrhosis and rapidly recurring pleural effusion. They failed to improve with diuretics and repeated thoracentesis. Refractory hepatic hydrothorax was successfully treated by minocycline-induced pleural symphysis. After pleurodesis, ventilatory function returned to normal in both patients. No recurrence of pleural effusion was noted. We suggest that minocycline pleurodesis is an alternative treatment for refractory hepatic hydrothorax because it is simple, safe and effective.

Aged↗

PubMed2002

[Percutaneous intrahepatic portosystemic shunting as a treatment for refractory hepatic hydrothorax].

Hepatic hydrothorax is an infrequent complication of portal hypertension in liver cirrhosis. Treatment with saline restriction and diuretics is usually effective but when this fails, the therapeutic approach is difficult and multiple complications occur. Transjugular percutaneous intrahepatic portosystemic shunt (IPS) is associated with a marked decrease in portal pressure and consequently this technique has been used in the treatment of refractory ascites. The aim of this study was to analyze the efficacy, safety and outcome of refractory hepatic hydrothorax treated by IPS. The procedure was performed in 5 patients who were all grade B or C in the Child-Pugh classification. Three patients showed complete response to the treatment, of whom 1 underwent transplantation 20 days later. The fourth patient showed partial response with a reduction in the need to perform thoracocentesis and the fifth patient showed no response to IPS and died after 17 days of follow-up. Albumin levels and Child classification remained unchanged. Two patients presented recurrence with reappearance of hydrothorax due to shunt dysfunction and 2 patients presented hepatic encephalopathy that responded to medical treatment. Refractory hepatic hydrothorax can be controlled by IPS in a large number of patients but its efficacy is restricted by shunt dysfunction, the risk of encephalopathy and by its limited effect on survival.

Aged↗

PubMed2003

Risk factors for spontaneous bacterial empyema in cirrhotic patients with hydrothorax.

BACKGROUND: Spontaneous bacterial empyema (SBEM) is a rare complication of portal hypertension. The characteristics and risk factors for SBEM are not well known. This study was performed to investigate the risk factors for SBEM in cirrhotic patients with hydrothorax. METHODS: From July 1996 to December 1998, 862 cirrhotic patients were studied. All patients underwent chest radiography, abdominal sonography or computed tomography after admission to detect the existence of pleural effusion. Pleural fluid was obtained after thoracentesis and sent for analysis. The clinical and laboratory data from patients with sterile hydrothorax and from SBEM at the time of first episode were compared. RESULTS: Seventeen patients had 26 episodes of SBEM during the study period, 56% (14 of 26) of these SBEM episodes were associated with spontaneous bacterial peritonitis (SBP) and 31% (8 of 26) were associated with bacteremia. The incidence of SBEM was 2% (17 of 862) in cirrhotic patients and 13% (17 of 132) in cirrhotics with hydrothorax. Patients with SBEM had a higher Child-Pugh score, lower serum albumin, prolonged prothrombin time, lower pleural fluid protein, and higher rate of associated SBP than patients with sterile hydrothorax. Multivariate analysis revealed that pleural fluid protein level (p = 0.0035) and presence of SBP (p = 0.0062) were predictive factors of SBEM. The hospitalization mortality rate of SBEM was 38%. CONCLUSIONS: Patients with advanced liver disease, low pleural fluid protein level, or SBP are predisposed to SBEM. A diagnostic thoracentesis should be performed in cirrhotic patients with pleural effusion when infection is suspected or clinical deterioration occurs.

Bacterial Infections↗

PubMed1992

[Hydrothorax of hepatic origin. Description of a clinical case, pathophysiology].

We admitted a 60 year old patient with severe right hydrothorax. He was known to suffer from decompensated non-alcoholic cirrhosis. His invaliding dyspnea was only temporarily improved by repeated thoracocentesis, due to the very rapid refilling of the thorax from the ascites; until the development of a "tension hydrothorax" with dangerous mediastinal deviation. By insertion a peritoneo-venous shunt described by LeVeen the clinical picture was improved, and the patient no longe required further pleural aspiration. Six per cent of cases of ascites complicating hepatic cirrhosis may be associated with hydrothorax of the same origin. The diaphragm is normally perforated by a multitude of tiny virtual holes, closed by the peritoneum and the thoracic pleura. The high intra-abdominal pressure in ascites tears these fragile membranes, and allows the peritoneal fluid to overflow into the pleural cavity. Usually treated by fluid restriction and diuretics, when this condition becomes intractable or when a tension hydrothorax appears, interfering with respiratory function a LeVeen peritoneo-venous shunt should be inserted.

Ascites↗

PubMed2006

[Two cases of intractable hepatic hydrothorax successfully treated with nasal CPAP].

Hepatic hydrothorax is often resistant to various treatments. A failure in the treatment for hepatic hydrothorax may be associated with poor prognosis. We report two cases of intractable hepatic hydrothorax successfully treated by combining chemical pleurodesis using OK-432 with nasal continuous positive airway pressure. Combination therapy may provide a minimally invasive and effective treatment for intractable hepatic hydrothorax.

Aged↗

PubMed2001

Hepatic hydrothorax.

Hepatic hydrothorax (HH) is an uncommon manifestation of cirrhosis with ascites. Pleural effusions form when ascitic fluid moves through diaphragmatic defects that have been opened by increased peritoneal pressure. The diagnosis is established clinically by finding a serous transudate and is confirmed by radionuclide imaging demonstrating communication between the peritoneal and pleural spaces. In end-stage liver disease, the management of hepatic hydrothorax is problematic and often does not respond to medical therapy. Therapeutic options for a refractory hepatic hydrothorax include therapeutic thoracentesis, talc slurry through a chest tube, peritoneovenous and pleurovenous shunting, thoracoscopic talc poudrage, transjugular intrahepatic portosystemic shunt (TIPS), thoracosopic diaphragmatic defect repair followed by talc poudrage, and lastly, liver transplant. TIPS can be used as a bridge for transplantation but is often complicated by encephalopathy. Video assisted thoracic surgery (VATS) with patching the defect and talc poudrage may provide symptomatic relief; however, the morbidity and mortality in these extremely ill patients is high. The only definitive treatment for refractory hepatic hydrothorax associated with end-stage cirrhosis is liver transplantation.

Journal Article↗

PubMed1997

Hepatic hydrothorax.

Ascites is a common manifestation of portal hypertension in patients with cirrhosis. Approximately 5% of patients with cirrhosis may develop a pleural effusion. This is usually right sided. In the absence of cardiac or lung disease, the presence of a pleural effusion in a cirrhotic patient is known as hepatic hydrothorax. Small volumes of fluid within the pleura may be associated with significant respiratory symptoms which require the clinician to rapidly remove the fluid. The development of hepatic hydrothorax is secondary to passage of ascites from the abdomen to the pleural space via defects in the diaphragm. Once the diagnosis of hepatic hydrothorax is established with certainty, medical therapy with salt restriction and diuretics is initiated. When these measures are ineffective the patient has refractory hepatic hydrothorax. Based on current studies, transjugular intrahepatic portal systemic shunts appear to be the most effective form of treatment for these patients.

Ascites↗

PubMed2002

Video-assisted thoracoscopic surgery with talc pleurodesis in the management of symptomatic hepatic hydrothorax.

OBJECTIVES: Video-assisted thoracoscopic surgery with talc pleurodesis is a therapeutic option for patients with hepatic hydrothorax that is refractory to medical therapy. We report the outcomes of 15 patients who underwent this procedure for significantly symptomatic disease. METHODS: Data on 15 consecutive patients presenting to our institution between November, 1996, and June, 2000, with refractory hepatic hydrothorax was retrospectively collected. Baseline demographical and clinical characteristics and outcomes after the procedure were analyzed. RESULTS: The mean age of our cohort was 51.5 yr, and eight (53%) of the 15 patients were male. The etiologies of liver disease were hepatitis C virus and/or alcohol (n = 12) and cryptogenic cirrhosis (n = 3). Nine patients were Child-Pugh class C and six class B. Success defined as control of symptomatic hydrothorax in the first 30 days after the procedure was achieved in 11 of 15 patients (73%). Eight of these patients remained asymptomatic at a median follow-up of 5.5 months after the procedure, but three patients experienced symptomatic fluid reaccumulation 45, 61, and 62 days after the initial procedure. After a second VATS procedure, control was achieved in two of these three patients. Complications included pain around the chest tube site, low grade fever with leukocytosis, pleurocutaneous fistula and empyema, all of which responded to medical therapy. Four patients did not respond to the procedure. There were no procedure-related deaths. Overall mortality and baseline clinical characteristics were similar between responders and nonresponders to VATS with pleurodesis. CONCLUSIONS: Symptomatic hepatic hydrothorax can be controlled with a single VATS with pleurodesis in as many as 53% of patients and with two procedures in 73% with no procedure-related mortality. The procedure may be considered as a palliative alternative in patients needing frequent thoracocentesis. It also provides an alternative to transjugular intrahepatic portosystemic shunts and is a bridge toward liver transplantation.

Adult↗

PubMed1998

Transjugular intrahepatic portosystemic shunts and liver transplantation in patients with refractory hepatic hydrothorax.

Hepatic hydrothorax is a relatively infrequent but potentially serious complication of cirrhosis resulting from the accumulation of ascitic fluid in the chest cavity. Medical management is initially directed at controlling ascites formation, but invasive therapeutic procedures may be required if symptoms persist. The aim of this study was to report on the long-term efficacy and safety of transjugular intrahepatic portosystemic shunt (TIPS) placement to reduce portal hypertension in 12 consecutive subjects with refractory hepatic hydrothorax. Most subjects had evidence of advanced cirrhosis of varying causes (Child-Pugh class A, 1; B, 5; C, 6). Mean subject age was 54 years, and subjects were followed up for a mean of 173 days (range, 7-926 days). The portosystemic pressure gradient after TIPS was reduced to <12 mmHg in all cases. Periprocedural morbidity was noted in 2 subjects, and 30-day survival after TIPS placement was 75%. Overall, 58% of subjects experienced either a complete or partial response following TIPS placement. Subject response did not correlate with age, baseline creatinine clearance, or Child-Pugh score. Cumulative subject survival was 42%, and 4 of the 5 long-term survivors required eventual liver transplantation. Subject age >65 years was associated with early mortality after TIPS placement, but this trend was not statistically significant. All 4 subjects undergoing liver transplantation required perioperative pleural fluid drainage, but only 1 subject has experienced recurrent effusion. We conclude 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.

Adult↗

PubMed1996

Late development of hydrothorax induced by a central venous catheter: report of a case.

We report herein the case of a 47-year-old woman who suffered a hydrothorax induced by a central venous catheter (CVC) which had been placed to facilitate total parenteral nutrition following a left sleeve pneumonectomy for lung cancer. The CVC was inserted into the superior vena cava (SVC) through the left subclavian vein after the operation; however, the tip inadvertently turned upward and came in contact with the lateral wall of the SVC. The patient suddenly developed dyspnea due to a right-sided hydrothorax 47 days after the insertion of the catheter. Indocyamine green administered through the catheter was thereafter found in the pleural fluid. The continuous mechanical force of the catheter tip against the SVC wall was thus considered to be the cause of this life-threatening delayed hydrothorax.

Catheterization, Central Venous↗