Hepatic encephalopathy

Description:

Hepatic encephalopathy is a complex often reversible in initial and the irreversible mental and neuromuscular disturbances in a final stage caused by a heavy liver failure.

Symptoms of Hepatic encephalopathy:

Acute hepatic encephalopathy develops at fulminantny and toxic hepatitis in such short time that it is difficult even to record clinical manifestations. Brightly there passes the excitement phase, the delirium or maniacal states is sometimes observed. Involuntary multiple twitchings of muscles which are a coma harbinger can be noted. The clapping tremor comes to light seldom. The condition of the patient worsens, intoxication, jaundice accrue, appetite disappears, the hiccups, nausea, vomiting join, body temperature increases, hemorrhages appear. When progressing hepatic encephalopathy visual and auditory hallucinations, dizziness, faints join, the speech is slowed down, stereotype of answers is observed. There are pains in right hypochondrium, the liver decreases. The last sign also as well as "a hepatic smell" from a mouth - the most terrible harbinger of a coma. To the terminal period of hepatic encephalopathy confusion of consciousness, motive and speech concern, acoustical, visual and tactile reactions are characteristic. The deep coma develops to a galopiruyusha and is complicated by the disturbances menacing for life in many bodies and systems. In an agonal state squint, disappearance of pupillary reflexes and a cerebrate rigidity are observed, the hyperthermia and a hyperventilation are possible. The sudden beginning, the short and extremely heavy current lasting from several hours to several days are characteristic of acute hepatic encephalopathy.

Subacute hepatic encephalopathy is characterized by passing psychological disturbances, the shown decrease in memory, a depression, drowsiness, sleeplessness, concern, excitability, a dysarthtia. At inspection the tremor and a diskoordination of small movements come to light, by the letter handwriting uneven. The patient is apathetic, simple calculations are difficult to him, ability of mental arithmetic is limited. In several days of change become more explicit. Reaction to irritants is slowed down, the clapping tremor attracts attention, the muscle tone is broken, the movements look slowed down, the ataxy sometimes develops. Further loss of orientation in time joins, retrograde amnesia, drowsiness, a disorientation in time and space develops. Then the hyperreflexia, pyramidal symptomatology (Babinsky's symptom, etc.), muscle tension, a stupor join; later consciousness and reactions to painful incentives disappear, breath becomes noisy and frequent. Subacute hepatic encephalopathy differs from acute generally in duration of development of symptoms and the slowed-down progressing in a coma (during 1-2 weeks). An example of such encephalopathy is cirrhosis in an end-stage.

Chronic hepatic encephalopathy is observed preferential at patients with cirrhosis with portal hypertensia. Allocate chronic recurrent and continuously current encephalopathy.

Reasons of Hepatic encephalopathy:

This syndrome most often develops at the chronic liver failure characteristic of late stages of cirrhosis, and also at the acute liver failure caused by a massive hepatic necrosis at patients with fulminant forms of an acute viral hepatitis, a syndrome to Reja, the heavy acute alcoholic hepatitis, acute toxic hepatitises caused by medicines, food or industrial poisons and at patients with endogenous toxic hepatoses - after operation of shutdown of a small bowel and at an acute fatty liver of pregnant women. At cirrhosis hepatic encephalopathy as a prestage of a hepatic coma should be considered as an independent clinical syndrome while psychological disturbances at patients with cirrhosis are observed for many months and even several years and are not transformed to a coma. Quite often symptoms of hepatic encephalopathy under the influence of treatment decrease or completely temporarily disappear for short or long term.

Treatment of Hepatic encephalopathy:

The standard approach to treatment - elimination and the prevention of a giperammoniyemiya for what there are several ways: a protein-free diet, enemas, antibiotics (for example, Neomycinum, 1 g in 3 times a day) for suppression or destruction of the bacteria forming urease, lactulose reception  (30-50 ml in 3 times a day) - the osmotic laxative acidifying contents of a large intestine. In some cases transplantation of a liver is effective.