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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pattern of neurological disease seen in Ethiopian patients hospitalized in general medical wards in two hospitals in Addis Ababa is analyzed and discussed. Cerebrovascular disease, most commonly cerebral thrombosis, accounted for 45% of the neurological diseases seen. The second commonest disorder was bacterial meningitis (12%). Hepatic encephalopathy and intracranial haemorrhage, the latter commonly due to hypertension, were found to be the commonest causes of admission in coma.
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PMID:Neurological diseases in Addis Ababa, Ethiopia. 12 34

Extra-hepatic obstruction of the portal vein is a well known cause of hypertension in childhood and 55 out of the 97 patients (57 per cent) seen with this condition presented before they were 15 years old. However, nearly half our cases (43 per cent) presented in adult life. Haematemesis was the commonest mode of presentation in both the adult and childhood group although splenomegaly was common, especially in the children. The severity and frequency of haematemesis increased during puberty in the children. Twelve children and three adults have now not bled for between five and 30 years, 10 of them ceasing spontaneously and five following surgery. Intra-abdominal infection or septicaemia precipitated the portal venous obstruction in 38 patients (39 per cent), though the exact cause of such obstruction in patients who had no cirrhosis was obscure in about half the cases. Ascites was present in 18/51 (35 per cent) of the children and 24/35 (69 per cent) of the adults. Its presence was associated with an increased mortality (p less than 0.01). Nineteen out of 42 (45 per cent) patients with ascites also had portal-systemic encephalopathy. Twenty-four patients died, nine having presented during childhood, variceal haemorrhage was responsible for death in 19 and infection in five. Sixty-four patients underwent 114 operations for variceal haemorrhage. Mortality was greater in the surgical group compared with those managed conservatively. Surgery is therefore indicated only in the rare case where bleeding cannot be controlled by medical means.
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PMID:The aetiology, presentation and natural history of extra-hepatic portal venous obstruction. 53 23

Brain edema and intracranial hypertension are a major cause of death in fulminant hepatic failure. We have shown that brain water measured in rats after hepatic devascularization (portacaval anastomosis followed in 24 to 48 hr by ligation of the hepatic artery) increases with the progression of encephalopathy. In this study, we examined whether intracranial hypertension develops in this model of fulminant hepatic failure. Using a fiberoptic pressure transducer, intracranial pressure rose from 3.3 +/- 1.1 mm Hg to 23.7 +/- 2.7 mm Hg (mean +/- S.E.M.) by the time the corneal reflex was lost; intracranial pressure was unchanged in control rats. Immediately after ligation of the hepatic artery, intracranial pressure was normal and remained stable until the last hours of the experiment, when it progressively rose, suggesting a loss of intracranial compliance. In addition, sudden and short episodes of marked increases in intracranial pressure (greater than 50 mm Hg) not related to seizure activity markedly decreased cerebral perfusion pressure. Internal carotid artery blood flow, an indirect measure of cerebral perfusion, decreased 29% +/- 12% by the end of the experiment. The time elapsed from ligation of the hepatic artery until loss of the corneal reflex (range 340 to 940 min) was related to the change in cerebral perfusion pressure, suggesting that an increase in systemic arterial pressure at the time of the initial rise in intracranial pressure may result in an increased length of survival. In this animal model, widely used to study the pathogenesis of hepatic encephalopathy, intracranial hypertension invariably appears in the terminal phase of the course. The development of intracranial pressure waves may be an indication that brain herniation is imminent.
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PMID:Intracranial pressure waves and intracranial hypertension in rats with ischemic fulminant hepatic failure. 191 75

Hepatic encephalopathy is a major complication of portal-systemic shunts with an incidence ranging up to 52%. A small fraction of these patients are refractory to medical therapy. Shunt ligation and colonic procedures are the main surgical approaches. The goal of the latter is to diminish the colonic absorption of nitrogenous substances which are involved in the pathophysiology of hepatic encephalopathy. Six patients, whose average age was 55.7 +/- 2.6 years, were operated for severe postshunt encephalopathy requiring 4.3 +/- 0.9 admissions for a total duration of 76 +/- 26 days over 1-11 years. One patient had undergone a splenoral shunt and 5 had a portacaval shunt. One ligation of the shunt and 5 colon exclusions were performed. The average postoperative hospital stay was 21.5 +/- 3.9 days. The mean follow-up was 47 +/- 20 months. The patient with the shunt ligation remains free of encephalopathy 94 months after the procedure and has not bled from his esophageal varices. Among the 5 colon exclusion patients, there were 1 death and 3 complications. Three patients were completely relieved of their hepatic encephalopathy. One of those 3 died of a subarachnoid hemorrhage 28 months after the surgery. The fourth still needs medication to control a persistent, although improved, encephalopathy that required 2 further hospitalizations. Colon exclusion is a useful intervention in very selected cases. It has a lower operative mortality than total colectomy and the advantage over shunt ligation of not reestablishing hypertension in the portal system.
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PMID:Surgical treatment of severe postshunt hepatic encephalopathy. 199 94

Cerebral herniation is a leading cause of death in patients with fulminant hepatocellular failure. Classical signs of elevated intracranial pressure are often absent in these patients. A reliable noninvasive method by which the presence of cerebral edema could be determined is much needed. To assess the efficacy of computed tomography of the brain in this setting, we compared the radiographic findings to the intracranial pressure measured by an epidural monitor in patients with fulminant hepatic failure. Unfortunately, a considerable difference existed between the presence of cerebral edema diagnosed by computed tomography of the brain and elevation of the intracranial pressure. Our observations suggest that in patients with fulminant hepatic failure and advanced hepatic encephalopathy, computed tomography of the brain is of little value in detecting cerebral edema. Pressure monitoring is most important to establish the presence and guide the therapy of intracranial hypertension.
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PMID:Elevated intracranial pressure and computed tomography of the brain in fulminant hepatocellular failure. 199 33

The authors report a case of toxic hepatitis in a woman of 22 years of age in the third trimester of her first pregnancy treated by methyldopa for hypertension of pregnancy which was diagnosed at 33 weeks of amenorrhoea. The prodromal symptoms were mild and consisted of nausea, vomiting and rise in temperature and this phase was associated with febrile jaundice without pruritus and it was only associated with coagulation disorders in the third stage of labour. This was a case of mixed cytolytic hepatitis (ASAT x 3N) and cholestasis (x 1.5N). The outcome was fatal. The patient died three days after delivery following haematemesis and renal failure as well as hepatic encephalopathy. The main diagnostic feature was acute hepatic stasis in spite of the absence of pruritus and the presence of a raised temperature after hematolytic, viral and obstructive causes had been eliminated. Histology confirmed that there was toxic hepatitis. This aetiology was suggested by the timing of the symptoms after MD (methyldopa) had been taken. Elkington described methyldopa hepato-toxicity in 1969. Fatal cases in the literature were in patients who were over 40 years of age. Methyldopa is used in pregnant women because of its safety as far as the fetus is concerned. Mechanism by which it causes toxic hepatitis is a combination of abnormal metabolism (the cytochrome P450 chain produces an antigen) and an immune reaction in response to this antigen and these explain why such severe and potentially fatal forms of the condition exist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fatal toxic hepatitis in pregnancy. A discussion of the role of methyldopa]. 232 42

Acute fatty liver of pregnancy is a rare clinical entity unique to pregnancy that can lead to hepatic failure and encephalopathy and, if the diagnosis is delayed, to death for the baby and the mother. The characteristic histological picture demonstrates microvesicular fatty infiltration of hepatocytes. Acute fatty liver of pregnancy is a disease of the third trimester of pregnancy. The most significant clinical findings are nausea or vomiting, abdominal pain, jaundice, hepatic encephalopathy, increased transaminase levels, decreased platelet count, increased prothrombin time, and renal failure. Hypertension and proteinuria are common. Liver biopsy is not always necessary for diagnosis but may be useful in atypical cases. The primary therapy is early delivery and supportive care. Both the obstetric team and the medical consultants must have a high index of suspicion for this disease because early delivery is lifesaving and has transformed the prognosis for the mother and the baby. Collaboration between obstetricians and gastroenterologists is necessary to make the diagnosis and also to improve our understanding of this disease of unknown etiology.
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PMID:Acute fatty liver of pregnancy: the hepatologist's view. 805 22

Oesophageal varices are abnormally dilated veins that develop beneath the mucosa of the lower oesophagus and upper stomach and cause profound gastrointestinal haemorrhage associated with a high mortality. Varices develop in the presence of protal hypertension, which, in Europe and the USA, is most commonly due to alcoholic cirrhosis of the liver. Alcoholic cirrhosis develops in 10-20% of chronic ethanol abusers as a result of prolonged hepatocyte damage, leading to centrilobular inflammation and fibrosis. The net effect on the portal venous system is an elevation of resistance, and/or increase of inflow, producing portal hypertension, and the development of collateral channels in the form of varices. Such parenchymal liver disease also causes ascites, clotting deficiencies, secondary malnutrition and hepatic encephalopathy, all of which contribute to the high mortality associated with variceal haemorrhage. Variceal bleeding is more likely to occur when the varices are large, long and numerous, with surface red markings, and may be precipitated to respiratory tract infection, non-steroidal anti-inflammatory drugs, alcohol, or may occur spontaneously. Once identified by endoscopy, the aims of management are to control the haemorrhage, to prevent recurrent haemorrhage, and to treat the underlying cause of portal hypertension. Attention to nutrition and long-term rehabilitation are particularly important in those alcoholic cirrhotic patients who survive.
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PMID:Alcohol and oesophageal varices. 855 40

Surgical porto-caval anastomosis and percutaneous intrahepatic porto-caval shunt are effective in the management of bleeding esophageal varices but are associated with liver failure and a high incidence of encephalopathy. The neurochemical consequences of ammonia detoxification may be important with regard to the development of hepatic encephalopathy. Maintenance of splanchnic venous hypertension leads to less post-shunt hepatic encephalopathy because of diminished absorption of ammonia. Results of medical treatment of hepatic encephalopathy are contradictory. However, mortality and controversial results of surgical treatment in hepatic encephalopathy restrict its indications to a small number of patients. Prevention of hepatic encephalopathy begins with the selection of patients for surgical or percutaneous shunting.
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PMID:[Physiopathology and surgical treatment of hepatic encephalopathy after porto-caval anastomosis]. 857 64

Intrahepatic cholestasis of pregnancy is a relatively common disease. It has an unknown etiology and may have a recurrent pattern. It commonly occurs in the 2nd-3rd trimester and characteristically presents with pruritus, jaundice and abnormal liver function tests. There is also an increased risk of preterm delivery and of cesarean section. Both maternal and neonatal prognosis is generally good. We describe a case of intrahepatic cholestasis of pregnancy with an atypical presentation and outcome. Our patient presented with acute renal and hepatic failure with hepatic encephalopathy, DIC and hypertension which was the cause of the fetal death in the third trimester of the pregnancy.
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PMID:[Intrahepatic cholestasis of pregnancy. A benign disease?]. 900 89


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