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Encephalopathy Wernicke: causes, symptoms, diagnosis, treatment
Last reviewed: 23.04.2024
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Wernicke's encephalopathy is characterized by a sharp onset, development of confusion, nystagmus, partial ophthalmoplegia and ataxia due to a lack of thiamine. The diagnosis is mainly based on clinical data. This disease can decrease on the background of treatment, persist or grow into Korsakov's psychosis. Treatment consists in the appointment of thiamine and general activities.
Wernicke's encephalopathy is the result of inadequate intake and absorption of thiamine in combination with continued use of carbohydrates. Often the basis is heavy alcoholism. Excessive consumption of alcohol interferes with the absorption of thiamine from the gastrointestinal tract and the accumulation of thiamine in the liver. Poor nutrition associated with alcoholism often prevents adequate intake of thiamine. Wernicke's encephalopathy can also be the result of other conditions that cause prolonged malnutrition or a deficiency of vitamins (eg, repeated dialysis, constant vomiting, fasting, stomach plication, oncology, AIDS). Carbohydrate loading of patients with thiamine deficiency (ie, feeding after fasting or IV injection of solutions containing dextrose to high-risk patients) can provoke the development of Wernicke's encephalopathy.
Not all patients who abuse alcohol and have thiamine deficiency develop Wernicke's encephalopathy, which indicates that other factors may be involved in its development. Genetic changes leading to the creation of pathological forms of transketolase, an enzyme involved in thiamine metabolism, can be involved in the development of this disease.
Characteristic of the lesion, symmetrically spreading around the third ventricle, the aqueduct, the 4th ventricle. Changes in mamillary bodies, dorsomedial thalamus, blue spot, gray matter around the aqueduct, oculomotor and vestibular nuclei are often revealed.
Symptoms of Wernicke's encephalopathy
Clinical changes are acute. Frequently observed oculomotor disorders, including horizontal and vertical nystagmus, partial ophthalmoplegia (eg, paralysis of vision, paralysis of conjugation). Disturbed pupillary reaction, flaccid or asymmetrical, may be noted.
Vestibular dysfunction is often observed without loss of hearing, the oculovestibular reflex may be disrupted. The ataxic gait can be the result of vestibular disorders or cerebellar dysfunction, gait sweeping, slow, with short steps.
Often there is general confusion, characterized by gross disorientation, indifference, inattention, drowsiness or stupor. The pain threshold of the peripheral nerves is often elevated, many patients develop severe autonomic dysfunction characterized by sympathetic hyperactivity (eg, tremor, agitation) or hypoactivity (eg hypothermia, postural hypotension, syncopal conditions). In the absence of treatment stupor can progress to whom, and then lead to death.
Diagnosis, prognosis and treatment of Wernicke's encephalopathy
The diagnosis is established on the basis of clinical data and depends on the recognition of the underlying malnutrition or deficiency of vitamins. There are no characteristic changes in cerebrospinal fluid caused by potentials, using brain imaging techniques, on EEG. However, these studies, as well as laboratory tests (for example, blood tests, blood glucose, blood formulas, functional liver tests, arterial blood gas analysis, toxicological screening) are necessary to exclude another etiology.
The prognosis depends on the timeliness of the diagnosis. Started on time treatment can adjust all deviations from the norm. Eye symptoms begin to subside within 24 hours after the early administration of thiamine. Ataxia and confusion can persist for days and months. In the absence of treatment, the disorder progresses; the mortality rate is 10-20%. Korsak's psychosis develops in 80% of surviving patients (this combination is called the Wernicke-Korsakov syndrome).
Treatment consists in the immediate administration of thiamine in a dose of 100 mg intravenously or intramuscularly, then every day for at least 3-5 days. Magnesium is a necessary cofactor in the metabolism of thiamine; hypomagnesemia needs to be corrected by prescribing magnesium sulfate at a dose of 1-2 g intramuscularly or intravenously every 6-8 h or magnesium oxide 400-800 mg orally once a day. General treatment consists of rehydration, correction of electrolyte disorders, restoration of nutrition, including the appointment of multivitamins. Patients with developed disorder need hospitalization. Termination of alcohol consumption is mandatory.
Since Wernicke's encephalopathy is preventable, all malnourished patients need to be given thiamine (usually 100 mg IM, then 50 mg per day) plus vitamin B 12 and folate (both 1 mg / day orally), especially if intravenous dextrose. It is prudent to administer thiamine before starting any treatment in patients with impaired consciousness. Poorly eating patients should continue taking thiamine after discharge from the hospital.
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