Obesity in our society is prevalent at an alarming rate. Obesity is linked to many chronic disease such as diabetes, gallbladder disease, heart disease and hypertension, depression as well as cancer of the colon, prostate, breast and ovaries among others. Many times however it is not the risk of disease and diminished quality of life that motivates this society but the social stigma that obesity carries with it. This has caused a great increase in the number of bariatric procedures being performed throughout the country. Bariatric surgery is often the last resort of those that have failed home diets and diets center approaches. It is also viewed by some as the easy way out “I will have the surgery and then my problem is over. Bariatric surgery may involve procedures such as making the stomach smaller with a device like a band, removal of part of the stomach. I usually encounter the patient for one of two reasons. The patient has regained the weight and is still searching for a way to get his or her weight under control. The patient has developed a nutrient deficiency neuropathy. Many times not only is the amount of food the patient can eat reduced but in addition the patient may develop absorption issues. These procedures can be life changing in more ways than one. Patients often times do not want to make the dietary lifestyle changes recommended to them post surgery that goes hand in hand with having the surgery. They do not take their vitamins and they don’t alter their eating habits. In addition, often times these patients fall through the cracks of the medical system after surgery and don’t get the continued long term follow up that they may need. Among the absorption issues that may develop thiamine, B12 and copper deficiencies can occur which lead to neuropathy. This typically manifest as pain, burning and numbness in the feet although other presentation are possible. This is when they come to my office seeking a functional medicine evaluation as well as High Power Laser Therapy treatment for their peripheral neuropathy. Once again, Peripheral neuropathy after bariatric surgery is a little known complication that those who want to undergo the procedure should be aware of and that those with neuropathy should know may be a possible cause of their symptoms. Below are articles from scientific literature regarding Bariatric Surgery and Neuropathy.
Semin Neurol.2010 Sep;30(4):433-5. Epub 2010 Oct 12.
Neuropathy following bariatric surgery.
St. Peter’s Hospital, Helena, Montana 59601, USA. email@example.com
Bariatric surgery is an increasingly common procedure for weight control and is associated with neurologic complications, including disorders of the peripheral nerve. The clinical features of these disorders, steps to take to prevent them, and their prognosis are discussed in this article.
© Thieme Medical Publishers.
Curr Treat Options Neurol. 2010 Jan;12(1):29-36.
Prevention and treatment of peripheral neuropathy after bariatric surgery.
Department of Neurology, University of Arkansas Medical School, 4301 West Markham Street, Slot 500, Little Rock, AR, 72205, USA, firstname.lastname@example.org.
OPINION STATEMENT: Given the ever-increasing problem of obesity, it is not surprising that the number of patients who undergo bariatric surgery continues to rise. For patients who have gastric banding, the amount of food they can consume is limited, and nausea and vomiting may further limit nutritional intake early on. More extensive procedures, such as the Roux-en-Y or biliopancreatic diversion with or without a duodenal switch, not only restrict intake but also limit absorption in the small intestine. As a result, deficiencies in vitamins, minerals, and trace elements may develop, leading to a variety of neurologic complications. The peripheral neuropathies best described with a clear-cut cause are an acute, frequently painful neuropathy or polyradiculoneuropathy associated with thiamine deficiency, and an isolated neuropathy or myeloneuropathy associated with deficiencies of either vitamin B12 or copper. Thiamine deficiency tends to occur in the first weeks or months after surgery, vitamin B12 deficiency may develop at any time from a few years to many years after surgery, and copper deficiency tends to be a fairly late complication, developing several years to many years following surgery. Patients who have undergone bariatric surgery may also have an increased risk of developing focal neuropathies, though these are less clearly related to specific nutritional deficiencies.Ideally, one would like to prevent these neuropathies, but there is no consensus of opinion as to what vitamins and micronutrients need to be taken following bariatric surgery. In addition, many patients who take supplements early on fail to maintain the regimen even though some of the neuropathies can occur fairly late. Supplements frequently recommended include a multivitamin, iron, vitamin D, folic acid, calcium citrate, and vitamin B12. Although thiamine is typically included in a multivitamin, the amount is fairly small, so I recommend adding 100 mg daily for at least the first year. Some have suggested zinc supplementation, but this is potentially problematic because exogenous zinc may interfere with copper absorption. Obtaining blood work every 6 months after surgery will help to identify and treat nutritional deficiencies early.For those patients who have had a bariatric procedure and then develop a neuropathy, evaluating levels of thiamine, copper, vitamin B12, methylmalonic acid, and homocystine is indicated. In addition, since one deficiency is frequently associated with others, obtaining levels of vitamin A, C, D, K, and E, as well as iron, zinc, selenium, and magnesium is worthwhile. Checking total protein, albumin, and cholesterol also gives a sense of general nutritional status. Occasionally, no clear-cut deficiency of a vitamin, mineral, or trace element can be identified in patients with various peripheral nervous system manifestations. Nevertheless, these patients may have at least some recovery with improving nutritional intake and vitamin supplementation, suggesting that we still do not fully understand how nutritional status affects the peripheral nervous system.
Neurology. 2004 Oct 26;63(8):1462-70.
A controlled study of peripheral neuropathy after bariatric surgery.
Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, MN 55905, USA.
BACKGROUND: Although peripheral neuropathy (PN) occurs after bariatric surgery (BS), a causal association has not been established.
OBJECTIVES: To ascertain whether PN occurs more frequently following BS vs another abdominal surgery, to characterize the clinical patterns of PN, to identify risk factors for PN, and to assess if nerve biopsy provides pathophysiologic insight.
METHODS: Retrospective review identified patients with PN after BS. The frequency of PN was compared with that of an age- and gender-matched, retrospectively evaluated cohort of obese patients undergoing cholecystectomy.
RESULTS: Of 435 patients who had BS, 71 (16%) developed PN. Patients developed PN more often after BS than after cholecystectomy (4/126; 3%) (p < 0.001). The clinical patterns of PN were polyneuropathy (n = 27), mononeuropathy (n = 39), and radiculoplexus neuropathy (n = 5). Risk factors included rate and absolute amount of weight loss, prolonged gastrointestinal symptoms, not attending a nutritional clinic after BS, reduced serum albumin and transferrin after BS, postoperative surgical complications requiring hospitalization, and having jejunoileal bypass. Most risk factors were associated with the polyneuropathy group. Sural nerve biopsies showed prominent axonal degeneration and perivascular inflammation.
CONCLUSIONS: Peripheral neuropathy (PN) occurs more frequently after bariatric surgery (BS) than after another abdominal surgery. The three clinical patterns of PN after BS are sensory-predominant polyneuropathy, mononeuropathy, and radiculoplexus neuropathy. Malnutrition may be the most important risk factor, and patients should attend nutritional clinics. Inflammation and altered immunity may play a role in the pathogenesis, but further study is needed.
PMID: 15505166 [PubMed - indexed for MEDLINE]