Blackwell Science, LtdOxford, UKJGHJournal of Gastroenterology and Hepatology0815-93192004 Blackwell Publishing Asia Pty LtdJanuary 2004191109112Case Report epatic

hydropericardiumTK Cheung et al. H

Journal of Gastroenterology and Hepatology (2004) 19, 109112

CASE REPORT

Hepatic hydropericardium
TING KIN CHEUNG, WILLIAM TAM, DYLAN BARTHOLOMEUSZ, HUGH HARLEY AND RICHARD JOHNSON

Department of Gastroenterology, Hepatology and General Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia

Abstract A 41-year-old man with chronic hepatitis C and cirrhosis presented with pericardial effusion and tamponade requiring pericardiocentesis. Nine liters of pericardial uid was drained with complete resolution of his ascites. He represented with recurrent pericardial effusions despite salt restriction and diuretic therapy. Subsequent radionuclide scans demonstrated a direct connection between the peritoneal and pericardial spaces. A pericardial window was formed but despite this there was recurrence of pericardial effusion and pleural effusion. The patient underwent orthotopic liver transplantation 7 months later and no recurrence of pleural or pericardial effusion was observed following transplantation. We believe this is the rst case report of pericardial effusion secondary to cirrhotic ascites and a communication between the peritoneal and pericardial cavities. 2004 Blackwell Publishing Asia Pty Ltd Key words: ascites, cirrhosis, hydropericardium, hydrothorax, pericardial effusion, tamponade.

CASE REPORT
A 41-year-old man presented with abdominal distention, left leg cellulitis and rigors. Past history included long-term intravenous drug use with multiple Staphylococcus aureus skin abscesses and chronic liver disease secondary to hepatitis C complicated by diuretic-resistant ascites. On clinical examination, he was febrile 38.5C with peripheral stigmata of chronic liver disease, tense ascites and peripheral edema with left leg cellulitis. Cardiorespiratory examination was unremarkable at that time with normal jugular venous pressure. Investigations included serum albumin 13 g/L, bilirubin 14 mol/L, alkaline phosphatase (ALP) 87 U/L, gamma-glutamyl transferase (GGT) 20 U/L, alanine aminotransferase (ALT) 25 U/L, creatinine 0.13 mmol/L and urea 14.2 mmol/L. Urinalysis showed the presence of blood, protein and casts and there was signicant proteinuria of 1.54 g/24 h. Hepatitis C RNA polymerase chain reaction (PCR) was positive with genotype 3. Chest Xray showed small bilateral pleural effusions and slight cardiomegaly. Renal biopsy conrmed the presence of

mesangiocapillary glomerulonephritis with minimal scarring. Liver biopsy showed chronic hepatitis with cirrhosis. The ascites was treated initially with sodium restriction, furosemide, spironolactone, and 4 L therapeutic paracentesis. The ascitic uid was discarded without biochemical analysis and the cellulitis was treated with intravenous ucloxacillin. During this admission, the patient developed increasing dyspnoea. Clinical examination showed a raised jugular venous pressure with positive Kussmauls sign, 15 mmHg of pulsus paradoxus and recurrence of tense ascites. Chest X-ray showed cardiomegaly and a small right basal effusion. An echocardiogram demonstrated a large pericardial effusion with tamponade (Fig. 1) and 3.7 L of clear yellow uid was aspirated. A bubble study conrmed that the catheter was in the pericardial space. Over the next 24 h, 9 L of uid drained through the pericardial catheter and his dyspnoea rapidly improved. Echocardiogram the next morning showed no residual pericardial uid and normal cardiac function and clinical examination revealed that his tense ascites had

Correspondence: Ting Kin Cheung, Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Woolloongabba, Queensland 4102, Australia. Email: cheungtingkin@yahoo.com Accepted for publication 24 February 2003.

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Figure 1 An echocardiogram showing the large pericardial effusion, as indicated by the white arrow.

Figure 3 Anterior image at 120 min showing accumulation of macroaggregated albumin (MAA) above the diaphragm, as indicated by the arrow.

Figure 4 Tomographic anterior coronal image of the thorax at 150 min showing distribution of macroaggregated albumin (MAA) in the pericardial cavity, as indicated by the arrow.

Figure 2 Anterior images at 15 min showing distribution of macroaggregated albumin (MAA) in the peritoneal cavity below the diaphragm and into the scrotum associated with a large inguinal hernia.

completely resolved. Biochemical analysis of the pericardial uid showed protein 3 g/L and albumin 1 g/L with a serum albumin 10 g/L. No bacteria were seen and the uid culture was negative. The catheter was removed and the patient was discharged several days later. The patient represented one month later with dyspnoea and ascites reaccumulation despite diuretic therapy. Repeat echocardiogram showed recurrent pericardial tamponade. Three liters of clear pericardial uid was drained. Biochemical analysis again conrmed the presence of transudative uid with no bacterial growth. Ascitic uid albumin was 3 g/L. A radionuclide scan was performed. Serial images and a tomographic (SPECT) study of the thorax were performed following injection of 40 MBq of 99mTc macroaggregated albumin (MAA) into the peritoneal cavity in the left iliac fossa (Figs. 24). This demonstrated a connection between the peritoneal and pericardial cavities. He presented one week later with another episode of pericardial tamponade and 1.8 L of blood-stained pericardial uid was drained with a positive culture for methicillin resistant Staphloccocus aureus (MRSA). The patient was treated with IV vancomycin for 6 weeks.

Hepatic hydropericardium In view of the frequent recurrence of pericardial tamponade, a 4 cm pericardial window was formed via a left posterolateral thoracotomy. Histopathology of the pericardium demonstrated acute organizing brinous pericarditis with MRSA on culture. The patient was accepted for liver transplantation. He had two further admissions with increasing shortness of breath. One episode required a 320 mL pericardiocentesis and on the other occasion clinical examination and chest X-ray conrmed large bilateral pleural effusions requiring thoracentesis. He underwent orthotopic liver transplantation after a 6-month period of abstinence from intravenous drug use. No further occurrence of pleural or pericardial effusions has been observed following transplantation up until the last review, although his ascites was slow to resolve postoperatively.

111 age from the thoracic duct, and passage of ascitic uid from the peritoneal cavity to the pleural space via lymphatic channels in the diaphragm. We postulate that there are fenestrations of both diaphragm and pericardium to allow accumulation of ascitic uid in the pericardial cavity. There was no evidence on the radionuclide scan that the pericardial uid accumulation was via the pleural space. There was no past history of surgery or trauma to account for this communication. The secondary infection of the pericardial cavity with MRSA and brinous pericarditis did not occlude the communication completely. Patients with hepatic hydrothorax usually have advanced liver disease and they can be potential candidates for liver transplantation. Management should aim at relieving symptoms and minimizing complications until transplantation is performed. Sodium restriction, diuretic therapy, paracentesis, thoracentesis, peritoneovenous shunt, and transjugular intrahepatic portosystemic shunt (TIPS) have been proposed as management strategies and the same strategies could also apply to hepatic hydropericardium. Sodium restriction together with diuretic therapy reduce the amount ascites formation and thus pleural (and pericardial) effusion. In many patients, it leads to a worsening of renal function and electrolyte imbalance.8 Peritoneovenous shunt is often associated with infection, venous thrombosis, disseminated intravascular coagulation and mechanical complications.8,14 Furthermore, they may not be useful in hydrothorax and hydropericardium as peritoneal uid may tend to move to the lower pressure pleural and pericardial space rather than the higher pressure venous system. There have been encouraging results using TIPS in patients with hepatic hydrothorax and ascites and in those without ascites.6,10,15 Repair of the defects in the diaphragm either by open thoracotomy or video-assisted thoracoscopy techniques has been reported to be successful but is associated with high morbidity and mortality.9,12 In our patient, recurrent pericardial effusion and cardiac tamponade ultimately required surgical intervention and a pericardial window was formed with moderate success, although the patient still underwent a further pericardiocentesis prior to liver transplantation.

DISCUSSION
To the best of our knowledge, pericardial effusion as a result of a communication between the peritoneal and pericardial cavities secondary to cirrhotic ascites has not been previously reported. In our patient, there is a strong suggestion of a direct communication between the peritoneal cavity and the pericardial cavity. The drainage of 9 L of transudative pericardial uid coincided with the immediate disappearance of tense ascites and the results of the subsequent radionuclide scan conrm the presence of a peritoneopericardial communication. The ascitic uid initially accumulated in the pericardial cavity in preference to the pleural space. Nther et al.1 reported a case of chronic pericardial effusion in a patient undergoing peritoneal dialysis. A radionuclide scan demonstrated communication between the abdominal and pericardial cavities. The effusion resolved after cessation of peritoneal dialysis. Shah et al.2 reported that 17 of 27 patients (63%) with alcoholic cirrhotic ascites had mild to moderate pericardial effusion compared with 3 of 28 controls (11%). It was postulated that this was related to uid retention and the possibility of a direct communication was not explored. The ultrasonic denition of pericardial effusion in this series was only 16 mL of pericardial uid.3,4 Hepatic hydropericardium could arise from the same mechanisms as hepatic hydrothorax.413 Hepatic hydrothorax is dened as the presence of a pleural effusion in a cirrhotic patient in the absence of pulmonary or cardiac disease.11,13 Hydrothorax occurs in 410% of patients with cirrhosis.5 It is usually right sided and may occur without detectable ascites.13 The exact mechanism of hepatic hydrothorax is controversial.8 Most cases are probably due to direct passage of ascitic uid through minute defects in the diaphragm, for example, congenitally thin central tendinous portion of the diaphragm or acquired defects (Liebermans holes). The negative pressure of the pleural space compared with the peritoneal cavity favors the one-way transfer of uid across these defects. A number of other theories have been proposed, including hypoalbuminaemia and a decrease in the colloid osmotic pressure, leakage of plasma from hypertensive azygos veins, lymphatic leak-

REFERENCES
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6 Degawa M, Hamasaki K, Yano K et al. Refractory hepatic hydrothorax treated with transjugular intrahepatic portosystemic shunt. J. Gastroenterol. 1999; 34: 12831. 7 Kirsch CM. Cirrhotic hydrothorax and the Law of unintended consequences. Chest 2000; 118: 24. 8 Lazaridis KN, Frank JW, Krowka MJ, Kamath PS. Hepatic hydrothorax: pathogenesis, diagnosis and management. Am. J. Med. 1999; 107: 2627. 9 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: 137. 10 Mitamura K. Further experiments are necessary to determine whether transjugular intrahepatic portosystemic shunt is the denitive treatment for refractory hepatic hydrothorax. J. Gastroenterol. 1999; 34: 1546.

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