(Wernicke’s encephalopathy)

Symptoms of Wernicke encephalopathy are acute onset of confusion, nystagmus, partial ophthalmoplegia and ataxia due to a thiamine deficiency. The diagnosis is primarily clinical. The disorder may remit by treatment persist or merge into a Korsakoff psychosis. The therapy involves the immediate administration of thiamine and supportive measures.

Wernicke’s encephalopathy is caused by a lack of thiamine or resorption in connection with unilateral carbohydrate intake. The most common cause is severe alcohol dependence. Excessive alcohol consumption affects the thiamine absorption from the gastrointestinal tract and the Thiaminspeicherung in the liver; typical for alcohol dependence malnutrition often leads to inadequate thiamine absorption.

Symptoms of Wernicke encephalopathy are acute onset of confusion, nystagmus, partial ophthalmoplegia and ataxia due to a thiamine deficiency. The diagnosis is primarily clinical. The disorder may remit by treatment persist or merge into a Korsakoff psychosis. The therapy involves the immediate administration of thiamine and supportive measures. Wernicke’s encephalopathy is caused by a lack of thiamine or resorption in connection with unilateral carbohydrate intake. The most common cause is severe alcohol dependence. Excessive alcohol consumption affects the thiamine absorption from the gastrointestinal tract and the Thiaminspeicherung in the liver; typical for alcohol dependence malnutrition often leads to inadequate thiamine absorption. Wernicke’s encephalopathy may also result from other diseases that a long-term malnutrition or a vitamin deficiency cause (eg. As repeated dialysis, hyperemesis, starvation, Magenplikatur, cancer, AIDS). The high-calorie, but vitamin diet of hospitalized patients with thiamine (d. H. Food structure during extreme emaciation or intervenous administration dextrosehaltiger solutions at high risk patients) may cause Wernicke encephalopathy. Not all alcoholics with thiamine deficiency also develop Wernicke encephalopathy; Therefore, other factors must be involved in the development. discussed a genetic variant of the thiaminabhängigen transketolase, which is particularly sensitive to thiamine deficiency. Characteristic the symmetrical lesions are at certain points of the brain (mamillary bodies, periaqueductal gray, quadrigemina, dorsomedial thalamic nuclei, Pulvinar, the bottom of the IV. Ventricle and cerebellar midline structures). Symptoms and signs The clinical changes occur suddenly. Eye motility such as horizontal and vertical nystagmus and partial ophthalmoplegias (z. B. paresis of Mm. Rect. Lat., Associated with strabismus) and pupil disorders are common. Vestibular dysfunction without hearing loss frequently occurs and the okulovestibuläre reflex may be damaged. A gait ataxia may occur due to vestibular disorders, cerebral dysfunction and / or polyneuropathy. The ataxia is broad and slowly with short steps. The typical general confusional state is characterized by pronounced disorientation, indifference, inattention, drowsiness or stupor. In the periphery, the pain threshold is often increased, and many patients develop severe autonomic dysfunction with sympathetic hyperactivity (z. B. tremor, agitation) or hypo activity (eg. As hypothermia, orthostatic hypotension, syncope). In untreated patients, the stupor can go into a coma and death. Diagnosis Clinical Investigation There are no specific diagnostic tests. The diagnosis is made clinically; it is crucial that the malnutrition or underlying vitamin deficiency is detected. Cerebrospinal fluid, irritable potentials, brain imaging or EEG show no disease-specific deviations. Nevertheless, these investigations and laboratory tests should (z. B. blood count, blood sugar, liver function tests, arterial blood gas measurements, toxicology screening) is to exclude other causes normally performed. Thiamine are not measured regularly as the thiamine in the blood do not always reflect the CSF levels and normal serum levels do not exclude the diagnosis of. Prognosis The prognosis depends on the timely diagnosis. With timely initiation of therapy, all disturbances are reversible. Eye symptoms can usually be shipped within 24 hours after timely Thiamingabe. Ataxia and confusion may persist days or months. Memory and learning impairment may not be able completely dissolve. Left untreated, the disease progresses; The mortality is 10-20%. 80% of surviving patients develop Korsakoff’s psychosis. (The combination is referred to as Wernicke-Korsakoff syndrome.) Parenteral therapy thiamine Parenteral magnesium Treatment consists of an immediate administration of thiamine 100 mg i.v. or i.m., which will continue for at least 3-5 days. Magnesium is an important cofactor in thiaminabhängigen metabolism; a magnesium deficiency should by magnesium sulphate 1-2 g i.m. or iv every 6-8 h or magnesium 400-800 mg p.o. be corrected 1-times daily. The supportive care includes, including rehydration, correction of electrolyte abnormalities and a general nutritional therapy. Vitamin doses. Advanced cases require hospitalization. Alcohol withdrawal is essential. Since prevention of Wernicke encephalopathy is possible, all apparently malnourished patients should thiamine parenterally (usually 100 mg i.m., followed by 50 mg in tablet form daily) and vitamin B12 and folate (both 1 mg po daily) receive, especially if an i.v. Dextrosezugabe necessary. Glucose infusions must always be added thiamine, because glucose increases thiamine. The administration of thiamine is also recommended before each treatment of patients with impaired consciousness. Malnourished patients should later outpatient continue to receive thiamine.

Comments

Leave a Reply

Sign In

Register

Reset Password

Please enter your username or email address, you will receive a link to create a new password via email.