Liver encephalopathy - Symptoms.

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

The degree of depression of consciousness is assessed using the Glasgow Depression Scale.

Functional tests	Nature of reaction	Score in points
Eye tearing	Spontaneous opening	4
	In response to a verbal command	3
	In response to painful irritation	2
	Absent	1
Physical activity	Purposeful in response to a verbal command	6
	Targeted in response to painful stimulation ("withdrawal" of limbs)	5
	Non-targeted in response to painful stimulation ("withdrawal" with flexion of the limbs)	4
	Pathological tonic flexion movements in response to painful stimulation	3
	Pathological extension movements in response to painful stimulation	2
	Lack of motor response to pain stimulation	1
Verbal answers	Maintaining orientation, quick correct	5
	Answers
	Confused speech	4
	Individual unclear words, inadequate answers	3
	Inarticulate sounds	2
	Lack of speech	1

The results of three functional tests are summed up - eye opening, motor activity, verbal responses. The overall result is calculated in points.

In hepatic encephalopathy, all parts of the brain are affected, so the clinical picture is a complex of various syndromes. It includes neurological and mental disorders. A characteristic feature of hepatic encephalopathy is the variability of the clinical picture in different patients. Encephalopathy is easy to diagnose, for example, in a patient with cirrhosis of the liver admitted to hospital with gastrointestinal bleeding or sepsis, whose examination reveals confusion and a "flapping" tremor. If the anamnesis is unknown and there are no obvious factors contributing to the deterioration of the course of the disease, the doctor may not recognize the onset of hepatic encephalopathy if he does not attach due importance to the subtle manifestations of the syndrome. In this case, data obtained from family members who have noticed a change in the patient's condition can be of great importance.

When examining patients with liver cirrhosis and neuropsychiatric disorders, especially in cases where they have appeared suddenly, the physician should consider 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 or other metabolic disorders.

Clinical signs and examination data in patients with hepatic encephalopathy vary, especially in the long-term course of chronic disease. The clinical picture depends on the nature and severity of the factors that caused the deterioration of the condition and on the etiology of the disease. In children, an extremely acute reaction may develop, often accompanied by psychomotor agitation.

In the clinical picture characteristic of hepatic encephalopathy, for ease of description, one can distinguish disorders of consciousness, personality, intellect and speech.

Hepatic encephalopathy is characterized by impaired consciousness with sleep disorder. Drowsiness in patients appears early, later the normal rhythm of sleep and wakefulness is inverted. Early signs of impaired consciousness include a decrease in the number of spontaneous movements, a fixed gaze, lethargy and apathy, and short responses. Further deterioration of the condition leads to the patient reacting only to intense stimuli. Coma initially resembles normal sleep, but as it worsens, the patient completely stops responding to external stimuli. These disorders can be suspended at any level. A 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 family. Such personality changes can be detected even in patients in remission, which suggests the involvement of the frontal lobes of the brain in the pathological process. These patients are usually sociable, friendly people with easy social contacts. They often have a playful mood, euphoria.

Intellectual disorders vary in severity from mild impairment of the organization of this mental process to severe ones, accompanied by confusion. Isolated disorders occur against the background of clear consciousness and are associated with impairment of optical-spatial activity. They are most easily detected 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, patients can be successively examined using the Reitan test for connecting numbers. Writing disorders are manifested in the form of disturbances in the writing of letters, so the patient's daily records reflect the development of the disease well. Impaired recognition of objects similar in size, shape, function and position in space subsequently leads to such disorders as urination and defecation in inappropriate places. Despite such behavioral disorders, patients often retain criticism.

The patients ' speech becomes slow, slurred, and their voice becomes monotonous. In deep stupor, dysphasia becomes noticeable, which is always combined with perseverations.

Some patients have a liver odor on their breath. This sour, fecal odor on the breath is caused by mercaptans, volatile substances that are normally formed in the feces by bacteria. If mercaptans are not removed through the liver, they are excreted by the lungs and appear in the exhaled air. The liver odor is not related to the degree or duration of encephalopathy, and its absence does not rule out liver encephalopathy.

The most characteristic neurological sign in hepatic encephalopathy is a "flapping" tremor (asterixis). It is associated with a disruption in the flow of afferent impulses from the joints and other parts of the musculoskeletal system to the reticular formation of the brainstem, which leads to the inability to maintain a posture. "Flapping" tremor is demonstrated on outstretched arms with spread fingers or during maximum extension of the patient's hand with a fixed forearm. In this case, rapid flexion-extension movements are observed towards the metacarpophalangeal and wrist joints, often accompanied by lateral movements of the fingers. Sometimes hyperkinesis affects the entire arm, neck, jaw, protruding tongue, retracted mouth and tightly closed eyelids, ataxia appears when walking. Tremor is most pronounced during maintaining a constant posture, less noticeable during movement and absent during rest. It is usually bilateral but not synchronous: the tremor may be more pronounced on one side of the body than on the other. It can be assessed by gently raising a limb or by the patient shaking the doctor's hand. The tremor disappears during coma. The "flapping" tremor is not specific for hepatic precoma. It is observed in uremia, respiratory failure, and severe heart failure.

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

Flexion plantar reflexes in deep stupor or coma become extension reflexes. Hyperventilation and hyperthermia may be observed in the terminal state. 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 patients' condition is unstable and they require enhanced monitoring.

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. Hepatic coma may quickly occur. In acute liver failure, the prognosis is determined by age (unfavorable in people under 10 and over 40 years of age); etiology (the prognosis is worse in viral compared to drug-induced disease); the presence of jaundice that appeared earlier than a week before encephalopathy.

Acute hepatic encephalopathy develops in acute viral, toxic, drug-induced hepatitis, as well as in patients with liver cirrhosis when acute necrosis is superimposed on cirrhotic changes in the terminal phase of the disease. As a rule, acute hepatic encephalopathy in patients with liver cirrhosis occurs with a sharp exacerbation of the disease, as well as with the influence of provoking factors: alcohol excesses, taking narcotic analgesics, sleeping pills, exposure to toxic hepatotropic substances, infection.

Subacute hepatic encephalopathy differs from acute only in the duration of the development of symptoms and the slow development of coma (over a week or more). Sometimes subacute encephalopathy becomes recurrent, and during periods of remission, patients feel satisfactory, since the symptoms of encephalopathy are significantly reduced.

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

Chronic recurrent and continuous encephalopathy are distinguished. Chronic hepatic encephalopathy is characterized by constant changes in the mental sphere of varying severity, which can periodically intensify (changes in character, emotions, mood, attention, memory, and intellect disorders), parkinsonian tremor, muscle rigidity, attention and memory disorders are possible. An important criterion for diagnosing chronic hepatic encephalopathy is the effectiveness of its correct and timely treatment.

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