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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic hydrothorax is a dreaded complication in patients with liver cirrhosis. Placement of chest tubes can alleviate respiratory distress, but patients often succumb due to excessive fluid and protein loss via the open drain. Our case illustrates that high-dose octreotide can strongly reduce hepatic hydrothorax drainage volume. This allows removal of the chest tube, which would otherwise not have been possible.
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PMID:Treatment of hepatic hydrothorax and reduction of chest tube output with octreotide. 1150 67

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.
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PMID:[Percutaneous intrahepatic portosystemic shunting as a treatment for refractory hepatic hydrothorax]. 1186 35

We report the first case of an adult presenting with respiratory symptoms caused by hepatic hydrothorax secondary to vitamin A intoxication. The patient was a 52-year-old woman who presented to the hospital with progressive dyspnea. Evaluation demonstrated mild elevation of her liver function tests, ascites, and a right pleural effusion. The patient consumed a variety of vitamins, including vitamin A. Her estimated vitamin A intake was at least 162,300,000 international units (IU) during 18 years. She dramatically escalated her dose the year before admission for a total acute dose of 98,550,000 IU, with a daily intake of 270,000 IU. The recommended daily allowance is 4,000 IU. A transjugular liver biopsy revealed histopathologic changes consistent with vitamin A toxicity: hypertrophy and hyperplasia of hepatic stellate cells, focal pericellular fibrosis, mild perivenular fibrosis, and minimal, predominantly microvesicular steatosis. Despite the absence of cirrhosis, pressure readings demonstrated portal hypertension. During her hospitalization, the patient's symptoms and biochemical profile improved. As the large and generally unregulated United States dietary supplement industry continues to grow, it is increasingly likely that individuals will present with the signs and symptoms of vitamin excess rather than vitamin deficiency. Physicians need to remain alert to the varied presentations and toxic manifestations of excessive vitamin use.
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PMID:Hepatic hydrothorax associated with vitamin a toxicity. 1187 12

Cryptogenic cirrhosis is a common cause of liver-related morbidity and mortality in the United States. Nonalcoholic fatty liver disease (NAFLD) is now recognized as the most common cause of cryptogenic cirrhosis. However, the diagnosis of cirrhosis in patients with NAFLD appears to be delayed compared with those with other chronic liver diseases and thus carries a higher mortality rate. This delay in diagnosis is illustrated in our case of a 53-year-old man who presented with hepatic hydrothorax and ascites, whose workup revealed cirrhosis due to NAFLD. Although a diagnosis of presumed NAFLD can be made noninvasively, a definitive diagnosis requires a liver biopsy specimen. A biopsy specimen is also important for detecting histologically advanced disease, which may be clinically silent and undetected by aminotransferases or diagnostic imaging. Although there are no proven treatments, recommendations for patients with NAFLD include avoidance of hepatotoxins and aggressive management of associated conditions, such as hypertriglyceridemia and type 2 diabetes mellitus.
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PMID:Nonalcoholic fatty liver disease: an underrecognized cause of cryptogenic cirrhosis. 1450 12

A hepatic hydrothorax is a pleural effusion that develops in a patient with cirrhosis and portal hypertension in the absence of cardiopulmonary disease. The pleural effusion is derived from ascitic fluid that enters the chest because of the negative pressure within the pleural space via defects in the diaphragm. The peritoneal-to-pleural flow of fluid can be demonstrated by nuclear scanning, even when the ascites is not clinically apparent. The pleural fluid usually has the characteristics of a transudate. However, an occasional patient with hepatic hydrothorax will develop spontaneous bacterial pleuritis manifest by increased pleural fluid neutrophils or a positive bacterial culture and will require antibiotic therapy. Treatment of the hydrothorax is directed at the underlying liver disease but a dyspneic patient can obtain relief from a thoracentesis or paracentesis. When medical therapy fails, liver transplantation is the treatment of choice. Both transjugular intrahepatic portosystemic shunting and thoracoscopic repair of diaphragmatic defects with pleural sclerosis can provide symptomatic relief, but the morbidity and mortality of these procedures are high because of the fragile nature of the patients.
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PMID:Hepatic hydrothorax. 1280 37

The majority of cirrhotic patients present dyspnea, but most of the time this is a consequence of ascites, hepatic hydrothorax or cardiopulmonary disease. Very few of these patients undergo the hepatopulmonary syndrome, an infrequent complication of chronic liver disease, especially when associated with portal hypertension and cirrhosis. Hepatopulmonary syndrome is characterised by dyspnea and, consequently, arterial hypoxemia, due to intrapulmonary vasodilation and shunting. The real pathogenesis of this vasodilation is still unknown, although many hypotheses have been suggested. Furthermore, no medical therapy appears to be really useful in the treatment of hepatopulmonary syndrome. At the present time, the only treatment that is efficacious for the resolution, or for the improvement of blood gas oxygenation abnormalities, is orthotopic liver transplantation.
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PMID:Hepatopulmonary syndrome. A review of the literature. 1285 33

Hepatic hydrothorax occurs in approximately 5 to 12% of patients with cirrhosis and portal hypertension. Various therapeutic modalities ranging from dietary and pharmacologic interventions to surgical approaches are available for the management of this condition. Treatment must be individualized based on the patient's response to conservative management as well as the severity of the underlying liver disease. Hepatic hydrothorax may be complicated by spontaneous bacterial empyema, which portends a poor prognosis with a mortality rate of up to 20%. All patients with hepatic hydrothorax should be evaluated for possible liver transplantation.
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PMID:Hepatic hydrothorax: pathophysiology, diagnosis, and management. 1467 28

Pleural effusion in patients with liver cirrhosis and intractable ascites is well known, but hepatic hydrothorax in the absence of ascites is a rare complication. We present the case of a 43-year old male, with a medical history of liver cirrhosis due to hepatitis C virus, who was admitted to the Pneumology Clinic for dyspnoea, worsening of general status and chronic asthenia. The pleural effusion, revealed on physical and laboratory examinations, persisted despite the therapy with diuretics and the frequent thoracocentesis. The thoracostomy followed by pleurodesis also failed. The pecularity of this case was the presence of refractory hydrothorax in the absence of ascites.
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PMID:Hydrothorax without ascites in liver cirrhosis. 1472 78

A 52-year-old man with history of post-hepatitic cirrhosis presented with ascitis and respiratory distress. Chest X-ray on admission showed a large right hydrothorax. Thoracentesis yielded a large volume of a clear transudate fluid. Peritoneal scintigraphy showed rapid migration of radiotracer into the right pleural cavity, confirming the abdominal origin of the pleural fluid and suspecting a large diaphragmatic defect. MR imaging study using ultrafast sequences confirmed the large diaphragmatic defect.
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PMID:Large diaphragmatic defect as the cause of hydrothorax in a cirrhotic patient: demonstration with peritoneal scintigraphy and magnetic resonance imaging. 1506 41

Hepatic hydrothorax in the absence of ascites is a rare complication of liver cirrhosis. A 56-year-old woman was referred to our hospital because of a massive pleural effusion on the right side, requiring continuous drainage. Although the patient was known to have chronic hepatitis C, she had no signs of hepatic failure including ascites. A laparoscopic examination revealed a nodular liver and a small volume of ascites in the peritoneal cavity. Indocyanine green sprayed into the intraperitoneal cavity was excreted from the pleural drain just after the spraying, indicating an intraperitoneal origin of the pleural fluid. Discontinuation of pleural drainage and an introduction of standard treatment for ascites due to liver cirrhosis (including restriction of salt intake and diuretic administration) resulted in a marked decrease of pleural effusion.
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PMID:Hepatic hydrothorax in the absence of ascites diagnosed by intraperitoneal spraying of indocyanine green. 1516 69


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