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Authors report a case of intraventricular hemorrhage with hepatic insufficiency. A 36-year-old man was admitted following the sudden onset of coma. For 10 years before admission he had suffered general fatigue and jaundice, which were treated with medication as acute hepatitis. On the day of admission he began to suffer from a severe headache. Within one hour he was comatose and began to have vomiting, followed by seizures characterized by tonic movement of the right extremities. Lumbar puncture showed an initial pressure over 400 mmH2O, with grossly bloody spinal fluid. Numerous hemorrhages were noted in both optic fundi. Bilateral carotid angiography demonstrated slight enlargement of left lateral ventricle. Computerized tomography revealed that the lareral, third and fourth ventricles were dilated. There were discrete areas of increased absorption coefficient with values measuring between 30 to 35 in the Hounsfield scale in all ventricles. Two burr holes in both frontal areas were performed. About 50ml of blood clot at left ventricle and 30 ml of blood clot with liquor at right ventricle were removed. The patient died 7 days after operation. Autopsy revealed clotted blood in the whole ventricular system, mainly in right anterior horn of lateral ventricle, and a markedly cirrhotic liver with hepatoma. In our review of the literature, the relationship between intraventricular hemorrhage and bleeding tendency caused by hepatic insufficiency was discussed.
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PMID:[Intraventricular hemorrhage with hepatic insufficiency--report of a case (author's transl)]. 23 Dec 14

A total of 60 patients were observed with acute hepatitis delta defined at examination of 200 adult subjects with acute HBsAg-positive hepatitis. Moderate and severe forms of the disease occurred more frequently, lethality reached 13.3%. An unfavorable prognosis was related to a short-term prejaundice period with intoxication (high body temperature, head ache, vertigo, recurrent vomiting, IgM antibodies presence in the serum at the height of the disease). No patients achieved cure within 9 months following the discharge from hospital. The process acquired the form of long-term convalescence with transformation into chronic hepatitis delta.
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PMID:[The clinical picture and outcome of acute delta infection]. 153 12

A retrospective study was done during 1984-1988 in the pediatric ward of Dr. Pirngadi Hospital revealing 41 cases of acute hepatitis, consisted of 61.0% boys and 39.0% girls. The majority of patients were below five years of age (68.3%). There were 37.1% cases with malnutrition. The common symptoms were fever, jaundice, vomiting and dark urine. On laboratory examination there were 10 cases with positive HBs Ag. Accompanying diseases were malnutrition, bronchopneumonia, anemia, bronchitis and pulmonary tuberculosis. A total of 63.4% of patients were healed, 29.3% discharged against medical advice and 7.3% died because of bronchopneumonia and hepatic coma.
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PMID:Acute hepatitis at the Department of Pediatrics, School of Medicine, University of North Sumatra/Dr. Pirngadi Hospital Medan. 189 96

Aprindine hydrochloride was administered IV and orally to 20 dogs with ventricular tachycardia. Seventeen of the 20 dogs had been unsuccessfully treated with conventional antiarrhythmic drugs. Fifteen of the 20 dogs converted to sinus rhythm after IV aprindine therapy, 4 dogs demonstrated marked slowing of their ventricular tachycardia, and 1 dog showed an increase in the rate of ventricular tachycardia. Emesis, ataxia, salivation, and nystamus were observed in 7 dogs after IV aprindine therapy. One dog developed clinical and laboratory evidence compatible with acute hepatitis.
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PMID:Aprindine for treatment of ventricular arrhythmias in the dog. 714 83

The clinical features, laboratory investigations and histopathology of 12 patients with idiopathic acute fatty liver of pregnancy are presented. Repeated vomiting, starting in the last trimester, was the cardinal symptom. Seven patients had proteinuria, hypertension and peripheral oedema before jaundice appeared. Caesarian section and induction of labour led to a lower than expected maternal mortality (33 X 3 per cent) and foetal mortality (66 X 7 per cent). There was a high incidence of twin and male births. Neutrophilia, thrombocytopenia and normoblasts were a uniform feature and uric acid levels were universally high. These findings may be useful in diagnosis in conjunction with liver function tests. Hepatic histology showed pathognomonic microvesicular fat in swollen hepatocytes with central nuclei and centrilobular distribution. However, a diffuse pattern and the presence of significant inflammation and fibrin deposits led to an initial misdiagnosis in two patients. Histology of fetal livers and five placentae was normal. Seven subsequent normal pregnancies occurred in four patients. Acute fatty liver of pregnancy may be confused with acute hepatitis or toxaemia on both clinical and histological grounds. Accurate diagnosis should lead to improved management and lessen maternal and fetal mortality. This justifies more intensive and urgent investigation of nausea, vomiting and jaundice in the last trimester of pregnancy.
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PMID:Idiopathic acute fatty liver of pregnancy in 12 patients. 715 26

A case of fulminant hepatitis with microvesicular steatosis resembling Labrea's fever, diagnosed in Vitoria (ES) is reported. The 16 year old boy presented with severe epistaxis, agitation, jaundice and hemorrhagic vomiting and died two days after admission to the emergency unit of the University Hospital. The disease started five days before with fever, myalgias, dark urine and jaundice and progressed with psychic agitation, torpor and coma. The liver and spleen were not palpable. HBsAg was negative in the serum. The autopsy showed acute hepatitis with lytic necrosis confluent in the midzonal and periportal areas with massive microvesicular steatosis in the remaining hepatocytes. Mononuclear cells predominated in the exudate. The reticulum showed condensation in the necrotic areas without typical bands of collapse. The portal tracts were edematous with mononuclear infiltration and mild bile duct proliferation. Absence of cholestasis. Except for the confluent midzonal and periportal necrosis this case showed several clinical and morphological aspects of the Labrea fever described from the East Amazon, demonstrating that the anatomical picture of this disease probably is not in related to a factor peculiar to the Amazon region.
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PMID:Labrea-like hepatitis in Vitoria, Espirito Santo State, Brazil: report of a case. 815 25

A 42-year-old female was admitted to a hospital, because of acute hepatitis A. Laboratory data were GOT 8210mU/ml. GPT 4650mU/ml, LDH 11860mU/ml, total bilirubin 4.7mg/dl, BUN 19.5mg/dl and creatinine 1.9mg/dl. Urinalysis showed proteinuria 3+ and occult blood 1+. Soon after admission, she suffered from anuric acute renal failure and was transferred to our hospital for hemodialysis. Her urine-volume was under 20 ml per day. Urinalysis showed proteinuria 4+, occult blood 1+ and casts. Laboratory data showed BUN 58.2mg/dl and creatinine 8.5mg/dl. She was treated by hemodialysis for 35 days, before recovering from renal failure. However, her renal function did not recover perfectly and her 24-hour creatinine clearance remained at 50ml/min after 6 months. Renal biopsy was performed on the 17th day after admission. Examination by light microscopy revealed the findings of acute tubular necrosis and examination by immunofluorescence antibody method was negative. Urinalysis of 8 patients with acute hepatitis A showed that all patients had proteinuria at the onset. Patients with acute hepatitis A have symptoms of appetite-loss, nausea, vomiting and/or diarrhea. These symptoms cause hypovolemia, and hepatic dysfunction causes discontrol of vasoactive hormones, which gives rise to disturbance of renal circulation. Subsequently, acute tubular necrosis and acute renal failure occur.
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PMID:[A case of acute hepatitis A associated with acute renal failure from the onset]. 823 Aug 22

Pericarditis is a frequent and serious complication of chronic uremia. The uremic pericarditis can get much improvement by aggressive heparin-free hemodialysis therapy. However, the presenting symptoms and signs are too nonspecific to identify at early stage. Cardiac tamponade is the late and fatal complication, and need the immediate & adequate management. A 35-year-old female patient suffered from nausea, vomiting and right upper quadrant dull pain in November 1993, and was admitted to a local hospital. Uremia (BUN: 210 mg/dl, serum Cr.: 13.2 mg/dl) and abnormal liver function (SGOT: 330 IU/L, SGPT: 449 IU/L) were found, then she received regular hemodialysis therapy. About 10 days later, acute exacerbation of liver function (SGOT: 2,488 IU/L, SGPT: 1,048 IU/L), consciousness disturbance and hypotension occurred during hemodialysis. She was referred to our ER immediately. At ER, she had been on comatous, shock state with pulseless electric activity. After resuscitation and serial evaluation, cardiac tamponade was diagnosed. Emergent pericardiocentesis and then bilateral partial pericardiectomy were done about 2 hours later. The pericardial effusion was bloody without evidence of malignancy, bacterial or TB infection. The pathology of pericardium revealed chronic inflammation only. HBsAg, Anti-HCV Ab, and anti-HAV IgM were undetectable. So the etiology of acute hepatitis was diagnosed as ischemic hepatitis. Her general condition and vital sign became stable thereafter. The liver function also improved rapidly. She was discharged one month later and received maintainance hemodialysis therapy and no evidence of recurrence till now.
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PMID:[Acute uremic pericarditis presented as cardiac tamponade with acute ischemic hepatitis: a case report]. 904 74

Ischemic hepatitis can occur as an acute episode in advanced congestive heart failure (CHF). The mechanism is massive necrosis of the central lobules resulting from acute hypoxia when low cardiac output further reduces oxygen supply, aggravating underlying congestion due to poor venous outflow. We describe a 70-year-old woman with congestive heart failure for 7 years who was admitted with jaundice, vomiting, abdominal pain and oliguria after an episode of hypotension. The diagnosis of ischemic hepatitis was established by a documented episode of severe hypotension, followed by elevation of serum transaminases, a rise in serum bilirubin and LDH levels, prolonged prothrombin time and acute renal failure. Other causes of acute hepatitis, such as a virus or drugs were excluded, and improved liver and renal function followed hemodynamic stabilization. We conclude that ischemic hepatitis should be considered whenever acute hepatitis follows a recent episode of systemic hypotension, especially in the context of concomitant CHF.
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PMID:[Ischemic hepatitis in congestive heart failure after an episode of hypotension]. 915 12

Most cases of acute hepatitis are caused by hepatitis viruses A, B or C. Diagnosis rests on the risk factor history and serological tests. In seronegative cases, consider other agents, such as Epstein-Barr virus and cytomegalovirus, drug reactions and autoimmune hepatitis. Hepatitis A and B can be prevented by appropriate use of highly effective, safe vaccines. Acute liver failure is an uncommon, devastating complication of acute viral hepatitis; continued vomiting, prolongation of prothrombin time and clouding of consciousness are indications for urgent transfer to a liver transplant unit. Hepatitis A is a simple, enterically transmitted illness that does not cause chronic hepatitis. 95% of adults recover from acute hepatitis B, whereas infection with hepatitis B virus acquired in childhood usually becomes chronic.
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PMID:Acute viral hepatitis. 964 Mar 8


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