Cases reported "Hepatorenal Syndrome"

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1/5. Successful treatment of hepatic hydrothorax with octreotide.

    Hepatic hydrothorax is a rare complication of cirrhosis. Controlling ascites formation is the goal of therapy. We report the case of an adult patient presenting with alcoholic cirrhosis who developed first a symptomatic hydrothorax, refractory to diuretics and fluid and sodium restriction, and then an hepatorenal syndrome. Treatment consisted of chest tube insertion and 5 days' intravenous infusion of octreotide. Complete clinical and biological data were reviewed. octreotide administration resulted in an increased urinary outflow and sodium output, concomitant with improved renal function. The patient has been free of symptoms after discharge from hospital for a follow-up period of 5 months. This observation raises interesting issues regarding the possible utility of splanchnic vasoconstrictors, reducing portal hypertension, in the treatment of refractory hepatic hydrothorax.
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2/5. Cases from the Osler Medical Service at Johns Hopkins University.

    A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen.On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. urinalysis revealed an elevated specific gravity and numerous muddy granular casts. hepatitis a, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm.What is the diagnosis?
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3/5. hepatorenal syndrome: resolution of ascites by continuous renal replacement therapy in an alcoholic coinfected with hepatitis b, C, and human immunodeficiency viruses.

    A 39-yr-old male with hepatorenal syndrome type 1 and refractory ascites was treated with continuous renal replacement therapy (CRRT) resulting in clinical improvement. He was positive for antibodies to hepatitis b, C, and human immunodeficiency viruses, and had a history of chronic alcohol and iv drug abuse. The patient had 4 hospital admissions during a 12-wk period. He first presented with advanced liver disease including pedal edema and a serum ammonia level of 56 micromol/L (reference range: 11 - 35 micromol/L). In subsequent admissions, he had asterixis, nausea, vomiting, jaundice, and worsening pedal edema. On his 4th admission, there was lethargy, tense ascites, decreased urinary output, bilateral edema of the lower extremities and scrotum, serum creatinine of 6.2 mg/dl (reference range: 0.6 - 1.5 mg/dl), and weight gain of 16 kg during the prior 8 wk. During the first 3 hospitalizations, he was treated with lactulose with slight improvement. On the 4th admission, he was started on low-dose dopamine (3 microg/kg/min) and 25% salt-poor albumin without clinical improvement. A pulmonary artery catheter was placed and hemofiltration by CRRT was performed for 5 days, with removal of 26.7 L of fluid and a net reduction of 11 kg of body weight. serum creatinine decreased to 4.2 mg/dl during CRRT and was 2.2 mg/dl at hospital discharge 2 weeks later. His PaO(2) improved from 66 to 78 mmHg and his systemic vascular resistance increased from 571 to 799 dyne.sec/cm(5). CRRT was effective in relieving severe fluid retention and producing marked clinical improvement. We suggest that CRRT should be considered for the treatment of refractory ascites including that caused by hepatorenal syndrome.
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4/5. Extensive white matter involvement in hemorrhagic shock and encephalopathy syndrome.

    Reported is a case of hemorrhagic shock and encephalopathy syndrome (HSE) with extensive white matter involvement. A three year old, previously healthy boy was presented with an acute onset of fever, loss of consciousness and convulsions. He had disseminated intravascular coagulation, metabolic acidosis, non-ketotic hypoglycemia and hepatorenal dysfunction. The computed tomography (CT) scan of his head on the second day of illness demonstrated symmetric, extensive low-density areas in the cerebral and cerebellar white matter. The child died on the 13th hospital day. A post-mortem histopathological examination of the liver revealed centrilobular necrosis and infiltration of fatty acid droplets. The concentrations of serum 2',5'-oligoadenylate synthetase and urinary neopterin were markedly elevated, indicating excessively activated cell-mediated immunity. This overproduction of inflammatory cytokines might play an important role in the pathogenesis of the brain lesion as well as in other clinical and laboratory manifestations. The patient had a decreased serum level of alpha l-antitrypsin, which may have been associated with the development of uncontrolled inflammation and coagulation disorder.
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5/5. Treatment with terlipressin as a bridge to liver transplantation in a patient with hepatorenal syndrome.

    hepatorenal syndrome is a rapidly lethal complication of cirrhosis. The present case provides further evidence of the efficacy of terlipressin in this context even with concomitant treatment with propranolol. A 56 year old male with HBV related cirrhosis developed renal failure characteristic of hepatorenal syndrome. He was also taking propranolol for primary prophylaxis of variceal bleeding. Terlipressin 6 mg/day was administered during haemodialysis and after 1 week plasma creatinine dropped from 6.2 to 2.8 mg%. Daily urinary volume, plasma sodium and natriuresis dramatically increased during the treatment. Discontinuation of the treatment led to a rapid relapse of renal failure (plasma creatinine from 1.8 to 2.2 mg%) and the drug was readministered until a successful liver transplantation could be performed 1 month after the beginning of the treatment. The patient has now a near normal renal function 3 months after transplantation.
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