Wernicke-Korsakoff Syndrome (WKS)

Thiamine before glucose - Giving a glucose load to a thiamine-depleted patient can precipitate or worsen Wernicke encephalopathy, so thiamine goes in before any dextrose-containing fluid, TPN or refeeding. The nuance worth knowing: a review of 19 papers concluded that correction of hypoglycemia should not be delayed, and that the risk tracks with prolonged glucose replacement without thiamine rather than a single acute correction. Treat symptomatic hypoglycemia immediately and give thiamine alongside it.

Always cover the refeeding period - In a patient with alcohol use disorder, thiamine during refeeding prevents acute thiamine deficiency with lactic acidosis. If you are starting nutrition perioperatively, thiamine is part of the order set, not an afterthought.

Replace magnesium or the thiamine will not work - Thiamine-dependent enzymes cannot operate in a magnesium-deficient state. Send a magnesium level with the rest of the electrolytes and correct it, or you will give thiamine and see no response.

Dosing - For acute deficiency with neurologic or cardiovascular signs, 200 mg IV or PO three times daily until symptoms resolve or improvement plateaus, then 10 mg/day orally. Regimens for suspected Wernicke-Korsakoff run considerably higher — 500 to 1500 mg IV three times daily for at least three days. Institutional protocols vary, so check yours. Anaphylaxis and bronchospasm have been reported with high-dose IV thiamine, so give it somewhere you can treat that.

Do not wait for a level - Prophylactic thiamine is relatively safe and should be started before the diagnosis is confirmed. Thiamine blood tests take days to result and must not delay empiric treatment.

You will miss it if you are not looking for it - Wernicke encephalopathy is missed in an estimated 68% of patients with alcohol use disorder and 94% of those without. Fewer than a third present with the full triad, and by one series fewer than 20% do. In the alcohol-using patient the Caine criteria — two of four signs — give 85% sensitivity and 100% specificity for a clinical diagnosis.

Ocular findings are the diagnostic lever - Nystagmus, ophthalmoplegia, sixth nerve palsy, diplopia, ptosis or painless vision loss in a malnourished or alcohol-using patient. These are the fastest to respond, usually within hours of thiamine, and if they do not improve the diagnosis should be reconsidered. Do not write off new nystagmus in PACU as residual anesthetic without asking about nutrition.

Confabulation makes the patient's history unusable - Korsakoff patients fill memory gaps with untrue material fluently and without any intent to deceive. Never take NPO status, last drink, medication list or prior anesthetic history from the patient alone — get a collateral source or the record.

Consent will not be retained - Anterograde amnesia profoundly limits new learning, and the executive deficits impair judgment, planning and problem-solving. Establish who holds decision-making authority before the day of surgery, and assume that anything explained in the preoperative area is gone by the time the patient reaches the OR.

Ataxia is a transfer and discharge problem - The gait is wide-based and short-stepped and many patients cannot stand or walk unassisted. Plan the transfer, the positioning for any block, and the discharge plan around that, and treat fall risk as present from arrival. About half of ataxic patients never recover fully.

Look for the non-alcoholic causes - Bariatric surgery, hyperemesis gravidarum, GI malignancy, prolonged vomiting, anorexia nervosa, starvation, chronic diuretic therapy, prolonged parenteral feeding and schizophrenia all cause this without any alcohol at all. The thin obstetric patient with intractable vomiting is the classic missed case.

Wet beriberi - the cardiac half - The same deficiency produces high-output heart failure with edema and fluid retention from impaired myocardial energy metabolism and dysautonomia. It is a medical emergency that can kill within days untreated, and the cardiac dysfunction improves within about 24 hours of starting thiamine. Dry beriberi gives symmetric peripheral neuropathy with impaired reflexes and motor and sensory deficits in the extremities — document that before any regional block.

Unexplained lactic acidosis - Thiamine mediates pyruvate metabolism, and deficiency raises lactate. A lactic acidosis you cannot account for in a malnourished or alcohol-using patient, particularly during refeeding, should prompt thiamine before you keep hunting for sepsis or hypoperfusion alone.

Alcohol brings the rest of its list - Withdrawal, cardiomyopathy, coagulopathy and altered anesthetic requirement travel with chronic use. See the alcohol substance abuse and alcoholic liver disease entries.

Be honest about the trajectory - Ocular signs clear fastest; roughly half of ataxic patients recover completely; only about one in five with an established amnestic state recovers fully; and about 25% require long-term institutional care. Mortality is 10% to 15% in severe cases. Do not tell a family the confusion is postoperative and will pass.

Wernicke-Korsakoff syndrome is thiamine (vitamin B1) deficiency injuring the brain. Thiamine pyrophosphate is the cofactor for pyruvate decarboxylation and for transketolase; without it, brain cell metabolism and ATP production fail and pyruvate is shunted to lactate, producing edema, neuronal loss and reactive gliosis. The damage falls on the mammillary bodies, dorsomedial thalami, periaqueductal gray, third ventricular walls and tectal plate, with the ocular findings from the abducens nuclei and midbrain gaze centers and the ataxia from the superior vermis.

Wernicke encephalopathy is the acute, often reversible half — confusion, ophthalmoplegia or nystagmus, ataxia. Korsakoff syndrome is the chronic and largely irreversible half — anterograde and retrograde amnesia with confabulation. Chronic alcohol use is the commonest cause, but stores deplete about four weeks after intake stops from any cause.