Bariatric Surgery and Thiamine Deficiency: Avoid the Catastrophe!

Vitamin B1, also known as Thiamine, is a member of the class of water-soluble B vitamins. Thiamine is converted in the human body to its active form, called Thiamine Pyrophosphate (TPP), which plays an important role in carbohydrate metabolism. Deficiency of vitamin B1 develops if there is insufficient dietary intake for 2-3 months, or even shorter in susceptible populations. The disease that is caused by deficiency of vitamin B1 has been called beriberi: from ‘I can’t, I can’t’ in the Sinhalese language (Sri Lanka), referring to its crippling effects. The World Health Organization’s report on Thiamine deficiency provides a global overview of this disorder.

In the UK and in other developed countries, chronic alcoholism and weight loss (bariatric) surgery have been highlighted as conditions at risk for thiamine deficiency. Nutrition is restricted intentionally by bariatric surgery, and renders patients vulnerable to various vitamin deficiencies. After a bariatric operation (gastric band, gastric bypass or sleeve gastrectomy), sufficient thiamine can be provided usually through a nutritionally balanced diet and daily multi-vitamin supplement tablets or capsules. But, deficiency can develop rapidly if there is persistent regurgitation of food or vomiting. There is special vulnerability in the early phase after weight loss surgery, when dietary intake is intentionally restricted to liquid and pureed consistency. Prolonged regurgitation and vomiting can occur simply because of difficulty to adjust to the altered anatomy. Mechanical complications of bariatric surgery, such as stenosis, band slippage or bowel obstruction, can lead to regurgitation and vomiting that persist until the problem is rectified. Whatever the cause, bariatric surgery patients with persistent vomiting or extraordinarily rapid weight loss are at risk of thiamine deficiency. The disease caused by thiamine deficiency in weight loss surgery patients has dubbed ‘bariatric beriberi’.

Thiamine deficiency can disrupt carbohydrate metabolism, leading to disorders in the: 1) central nervous system (called Wernicke’s encephalopathy and Korsakov’s psychosis); 2) peripheral nervous system (called polyneuropathy); and 3) cardiovascular system. Thiamine deficiency does not necessarily cause symptoms related to all three systems; often, symptoms related to one system predominate.

The classic presentation of Wernicke’s encephalopathy is a triad of mental status changes, eye movement abnormalities, and cerebellar dysfunction. Altered mental status may result in confusion, memory deficits or impaired consciousness. Korsakov’s psychosis is acute manifestation of severe loss of memory for recent events and confabulation (fabrication of memories). Abnormalities in eye movement may present as nystagmus (involuntary eye movements), opthalmoplegia (paralysis of the muscles of the eyeball) or diplopia (double vision). A devastating symptom is acute, bilateral blindness. Dysfunction of the cerebellum (the hind-brain) can lead to gait abnormalities and ataxia (imbalance).

Polyneuropathy – disease of peripheral nerves – may produce paraesthesiae (sensations of tingling and numbness), weakness and muscle wasting in the arms and particularly in the legs.

Cardiovascular dysfunction – disorder of the heart and circulatory system – arises because of cardiopathy (dysfunction of the muscles of the heart). Common symptoms are palpitations (because of sinus tachycardia) and oedema, mainly of the legs (because of high output ventricular failure). If thiamine deficiency presents with prominent cardiac symptoms, it can be called ‘wet beriberi’ (referring to fluid overload), as opposed to ‘dry beriberi’ with polyneuropathy.

Finally, there can be vague symptoms related to the gastrointestinal tract, including loss of appetite and constipation (possible because of altered gut motility).

An oft-quoted review of Wernicke’s encephalopathy following bariatric surgery highlights that 94% of patients were admitted to hospital within 6 months after surgery. Recurrent vomiting was reported in 90% of cases, and had lasted for a median duration of 21 days. When vomiting was not reported, patients had rapid weight loss, loss of appetite or eating avoidance, or did not take vitamin supplements. The classic triad of eye movement abnormalities, mental status changes and ataxia was present in 38%; 2 signs were present in 43%; and one sign was present in 19%. Blurred vision or impaired visual acuity was noted in 20%. Peripheral polyneuropathy (both motor and sensory) was noted in 76%, and it was more common in the lower limbs than in the upper limbs. Complete recovery was observed in 51%; the remainder was considered to have incomplete recovery. Frequent sequelae were cognitive impairments, gait difficulties and nystagmus.

Persistent vomiting, regurgitation, excess alcohol intake or rapid weight loss after bariatric surgery create susceptibility to thiamine deficiency. Patients at risk for thiamine deficiency should be prescribed thiamine tablets (200-300 mg day). Thiamine should be given intravenously to patients who are unable to take medicines orally or if there are symptoms of thiamine deficiency. If thiamine deficiency is suspected because of the presence of symptoms, intravenous treatment should be started immediately and should not be delayed pending test results. The recommended dose of intravenous thiamine is 500 mg/day for 3-5 days, followed by 250 mg/day for 3 to 5 days until resolution of symptoms, and then 100 mg/day, orally, usually indefinitely or until risk factors have resolved. If thiamine deficiency does not resolve with thiamine supplementation then small bowel bacterial overgrowth should be considered.

Oral or intravenous glucose must not be given to patients at risk of or with suspected thiamine deficiency as it can precipitate Wernicke-Korsakoff syndrome. Thiamine is a co-factor in glucose metabolism, and glucose administration can cause thiamine deficiency to manifest acutely, perhaps by using up remaining thiamine stores. If thiamine deficiency is suspected, thiamine administration should precede glucose.

In summary, investigations should never delay thiamine administration in patients with possible Wernicke’s encephalopathy. Investigations may help to confirm Wernicke’s encephalopathy and exclude other diseases, but cannot replace clinical diagnosis.