Hepatic encephalopathy - Stages

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

• consciousness is preserved, patients complain of severe general weakness, loss of appetite, nausea, bitterness in the mouth, hiccups, pain in the right hypochondrium, dizziness, “flickering spots” before the eyes, headache, tinnitus;
• patients adequately answer questions, recognize others, but periodically lose their bearings in time and space (they may not understand where they are, not be able to name the day of the week, etc.);
• excitement, fussiness, emotional lability, euphoria are often observed (they claim that they feel great);
• the ability to concentrate is impaired, patients often repeat the same words and cannot finish a sentence;
• sometimes patients commit unmotivated acts, look for non-existent objects, etc.;
• patients have difficulty performing the simplest mental tasks (make mistakes when counting, adding prime numbers). This is especially noticeable when performing a number connection test (the patient cannot connect a group of numbers from 1 to 25 in 30 seconds);
• the coordination of fine movements is disrupted, which is clearly visible in the “written test” (handwriting becomes unclear and difficult to understand);
• the sleep formula is disrupted (patients are sleepy during the day and suffer from insomnia at night);
• according to the Glasgow scale, the sum of points is 13-14;
• pupils are dilated, pupillary reaction is weakened;
• there are no changes on the electroencephalogram; some patients may have disturbances in the a-rhythm (irregularity, disorganization, tendency to increase the amplitude of the waves), and a decrease in the response to opening the eyes;
• Moderate hemorrhagic phenomena (skin hemorrhages, nosebleeds) are possible.

Stage II (somnolence, precoma II) is a more pronounced stage of hepatic encephalopathy, heralding the onset of stupor. It is characterized by the following manifestations:

• the excitability and euphoria of patients is replaced by apathy, a feeling of melancholy, doom, hopelessness; patients are inhibited, drowsy;
• upon awakening, consciousness is confused, patients are disoriented in time, space, and faces; they carry out simple commands, but cannot perform tasks that require attention (for example, counting);
• periodically, patients briefly lose consciousness;
• against the background of inhibition, lethargy, drowsiness, agitation, delirium, hepatic delirium, auditory and visual hallucinations, inappropriate behavior periodically occur, patients try to jump up, run, throw themselves out of the window, scream, swear, become aggressive;
• sometimes tonic spasms of the muscles of the arms and legs and twitching of various muscle groups occur;
• a symptom of flapping tremor appears (asterixis - translated from Greek as "inability to maintain a fixed position"). To identify the symptom, the patient is asked to stretch his arms forward in a sitting position, spread his fingers and tense them. Chaotic twitching of the fingers in the lateral and vertical directions, flexion and extension of the wrist appear, combined with a large tremor of the arm muscles, which is somewhat reminiscent of the flapping of birds' wings. You can ask to bend the hand in the dorsal position of the outstretched arm - in this case, a flapping tremor also appears;
• Glasgow scale score 11-12;
• the electroencephalogram shows an increase in the amplitude of the waves, the rhythm is sharply slowed (7-8 oscillations per second), stable theta and delta waves appear;
• tendon and pupillary reflexes are sharply reduced;
• breathing becomes more rapid;
• dyspeptic disorders, intense jaundice, and liver odor from the mouth are expressed;
• a decrease in liver size is observed (in patients with acute liver damage; in liver cirrhosis, a decrease in liver size is practically not observed or is expressed very slightly).

Stage III (stupor, shallow coma, coma I)- corresponds to the transition from precoma to coma, characterized by the following symptoms:

• a pronounced disturbance of consciousness, characterized by stupefaction with awakening after sharp stimulation, while short-term excitement with delirium and hallucinations is observed;
• pupils are dilated, with a complete lack of reaction to light; the symptom of “floating eyeballs” is characteristic; tendon reflexes are increased;
• pathological reflexes of Babinski, Gordon, Rossolimo, clonus of the foot muscles are determined;
• rigidity of skeletal muscles, paroxysmal clonic seizures, sometimes fibrillary muscle twitching, tremors are observed;
• identification of the symptom of “flapping tremor” is impossible (the patient is practically unconscious and cannot participate in determining the symptom);
• Glasgow scale score of 10 or less;
• the face becomes mask-like;
• a liver odor is detected from the mouth;
• jaundice increases sharply, the size of the liver continues to decrease (mainly in patients with acute liver pathology);
• paresis of the smooth muscles of the intestine (atony, severe flatulence) and bladder develops;
• the symptoms of hemorrhagic diathesis increase;
• On the electroencephalogram, a- and beta activity disappears, and hypersynchronous three-phase 8-waves are recorded.

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

• consciousness is completely lost; pupils are dilated, do not react to light;
• Kussmaul breathing (a sign of metabolic acidosis), liver odor from the mouth, subsequently Cheyne-Stokes or Biot breathing appears, indicating severe depression of the respiratory center;
• rigidity of the muscles of the back of the head and limb muscles is noted, opisthotonus may be observed; convulsions periodically appear due to hypoglycemia and hypokalemia, however, with deep coma, severe hypotension develops;
• tendon reflexes disappear, pathological reflexes of Babinski, Gordon, Zhukovsky, and in some cases grasping and proboscis reflexes are often detected;
• "flapping tremor" is not detected;
• jaundice is pronounced, the liver size is reduced (in hepatic coma, which is the terminal phase of liver cirrhosis, the reduction in liver size is not always clearly expressed);
• Cardiovascular disorders are characterized by tachycardia, a sharp decrease in blood pressure, muffled heart sounds; the development of hepatocardial syndrome is possible (premature appearance of the second heart sound - "woodpecker knock", prolongation of the QT interval, widening of the T wave), caused by myocardial dystrophy;
• anuria develops;
• the phenomena of hemorrhagic diathesis (skin hemorrhages, nasal, gastric, intestinal, uterine bleeding) may be significantly expressed;
• increased body temperature;
• hypersynchronous delta waves dominate the electroencephalogram; in the final stage, the electroencephalogram approaches the isoline.

Variants of the course of hepatic coma

A distinction is made between hepatic coma with an acute and slow onset. With an acute onset, the prodromal period lasts 1-3 hours, then coma sets in, and death can occur within a few days. A lightning-fast course of hepatic coma is possible, with a fatal outcome occurring within a few hours.

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

Depending on the etiopathogenetic features of digestion, the followingtypes of hepatic coma are distinguished:

• endogenous hepatic (true) coma - develops as a result of 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 - caused by the presence of portocaval anastomoses;
• mixed hepatic coma - occurs with the development of necrosis of the liver parenchyma in patients with liver cirrhosis with pronounced portocaval anastomoses; this usually occurs with high activity of the pathological process in the liver;
• false hepatic (electrolyte) coma - develops in patients with liver cirrhosis against the background of electrolyte disturbances (hypokalemia, hypochloremia, hyponatremia), while, as a rule, there is hypokalemic metabolic alkalosis, which promotes the penetration of ammonia into brain cells.

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