Hepatic encephalopathy
From Medical-Wiki
Hepatic encephalopathy (HE) is a form of altered consciousness that occurs in patients with acute or chronic liver disease. It is primarily characterized by changes in personality, consciousness, and neuromuscular function. The very earliest manifestations include reversal of sleep pattern, apathy, hypersomnia, irritability, and personal neglect. This may progress to delirium and eventually coma.
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Possible physiological origins of hepatic encephalopathy
On autopsy, Alzheimer type II astrocytosis has been found in the brains of patients who died in hepatic coma. PET scans have demonstrated a significantly decreased glucose utilization in the cerebral cortex and concomitant increased utilization in the thalamus, caudate lobe, and cerebellum. These findings suggest that there is a state of hypometabolism responsible for HE.
It has not been possible to identify any single cause for this hypometabolism. The assumption is that it is multifactoral. One of the suggested processes is accumulation of brain toxins produced in the gut. Ammonia may influence the blood brain barrier allowing these toxins to cross into brain.
A second process is an alteration in amino acid composition. This leads to an accumulation of “false” transmitters.
The final process is increase of neuroinhibitory substances, such as manganese, monoamines, or endogenous opiates. [1]
Diagnosing hepatic encephalopathy
Neurlogical signs
The diagnosis of HE is clinical. The progressive form of the disease is rather easy to recognize—a gradual decrease in the level of consciousness (from lethargy to somnolence to stupor and, eventually, coma), impairment of intellectual capacity (eg, reasoning, orientation), and progressive neurologic deficits.
The subclinical form may require a more subtle interpretation of neurological signs, but there is no pathognomonic sign or finding.
Specific neurologic signs may include hyperreflexia, rigidity, myoclonus and asterixis. It should be noted that asterixis is not a specific sign of hepatic encephalopathy — it may occur in a variety of other forms of metabolic encephalopathies. The severity of the encephalopathy may be classified as acute, acute recurrent, chronic recurrent and chronic permanent encephalopathy.
Laboratory findings
Laboratory work should be done to exclude other causes, but there is no specific test for hepatic encephalopathy. An elevated serum ammonia is a common finding but by no means present in all cases. It does not correlate with the degree of derangement. Cerebrospinal fluid is often normal although it may show an elevated protein with increased GABA levels.
Lumbar puncture and CT scanning are appropriate to rule out other disease processes. The EEG shows a slow, triphasic wave activity over the frontal areas—a nonspecific finding. [2]
Treatment for hepatic encephalopathy
The goal of therapy is to decrease intestinally derived toxins produced by excessive bacterial activity and increased formation of ammonia. There are a number of possible treatments based upon the suspected pathophysiology, but none are supported by large studies. [3]
