Article: Thiamine Deficiency May Complicate Gastric Bypass
This was in my Medscape Daily News today: It’s set up for continuing
medical education credits, and I’ve included part of that information, too,
because it summarizes.
Thiamine Deficiency May Complicate Gastric Bypass CME
News Author: Laurie Barclay, MD
CME Author: Charles Vega, MD, FAAFP
To earn CME credit, read the news brief along with the CME information that
follows and answer the test questions.
Release Date: December 30, 2005; Valid for credit through December 30, 2006
Credits Available
Physicians - up to 0.25 AMA PRA Category 1 continuing medical education
credits for physicians ;
Family Physicians - up to 0.25 AAFP Prescribed continuing medical education
credits for physicians
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
Learning Objectives for This Educational Activity
Upon completion of this activity, participants will be able to:
* Describe neurologic complications of bariatric surgery.
* List classic symptoms associated with Wernicke encephalopathy.
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.
Pearls for Practice
* Possible neurologic complications of bariatric surgery include
myelopathy, ataxia, and neuropathies.
* The classic triad of Wernicke encephalopathy includes oculomotor
abnormalities, altered mental status, and ataxia.