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Signs are Not Always Clear for Wernicke Encephalopathy After Bariatric Surgery
What to Look for

Patients who have bariatric surgery can develop Wernicke encephalopathy, a constellation of neurologic symptoms caused by thiamine (vitamin B1) deficiency, according to a review article in the Mar. 13 issue of Neurology (68:807–811).

“The index of suspicion should be highest in the first few weeks after surgery, because Wernicke encephalopathy seems to occur between four and 12 weeks after surgery,” the authors wrote. “The half-life of thiamine is 10 to 20 days, and the occurrence of symptoms four to 12 weeks after surgery would thus reflect depletion of thiamine stores. However, Wernicke encephalopathy can occur as early as 2 weeks to as late as 18 months after surgery.”

The investigators identified 32 cases after reviewing the literature for case reports, case series, and cohort studies of Wernicke encephalopathy after bariatric surgery. The patients had two of four classic symptoms of Wernicke encephalopathy: dietary deficiencies, oculomotor abnormalities, cerebellar dysfunction, and altered mental state or mild memory impairment. Most had MRI findings of hyperintense signals in the periaqueductal gray area and dorsal medial nucleus of the thalamus, but MRI results were normal in 15 patients. Serum thiamine levels were low in four patients and normal in two patients, but information about thiamine supplementation was unavailable in most reports.


Dr. Pariwat Thaisetthawatkul said “bariatric surgery can cause complications, especially metabolic complications related to nutritional deficiency,” but the good news is that “Wernicke encephalopathy is potentially treatable.”

As more obese people are treated with this surgery, neurologists need to be prepared to diagnose and treat Wernicke encephalopathy, even without the full gamut of symptoms, signs, and normal neuroimaging studies, said the principal study author Sonal Singh, MD, in a phone interview. Dr. Singh is an instructor of internal medicine at Wake Forest University Health Sciences in Winston-Salem, NC.

Patients could have atypical features such as numbness of the arms and legs [8 cases], visual disturbances and convulsions [one case], as well, he said. “It's important to know that this syndrome occurred most commonly in young women who were vomiting one to three months after the surgery. This time period coincides with the time required for thiamine deficiency to develop.”

Dr. Singh added: “Because the treatment, parenteral thiamine, is harmless, and patients could die of Wernicke encephalopathy, neurologists should feel comfortable making the diagnosis based on clinical findings and then treating patients even if they do not have all three features and even if brain-imaging results are normal.”

Dr. Singh noted that prospective studies are needed to determine the incidence of postoperative Wernicke encephalopathy. “Wernicke encephalopathy typically occurs in alcoholics,” he said, adding that neurologists need to remember that bariatric surgery is also a risk.


Commenting on the study, Joseph R. Berger, MD, told Neurology Today: “It's important for neurologists to know that after bariatric surgery, patients are at risk of neurologic complications. The most important and serious of these is Wernicke encephalopathy, because of the morbidity and possible irreversibility associated with it.” Dr. Berger, the Ruth L. Works Professor and chair of neurology at the University of Kentucky College of Medicine in Lexington, has conducted research on the neurologic complications of bariatric surgery (Arch Neurol 2004;61:1185–1189).

Dr. Berger agreed with Dr. Singh that Wernicke encephalopathy could occur without all three symptoms. “Some individuals have only one or two of the triad,” he said. “The neurologist is often called in when the patient is confused or has features of peripheral neuropathy. But this condition can start with ocular motility disorders, seizures, or other neurologic manifestations. If neurologists are not aware that this is a consequence of thiamine deficiency, they can overlook it and not treat it quickly enough.”

One contributing issue is the short hospitalization associated with bariatric surgery, typically two or three days, and the fact that patients don't develop thiamine deficiency until they have been home for some time. “It generally takes weeks for thiamine to be depleted, which is why the authors were seeing it one to three months after surgery,” he said. “To give intravenous thiamine on day one or two would be insufficient. A day, two days, or a week of vomiting is not enough to lead to this disorder.”

There are no guidelines for monitoring of postoperative neurologic complications after bariatric surgery, he said, noting that centers with a high volume of bariatric surgery typically have dietitians who are aware of the mineral deficiencies that may be seen postoperatively. “As we perform this surgery more often, there will be guidelines written regarding these deficiencies and how to manage appropriately,” he said.

For now, neurologists need to be concerned about the possibility of Wernicke encephalopathy in people with isolated altered mental status after bariatric surgery, those with nystagmus, and those with peripheral neuropathy. “Rapid administration of parenteral thiamine could be critical to preserving or restoring normal neurologic functioning,” he said.

Although the authors found that most patients received parenteral thiamine and made a complete recovery, Dr. Berger expressed concern that, not infrequently, patients live with residual features of Wernicke encephalopathy.

Dr. Berger agreed that a prospective study is needed to monitor bariatric surgery patients' postoperative vitamin and mineral levels and their dietary history, as well as nausea and vomiting. “In centers where a large number of these surgeries are being performed, we need to identify the factors that increase the risk,” he said. “This is a population growing ever larger year by year. As physicians we need to be aware of the complications that occur in them.”


“Bariatric surgery can cause complications, especially metabolic complications related to nutritional deficiency,” said Pariwat Thaisetthawatkul, MD, an assistant professor of neurology at the University of Nebraska in Lincoln, in a phone interview. But the good news: “Wernicke encephalopathy is potentially treatable.” While at the Mayo College of Medicine, he and co-investigators published a prospective study about peripheral neuropathy after bariatric surgery (Neurology 2004;63:1462–1470).


As more obese people are treated with bariatric surgery, neurologists need to be prepared to diagnose and treat Wernicke encephalopathy, even without the full gamut of symptoms, signs, and normal neuroimaging studies.


• Singh S, Kumar A. Wernicke encephalopathy after obesity surgery: a systematic review. Neurology 2007;68:807–811.
• Berger JR. The neurologic complications of bariatric surgery. Arch Neurol 2004;61:1185–1189.
• Thaisetthawatkul P, Collazo-Clavell ML, Dyck PJ, et al. A controlled study of peripheral neuropathy after bariatric surgery. Neurology 2004;63:1462–1470.