Peripheral Neuropathy and Severe Malnutrition ...

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tion of bariatric surgery is beriberi, which is caused by deficiency in thiamine (vitamin B-1). The body's stores of thiamine may be depleted in 18–20 days, and ...
OBES SURG DOI 10.1007/s11695-008-9539-2

CASE REPORT

Peripheral Neuropathy and Severe Malnutrition following Duodenal Switch Erlend T. Aasheim & Dag Hofsø & Jøran Hjelmesæth & Rune Sandbu

Received: 12 March 2008 / Accepted: 15 April 2008 # Springer Science + Business Media, LLC 2008

Abstract Severe thiamine (vitamin B-1) deficiency is a medical emergency that has long been recognized as a potential complication of bariatric surgery. The incidence of this rare complication is largely unknown. We describe a super-obese male patient with extreme lower limb weakness 3 months following a duodenal switch operation, occurring in association with persisting vomiting. Excessive malabsorption led to severe malnutrition, with lower limb edemas and clinical evidence of ascites and pleural effusion. Blood tests revealed low levels of albumin, hemoglobin, potassium, vitamins A, B-1, and B-6, and elevated prothrombin time. The symptoms of neuropathy improved after extensive nutritional therapy. Weight eventually stabilized following elongation of the common channel. This case report demonstrates the importance of awareness of neurological complications following bariatric surgery. These complications require urgent and vigorous therapy when they occur. Keywords Morbid obesity . Bariatric surgery . Thiamine . Malnutrition . Peripheral neuropathy

E. T. Aasheim Department of Medicine, Aker University Hospital and Faculty Division Aker University Hospital, University of Oslo, Oslo, Norway D. Hofsø : J. Hjelmesæth : R. Sandbu Morbid Obesity Center, Vestfold Hospital Trust, Tønsberg, Norway E. T. Aasheim (*) Aker University Hospital Research Center, Trondheimsvn. 235, 0514 Oslo, Norway e-mail: [email protected]

Introduction Bariatric surgery is at present the preferred treatment to induce a substantial and sustained weight loss in morbidly obese patients and has proven benefits on obesity-related diseases such as type 2 diabetes and sleep apnea [1]. The operative morbidity and mortality associated with bariatric surgery is low, as compared with other major surgical procedures [2]. However, nutritional and metabolic complications may also occur. For instance, severe malnutrition led to a need for revision surgery in 5% in one series of duodenal switch patients [3]. Another potential complication of bariatric surgery is beriberi, which is caused by deficiency in thiamine (vitamin B-1). The body’s stores of thiamine may be depleted in 18–20 days, and severe deficiency may lead to symptoms from both the cardiovascular system and nervous system [4]. The neurological conditions (Wernicke’s encephalopathy and peripheral neuropathy) seem to dominate in patients undergoing obesity surgery [5]. More than 30 cases of Wernicke’s encephalopathy have been reported following bariatric procedures [6]. Polyneuropathy was observed in as many as 71 of 435 bariatric surgery patients (17%) [7]. We report a patient with polyneuropathy and severe malnutrition following duodenal switch.

Case Report A 49-year-old super-obese (BMI 61.9 kg/m2, weight 212 kg, height 1.85 m) white man with hypertension, gallbladder disease, sleep apnea, and a former gastric banding procedure underwent an open biliopancreatic diversion with duodenal switch and cholecystectomy at a

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foreign institution in June 2004. The operation and immediate postoperative period was uneventful, and supplementation with multivitamins, calcium, and iron was recommended upon discharge. The patient presented at our outpatient clinic 3 months following surgery, complaining of fatigue and dizziness. He had been unable to take his multivitamin pills because of nausea and had lost 48 kg of weight. Blood tests were notable for elevated prothrombin time and mild anemia (Table 1). Frequent small protein-rich meals and compliance with vitamin and mineral supplementation were recommended. One month later, the patient had a total weight loss of 59 kg and was admitted to hospital. He reported lethargy, persisting vomiting, and unsteadiness. Gait function deteriorated during his stay. Within a few days, severe lower limb weakness made the patient unable to walk, and he ambulated by crawling. A barium swallow indicated a narrow lumen, but no stenosis was identified by endoscopy, which revealed gastritis and an intact duodenoileal anastomosis. A proton pump inhibitor, small mashed meals and nutrition drinks were prescribed. After 2 weeks, the patient had improved, but he was still unable to walk without support. His symptoms were eventually suspected to be related to thiamine deficiency, and treatments with thiamine (a total of 2,000 mg i.m. during

1 month) and vitamin B-12 were initiated. The patient was discharged to a nursing home for 3 weeks. Six months after discharge from our hospital, the patient had lost 100 kg, and still felt lethargic. He could walk but had difficulties mounting stairs and standing up from a squatting position. Examination revealed somewhat atrophic lower extremity muscles. Blood tests revealed severe deficiency in thiamine despite previous supplementation (Table 1). Intramuscular injections with B-vitamins (containing 10 mg of thiamine) were given three times weekly. A blood thiamine level 2 months later was within the normal range and his general health was improving. He still had difficulties standing up from a squatting position. MR imaging of the brain and spinal cord was normal. During the following 3 months, gait function improved further, but despite vigorous supplementation regimens, the patient remained deficient in vitamin A, and the elevated prothrombin time suggested severe protein and/or vitamin K deficiencies. The patient kept losing weight and had eventually lost 119 kg 17 months following surgery. Clinical examination was remarkable for lower limb edemas and signs of ascites and pleural effusion. Biochemical signs of nutritional derangement included low blood levels of albumin, hemoglobin, and potassium (Table 1). An elongation of the common channel was deemed

Table 1 Nutritional status Time since surgery (months)

Reference

3 Nausea

Weight (kg) BMI (kg/m2) Vitamin B-1 (nmol/l) Vitamin B-6 (nmol/l) S-Folate (nmol/L) Vitamin B-12 (pmol/l) Vitamin A (μmol/l) Vitamin E (μmol/l) 25(OH)-vitamin D (nmol/l) PTH (pmol/l) Albumin (g/l) Hemoglobin (g/dL) MCV (fL) Ferritin (μg/l) Prothrombin time (INR) Cholesterol, total (mmol/l) Na (mmol/l) K (mmol/l) Ca, albumin corr. (mmol/l) Phosphate (mmol/l)

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