The hepatic coma is a severe condition of central nervous system depression and its functions associated with disorders in the circulatory system that arise due to severe liver failure, due to a significant drop in the portal blood system.
Hepatic coma, as a rule, occurs under the influence of heavy intoxication on the body, as a result of mechanical damage to the integrity of the liver or the death of the majority of the body cells, as a result of various diseases, acute and chronic. On a share of the patients who have got in a hospital with signs of a hepatic coma, it is necessary about 1/3 patients in the age of till 40th years. Everyone without exception has a history of liver failure.
Causes of hepatic coma
The rate of onset of a pathological condition is directly proportional to the degree of damage to the central nervous system. Not the least role is played by such toxins as ammonia, aromatic acids, phenolic derivatives. These substances affect the brain in a toxic way, which leads to a reduction in energy costs, damage to the neurotransmitters, and a change in the membrane potential. And if a disturbance of the water-electrolyte balance is observed, as in the case of dehydration, their effect is enhanced. The formation of ammonia from urea is carried out by microorganisms in the small intestine. His final metabolism is always in the liver and ammonia should not be determined in the blood.
Hyperaminoacidemia and hyperammonemia are explained by the development of portal anastomoses in patients with a history of liver cirrhosis , which leads to the inability of liver cells to synthesize urea. Therefore, the accumulation of degradation products in the body is of great importance for the development of the pathological state, which leads to metabolic acidosis , with a further transition to alkalosis .
According to this, doctors classify the causes of hepatic coma development into endogenous and exogenous.
Endogenous hepatic coma occurs in individuals who have recovered from acute viral hepatitis, or the so-called Botkin disease, which causes necrosis of liver tissue. The endogenous cause can also be the use of large doses of alcohol, the abuse of drugs or the consumption of poisonous fungi. These include mechanical causes, such as acute liver vein thrombosis in the acute stage, schistosomiasis or an error during the operative ligation of the hepatic artery. Less common are hepatosis of pregnant women, liver cancer , hemotransfusion of blood incompatible by group affiliation and others.
Exogenous hepatic coma suffer patients with cirrhosis of the liver aggravated by processes of circulatory disturbances in the portal vein. Mixed hepatic coma on etiology is relevant when combined and those and other factors.
Symptoms of the hepatic coma
The clinic grows most often slowly, but in a small percentage of cases in patients suffering from cirrhosis of the liver as a result of a history of hepatitis, the onset is acute.
Symptoms of a hepatic coma progress for 1-2 weeks. First, patients complain of loss of appetite, lack of taste and increased fatigue. There is a severe headache , patients sleep badly, note abdominal pains and intolerable skin itching . Sometimes bleeding occurs in the mucous membranes. Then the patient's clinical picture deteriorates sharply. There is a psychomotor agitation, complicated by epileptiform seizures, often accompanied by a twitching of certain muscle groups of the body.
In terms of the degree of expression of the expressive motor behavior, taking into account changes in the waves of the electroencephalogram, the following stages of the hepatic coma are distinguished:
♦ During the period of the prekom, the anxious state is characterized by a sense of wanton anguish and apathy. Thinking slows down, there are problems with falling asleep. The answers to the questions are adequate, others will know, but there is no concentration of attention, the patient can hardly solve even the most simple tasks for logic. There are no significant abnormalities on the electroencephalogram.
♦ The next stage is a menacing hepatic coma. There is an alternation of bouts of excitement, bouts of sleepiness and deep depression . Developed violations of hepatic-cell nature: a characteristic sweet-putrefactive smell of the mouth, jaundice of the skin and others. The clinical signs of hemorrhagic syndrome are clearly expressed: the accumulation of blood in the organs of the gastrointestinal tract and in the area of the mucous membranes of the oral cavity. The amplitude of the waves on the electroencephalogram is increased, the rhythm is slowed down to 7-8 oscillations per second.
♦ At the stage of the coma itself, complete absence of consciousness, pupils dilated, there is no reaction to light. There are clonic convulsions, in rare cases fibrillar paroxysmal contractions of muscles. The severity of the skeletal musculature is determined. The face of the patient resembles a mask - the nasolabial and frontal folds are smoothed, the ocular gap is wider, the corner is lowered at the mouth. The oppression of the respiratory center is manifested by the appearance of pathological respiration of the Biot or Kussmaul, which is a sign of acidosis. Cardiovascular changes are characteristic: pulse is quickened, blood pressure drops sharply, heart sounds are poorly heard, strange noises appear. The body temperature is increased, often sepsis is possible. It is possible that oliguria and leukocytosis of the blood develop. The electroencephalogram produces hypersynchronous delta waves that are replaced by an isoniazia.
Treatment of hepatic coma
For the appointment of adequate treatment, it is necessary to conduct differential diagnosis with cerebrovascular disturbances and neuropsychiatric disorders in patients with alcoholism before it starts.
"Hepatic" odor, an increase in the blood test of bilirubin, hemorrhagic diathesis and similar signs, more characteristic of the clinical picture of the hepatic coma in these cases is not observed.
If the diagnosis is correct, the patient begins treatment based on the stage of the coma with which he was hospitalized. In the precoma stage, the content of daily protein in the diet is limited to 50 g, and when the symptoms increase, it is completely excluded. Assign cleaning enemas and purgatives for the purpose of reducing intoxication. To suppress the intestinal microflora inside accept semisynthetic antibiotics of the penicillin group, as an option - Ampicillin at a dose of 6 g per day. Emergency treatment is carried out in the hospital or in the intensive care unit.
Treatment of the hepatic coma is aimed primarily at increasing the functional parameters of the organ, by balancing the water-electrolyte balance. Intravenous drip is prescribed 5% Glucose 800 ml solution with the addition of 30 ml Asparkam solution. A large dose of a hormone such as Prednisolone up to 1000 mg per day is required to prevent necrotic death of liver cells.
To normalize the functions of the body, prescribe 1% solution of nicotinic acid per 10 ml intramuscularly, 1% Ribaflavin solution to 3 ml intravenously, 5% solutions of vitamin B1 and vitamin B6, 5 ml each, intramuscularly.
Struggle with high acidity of blood is carried out by introducing a 4% solution of Sodium Chloride for intravenous drip injection in a volume equal to 500 ml, alkalosis is neutralized by the introduction of potassium preparations.
Of modern methods of treatment, hemosorption and plasmapheresis of drugs through the catheter in the umbilical vein are popular. With a strong excitation, Haloperidol is relevant for 1 g in enema, with clonic convulsions, Relanium is administered intravenously in 2.0 ml. Diuretics are strictly prohibited.
To prevent oxygen starvation of the brain and liver, inhalations with humidified oxygen are prescribed, oxygenated foam is injected into the stomach and a oxygenation of about 2 hours is performed in the pressure chamber.
With a favorable prognosis after the patient comes out of a coma, it is advisable to appoint a plentiful drink and a special diet enriched with carbohydrates, with a minimum amount of fats and proteins. According to the indications, symptomatic therapy continues: anticonvulsant, soothing, cardiovascular and other means.
If symptoms of DVS-syndrome are noted, it is necessary to administer Heparin, the amount of which is controlled by a coagulogram. Droperidol and Euphyllin are prescribed to improve blood supply to the liver. Proteolytic processes in the organ reduce Gordoks, Kontoikal, which are inhibitors of proteolytic enzymes.
If therapy remains impotent, hepatic failure develops, which leads to the need for extracorporeal dialysis. Liver transplantation in this case is questioned, since its effectiveness has not yet been proven.
Forecast of hepatic coma
It is important to understand that the prognosis is of great importance for those who study methods of treatment of extremely severe forms of hepatic coma, characterized by high lethality (about 80%). This can be explained by the fact that there is no treatment for the causes of this disease and the result depends on the regenerative capacity of the liver. With this in mind, it can be safely said that factors such as age, the period of time from the onset of jaundice to the first signs of coma, the parameters of the electroencephalogram, the intensity of the progression of neuropsychiatric signs, and others, give the right to formulate an initial prognosis.
With timely treatment begun, the prognosis of the hepatic coma is favorable, but if the history of chronic renal failure is unfavorable, since coma is capable of regression and is prone to relapse for several months. No less important is the depth of lesions, therefore at early stages there is a chance for complete recovery, and with the clinical signs of coma itself, this process is unfortunately irreversible.