Portosystemic encephalopathy

Called "portosystemic encephalopathy" (portal-systemic encephalopathy) Sherlock employees (1954) described the disease of the nervous system that occur in patients with diffuse liver diseases, especially cirrhosis. The development of this condition is due to the fact that nitrogen-containing substances pass liver or pass through it in unmodified form, and then get into the bloodstream and cause of brain impairment. Ammonia compounds can be formed of protein from food, blood, shed abroad in the stomach bleeding from varikozno expanded veins; known value in their education belongs abnormal microflora of the intestine. Nitrogen-containing toxic products can bypass the liver parenchyma on natural or created operational by portocaval anastomoses or developed through intrahepatic messages between the branches of the portal and hepatic veins. In severe liver failure are not even required collateral circulation in order ammonia fell into total current circulation. The most subtle method of recognition of portosystemic encephalopathy is electroencephalography.
The main clinical sign of this syndrome is a disorder of consciousness, reflected in the periodically coming stupor and sometimes in a coma. Before the onset of ammonium coma changes occur in the psyche of a patient: agitation, behaviour, inadequate environment. There is a considerable tremor, involuntary movements of the fingers, taxicera gait, twitching facial muscles, often ptosis age, language, sometimes hanging out of his mouth. Reflexes and muscle tone, initially elevated, in the coma reduced, sometimes there comes full areflexia. Less likely to cause sleep disturbances, hallucinations, visual impairment and speech. The attacks can end abruptly: consciousness returns, the symptoms of nervous system lesions disappear. Sometimes the patient dies in a coma due to liver failure.
Unlike the so-called true hepatic coma associated with progressive loss of liver parenchyma, described the state of coma is not always, and if it is, then it is usually reversible. Kalk (1957) discerns even the so-called false hepatic coma with a loss of consciousness caused primarily by hypovolemia. Because ammonia poisoning and hypovolemia play a significant role in the Genesis of the so-called true hepatic coma, to distinguish one from the false hepatic coma is very difficult. Leevy, Davidson (1968) indicate that when a coma, which is a manifestation of portosystemic encephalopathy, is not observed rise of biochemical signs of liver failure, sometimes the latter are simply missing.