Hepatic encephalopathy: symptoms

Symptoms of hepatic encephalopathy include nonspecific symptoms of mental disorders, neuromuscular manifestations, asterixis, changes in the electroencephalogram.

Assessment of the degree of severity of depression is done according to the Glasgow scale.

Functional tests	The nature of the reaction	Score in points
Tearing off the eyes	Spontaneous opening	4
	In response to a verbal order	3
	In response to painful irritation	2
	Absent	1
Physical activity	Purposeful in response to verbal orders	6th
	Purposeful in response to painful irritation ("withdrawal" of limbs)	5
	Unselected in response to painful irritation ("withdrawal" with flexion of limbs)	4
	Pathological tonic flexion in response to pain stimulation	3
	Pathological extensor movements in response to pain stimulation	2
	Absence of motor reaction to painful irritation	1
Verbal responses	Preservation orientation, fast correct	5
	Answers
	Confused speech	4
	Some vague words, inadequate answers	3
	Inarticulate sounds	2
	Lack of speech	1

The results of three functional tests are summarized: eye opening, motor activity, verbal responses. The grand total is calculated in points.

When hepatic encephalopathy affects all parts of the brain, so the clinical picture is a complex of different syndromes. It includes neurological and mental disorders. A characteristic feature of hepatic encephalopathy is the variability of the clinical picture in various patients. It is easy to diagnose encephalopathy, for example, when entering a hospital with gastrointestinal bleeding or sepsis, a patient with cirrhosis of the liver, when examined, reveals confusion and a "clapping" tremor. If the anamnesis is unknown and there are no obvious factors contributing to the worsening of the course of the disease, the doctor may not recognize the onset of liver encephalopathy unless it gives proper significance to the subtle manifestations of the syndrome. Great value in this case can have data obtained from family members who have noticed a change in the patient's condition.

When examining patients with cirrhosis of the liver with neuropsychiatric disorders, especially in cases when they suddenly appeared, the doctor should take into account the possibility of developing neurological symptoms in rare patients with intracranial hemorrhage, trauma, infection, brain tumor, as well as brain damage as a result of taking medications drugs or other metabolic disorders.

Clinical signs and examination data in patients with hepatic encephalopathy differ among themselves, especially in the long-term course of a chronic disease. The clinical picture depends on the nature and severity of the factors that caused the deterioration, and the etiology of the disease. Children can develop an extremely acute reaction, often accompanied by psychomotor agitation.

In the clinical picture, characteristic for hepatic encephalopathy, for the convenience of description can be distinguished disorders of consciousness, personality, intellect and speech.

For hepatic encephalopathy, a disorder of consciousness with a sleep disorder is characteristic . Drowsiness in patients appears early, later the inversion of the normal rhythm of sleep and wakefulness develops. Early signs of a disorder of consciousness include a decrease in the number of spontaneous movements, a fixed look, inhibition and apathy, a brevity of answers. Further deterioration of the condition leads to the fact that the patient reacts only to intense stimuli. The coma at first resembles a normal dream, however, as it becomes heavier, the patient completely ceases to react to external stimuli. These violations can be suspended at any level. Rapid change in the level of consciousness is accompanied by the development of delirium.

Personality changes are most noticeable in patients with chronic liver disease. They include childishness, irritability, loss of interest in the family. Such personality changes can be detected even in patients in a state of remission, which involves the involvement of the frontal lobes of the brain in the pathological process. These patients, as a rule, are sociable, kind people with facilitated social contacts. They often have a playful mood, euphoria.

Intelligence disorders vary in severity from a mild disruption of the organization of this mental process to a pronounced, confused consciousness. Isolated disorders arise against a background of clear consciousness and are associated with a violation of optic-spatial activity. Most easily they are revealed in the form of constructive apraxia, expressed in the inability of patients to copy a simple pattern of cubes or matches. To assess the progression of the disease, one can consistently examine patients using the Reitan test to connect the numbers. Disorders of the letter are manifested in the form of violations of the letters, therefore the patient's daily records reflect the development of the disease. Violation of the recognition of objects that are similar in size, shape, function and position in space, further leads to such disorders as urination and defecation in unsuitable places. Despite such behavioral disorders, patients often remain critical.

Speech in patients becomes slow, indistinct, and voice - monotonous. In a deep comparison, dysphasia becomes noticeable, which is always combined with perseverations.

Some patients experience hepatic odor from the mouth. This acidic feces smell when breathing is caused by mercaptans - volatile substances, which are normally produced in stool by bacteria. If mercaptans are not removed through the liver, they are excreted by the lungs and appear in the exhaled air. The hepatic odor is not associated with the extent or duration of encephalopathy, its absence does not allow excluding hepatic encephalopathy.

The most characteristic neurological sign in hepatic encephalopathy is the "clapping" tremor (asterixis). It is associated with a violation of the inflow of afferent impulses from the joints and other parts of the musculoskeletal system into the reticular formation of the brainstem, which leads to inability to hold the pose. The "flapping" tremor is demonstrated on elongated arms with the fingers arranged or at the maximum extension of the hand of the patient with a fixed forearm. At the same time, rapid flexion-extensor movements are observed to the metacarpophalangeal and radiocarpal joints, often accompanied by lateral finger movements. Sometimes hyperkinesis captures the entire arm, neck, jaw, sticking out tongue, drawn mouth and tightly closed eyelids, there is ataxia when walking. Tremor is most pronounced while maintaining a constant posture, less noticeable during movement and absent during rest. Usually it is two-sided, but not synchronous: the tremor can be more pronounced on one side of the body than on the other. It can be assessed by carefully lifting the limb or by shaking the patient's hands with a doctor. During coma, the tremor disappears. The "flapping" tremor is not specific for hepatic precoma. It is observed with uremia, respiratory and severe heart failure.

Deep tendon reflexes are usually elevated. At some stages of hepatic encephalopathy, muscle tone is increased, and muscle rigidity is often accompanied by a prolonged clonus of the feet. During coma, patients become flaccid, reflexes disappear.

Flexural plantar reflexes in deep copula or coma turn into extensor reflexes. In the terminal state, hyperventilation and hyperthermia can occur. The diffuse nature of cerebral disorders in hepatic encephalopathy is also evidenced by excessive appetite of patients, muscle twitching, grasping and sucking reflexes. Visual disturbances include reversible cortical blindness.

The condition of the patients is unstable, followed by increased surveillance.

Clinical manifestations of hepatic encephalopathy depend on its stage and type of course (acute, subacute, chronic).

Acute hepatic encephalopathy is characterized by a sudden onset, a short and extremely severe course, lasting from several hours to several days. A hepatic coma can quickly occur. In acute liver failure, the prognosis is determined by age (unfavorable in persons younger than 10 and older than 40, etiology (the prognosis is worse when viral compared to the medicinal nature of the disease), the presence of jaundice that appeared earlier than a week before encephalopathy.

Acute hepatic encephalopathy develops with acute viral, toxic, medicamentous hepatitis, as well as in patients with cirrhosis of the liver with acute necrosis deposition on cirrhotic changes in the terminal phase of the disease. As a rule, acute hepatic encephalopathy in patients with cirrhosis occurs with severe exacerbation of the disease, as well as under the influence of provoking factors: alcoholic excesses, the use of narcotic analgesics, hypnotics, exposure to toxic hepatotropic substances, infection.

Subacute hepatic encephalopathy differs from acute only duration of development of symptoms and delayed development of coma (for a week or more). Sometimes subacute encephalopathy acquires a recurring course, during the periods of remission patients feel satisfactory, as the phenomena of encephalopathy significantly decrease.

Chronic hepatic encephalopathy is observed mainly in patients with cirrhosis of the liver with portal hypertension.

Isolate chronic recurrent and continuous flow of encephalopathy. Chronic hepatic encephalopathy is characterized by constant changes in the mental sphere of varying severity, which can periodically increase (changes in character, emotions, mood, attention, memory, intellect), parkinsonian tremor, muscle stiffness, attention disturbance, memory are possible. An important criterion for the diagnosis of chronic hepatic encephalopathy is the effectiveness of correct and timely treatment.

[1], [2], [3], [4]