Bariatric surgery is being performed more often to alleviate the symptoms of severe obesity. There are complications to this surgery that need to be understood, however. To help understand the pathophysiology of neuromuscular complications after bariatric surgery, this article reviews the techniques and surgical and metabolic complications of bariatric surgery. Then, neuromuscular complications after the surgery are reviewed.
Obesity is defined as a body mass index (BMI) of greater than or equal to 30 kg/m 2 . Severe obesity is defined as 100 lb above ideal body weight or as a BMI above 35 kg/m 2 . Obesity has been shown to be associated with many comorbidities, such as cardiovascular-related disease, stroke, obstructive sleep apnea, type 2 diabetes mellitus, dyslipidemia, hypertension, hepatobiliary disease, cancer, endocrine disorders, psychosocial problems, and many orthopedic complications . Management options for severe obesity can be divided into nonsurgical or surgical approaches. The nonsurgical approach includes behavioral treatment , nutritional modification , and drug treatment . In the case of morbid obesity, however, conservative management has been disappointing . In 1991, the National Institutes of Health issued a statement from a consensus conference panel recommending that surgical options or bariatric surgery be strongly considered in selected patients who have morbid obesity . This type of surgery was developed around the 1950s as a result of observations on the consequence of patients who had short bowel syndrome . After that, the procedures have been performed increasingly and become more popularized. The number of the procedures performed increased from 20,000 in 1993 to more than 120,000 in 2003 . Bariatric surgery is very effective in initiating and maintaining weight loss, and in reducing comorbidities . The procedures have been adopted by people from all walks of life. Generally, indications to consider bariatric surgery include 1) adult patients who have a BMI greater than 40 kg/m 2 or 2) adult patients who have a BMI between 35 and 40 kg/m 2 and have comorbid conditions such as cardiovascular diseases, severe diabetes mellitus, or hypertension . To understand the pathophysiology of neuromuscular complications after bariatric surgery, it would be very helpful to review first the techniques: surgical and metabolic complications of bariatric surgery. Then, neuromuscular complications after the surgery will be reviewed.
Techniques of bariatric surgery and surgical complications
Bariatric surgery may be divided into three main types: restrictive, malabsorptive, and combined procedures . Vertical banded gastroplasty (VBG) and gastric banding (GB) are examples of restrictive procedures.
In VBG, a small proximal gastric pouch (usually less than 20 mL in size) will be created . This pouch is drained through a small outlet (usually 10 to 12 mm in diameter) along the lesser curvature of the stomach . In pure restrictive procedures, normal absorption of nutrients through the small intestines is left intact. The procedure produces early satiety, and weight loss is achieved through reduced calorie intake. Because of this, nutritional deficiencies very uncommonly occur, unless there are complications such as severe nausea and vomiting, which can occur in about 8% of patients , or marked changes in eating habits .
Biliopancreatic diversion (BPD) is an example of malabsorptive procedure. This procedure was developed and popularized in Europe . The procedure creates fat malabsorption by rerouting bile from entering the usual route, at proximal small intestine, to a common limb created at the distal ileum . In BPD, a proximal gastric pouch, the size of which is about 100 to 150 mL, is created along the lesser curvature of the stomach . The distal ileum is divided at about 250 cm from the ileocecal valve, and the distal stump is lifted and anastomosed to the created stomach pouch as an alimentary limb The proximal stump is anastomosed to the alimentary limb as a side-to-side entero-enterostomy at about 50 to 100 cm from the ileocecal valve, thus creating a common channel, where the food, bile, and digestive enzymes can be mixed. The length of this common limb depends on how severe malabsorption is required in each individual. To reduce the risk of developing proximal duodenal ulcers after the procedure, distal gastrectomy may be performed . This procedure results in significant weight loss but has many adverse effects, such as diarrhea, gall stones, malodorous stool and gas, vitamin and mineral deficiencies, especially fat-soluble vitamins, protein–calorie malnutrition, and bacterial overgrowth. The patients who have this procedure will need to have a close and life-long follow-up and nutritional care .
The most commonly performed bariatric procedure in the United States is Roux-en-Y gastric bypass (RYGB) . This combined procedure uses a small gastric pouch (10 to 30 mL), which is drained to 75 to 150 cm Roux limb. The Roux limb is created from a distal stump of the jejunum divided at about 30 to 50 cm distal to the ligament of Trietz . The proximal stump then is anastomosed as entero-enterostomy to the Roux limb. The point of anastomosis dictates the length of the Roux limb. Even though RYGB is considered a gold-standard of gastric bypass procedure, this technique could be modified in numerous ways, such as variation in size of gastric pouch and gastrojejunostomy, length of the Roux limb, and method to create the gastric pouch . RYGB has been shown to result in long-term and sustained weight loss in about 70% of patients . Compared with pure restrictive procedures, RYGB has been shown to be more effective in terms of absolute amount and maintenance of weight loss .
Jejunoileal bypass merits mentioning even though the procedure no longer is performed because of the occurrence of fatal complications following the surgery. There were many patients, however, who had this operation and could remain subjected to its long-term complications. In this type of surgery, the jejunum was divided at 35 cm distal to the ligament of Treitz, and the proximal stump was anastomosed in an end-to-side manner to the terminal ileum, about 10 cm from the ileocecal valve . About 300 to 500 cm of bowel was bypassed in this procedure. Jejunoileal bypass was popular and remained standard procedure for about 15 to 20 years but was found later to be associated with fatal hepatic failure and cirrhosis in most patients. Many patients also developed an autoimmune process causing fever, joint pain, and cutaneous eruption. Other complications included severe protein malnutrition, calcium oxalate nephropathy, electrolyte imbalance, severe vitamin and mineral deficiencies, diarrhea, bacterial overgrowth, and osteoporosis . The procedure eventually was abandoned.
Complications after bariatric surgery could be perioperative, short-term (within the first year) or long-term . The most common early perioperative complication is leakage of anastomosis , followed by obstruction and pulmonary embolism. Short-term complications include mainly issues related to weight loss and gall stone formation. Other commonly seen problems in this period include gastrointestinal (GI) symptoms such as nausea, vomiting, dumping syndrome, diarrhea, food intolerance, dehydration, and anastomotic ulcers .
Some GI symptoms will be focused on here, because they are related to the occurrence of neuromuscular complications after the surgery. Nausea and vomiting are the most common complaints after bariatric surgery . These symptoms are seen more often in patients who have undergone restrictive procedures . A very common cause is noncompliance to the recommended diet regimen after surgery . This includes eating too fast, too much food volume in each meal, eating a big chunk of meat, especially red meat and poultry, and inadequate chewing. It is very important to rule out surgical complications such as stoma or outlet obstruction in patients who present with progressive vomiting or sudden intolerance to all types of food . Dietary recommendations to prevent vomiting includes chewing thoroughly, eating meals slowly (longer than 20 minutes), small meal volume (less than 45 mL), and avoidance of meat in case of meat intolerance . Dumping syndrome is seen more commonly after a combined procedure such as RYGB or in some patients who had malabsorptive procedures such as BPD . The symptoms start in these patients soon after taking in a diet with high sugar content . The symptoms of dumping syndrome can be divided into two phases, early and late, and have both GI and vasomotor, or autonomic, symptoms . GI symptoms include nausea, abdominal cramps, and diarrhea. Vasomotor symptoms consist of tremulousness, profuse sweating, lightheadedness, flushing, and syncope . The early phase of dumping syndrome is caused by rapid transit of hyperosmolar food content, especially food rich in carbohydrates, into the small intestine, causing fluid shift from the vascular space into the GI tract . Another factor precipitating the early phase is increased surge of enteropeptides. The late phase of dumping syndrome occurs about 1 to 3 hours after eating and is caused by reactive hyperinsulinemic hypoglycemia . Management includes avoiding food high in sugar or fat, small meals, and use of somatostatin or its analog . Diarrhea is frequently seen after RYGB and BPD. After RYGB, diarrhea can be a presentation of dumping syndrome . After BPD, diarrhea, malodorous stool, and gas occur mainly as a result of fat malabsorption and are seen less frequently when the common’ limb is 100 cm . The other causes of diarrhea include infection, bacterial overgrowth, and food or lactose intolerance .
Metabolic complications after bariatric surgery and its neurological disorders
Because the aim of bariatric surgery is to significantly reduce amount of food intake and alter the route of food absorption, metabolic complications, particularly from protein–calorie malnutrition and vitamin and mineral deficiencies tend to occur . The type and severity of metabolic complications depend on the type of surgery. Of note is that about 20% to 30% of obese patients who underwent bariatric surgery were found to have micronutrient deficiency even before surgery . This mandates a careful preoperative evaluation of the nutritional status . The mechanisms by which neurologic injury occur after bariatric surgery are related mostly to metabolic or nutritional complications. Detailed general discussion about all nutritional deficiency is beyond the scope of this article. Only the nutrient deficiency that potentially causes neuromuscular complications after bariatric surgery will be focused on here. These are vitamin B12 (cobalamin), vitamin B1(thiamine), copper, calcium and vitamin D, folate, and vitamin B6 (pyridoxine).
Vitamin B12 is essential in DNA synthesis, being a cofactor for folate-dependent methionine synthase and mitochondrial–β-oxidation of fatty acids, being a cofactor for methylmalonyl coA mutase . It is also probably essential for neurologic function, because the deficiency may cause both central and peripheral neurological disorders . After bariatric surgery, vitamin B12 deficiency occurs commonly. The prevalence is from 12% to 70% . Mechanisms of deficiency include reduced acidity in the stomach pouch, meat intolerance, and reduced intrinsic factor secretion after bariatric surgery . Vitamin B12 deficiency is seen most frequently after RYGB and BPD . It occurs more frequently in patients who develop meat intolerance and nonvitamin users after the surgery . B12 deficiency causes hematological, GI, and neurological disorders. The most well-known neurological disorder arising from B12 deficiency is subacute combined degeneration of spinal cord. After bariatric surgery, parenteral (subcutaneous or intramuscular) administration of 1000 μg once a month is recommended for B12 supplementation , even though oral B12 supplementation at the dose of 350 μg daily has been reported to be effective . Interestingly, even though low serum levels of vitamin B12 are common after bariatric surgery, most cases are asymptomatic . Subacute combined degeneration from B12 deficiency has been reported after partial gastrectomy from the other indications and has been reported after bariatric surgery only recently .
Vitamin B1 plays an important role in both metabolic and nerve functions, including acetylcholine receptor clustering and acetylcholine biosynthesis . Vitamin B1 is reabsorbed predominantly in duodenum and jejunum, through a carrier-mediated transport (at lower intakes) and passive diffusion (at higher intakes) . Only a small amount is stored in the body, mainly in the muscles and the rest in heart, liver, kidneys, and the nervous tissue . In bariatric surgery, reduced absorption of vitamin B1 occurs from reduced acid production from stomach and, most importantly, following prolonged and severe nausea and vomiting The prevalence of thiamine deficiency after bariatric surgery is unknown but is associated mostly with VBG, where reduced food intake is the main cause . Vitamin B1 deficiency causes peripheral (beriberi) and central (Wernicke’s encephalopathy) neurological disorders . In Western populations, B1 deficiency manifesting as Wernicke’s encephalopathy and beriberi is very rare, seen mainly in alcoholics. On the other hand, beriberi is seen predominantly in Asian populations, especially in people who eat milled rice and have high carbohydrate intake but low meat intake. This difference in clinical predisposition is of unclear cause, but different genetic background may play a role . Beriberi, however, has been reported in adolescents who underwent RYGB . It is very important to recognize the syndrome, because prompt treatment results in dramatic improvement, and late treatment can result in permanent neurologic sequelae. The recommended treatment is immediate intravenous administration of thiamine 100 mg, followed by 100 mg intramuscularly daily for 5 days and oral maintenance permanently . Intravenous glucose without thiamine can precipitate Wernicke’s encephalopathy in a severely malnourished patient. To confirm the diagnosis of vitamin B1 deficiency, measurement of erythrocyte transketolase activity is the most reliable . The prevalence of Wernicke’s encephalopathy after bariatric surgery is unknown. Wernicke’s encephalopathy after bariatric surgery has been reviewed recently . The onset was mostly 4 to 12 weeks after surgery. The syndrome was seen after both restrictive and combined procedures. Vomiting was the most common predisposing factor. Most patients had the clinical triad of the syndrome. Treatment with parenteral thiamine results in a complete recovery in most patients.
Copper deficiency recently has emerged as a cause of neurological disorders following gastric surgery . Copper absorption into intestinal mucosa requires copper transporters (Ctr1 copper transporter and DCT-1) . It then is transported to ATP7A to be exported from the intestinal cells into the circulation. Clinically, copper deficiency causes hematologic and neurologic manifestations . Neurological symptoms start subacutely in the form of myeloneuropathy. The frequency of copper deficiency after bariatric surgery remains unknown. So far, there has been no general recommendation regarding copper supplement after bariatric surgery. The clinical syndrome, however, needs to be recognized and the deficiency corrected promptly if it happens.
Calcium and vitamin D have a major function in maintaining bone health in the human body . Vitamin D works through its active form, 1, 25(OH) 2 D. The primary action of 1, 25 (OH) 2 D is to promote intestinal absorption of calcium and phosphorus through the small intestine. This reaction is regulated by parathyroid hormone. Moreover, calcium is also important in nerve and muscle functions . Calcium is absorbed mainly in the duodenum and proximal jejunum, whereas vitamin D is absorbed mainly in the jejunum and ileum . After RYGB and BPD, calcium and vitamin D deficiency predictably occurs. Possible causes include bypassing the duodenum and proximal jejunum, food intolerance, and fat malabsorption. The frequencies of calcium and vitamin D deficiencies were reportedly 10% and 50%, respectively, after RYGB . The deficiency results in osteoporosis and osteomalacia. Neurologically, osteomalacia and vitamin D deficiency long have been known to be associated with proximal myopathy (osteomalacic myopathy) . Measurement of serum vitamin D, urine calcium, serum bone alkaline phosphatase (BAP), and serum parathyroid hormone (PTH) levels would help establishing the diagnosis. In general, serum vitamin D and 24-hour urine calcium are decreased (total 25–OH D less than 15 ng/mL), and the levels of BAP and PTH are elevated . Treatment with vitamin D supplement results in definite improvement in strength and pain. The recommended vitamin D supplementation after bariatric surgery is to administer 50,000 IU of vitamin D3 (cholecalciferol) or vitamin D2 (ergocalciferol) once per week . A case of osteomalacic myopathy after jejunoileal bypass has been reported .
Folate or folic acid consists of pterin linked to p-aminobezoic acid. The most common tissue form of folic acid is methyl-tetrahydrofolate (methyl-THF) . Vitamin B12 acts as a coenzyme in the conversion of methyl-THF to THF, the biologically active form. B12 deficiency then can cause folate deficiency . Folate is absorbed mainly at the proximal intestine, mediated by a saturable, specific carrier . Absorption by diffusion, however, may also occur at high concentrations . After bariatric surgery, folate deficiency occurs as a result of reduced food intake and reduced gastric acid secretion that facilitates folate absorption . The incidence could be as high as 35% . Folate deficiency after bariatric surgery may present with megaloblastic anemia or could be asymptomatic . Neurologically, folate deficiency has been reported to be associated with peripheral neuropathy or neuropsychiatric disorders . In some cases, the clinical features of subacute combined degeneration have been observed . The incidence of neurological complications is very low, however, and the association of these neurologic manifestations to folate deficiency has been debated . The recommended dose of folate supplement after bariatric surgery is 1 mg/d .
Vitamin B6 consists of three main active derivatives: pyridoxal, pyridoxine, and pyridoxamine . The incidence of B6 deficiency after bariatric surgery is about 17% Neurological disorders resulting from B6 deficiency after bariatric surgery never have been reported, however.
Metabolic complications after bariatric surgery and its neurological disorders
Because the aim of bariatric surgery is to significantly reduce amount of food intake and alter the route of food absorption, metabolic complications, particularly from protein–calorie malnutrition and vitamin and mineral deficiencies tend to occur . The type and severity of metabolic complications depend on the type of surgery. Of note is that about 20% to 30% of obese patients who underwent bariatric surgery were found to have micronutrient deficiency even before surgery . This mandates a careful preoperative evaluation of the nutritional status . The mechanisms by which neurologic injury occur after bariatric surgery are related mostly to metabolic or nutritional complications. Detailed general discussion about all nutritional deficiency is beyond the scope of this article. Only the nutrient deficiency that potentially causes neuromuscular complications after bariatric surgery will be focused on here. These are vitamin B12 (cobalamin), vitamin B1(thiamine), copper, calcium and vitamin D, folate, and vitamin B6 (pyridoxine).
Vitamin B12 is essential in DNA synthesis, being a cofactor for folate-dependent methionine synthase and mitochondrial–β-oxidation of fatty acids, being a cofactor for methylmalonyl coA mutase . It is also probably essential for neurologic function, because the deficiency may cause both central and peripheral neurological disorders . After bariatric surgery, vitamin B12 deficiency occurs commonly. The prevalence is from 12% to 70% . Mechanisms of deficiency include reduced acidity in the stomach pouch, meat intolerance, and reduced intrinsic factor secretion after bariatric surgery . Vitamin B12 deficiency is seen most frequently after RYGB and BPD . It occurs more frequently in patients who develop meat intolerance and nonvitamin users after the surgery . B12 deficiency causes hematological, GI, and neurological disorders. The most well-known neurological disorder arising from B12 deficiency is subacute combined degeneration of spinal cord. After bariatric surgery, parenteral (subcutaneous or intramuscular) administration of 1000 μg once a month is recommended for B12 supplementation , even though oral B12 supplementation at the dose of 350 μg daily has been reported to be effective . Interestingly, even though low serum levels of vitamin B12 are common after bariatric surgery, most cases are asymptomatic . Subacute combined degeneration from B12 deficiency has been reported after partial gastrectomy from the other indications and has been reported after bariatric surgery only recently .
Vitamin B1 plays an important role in both metabolic and nerve functions, including acetylcholine receptor clustering and acetylcholine biosynthesis . Vitamin B1 is reabsorbed predominantly in duodenum and jejunum, through a carrier-mediated transport (at lower intakes) and passive diffusion (at higher intakes) . Only a small amount is stored in the body, mainly in the muscles and the rest in heart, liver, kidneys, and the nervous tissue . In bariatric surgery, reduced absorption of vitamin B1 occurs from reduced acid production from stomach and, most importantly, following prolonged and severe nausea and vomiting The prevalence of thiamine deficiency after bariatric surgery is unknown but is associated mostly with VBG, where reduced food intake is the main cause . Vitamin B1 deficiency causes peripheral (beriberi) and central (Wernicke’s encephalopathy) neurological disorders . In Western populations, B1 deficiency manifesting as Wernicke’s encephalopathy and beriberi is very rare, seen mainly in alcoholics. On the other hand, beriberi is seen predominantly in Asian populations, especially in people who eat milled rice and have high carbohydrate intake but low meat intake. This difference in clinical predisposition is of unclear cause, but different genetic background may play a role . Beriberi, however, has been reported in adolescents who underwent RYGB . It is very important to recognize the syndrome, because prompt treatment results in dramatic improvement, and late treatment can result in permanent neurologic sequelae. The recommended treatment is immediate intravenous administration of thiamine 100 mg, followed by 100 mg intramuscularly daily for 5 days and oral maintenance permanently . Intravenous glucose without thiamine can precipitate Wernicke’s encephalopathy in a severely malnourished patient. To confirm the diagnosis of vitamin B1 deficiency, measurement of erythrocyte transketolase activity is the most reliable . The prevalence of Wernicke’s encephalopathy after bariatric surgery is unknown. Wernicke’s encephalopathy after bariatric surgery has been reviewed recently . The onset was mostly 4 to 12 weeks after surgery. The syndrome was seen after both restrictive and combined procedures. Vomiting was the most common predisposing factor. Most patients had the clinical triad of the syndrome. Treatment with parenteral thiamine results in a complete recovery in most patients.
Copper deficiency recently has emerged as a cause of neurological disorders following gastric surgery . Copper absorption into intestinal mucosa requires copper transporters (Ctr1 copper transporter and DCT-1) . It then is transported to ATP7A to be exported from the intestinal cells into the circulation. Clinically, copper deficiency causes hematologic and neurologic manifestations . Neurological symptoms start subacutely in the form of myeloneuropathy. The frequency of copper deficiency after bariatric surgery remains unknown. So far, there has been no general recommendation regarding copper supplement after bariatric surgery. The clinical syndrome, however, needs to be recognized and the deficiency corrected promptly if it happens.
Calcium and vitamin D have a major function in maintaining bone health in the human body . Vitamin D works through its active form, 1, 25(OH) 2 D. The primary action of 1, 25 (OH) 2 D is to promote intestinal absorption of calcium and phosphorus through the small intestine. This reaction is regulated by parathyroid hormone. Moreover, calcium is also important in nerve and muscle functions . Calcium is absorbed mainly in the duodenum and proximal jejunum, whereas vitamin D is absorbed mainly in the jejunum and ileum . After RYGB and BPD, calcium and vitamin D deficiency predictably occurs. Possible causes include bypassing the duodenum and proximal jejunum, food intolerance, and fat malabsorption. The frequencies of calcium and vitamin D deficiencies were reportedly 10% and 50%, respectively, after RYGB . The deficiency results in osteoporosis and osteomalacia. Neurologically, osteomalacia and vitamin D deficiency long have been known to be associated with proximal myopathy (osteomalacic myopathy) . Measurement of serum vitamin D, urine calcium, serum bone alkaline phosphatase (BAP), and serum parathyroid hormone (PTH) levels would help establishing the diagnosis. In general, serum vitamin D and 24-hour urine calcium are decreased (total 25–OH D less than 15 ng/mL), and the levels of BAP and PTH are elevated . Treatment with vitamin D supplement results in definite improvement in strength and pain. The recommended vitamin D supplementation after bariatric surgery is to administer 50,000 IU of vitamin D3 (cholecalciferol) or vitamin D2 (ergocalciferol) once per week . A case of osteomalacic myopathy after jejunoileal bypass has been reported .
Folate or folic acid consists of pterin linked to p-aminobezoic acid. The most common tissue form of folic acid is methyl-tetrahydrofolate (methyl-THF) . Vitamin B12 acts as a coenzyme in the conversion of methyl-THF to THF, the biologically active form. B12 deficiency then can cause folate deficiency . Folate is absorbed mainly at the proximal intestine, mediated by a saturable, specific carrier . Absorption by diffusion, however, may also occur at high concentrations . After bariatric surgery, folate deficiency occurs as a result of reduced food intake and reduced gastric acid secretion that facilitates folate absorption . The incidence could be as high as 35% . Folate deficiency after bariatric surgery may present with megaloblastic anemia or could be asymptomatic . Neurologically, folate deficiency has been reported to be associated with peripheral neuropathy or neuropsychiatric disorders . In some cases, the clinical features of subacute combined degeneration have been observed . The incidence of neurological complications is very low, however, and the association of these neurologic manifestations to folate deficiency has been debated . The recommended dose of folate supplement after bariatric surgery is 1 mg/d .
Vitamin B6 consists of three main active derivatives: pyridoxal, pyridoxine, and pyridoxamine . The incidence of B6 deficiency after bariatric surgery is about 17% Neurological disorders resulting from B6 deficiency after bariatric surgery never have been reported, however.
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