Cases reported "Hepatorenal Syndrome"

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1/45. Falsely low calcium measurements after high volume plasma exchange in a patient with liver failure.

    A 63-year-old male with lactic acidosis secondary to fialuridine-induced liver failure underwent seven plasma exchanges while awaiting orthotopic liver transplantation. Following plasma exchange, total serum calcium concentrations measured by conventional clinical chemistry methods were significantly lower than the elemental calciums determined by atomic absorption spectroscopy (P = 0.004). The difference in calcium measured by atomic absorption and by conventional methods correlated with serum citrate concentration (R = 0.77) Following the first exchange, the serum lactic acid concentration decreased from 10.2 to 4.4 mmol/L. These results suggest that plasma exchange may aid in the removal of metabolic products such as lactic acid in patients with liver failure. However, the accumulation of unmetabolized citrate may also result in falsely low total calcium measurements in some patients who undergo plasma exchange. ( info)

2/45. Alcoholic hepatitis-the case for intensive management.

    Alcoholic hepatitis is a common condition with a high mortality. Although treatment options for established alcoholic hepatitis are limited, many of the complications of this condition are preventable. This case report and discussion illustrate the important role of early diagnosis and intervention in this patient group. Important management points are stressed to aid physicians who may encounter this condition rarely. ( info)

3/45. 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. ( info)

4/45. 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? ( info)

5/45. Severe systemic reaction to (99m)Tc-methylene diphosphonate: a case report.

    We report an unusual severe systemic reaction that occurred in a woman after a (99m)Tc-methylene diphosphonate bone scan and for which no alternative explanation could be found. The bone scintigram showed diffusely increased uptake in the liver and kidneys accompanied by reversible dysfunction of these organs and dermatologic manifestations. We speculate that an immune-mediated mechanism may have caused this unusual reaction. ( info)

6/45. Terlipressin plus hydroxyethyl starch infusion: an effective treatment for hepatorenal syndrome.

    ornipressin is a vasopressin analogue that can cause potent splanchnic vasoconstriction. It has been shown that, in combination with albumin infusion, ornipressin is able to reverse hepatorenal syndrome. However, its clinical use is limited by possible severe ischaemic complications. In our case, a 47-year-old man received a right hemihepatectomy for cholangiocellular carcinoma. On post-operative day three, he developed hepatorenal syndrome with ascites, peripheral oedema and oliguria (250-500 ml/day). Serum creatinine was increased to 3.5 mg/dl. The patient was treated with terlipressin, another vasopressin analogue with fewer side effects than ornipressin, (1 mg every 4 h intravenously) and hydroxyethyl starch (500 ml/day). urine output increased to 3000 ml/day, serum creatinine decreased to normal range within 4 days and ascites and oedema disappeared. We hereby report the first case of successful treatment of hepatorenal syndrome with terlipressin and hydroxyethyl starch, which appears to be a safe and effective treatment. ( info)

7/45. Is spontaneous bacterial peritonitis an inducer of vasopressin analogue side-effects? A case report.

    In recent years, the use of vasopressin analogues in the treatment of hepatorenal syndrome has become an effective therapeutic strategy leading to improved survival and often allowing the completion of liver transplantation. Terlipressin, in particular, has proven to be safe and effective. Due to the limited number of patients treated so far, it is, however, difficult to draw any definite conclusions on the optimal dosage and on the occurrence of side-effects in these patients. The case is reported of an ascitic cirrhotic patient who developed spontaneous bacterial peritonitis followed by a type-I hepatorenal syndrome. Treatment with terlipressin boluses (0.5 mg/4 h) associated with albumin infusion was then started. The course of the disease was monitored by clinical and laboratory means. After 10 boluses of terlipressin, rectorrhagia and severe ischaemic complications involving the skin of the abdomen, lower limbs, scrotus, and penis, occurred. These ischaemic complications improved after terlipressin withdrawal, while renal failure evolved leading to the patient's death. This case report shows that, in patients with type-I hepatorenal syndrome, the use of terlipressin, even at low dosages, may induce life-threatening ischaemic complications and, moreover, suggests that the recent occurrence of spontaneous bacterial peritonitis, even if properly treated, may significantly increase the risk of major ischaemic complications. ( info)

8/45. Combined treatment of liver failure and hepatorenal syndrome with orthotopic liver transplantation.

    hepatorenal syndrome (HRS) is a severe complication of liver failure with high mortality. The pathogenesis of this reversible functional renal failure is not yet clearly understood. Diagnosis is based upon the association of clinical and biological criteria. A patient was admitted to our institution for severe liver failure secondary to an exacerbation of cirrhosis, where he developed a fulminant hepatorenal syndrome. Both, the renal and hepatic failure were successfully treated by orthotopic liver transplantation. Special attention was paid to the immunosuppressive treatment with cyclosporine whose use, we believe, should be delayed until function has partially recovered. ( info)

9/45. calciphylaxis associated with acute, reversible renal failure in the setting of alcoholic cirrhosis.

    We describe a case of calciphylaxis in a 47-year-old man with alcohol-induced end-stage liver disease and acute renal failure secondary to hepatorenal syndrome. Possible contributing factors included transiently impaired renal function, protein c and S deficiencies, elevated calcium-phosphate product, hyperphosphatemia, low serum albumin, repeated albumin infusions, and elevated alkaline phosphatase level. ( info)

10/45. A case of budd-chiari syndrome secondary to multiple thrombogenic conditions: a case report and review of literature.

    This report describes a case of budd-chiari syndrome caused by latent polycythemia vera and factor v Leiden mutation. This syndrome usually occurs due to thrombosis of hepatic veins or membranous obstruction of inferior vena cava. The most common reasons for thrombosis are manifest polycythemia vera and the other prothrombotic conditions. Recently, latent polycythemia vera and factor v Leiden mutation have been reported in increasing frequency. In this report, we aimed to emphasize that all prothrombotic conditions must be evaluated while investigating the etiology of budd-chiari syndrome, including latent polycythemia vera and factor v Leiden mutation, and appropriate antithrombotic and surgical therapies must be performed without delay. ( info)
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