Nutrional issues after bariatric surgery www.gastricbypassproblems.org

Early deficiency produces fatigue, irritation, poor memory, sleep disturbances, precordial pain, anorexia, abdominal discomfort, and constipation.

The syndrome of peripheral neurologic changes due to thiamine deficiency is called dry beriberi. These changes are bilateral and symmetric, involving predominantly the lower extremities, and begin with paresthesias of the toes, burning of the feet (particularly severe at night), muscle cramps in the calves, and pains in the legs. Calf muscle tenderness, difficulty in rising from a squatting position, a decrease in the vibratory sensation in the toes, and plantar dysesthesia are early signs. A diagnosis of mild peripheral neuropathy can be made when ankle jerks are absent. Continued deficiency causes loss of knee jerk, loss of vibratory and position sensation in the toes, atrophy of the calf and thigh muscles, and finally footdrop and toedrop. The arms may be affected after leg signs are well established.

Cerebral beriberi (Wernicke-Korsakoff syndrome) results from severe acute deficiency superimposed on chronic deficiency. Mental confusion, aphonia, and confabulation constitute the early stage, called Korsakoff's syndrome. Cerebral blood flow is markedly reduced and vascular resistance increased. Wernicke's encephalopathy consists of nystagmus, total ophthalmoplegia, coma, and, if untreated, death.

Cardiovascular (wet) beriberi (Shoshin beriberi) occurs in thiamine deficiency when myocardial disease is prominent. This causes a high cardiac output with vasodilation and warm extremities. Before heart failure occurs, tachycardia, a wide pulse pressure, sweating, warm skin, and lactic acidosis develop. With heart failure, orthopnea and pulmonary and peripheral edema occur; vasodilation continues, sometimes resulting in shock.

Nutritional counseling and follow-up is important for preventing negative neurological side effects following obesity surgery

Bariatric surgery for morbid obesity is associated with neurological complications according to a systematic study of peripheral neuropathy after bariatric surgery. The study, in the Oct. 26, 2004 issue of the journal Neurology, identified the factors that may put people at risk for these complications, according to P. James B. Dyck, M.D., principal investigator in the study.

"Obesity is at epidemic proportions in the United States. The National Institutes of Health (NIH) estimates that 64 percent of adult Americans are overweight or obese. As more people elect to have bariatric surgery for morbid obesity, it's important to monitor our experience with these surgeries and make them as safe as possible," said Dr. Dyck, associate professor of neurology at the Mayo Clinic College of Medicine in Rochester, Minn. "We found that people were at risk for neurological complications (peripheral neuropathy or PN) following bariatric surgery. Nutritional support before and after surgery seems to a key factor in determining whether people had PN complications."

"Diseases of the peripheral nervous system, PN, can be focal, like carpal tunnel syndrome which affects fingers and hands; or more generalized, causing wide spread pain or weakness," Dr. Dyck said. "The peripheral nerves are the 'wires' that go throughout the body and conduct motor and sensory information."

Dr. Dyck spoke today at an American Medical Association's 23rd Annual Science Reporters Conference in Washington D.C.

In the study, the charts of 435 people who had one of two types of bariatric surgery approved for treatment of the morbidly obese by the NIH (gastric bypass and 'stomach stapling') were compared with the charts of 123 obese patients who had gall bladder surgery to determine whether bariatric surgery or abdominal surgery in general was associated with PN. All patients were obese, and were compared on indices including age, gender, rate of weight loss, degree of obesity (body mass index or BMI), time to reach maximum weight loss, and taking multivitamin and calcium supplements, to determine which factors were correlated with neurological complications.

"People who had had bariatric surgery were significantly more likely to have PN than the people in the control group," Dr. Dyck said. "The most common PNs were carpal tunnel syndrome and sensory neuropathy, but a small number had a more severe form of PN which can lead to extreme pain and weakness, sometimes confining people to a wheelchair."

"The risk factors that we found correlated with PN included very rapid weight loss, not taking vitamins and prolonged nausea and vomiting. Factors including age, gender, pre-surgery BMI and general health had no association," Dr. Dyck said. "A major risk factor correlated with PN after surgery was failure to attend a nutritional clinic. The evidence was very strong that PN complications were associated with malnutrition."

"Our study offers a clear message that PN after bariatric surgery is largely preventable and that a multidisciplinary approach to bariatric surgery that includes good follow-up and good nutritional counseling is the key to a successful outcome," Dr. Dyck concluded. "This gives people a good way to evaluate programs that offer bariatric surgery and assure a better outcome."

NEW YORK (Reuters Health) Jul 20 - In the July 21st issue of The New England Journal of Medicine, researchers describe the development of hyperinsulinemic hypoglycemia with nesidioblastosis in six patients who underwent Roux-en-Y gastric bypass surgery.

The authors believe that this was due to an increase in beta-cell trophic factors caused by the operation rather than to hyperfunction of pancreatic islets.

Between 2000 and 2004, the patients underwent gastric bypass for extreme obesity. Dr. F. John Service and colleagues, from the Mayo Clinic in Rochester, Minnesota, note that the onset of spontaneous postprandial hypoglycemia began between 0.5 and 8 years after gastric bypass. The main symptoms were confusion in three patients, loss of consciousness in two, and tunnel vision in one.

During the hypoglycemic episodes, serum glucose levels ranged from 31 to 53 mg/dL, while insulin levels were 3.1 to 28 U/mL. Sulfonylurea levels were undetectable in the five patients who underwent testing.

Aside from equivocal results in one patient, radiologic evaluation showed no evidence of insulinoma. All of the subjects had positive arterial calcium-stimulation tests, which were used to guide pancreatic resection. Analysis of the resected specimens revealed nesidioblastosis in all of the subjects and multiple insulinomas in one patient.

"There is emerging recognition that postprandial hypoglycemia may be due to endogenous hyperinsulinemia from abnormal islets, as a result of either nesidioblastosis or insulinoma," the authors state. The present results extend this finding to patients with postprandial neuroglycopenia following gastric bypass surgery, they add.

In a related editorial, Dr. David E. Cummings, from the University of Washington, Seattle, comments that "the possibility that Roux-en-Y gastric bypass stimulates beta-cell-trophic factors should spur research to identify these entities...so that their physiological effects can be harnessed and used pharmacologically to treat diabetes."

N Engl J Med 2005;249-254,300-301.

Postgastroplasty syndrome: Polyneuropathy

Selenium Deficiency (it is unknown whether gastric bypass patients can digest and absorb the micronutrients like selenium, chromium etc.)

Thiamine (vitamin B1 deficiency)