Thiamine Def/Gastric Bypass

From MedScape Medical News Thiamine Deficiency May Complicate Gastric Bypass CME News Author: Laurie Barclay, MD CME Author: Charles Vega, MD, FAAFP Dec. 30, 2005 -- Thiamine deficiency with a nonclassic presentation may follow gastric bypass for obesity, according to a case report in the December 27 issue of Neurology. "The neurological complications following gastric bypass surgery are diverse," coauthor Raul N. Mandler, MD, from George Washington University in Washington, DC, said in a news release. "Vitamin B1 deficiency and Wernicke encephalopathy should be carefully considered in surgically treated obese patients." The authors describe a 35-year-old woman who developed many symptoms following bariatric gastric bypass, including nausea, anorexia, fatigue, apathy, hearing loss, psychomotor slowing, forgetfulness, ataxia, and bilateral hand paresthesias. By the twelfth postoperative week, she had lost 40 lb and had lethargy, confusion, and difficulty walking, which necessitated hospitalization. Examination showed inattention, fluent speech with decreased comprehension, decreased hearing, strength 3/5 in the lower extremities, vibratory sense decreased in the feet, deep tendon reflexes absent, and wide-based gait. Laboratory abnormalities were a slight elevation in liver enzymes, high serum glucose level (163 mg/dL), and low serum potassium level (2.6 MEq/L). Her mental status continued to decline despite treatment for dehydration. When hospitalized, her heart rate was 125 beats per minute; she opened her eyes to nail bed pressure but followed no commands and was nonverbal. Pupils were round and fixed at 3 mm; oculocephalic and deep tendon reflexes were absent; and general muscle tone was flaccid without spontaneous movements or withdrawal to painful stimuli. Cerebral spine fluid protein level was 90 mg/dL, and there was diffuse slowing on electroencephalogram. Brain magnetic resonance imaging (MRI) revealed bilateral symmetric hyperintense signal on T2-weighted and fluid attenuated inversion recovery images at the floor of the fourth ventricle, periaqueductal gray matter, the medial portions of both thalami, and the premotor and motor cortices, with contrast enhancement in all T2 hyperintense regions. When she was given intravenous (IV) vitamin B1, 100 mg every 8 hours, her oculocephalic reflexes gradually returned to normal, and she eventually became responsive. Follow-up brain MRI 11 days after thiamine repletion showed interval improvement, with less contrast enhancement, but with increased signal on precontrast T1-weighted images in the premotor and motor cortices, likely representing petechial hemorrhages. "Wernicke encephalopathy is a well-defined syndrome, but difficult to identify in the absence of the classic triad of oculomotor abnormalities, ataxia, and confusion," the authors write. "When a patient presents with unusual symptoms (in our case with progressive hearing loss, most likely secondary to thalamic involvement), then blood work (red blood cell transketolase levels) and MRI become helpful tools in making the diagnosis." The authors have disclosed no relevant financial relationships. "This case highlights the variability of Wernicke encephalopathy where the classic trio of eye movement abnormalities, confusion, and ataxia are seen in less than 20% of patients," says Heidi Schwarz, MD, who wrote a related commentary. "It is unusual because the patient also had hearing loss." Dr. Schwarz notes that bariatric surgery may have other complications, including anemia, vitamin D deficiency and bone resorption, rhabdomyolysis, vitamin A deficiency, and hypocalcemia. Neurologic complications are common, especially when there is intractable vomiting causing myelopathy and ataxia due to deficiencies in vitamin B12, copper, or vitamin E; or peripheral neuropathy, plexopathies, and mononeuropathies due to vitamin or micronutrient deficiencies or as yet unknown causes. "Although thiamine deficiency was not documented serologically [in this case report], the course, MRI findings, and response to thiamine establish the diagnosis," Dr. Schwarz writes. "Patients who have had bariatric surgery require a high index of suspicion for Wernicke encephalopathy so that prompt treatment can be given to prevent devastating and often permanent disability." Neurology. 2005;65:1847, 1987 Clinical Context Bariatric surgery is an effective treatment for many patients with morbid obesity, but this procedure has attendant risks. Neurologic complications are particularly serious potential complications of bariatric surgery, including myelopathy and ataxia associated with deficiencies in vitamin B12, vitamin E, and copper. Patients might also experience neuropathies related to other deprivation of essential vitamins and micronutrients. The classic presentation of Wernicke encephalopathy includes oculomotor abnormalities, mental status changes, and ataxia. Unfortunately, this classic presentation occurs in only 20% of cases of Wernicke encephalopathy. Examining risk factors for thiamine deficiency, including bariatric surgery, can help physicians diagnose this disorder, and the current case report highlights an atypical presentation of Wernicke encephalopathy following surgery. Study Highlights ? The authors describe a 35-year-old woman who underwent gastric bypass surgery for obesity. Following the surgery, she developed anorexia, nausea, vomiting, and fatigue. The patient was rehospitalized, where she experienced hearing loss, psychomotor slowing, apathy, forgetfulness, and bilateral hand paresthesias. ? By the twelfth postoperative week, the patient had lost 40 lb and had become increasingly confused. ? On examination, the patient experienced a gradual deterioration in neurologic function, beginning with decreased lower extremity power, absent deep tendon reflexes, and wide-based gait. Subsequently, her pupils became fixed, and spontaneous movements stopped. Eventually, the patient became unresponsive, even to painful stimuli. ? The patient developed elevated serum glucose levels. At the initial evaluation an electroencephalogram was normal, but the patient exhibited diffuse slowing on a second test. MRI of the brain demonstrated bilateral symmetric hyperintense signals at the floor of the fourth ventricle, periaqueductal gray matter, the medial portions of both thalami, and the premotor and motor cortices. ? Initial treatment with 100 mg of thiamine IV yielded no response, but increasing the dose to 100 mg IV every 8 hours produced a good clinical result. On hospital day number 4, the patient regained consciousness, and both pupillary reflexes and extraocular muscle movements returned. She also developed horizontal and gaze-evoked nystagmus at this time. A repeat MRI demonstrated less signal intensity, and there was evidence of petechial hemorrhages in the premotor and motor cortices. Something to think about. Darlene

Darlene, thanks for sharing. I've had some B-1 (thiamin) deficiencies and can relate to some of these symptions. I have to take additional B-1 everyday. I also deal with low potassium. I am having to take prescribed potassium again. Dana