Bariatric Beriberi: Thiamin Deficiency in the Bariatric Patient

This Month’s Contributor: Laura Frank, PhD, RD, CD, MPH

Dr. Frank is currently a Clinical Assistant Professor for Washington State University in the Program of Nutrition and Exercise Physiology. She is also director of clincial sites for the Coordinated Program of Dietetics. Dr. Frank is a clinical dietitian at Madigan Army Medical Center (MAMC) in bariatrics. She also writes articles and presents on nutrition topics related to bariatric surgery.

Bariatric Times. 2011;8(1):14

Introduction
Thiamin (vitamin B1) is a water-soluble vitamin found in many food products, including meat (with pork being the best source of thiamin), legumes, and whole- or enriched-grain products.[1] Thiamin is important for the body as a cofactor in several enzymes associated with carbohydrate metabolism and energy production. Thiamin deficiency historically has been termed beriberi, derived from the Singhalese word “beri,” meaning weakness, and refers to clinical manifestations associated with a deficient state of thiamin.[2] Beriberi can present as “wet” beriberi with cardiac involvement including cardiac hypertrophy and dilation, tachycardia, and edema, especially in the lower extremities.[3] “Dry” beriberi is manifested by polyaxialneuropathy, muscle weakness, pain, and paralysis.3 More seriously, thiamin deficiency can manifest as Wernicke’s Korsakoff (WK) syndrome, which is also known as Wernicke’s encephalopathy.[2] Classic components of WK include a combination of ataxia, opthalmoplegia, nystagmus, and mental confusion.[4] A systematic review regarding bariatric encephalopathy after bariatric surgery has been published.[2]

Thiamin deficiency after bariatric surgery has been well documented and has been termed bariatric beriberi.[3] Among the most commonly reported bariatric surgery to be associated with WK is Roux-en Y gastric bypass (RYGBP),[4–9] However, WK has also been reported to be associated with post-adjustable gastric band10 gastrectomy,[11] intragastric balloon (BIB),[4] and gastroplasty.[12] Most reported cases of WK and polyneuropathy after bariatric surgeries are associated with protracted vomiting,[2] typically occurring within the first 2 to 3 months after surgery.[4] Rapid and/or appreciable weight loss and dietary insufficiency have also been implicated in the etiology of thiamin deficiency,[2,4,9] as well as loss of appetite, eating avoidance, and nonadherence to vitamin supplementation.[2]

Thiamin assessment prior to repletion may be used to confirm suspicions of thiamin deficiency in bariatric patients; however, practical limitations may influence the practitioner to treat the patient without confirmation of deficiency and monitor and evaluate resolution of signs and symptoms of thiamin deficiency. Ideally, all patients should be tested for subnormal thiamin concentrations as demonstrated by plasma or urine thiamin levels, erythrocyte transketolase activity or by stimulation of this enzyme using thiamin pyrophosphate (TPP).[13] It is important to note that some of these tests are expensive and may not be readily available.

Computed axial tomography or magnetic resonance imaging (MRI) can be done to search for central nervous system morphology in patients with suspected WK.[4]

There is insufficient evidence from controlled trials to generate practitioner guidelines in the dose, frequency, route, or duration of thiamin treatment in patients with suspected deficiency.[14] Positive diagnostic evidence includes several precipitating factors, specific clinical manifestations, and a favorable response to thiamin repletion. Parenteral doses of 100mg per day for the first seven days followed by daily oral doses 50mg per day until complete recovery have been recommended.[15] There are other reports recommending 100mg thiamin intravenous (IV) or intramuscular (IM) daily until symptoms have improved.[16]

The importance of thiamin’s role in metabolism and neurological function should not be minimized. Multidisciplinary approaches to the prevention, diagnosis, and treatment of thiamin deficiency are important in improving clinical outcomes in the bariatric surgery patient.

References
1.    Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism, Fifth Edition. Canada: Wadsworth Cengage Learning; 2009;9:323–333.
2.    Aasheim ET. Wernicke encephalopathy after bariatric surgery. A systematic review. Ann Surg. 2005;248(5):714–720
3.    Gollobin C, Marcus WY. Bariatric beriberi. Obes Surg. 2002;12:309–311.
4.    Lopes Chaves LC, Faintuch J, Kahwage S, de Assis Alencar F. A cluster of polyneuropathy and Wernicke-Korsakoff syndrome in a bariatric unit. Obes Surg. 2002;12:328–334.
5.    Salas-Salvado J, Garcia-Lorda P, Cuatrecasas G, et al. Wernicke’s syndrome after bariatric surgery. Clin Nutr. 2000;19(5):371–373.
6.    Escalona A, Perez G, Leon F, et al. Wernicke’s encephalopathy after Roux-en Y gastric bypass. Obes Surg. 2004;14:1135–1137.
7.    Loh Y, Watson WD, Verma A, et al. Acute Wernicke’s encephalopathy following bariatric surgery: clinical couse and MRI correlation. Obese Surg. 2004;14:129–132.
8.    Worden RW, Allen HM. Wernicke’s encephalopathy after gastric bypass that masqueraded as acute psychosis: a case report. Curr Surg. 2006;63:114–116.
9.    Juhasz-Pocsine K, Rudnick SA, Archer RL, Harik SI. Neurological complications of gastric bypass surgery for morbid obesity. Neurology. 2007;68:1843–1850.
10.    Bozbora A, Coskun H, Ozarmagan S, et al. A rare complication of adjustable gastric banding: Wernicke’s encephalopathy. Obes Surg. 2000;10:274–275.
11.    Koike H, Misu K, Hattori N, et al. Postgastrectomy polyneuropathy with thiamine deficiency. J Neurol Neurosurg Psychiatry. 2001;71:357–362.
12.    Toth C, Voll C. Wernicke’s encephalopathy following gastroplasty for morbid obesity. Can J Neurol Sci. 2001;28:89–92.
13.    Halverson JD. Micronutrient deficiencies after gastric bypass for morbid obesity. Am Surg. 1986;52:594–598.
14.    Day E, Bentham P, Callaghan R, et al. Thiamine for Wernicke-Korsakoff syndrome in people at risk from alcohol abuse. Cochrane Database Syst Rev. 2004;CD004033.
15.    Aills L, Blankenship J, Buffington C, et al. Bariatric Nutrition: suggestions for the surgical weight loss patient. Surg Obes Relat Dis. 2008. Suppl;4(45).
16.    Heye N, Terstegge K, Sirtl C, et al. Wernicke’s encephalopathy—causes to consider. Intensive Care Med. 1994;20:282–286.

Category: Nutritional Considerations in the Bariatric Patient, Past Articles