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

The clinical course of a 26 year old female patient with acute liver necrosis and coma due to hepatitis B is reported. The disturbances of conciousness had improved. The patient survived 41 days after the beginning of the coma and developed liver cell regeneration and an acute post-hepatitic liver cirrhosis. As a grave complication a septicemia with aspergillus was observed. The patient died because of gastro-intestinal hemorrhage. At autopsy there were no signs of brain edema. The treatment consisted in: daily infusions with coenzyme A, nicotinamid-adenin-dinucleotide, alpha lipoic acid and cocarboxylase to improve the metabolic disorders and the clinical picture; mannitol intravenously to prevent and to treat cerebral edema; 33 charcoal-hemoperfusions to remove toxic substances of acute liver failure. Treatment of the aspergillus infection with 5-fluorocytosine and amphotericine B and infusion of concentrated ascites led to a decompensation of liver functions. From this observation the following conclusions can be drawn: after an acute viral hepatic necrosis, new synthetic functions and improvements of the disturbed intermediary metabolism in regenerated liver-cells can eventually be seen only after twenty-four to thirty days. With systematically applicated mannitol infusions it is possible to treat cerebral edema effectively.
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PMID:Treatment of fulminant hepatic failure with infusions of Co-factors and mannitol and charcoal-hemoperfusions during Forty-one days. 50 61

A 42-year-old male was admitted with subarachnoidal hemorrhage. Dexamethasone 224 mg was used to reduce brain edema. His operation was successful without blood transfusion. No remarkable signs and symptoms were found except HBsAg positive and mild GPT elevation during his admission. He was discharged on the 33rd day. But 2 weeks later, he felt general fatigue and became worse day by day. He was re-admitted on the 75th day. Several therapies were given but he died of hepatic failure on the 85th day. The autopsy showed liver cirrhosis with massive necrosis. We believed that the steroid-withdrawal-phenomenon caused excessive immunological response and this process caused his hepatic failure leading to death.
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PMID:[A case of HBsAg positive liver cirrhosis who died after withdrawal of steroid]. 140 69

We studied 18 formalin-fixed brains using MRI, and correlated our data with subsequent gross and microscopic examinations. 9 of our patients died from brain diseases (stroke due to infarction 4, stroke due to hemorrhage 1, encephalitis 2, head injury 1, brain tumor 1). 9 of our patients died from non-CNS diseases (stomach cancer 1, colon cancer 1, liver cirrhosis 1, myocardial infarction 2, trauma 4). In MRI of postmortem brain, T1WI and T 2WI was able to clearly show the myelination process of brainstem, basal ganglia, internal capsule and optic radiation in a 2 months-old-boy. The findings were similar to MRI of live infants. In normal adult postmortem brains, the T1WI showed a relatively low signal intensity of white matter as compared to gray matter. The pictures were similar to proton density images, not T1WI of normal adult brains. The reason why the signal intensity of the white matter was lower than the gray matter may have been due to lysis of lipid of myelin sheath in the formalin solution. Postmortem MRI was able to detect the periventricular hyperintensity (corresponding to arteriosclerotic encephalopathy) and subcortical hyperintensity spots (which corresponding to the widening of the Virchow-Robin perivascular space because of arteriosclerosis) in the brains of our elderly patients. Postmortem MRI detected the intracerebral hemorrhage, which appeared as a dark signal in both short and long TR images. However, MRI did not show blood in the ventricles, sulci, or superficial hemorrhages in the cortex of brain. Brain edema was revealed in the postmortem MRI and appeared as low signal intensity in T1WI and hyperintensity in T2WI. It was associated with a significant mass effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[MRI of postmortem brains]. 820 68

Hepatic encephalopathy is a well-recognized clinical complication of chronic liver disease. About 30% of patients with cirrhosis die in hepatic coma. Hepatic encephalopathy can occur in patients with fulminant liver disease without evidence of portal-systemic shunting. These patients have increased intracranial pressure and brain edema with a deleterious clinical course and poor prognosis unless liver transplantation is available. The pathogenesis of portal-systemic hepatic encephalopathy probably is multifactorial, although the predominant causative agent appears to be ammonia. The molecular basis of neurotoxicity of ammonia or other agents implicated in the condition is poorly understood. Therapy includes timely recognition and correction of precipitating factors. Once the condition is manifested, standard therapy is acute administration of lactulose, a disaccharide that is undigested in the small intestine. Its beneficial action is not fully understood. The use of oral antibiotics and BCAAs is of some benefit in patients who do not respond to lactulose. Limitation of protein in the diet may be useful for short periods but is not recommended for long-term use because of potential worsening of already poor nutrition. Several experimental therapies based on potential pathogenetic mechanisms have not resulted in improved outcomes over standard therapy with lactulose. However, future research will likely focus on the correction of alterations in neurotransmission. It is hoped that newer therapies will provide protection from the putative neurotoxins that cause secondary defects in neurotransmission.
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PMID:Hepatic encephalopathy. Metabolic consequence of cirrhosis often is reversible. 1127 94

In patients with severe liver failure, brain edema is a frequent and serious complication that may result in high intracranial pressure and brain damage. This short article focuses on basic physiologic principles that determine water flux across the blood-brain barrier. Using the Starling equation, it is evident that both the osmotic and hydrostatic pressure gradients are imbalanced across the blood-brain barrier in patients with acute liver failure. This combination will tend to favor cerebral capillary water influx to the brain. In contrast, the disequilibration of the Starling forces seems to be less pronounced in patients with cirrhosis because the regulation of cerebral blood flow is preserved and the arterial ammonia concentration is lower compared with that of patients with acute liver failure. Treatments that are known to reverse high intracranial pressure tend to decrease the osmotic pressure gradients across the blood-brain barrier. Recent studies indicate that interventions that restrict cerebral blood flow, such as hyperventilation, hypothermia, and indomethacin, are also efficient in preventing edema and high intracranial pressure, probably by decreasing the transcapillary hydrostatic pressure gradient. In our opinion, it is important to recall that rational fluid therapy, adequate ventilation, and temperature control are of direct importance to controlling cerebral capillary water flux in patients with acute liver failure. These simple interventions should be secured before more advanced experimental technologies are instituted to treat these patients.
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PMID:Brain edema in liver failure: basic physiologic principles and management. 1242 10

Hepatic encephalopathy (HE) in acute liver injury signifies a serious prognosis. Brain edema and intracranial hypertension are major causes of death in this syndrome. Comparison of HE in acute liver failure (ALF) with that of cirrhosis allows recognition of important differences and similarities. A key role for ammonia in the pathogenesis of both HE and brain edema is now firmly supported by clinical and experimental data. Additional factors, such as infection, products of the necrotic liver, and synergistic toxins, may contribute to an altered mental state. A low plasma osmolarity, high temperature, and both high and low arterial pressure may affect brain water content. A combined derangement of cellular osmolarity coupled with cerebral hyperemia can explain the development of brain edema in ALF. Increasingly, study of the mechanisms responsible for brain swelling provides critical information for understanding the pathogenesis of HE.
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PMID:Pathogenesis of hepatic encephalopathy in acute liver failure. 1452 79

Hepatic encephalopathy and brain edema are important complications in the course of a patient with acute liver failure. Presumed unrelated for many years, increasing evidence suggests that an increase in brain water is seen in all forms of hepatic encephalopathy. Ammonia, traditionally linked to the pathogenesis of hepatic encephalopathy, plays an important role in the increase in brain water. In acute liver failure, an osmotic disturbance in the astrocyte, in combination with an alteration of cerebral blood flow results in overt brain edema and intracranial hypertension. In cirrhosis, magnetic resonance techniques indicate the presence of a brain osmotic disturbance. Several clinical factors modulate the development of brain swelling.
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PMID:Brain edema in acute liver failure. A window to the pathogenesis of hepatic encephalopathy. 1509 1

The clinical presentation of acute liver failure and hepatic encephalopathy (HE) in patients with cirrhosis differs significantly. The most serious neurological complication of acute liver failure is the development of devastating brain oedema. Therefore, intracranial pressure monitoring is urgently needed in these patients. Brain oedema is amplified by hypoglycemia, hypoxia and seizures, which are also frequent complications of acute liver failure. Therefore, these parameters must also be monitored. In contrast to acute liver failure in which cerebral dysfunction progresses rapidly, cognitive decline may be clinically undetectable for a long time in cirrhotic patients, until clinically overt symptoms such as psychomotor slowing, disorientation, confusion, extrapyramidal and cerebellar symptoms or a decrease in consciousness occur. Clinically, overt HE is preceded by minimal alterations of cerebral function that can only be detected by neuropsychological or neurophysiological measures, but which nevertheless interfere with the patient's daily living. Rapidly progressing spastic paraparesis (hepatic myelopathy) is a rare complication of cirrhosis. In contrast to HE, it does not respond to blood ammonia lowering therapies but must be considered as an indication for urgent liver transplantation. Cognitive dysfunction has recently been detected in hepatitis C virus (HCV)-infected patients with normal liver function. The patients presented with severe fatigue, cognitive dysfunction and mood disorders. Alterations in brain metabolites, as detected by magnetic resonance spectroscopy, indicated central nervous system alteration in these patients. In contrast to patients with HE, HCV-infected patients did not show motor symptoms or deficits in visual perception, but considerable deficits in attention and concentration ability.
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PMID:Neurological and neuropsychiatric syndromes associated with liver disease. 1625 35

The availability of an animal model is crucial in studying the pathophysiological mechanisms of disease and to test possible therapies. Now, there are several models for the study of liver diseases, but there still remains a lack of a satisfactory animal model of chronic liver disease with hepatic encephalopathy (HE) and abnormalities in nitrogen metabolism, as seen in humans. In rats, two models of chronic HE are widely used: rats after portacaval anastomosis (PCA) and rats with chronic hyperammonemia. The first one mimics the situation induced in cirrhosis by collateral circulation, and has the problem of the absence of hepatocellular injury. The model of hyperammonemia is useful to study the effect of ammonia as a brain toxic substance, but also lacks liver failure. Bile-duct ligation has been used to induce cirrhosis and could also be a model of HE, probably with the addition of a precipitant factor. An ideal model of HE in chronic liver disease must have liver cirrhosis and a precipitant factor of HE; it must also show neuropathological characteristic findings of HE, neurochemical alterations in the main pathways impaired in these complications of cirrhosis, and low-grade brain edema.
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PMID:Animal models in the study of episodic hepatic encephalopathy in cirrhosis. 1638 50

Brain water may increase in hepatic encephalopathy (HE). Diffusion tensor imaging was performed in patients with cirrhosis with or without HE to quantify the changes in brain water diffusivity and to correlate it with neuropsychological (NP) tests. Thirty-nine patients with cirrhosis, with minimal (MHE) or overt HE, were studied and compared to 18 controls. Mean diffusivity (MD) and fractional anisotropy (FA) were calculated in corpus callosum, internal capsule, deep gray matter nuclei, periventricular frontal, and occipital white matter regions in both cerebral hemispheres. The MD and FA values from different regions in different groups were compared using analysis of variance and Spearman's rank correlation test. In 10 patients with MHE, repeat studies were performed after 3 weeks of lactulose therapy to look for any change in MD, FA, and NP scores. Significantly increased MD was found with insignificant changes in FA in various regions of brain in patients with MHE or HE compared with controls, indicating an increase in interstitial water in the brain parenchyma without any microstructural changes. A significant correlation was found between MD values from corpus callosum, internal capsule, and NP test scores. After therapy, MD values decreased significantly and there was a corresponding improvement in NP test scores. Further analysis showed that MD values were different for different grades of minimal or overt HE. In conclusion, the increase in MD with no concomitant changes in FA in cirrhosis with minimal or early HE indicates the presence of reversible interstitial brain edema.
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PMID:Demonstration of interstitial cerebral edema with diffusion tensor MR imaging in type C hepatic encephalopathy. 1732 10


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