Figure 52-1 Sural nerve biopsy from a patient with peripheral neuropathy after bariatric surgery demonstrating very active axonal degeneration. Teased fiber preparations (upper left) show almost all fibers are undergoing early axonal degeneration at the same stage of degeneration, suggesting a common time of histologic insult; epoxy semithin sections stained with methylene blue (upper right) show frequent degenerating fiber profiles (arrows); paraffin cross-sections immunostained with CD68 (lower left) show a fascicle with frequent macrophages in the endoneurium (involved in removal of axonal degeneration products); and a paraffin cross-section immunostained with CD45 (lower right) shows rare endoneurial lymphocytes. There was little evidence of an inflammatory/immune process on this nerve biopsy.
The patient was seen in the nutritional clinic and treated aggressively with a structured dietary schedule of multivitamins and mineral supplements, and monitored fluid and calorie intake. Although subacute inflammatory polyradiculoneuropathy (GBS) was considered, immune therapy was not used because the electrophysiologic and pathologic nerve findings were attributed to poor dietary and vitamin intake rather than to an autoimmune disorder. An endocrinology consultation was obtained, and her hyperthyroidism was treated. At last follow-up visit, she continued to lose weight (12 kg more). Her weakness had stopped progressing, but she still was unable to stand by herself.
Our case shows that neurologic complications can occur after bariatric surgery. Peripheral neuropathy (as in this case) has been reported to be the most frequent complication following weight reduction surgery.1 The frequency of peripheral neuropathy after bariatric surgery is reported to be about 16%.2 The neuropathy pattern after bariatric surgery usually occurs in three forms: sensory-predominant polyneuropathy, mononeuropathy, or radiculoplexus neuropathy. Our patient had a radiculoplexus neuropathy (severe pain and weakness in proximal and distal lower limb segments and proximal upper limb segments) and possibly also a sensory-predominant polyneuropathy. A large controlled study on peripheral neuropathy following bariatric surgery showed that major risk factors for postoperative peripheral neuropathy included rapid and large absolute degrees of weight loss, prolonged postoperative gastrointestinal symptoms (nausea, vomiting, diarrhea, or dumping syndrome) for more than 3 months after the surgery, not attending a nutritional clinic regularly after the surgery, having markers indicating malnutrition (reduced serum albumin and transferring) postoperatively, having postoperative complications requiring hospitalization, and having jejunoileal bypass.2 This patient had many of these risk factors. She had rapid weight loss, she did not attend a nutritional clinic on a regular basis, she did not follow physician’s instructions, and she did not take nutrition supplementation. She also developed gastrointestinal symptoms (nausea and vomiting after the surgery). Even though the gastrointestinal symptoms were not prolonged, they were severe enough to bring her back to medical attention. She also had decreased serum prealbumin and total iron-binding capacity, which indicated a malnourished state. All of these conditions predisposed her to develop a peripheral neuropathy.
The cause of our patient’s peripheral neuropathy was unclear. Metabolic complications and nutritional deficiency after bariatric surgery have been described extensively, including protein-calorie malnutrition; and vitamin B12, folate, vitamin B1, vitamin D, calcium, and copper deficiency.3 Many of these complications can precipitate a peripheral neuropathy in susceptible individuals. This patient had extensive work-up regarding nutritional and metabolic status, but no specific vitamin deficiency was identified. Severe pain in the calves (as our patient described) has been reported in acute peripheral neuropathy caused by thiamine deficiency.4 Even though whole blood thiamine level was normal, an erythrocyte transketolase level of thiamine would have been a more reliable indication of thiamine deficiency.5 She was eventually treated with multivitamins, minerals, and other nutritional supplements, including thiamine, but at last evaluation, she has only improved minimally. Some patients who developed acute sensorimotor neuropathy following bariatric surgery had large inflammatory cell collections seen on their sural nerve biopsies.2 The cause of these inflammatory reactions raised the possibility of an immune etiology for peripheral neuropathy after bariatric surgery. We did perform a sural nerve biopsy in this case to determine if there was inflammatory cause to her neuropathy. Inflammation of the kind seen in GBS was not observed; the macrophage increase in the endoneurium was explained by the fiber degeneration. The nerve biopsy findings of severe, extensive axonal degeneration are not specific but imply a very active disorder, as could be seen from many causes.6
Regardless of whether bariatric surgery causes a neuropathy of the kind encountered here and is due to malnutrition, vitamin deficiency, or autoimmunity, this case emphasizes the importance of both preoperative and postoperative management of bariatric surgery. There is evidence, albeit somewhat uncertain, that careful postoperative management of enteric intake of calories, protein, minerals and vitamins is associated with a lower occurrence of sensorimotor polyneuropathy. Our patient was advised that intensive enteric care was needed during the pre- and postoperative period and decided not to have her bariatric surgery at Mayo Clinic because she found our program too intrusive. We suggest that in caring for bariatric surgery patients, it is important to lose weight in a controlled manner, address postoperative complications promptly, have a comprehensive postoperative nutritional program, and have regular follow-up examination in a nutritional clinic. By addressing these risk factors, we hope to decrease the occurrence of peripheral neuropathy.