Definition Wernicke’s encephalopathy is a serious neurological condition that results primarily from a deficiency of the nutrient thiamine which
is also known as Vitamin B1. This condition is an inflammatory, hemorrhagic, degenerative condition of the brain. It is characterized by lesions in several parts of the brain, including the hypothalamus, mammillary bodies, and tissues surrounding the ventricles and aqueducts, double vision, ophthalmoplegia, involuntary and rapid movements of the eyes, lack of muscular coordination, and decreased mental function, which may be mild or severe. The disease is comprised of three main symptoms: mental confusion, lack of muscle coordination, and a paralysis of the muscles which control eye movements. Frequency
The male-to-female ratio is 1.7:1, likely owing to alcoholism being 3-4 times more frequent in men than in women. Wernicke encephalopathy have placed the incidence between 0.8% and 2.8% of the general population The incidence can be as high as 12.5% in a population of alcoholics This disease is caused by a lack of thiamin (vitamin B1), which leads to problems with the normal functioning of the brain. Thiamine deficiency is characteristically associated with chronic alcoholism, because it affects thiamine uptake and utilization. Most cases of Wernicke’s encephalopathy are rooted in chronic alcohol abuse. Alcohol can, over time, severely impair the body’s ability to absorb thiamine, gradually leading to a deficiency of this nutrient. When someone who is known to abuse alcohol has symptoms such as confusion and gait ataxia, meaning lack of coordination in walking, Wernicke’s encephalopathy should be considered as a possible cause.
Wernicke encephalopathy may develop in nonalcoholic conditions such as:
1. prolonged starvation 2. hyperemesis gravidarum (continuous nausea and vomiting during pregnancy) 3. bariatric surgery and other gastric bypass surgeries 4. HIV-AIDS 5. healthy infants given the wrong formulas 6. malnutrition 7. complication of GI tract disease 8. Cancers that have spread throughout the body 9. Heart failure (when treated with long-term diuretic therapy) 10. Long periods of intravenous (IV) therapy without receiving thiamine supplements 11. Long-term dialysis 12. Very high thyroid hormone levels (thyrotoxicosis)
Abnormal eye movement (back and forth movements called nystagmus) – most common 2. Thiamine deficiency often affects the temperature-regulating center in the brainstem. Gait ataxia is often a presenting symptom. Encephalopathy is characterized by a global confusional state. abducens.
Loss of muscular coordination (ataxia) – Leg tremor. ataxic gait. Hypothermia. Carbohydrate loading in the presence of marginal thiamine stores (feeding after starvation) 15. disinterest. Double vision 3. The most constant symptoms of Wernicke encephalopathy are the mental status changes. or agitation. cerebellar damage. which can result in hypothermia. Swallowing difficulties. Hypotension can be secondary to thiamine deficiency either through cardiovascular beriberi or thiamine deficiency–induced autonomic dysfunction.
. and vestibular paresis. Ataxia is likely to be a combination of polyneuropathy. bilateral lateral rectus palsies 5.
Ocular Abnormalities. is universally impaired in the acute stages of Wernicke encephalopathy. ptosis. Coma Wet beriberi Nutritional polyneuropathy Muscle atrophy. and anisocoria OTHER SYMPTOMS
Vestibular dysfunction Hypotension.13. inattentiveness. usually without hearing loss. Stupor and coma are rare. pupillary abnormalities such as sluggishly reactive pupils. Vestibular dysfunction. Congenital transketolase function abnormalities Signs and Symptoms TRIAD SYMPTOMS The 3 components of the classic triad of Wernicke encephalopathy are encephalopathy. can be profound. Ocular abnormalities are the hallmarks of Wernicke encephalopathy. Absence of thiamine from the diet (in the case of infants fed formula without the addition of thiamine) 16. Eyelid drooping 4. The oculomotor signs are:
1. Chronic renal failure 14. and vestibular nuclei 6. and some variant of oculomotor dysfunction. Loss of memory. scotomata. Cold skin.
Encephalopathy. conjugate gaze palsies reflecting cranial nerve involvement of the oculomotor.
Toxic drug screening is performed to exclude some causes of drug-induced altered mental status. Staggering gait.
Double vision. Wernicke encephalopathy is a clinical diagnosis.
. and continue until the patient resumes a normal diet.
Diagnosis No specific laboratory test is available for diagnosing Wernicke encephalopathy. Difficulty with speech. Reduced eye movement.
Intravenous thiamine is given to the patient for a few days until it can be given by mouth. There are blood and urine tests available to check the level of thiamin. Eye movement abnormalities. Serum albumin. an important enzyme in aerobic metabolism. Dry skin. Serum vitamin B1 levels 3. These tests are sensitive and helpful. The level of this is reduced in people with thiamine deficiency. A Diagnosis can be made by treating the patient with thiamin and watching the symptoms improve. Start thiamine prior to or concurrently with treatment of intravenous glucose solutions.
When a person appears poorly nourished (malnourish). The motto should be “If in doubt. as thiamine is a cofactor of the pyruvate dehydrogenase enzyme. This test relates to the person’s general nutrition 2.” as administration of thiamine does not pose potential harm. The most effective treatment is to eat properly. treat. This is particularly the case where malnutrition is likely to be present.
Blood pyruvate and lactate measurements. Transketolase activity in the red blood cells. To exclude hypoglycemia and hyperglycemia. Abnormal eye movements. and normal electrolyte levels may only give false reassurance and delay therapy. Confabulation (making up stories). Complete blood cell (CBC) count rules out severe anemias and leukemias as causes of altered mental status. The following should be done to check the patient’s nutrition level:
1. but giving the patient thiamin and seeing the response is the best way to diagnose this condition. Inability to form new memories. serum glucose levels should be obtained.
allrefer. ensure oxygenation and maintain the patient’s blood pressure as patients with Wernicke’s encephalopathy present with an altered mental status in prehospital settings. Providing proper nutrition.
Patients with Wernicke encephalopathy are likely hypomagnesemic and should be treated empirically with parenteral magnesium sulfate. as they may be unresponsive to parenteral thiamine in the presence of hypomagnesemia. the blood transketolase activity can return to normal and clearing of the clinical signs may occur. After correction of hypomagnesemia in conjunction with thiamine repletion.com
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