Hepatic coma is the final stage of progressive hepatic insufficiency. Against the backdrop of severe intoxication caused by pathological or mechanical damage, or the death of a significant part of the liver as a result of trauma, necrosis or its removal, as a result of acute and chronic liver diseases, there are symptoms of severe damage to the central nervous system, as well as other organs and systems.
Hepatic coma is divided into two types: hepatocellular, which occurs as a result of severe damage to a significant part of the hepatic cells in viral hepatitis (Botkin's disease), intoxication with chemicals, poisoning by certain species of fungi and other pathological conditions of the body (diseases of an infectious and non-infectious nature ).
Shunt coma or "bypass" develops if the outflow of blood from the intestine passes not through the liver, but through the portocaval anastomoses. Maybe a mixed version of the hepatic coma, in which both the decay of the liver cells takes place and the portal system is shunted.
The main reasons for the development of hepatic coma include: alcohol, drug intoxication, drugs. Shunto who can be provoked by ingestion of protein-rich foods. A predisposing factor for the development of hepatic coma is the poisoning of ammonium derivatives and aromatic amino acids, the formation of non-toxic products from them occurs precisely in the liver.
The hepatic coma develops gradually: the patient has a feeling of inexplicable anxiety, anguish, apathy, euphoria. There is a slowing of thinking, disorientation, sleep disorder in the form of activity at night and insuperable sleepiness during the day. Shunt coma is characterized by transient disorders of consciousness. Then the symptomatology is aggravated: the mind becomes confused, the patient moans or cries, at times reacts to external stimuli (pain upon palpation of the liver). Often observed jerking of the muscles of the face and extremities, trism (tonic spasm of the chewing muscles) of the jaw.
In the clinic there are meningeal symptoms of Kerning and Brudzinsky, a positive symptom of Babinsky, tendon reflexes are increased. There are specific symptoms: from the mouth "liver" odor, jaundice (may be absent with extensive necrosis of the parenchyma), tremor of hands.
Hemorrhagic syndrome is expressed by petechial (capillary, point) hemorrhages in the mucous membrane of the oral cavity and gastrointestinal tract.
In the abdominal cavity a free liquid accumulates - edematous ascites syndrome.
With extensive necrosis of liver parenchyma, severe pains appear in the right upper quadrant. The breathing of Chain-Stokes, Kussmaul, is developing.
The terminal stage is characterized by hepatic insufficiency with infection and the development of sepsis, the level of total bilirubin is increasing. After this, the deep coma itself develops. The patient becomes motionless, motor excitement ceases, sometimes convulsions are observed, the face is masklike. Pupils are dilated, do not respond to light.
There is areflexia, rigidity of the occipital muscles. Arterial blood pressure is sharply reduced, pulse is threadlike, heart sounds are deaf, tachycardia is increasing. Corneal reflexes go out, paralysis of sphincters, stopping of breathing occurs.
The clinical picture of the development of the hepatic coma is represented by three stages: precoma, which threatens the hepatic coma and the developed hepatic coma.
Precoma is characterized by impaired orientation, thinking, sleep disorder (drowsiness during the day and wakefulness at night).
At the stage of a threatening hepatic coma there is confusion. Attacks of excitement are replaced by drowsiness and depression. There is a disorder of coordination of movements, a tremor of fingers of fingers, speech disturbance.
For the developed hepatic coma is characterized by a complete lack of consciousness, rigidity of the occipital muscles and muscles of the extremities, pathological reflexes. Progression of jaundice, increased "liver" odor, the phenomenon of hemorrhagic diathesis. The body temperature rises, sepsis often joins. The oliguria develops and leukocytosis grows.
The outcome of a hepatic coma depends on the timeliness and intensity of the treatment started. If it is started at the first signs of the disease, then the chances of a favorable outcome of the disease are much greater. The success of the results depends on active complex therapy aimed at combating intoxication and improving the functional capacity of liver cells.