Hepatic encephalopathy: stages

Stage I (harbingers of coma, precoma I) is characterized by the following symptoms:

• Consciousness is preserved, patients complain of pronounced general weakness, lack of appetite, nausea, bitterness in the mouth, hiccups, pain in the right hypochondrium, dizziness, "flashing of flies" before the eyes, headache, tinnitus;
• patients adequately answer questions, recognize others, but periodically cease to navigate in time, in space (they may not understand where they are, do not call the day of the week, etc.);
• often there is excitement, fussiness, emotional lability, euphoria (they say they feel fine);
• impaired ability to concentrate attention, patients often repeat the same words, can not finish the sentence started;
• Sometimes patients commit unmotivated acts, look for non-existent items, etc .;
• patients with difficulty perform the simplest mental tasks (making mistakes when counting, adding up simple numbers). This is especially noticeable when performing a number-number test (the patient can not connect a group of numbers from 1 to 25 in 30 seconds);
• the coordination of small movements is violated, which is well revealed in the "written sample" (handwriting becomes fuzzy, incomprehensible);
• the sleep formula is broken (patients are sleepy during the day and suffer from sleeplessness at night);
• on the Glasgow scale, the score is 13-14;
• pupils dilated, pupillary reaction weakened;
• there are no changes on the electroencephalogram, some patients may have abnormalities (irregularity, disorganization, a tendency to increase the amplitude of the waves), a decrease in the reaction to opening the eyes;
• moderate hemorrhagic phenomena (skin hemorrhages, nasal bleeding) are possible.

Stage II (somnolentia, precoma II) is a more pronounced stage of hepatic encephalopathy, predicting the onset of the soporus. It is characterized by the following manifestations:

• excitability and euphoria of patients is replaced by apathy, a sense of anguish, doom, despair; patients are hindered, sleepy;
• when awakening, the consciousness is confused, the sick are disoriented in time, space, faces; the simplest commands are performed, but tasks that require attention (for example, an account) can not be performed;
• periodically the patients briefly lose consciousness;
• on the background of inhibition, lethargy, drowsiness, excitement, delirium, hepatic delirium, auditory and visual hallucinations, inadequate behavior, patients try to jump up, run, throw themselves out of the window, shout, scold, become aggressive;
• sometimes there are tonic spasms of the muscles of the hands and feet, twitching of different muscle groups;
• there is a symptom of a clapping tremor (asterixis - in translation from the Greek "inability to maintain a fixed position"). To identify a symptom in a sitting position, it is suggested that you stretch your arms forward, push your fingers apart and strain them. There are chaotic twitching of fingers in the lateral and vertical directions, flexion and extension of the wrist, combined with a large tremor of the muscles of the hands, which somewhat resembles the flapping of the wings of birds. You can suggest to bend the brush in the dorsal position of the outstretched arm - thus also appears a clapping tremor;
• the sum of points on the Glasgow scale 11 -12;
• on the electroencephalogram there is an increase in the amplitude of the waves, the rhythm is sharply slowed down (7-8 oscillations per second), stable theta and delta waves appear;
• tendon and pupillary reflexes are sharply reduced;
• breathing becomes rapid;
• expressed dyspepsia, severe jaundice, liver odor from the mouth;
• there is a decrease in liver size (in patients with acute liver damage, with liver cirrhosis, a decrease in liver size is practically not observed or very little expressed).

Stage III (sopor, shallow coma, coma I) - corresponds to the transition of the precoma into a coma, characterized by the following symptomatology:

• marked impairment of consciousness, characterized by stunnedness with awakening after a sharp stimulation, while there is a brief excitement with delirium and hallucinations;
• pupils are wide, with a complete lack of reaction to light; a symptom of "floating eyeballs" is characteristic; tendon reflexes increased;
• pathological reflexes of Babinsky, Gordon, Rossolimo, and the clone of the foot muscles are determined;
• stiffness of skeletal muscles, paroxysmal clonic convulsions, sometimes fibrillar muscle twitching, tremor;
• detection of the symptom of "clapping tremor" is impossible (the patient is practically unconscious and can not participate in the definition of the symptom);
• the sum of points on the Glasgow scale is 10 or less;
• the face becomes masklike;
• the hepatic odor from the mouth is determined;
• sharply increased jaundice, continue to decrease the size of the liver (mainly in patients with acute liver disease);
• develops paresis of smooth muscles of the intestine (atony, pronounced meteorism), bladder;
• the phenomena of hemorrhagic diathesis increase;
• A-and beta-activity disappears on the electroencephalogram, and hypersynchronous three-phase 8-waves are recorded.

Stage IV (coma) is the most severe degree of hepatic encephalopathy. Hepatic coma has the following clinical symptoms:

• consciousness is completely lost; pupils dilated, do not respond to light;
• respiration of Kussmaul (a sign of metabolic acidosis), liver odor from the mouth, followed by the emergence of Cheyne-Stokes or Biot respiration, indicating a severe depression of the respiratory center;
• stiffness of the muscles of the occiput and muscles of the extremities is noted, opisthotonus can be observed; Periodically there are convulsions due to hypoglycemia and hypokalemia, however, with severe coma develops pronounced hypotension;
• tendon reflexes disappear, pathological reflexes of Babinsky, Gordon, Zhukovsky, and in some cases, grasping and proboscis reflexes are revealed;
• "Clapping tremor" is not determined;
• pronounced jaundice, reduced liver size (with hepatic coma, which is the terminal phase of liver cirrhosis, a decrease in liver size is not always clearly pronounced);
• cardiovascular disorders characterized by tachycardia, a sharp decrease in blood pressure, deafness of the heart tones; possibly the development of hepatocardial syndrome (premature appearance of II tone - "knocking woodpecker", prolongation of the QT interval, widening of the T wave) due to myocardial dystrophy;
• anuria develops;
• can be significantly expressed the phenomenon of hemorrhagic diathesis (skin hemorrhages, nasal, gastric, intestinal, uterine bleeding);
• increased body temperature;
• the electroencephalorrhme is dominated by hypersynchronous delta waves, in the final stage the electroencephalogram approaches the isoline.

Variants of a current of a hepatic coma

Distinguish between the hepatic coma with an acute and slow onset. With an acute onset, the duration of the prodromal period is 1-3 hours, then coma occurs, death may occur within a few days. Perhaps lightning fasting of the hepatic coma, with a lethal outcome may occur in a few hours.

The slow onset of the hepatic coma is characterized by the fact that the prodromal period lasts several days and even weeks, then within the first 1-4 days the second stage of hepatic encephalopathy develops, giving way to complete coma with all clinical manifestations.

Depending on the etiopathogenetic digestion characteristics distinguish the following types of hepatic coma:

• endogenous hepatic (true) coma - develops due to massive necrosis of the liver parenchyma, usually the outcome of a severe course of acute viral, toxic, drug-induced hepatitis;
• Portosystemic (portocaval, bypass, exogenous) hepatic coma - is caused by the presence of portocaval anastomoses;
• mixed hepatic coma - occurs with the development of necrosis of the hepatic parenchyma in patients with cirrhosis of the liver with pronounced portocaval anastomoses; This usually happens with a high activity of the pathological process in the liver;
• false hepatic (electrolyte) coma - develops in patients with cirrhosis of the liver against electrolyte disorders (hypokalemia, hypochloraemia, hyponatremia), and as a rule there is hypokalemic metabolic alkalosis, which contributes to the penetration of ammonia into the cells of the brain.

[1], [2], [3], [4], [5], [6]