Acute Wernicke's Encephalopathy following Bariatric Surgery: Clinical Course and MRI Correlation

Abstract

Postoperative complications and nutritional deficits resulting from bariatric surgery can lead to severe vitamin-deficiency states, such as Wernicke's encephalopathy (WE). Patients with acute WE generally present with the classic clinical triad of inattentiveness, ataxia, and ophthalmoplegia. We describe a patient who presented with acute WE at 2 months after laparoscopic bariatric surgery. Initial MRI of the brain demonstrated the characteristic injuries of WE, and repeat imaging showed resolution after 4 months of thiamine supplementation, at which time the patient had normal gait but persistent memory deficits. Even with early recognition and aggressive therapy, acute WE commonly results in permanent disability due to the irreversible cytotoxic effects on specific regions of the brain. Since the clinical onset of acute WE follows a predictable time-course in post-bariatric surgery patients with malnutrition, we recommend prevention by administration of parenteral thiamine beginning at 6 weeks postoperatively in malnourished patients.

Practical Recommendations of the Obesity Management Task Force of the European Association for the Study of Obesity for the Post-Bariatric Surgery Medical Management

“…Therefore, a short period of persistent vomiting impairing regular food intake can precipitate thiamine deficiency [5,25]. Symptomatic thiamine deficiency has been described after a few weeks of intractable vomiting after any bariatric procedure, usually as a consequence of mechanical problems such as stoma stenosis after gastric bypass [32], excessive band tightness or band slippage after gastric banding [33] and stomach oedema with impaired nutrition after sleeve gastrectomy [34]. Cases of thiamine deficiencies have been reported also after biliopancreatic diversion [35].…”

Wernicke's Encephalopathy in a Patient with Schizophrenia

“…17,22 Even with early recognition and aggressive therapy, permanent disability often occurs due to the irreversible cytotoxic effects on specific regions of the brain. 1 While alcohol abuse is the predominant risk factor for WE, numerous other conditions have been associated with its development, all of which predispose to malnutrition or vitamin deficiency (Table 2). [1][2][3][4][5][6][7][8][9][10][11] Wernicke's encephalopathy can occur in both acute and chronic malnutrition states, as body stores of thiamine are only sufficient for up to 18 days.…”

“…1 While alcohol abuse is the predominant risk factor for WE, numerous other conditions have been associated with its development, all of which predispose to malnutrition or vitamin deficiency (Table 2). [1][2][3][4][5][6][7][8][9][10][11] Wernicke's encephalopathy can occur in both acute and chronic malnutrition states, as body stores of thiamine are only sufficient for up to 18 days. 23 Previous published case reports suggests that there is an approximate lag time of 4 to 6 weeks from onset of thiamine-deficient diet to symptomatic presentation of WE.…”

“…[1][2][3][4][5][6][7][8][9][10][11] Data from autopsy series note the prevalence of nonalcoholic WE to range from 0.8% to 2.8%. 12,13 In one report, 20% of cases were diagnosed before death.…”

Wernicke encephalopathy following splenectomy in a patient with liver cirrhosis: a case report and review of the literature

“…This triad of symptoms is seen, however, in only 16% of patients (Sechi and Serra, 2007;Cho et al, 2009), and considerable discrepancy exists between pathologic features and presenting signs (Doherty et al, 2002;Loh et al, 2004).…”