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 Table of Contents  
Year : 2016  |  Volume : 1  |  Issue : 1  |  Page : 9-12

Peroneal palsy after bariatric surgery

1 Department of Surgery, National University Hospital, University of Manchester, Singapore
2 Department of Surgery, National University Hospital, Singapore

Date of Web Publication25-Oct-2016

Correspondence Address:
A Shabbir
NUHS Tower Block, Level 8, 1E Kent Ridge Road, Singapore 119228
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2542-4629.193039

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The rise in popularity of bariatric surgery has been accompanied by a considerable increase in complications observed. Foot drop is a rare, but recognized complication after bariatric surgery. Early studies suggested the combination of rapid weight loss in the setting of postural compression of the nerve as main contributory factors. However, further research has also emphasized the role of postbariatric malnutrition and inflammation in the development of this neuropathy. The cause of this neuropathy is likely to be multifactorial, and understanding these mechanisms will assist multidisciplinary specialists in providing care to postbariatric patients suffering from this condition.

Keywords: Bariatric surgery; foot drop; obesity; peroneal nerve palsy; weight loss

How to cite this article:
Zhen C, Bautista T, Shabbir A. Peroneal palsy after bariatric surgery. Saudi J Laparosc 2016;1:9-12

How to cite this URL:
Zhen C, Bautista T, Shabbir A. Peroneal palsy after bariatric surgery. Saudi J Laparosc [serial online] 2016 [cited 2023 Mar 23];1:9-12. Available from: https://www.saudijl.org/text.asp?2016/1/1/9/193039

  Introduction Top

Obesity - once considered as a deviation from the norm - is now regarded as a disease. [1] The increasing prevalence of obesity [2] has resulted in a rising number of bariatric procedures being done, as surgery remains the most reliable treatment option for sustained weight loss and remission of obesity related comorbidities. [3],[4],[5] Consequently, there has been an observed increase in the incidence of both early and late postoperative complications. [6] Peroneal nerve palsy is a rare neurologic complication that has been reported to occur after bariatric surgery. This article will review the possible etiologies and management of this complication.

  Pathophysiology Top

Neurologic complications can present months or years following surgery. It is reported to occur in 5-16% of all patients undergoing any type of bariatric surgery. [7] In a literature review of fifty case reports, which yielded 96 patients following bariatric surgery, the most reported neurologic complication was peripheral neuropathy (62%) followed by encephalopathy (31%). Amongt the patients who had peripheral neuropathy, 40 (67%) presented with polyneuropathies and 18 (30%) with mononeuropathies. [8] Commonly reported mononeuropathies after bariatric surgery are carpal tunnel syndrome (median nerve neuropathy), and foot drop (peroneal nerve neuropathy), while mononeuropathies of the ulnar, radial, and sciatic nerves are less common.

Even during the prebariatric era, foot drop had already been implicated in patients with weight loss. In 1929, Woltman [9] was the first to report the correlation between peroneal nerve injury and excessive weight loss in aging and severely ill patients. He also observed that another significant cause, which contributed to the nerve insult was the habitual leg-crossing of his patients. Similarly, in 1958 Sprofkin [10] reported nine cases of foot drop in which the nerve palsy of the patients was attributed to the leg-crossing habit in the setting of weight-reduction. The authors proposed that it was the loss of the protective subcutaneous fat that previously cushioned the nerve, which made it susceptible to traumatic compression from the fibular head.

Other studies have suggested that the rapid and massive weight reduction itself is the culprit. In one study, all the thirty patients out of 150 who developed peroneal nerve palsies had an average weight of loss of 10.9 kg over a mean period of time of 2.9 months with diet alone. [11] In a study conducted by Weyns et al., [12] nine out of the 160 patients developed foot drop after bariatric surgery (gastric banding and gastric bypass), and eventually received definitive surgery. It was demonstrated that these patients had a mean weight loss of 45 kg over a mean period of 8.6 months compared to their control group of ten patients who underwent bariatric surgery but did not develop foot drop, in which the mean weight loss was 42.6 kg over a mean period of 21.7 months. Thaisetthawatkul et al. [13] studied characteristics and outcomes of 435 postbariatric patients. The types of bariatric procedures done were vertical banded gastroplasty, gastric bypass, pancreaticobiliary bypass, and jejunoileal bypass. They reported that patients who developed neuropathies lost more weight and reached maximum weight loss faster than those who did not develop neuropathies (mean 43 kg in mean 8 ± 4 months vs. mean 33 kg in 19 ± 13 months, respectively). These authors concluded that substantial weight loss in a short period of time is associated with a higher risk of developing foot drop.

Further research into the mechanism of foot drop after weight loss has shown that it is specifically the malnutrition resulting from the rapid weight loss that is associated with foot drop. Denny-Brown [14] was the first to publish an extensive report on neurologic complications occurring after harsh dietary restriction seen in the World War II prisoners of war. Ten percent of the prisoners developed transient foot drop, which the author attributed to severe malnutrition. In 1977, Sherman and Easton [15] noted weight reduction as the common feature in their patients who developed peroneal nerve palsy. Although at this time, they could only speculate that nutritional deficiency was the cause, they observed that their patients recovered completely with the cessation of further weight loss and the initiation of a supplementary intake of multivitamins. The most frequent nutritional deficiencies after bariatric surgery are Vitamins B1, B12, C, A, D, E, K, folic acid, along with the trace minerals iron, zinc, selenium, and copper [11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29] Vitamin deficiency after bariatric surgery is common. Malinowski [18] reported that 50% of cases studied had vitamin deficiency at the end of the 1 st postoperative year.

Neurologic complications have also been described in adolescent obese patients. Towbin et al. [19] described postoperative neurologic complications of Roux-en-Y gastric bypass (RYGB) surgery caused by micronutrient deficiencies. The study reported three adolescent obese patients who presented with painful soles, lower extremity weakness and numbness, and depressed tendon reflexes among the array of other neurologic symptoms associated with the syndrome of Beriberi, a thiamine (Vitamin B1) deficiency.

Bariatric surgery, specifically the bypass procedure, is well known to alter nutrient levels. In the RYGB, it produces malnutrition via both restrictive and malabsorptive mechanisms. It causes gastric restriction via the small (≤30 ml) gastric pouch which promotes early satiety and thus limits food intake. The malabsorptive component is formed by the exclusion of the distal stomach, duodenum, and proximal jejunum, which decreases the absorptive and secretory surface area necessary for nutrient metabolism. When postbariatric patients were compared to postcholecystectomy patients, it was observed that neurologic complications seen in postbariatric patients were associated with the consequent malabsorption that was specific to the bypass procedure rather than abdominal surgery itself. [13]

Finally, Thaisetthawatkul et al. [13] also demonstrated the role of inflammation in neuropathies following bariatric surgery. Sural nerve biopsies taken from these patients revealed active axonal degeneration as the main pathological process in the nerve fibers. The nerve damage was confirmed by the presence of an increased number of mononuclear inflammatory cells and hemosiderin-laden macrophages involving the epineurium and endoneurium with neovascularization around the nerves.

Peroneal palsy, as a complication of weight loss or malnutrition, has been demonstrated in a variety of studies over the last century. These studies have posited the role of nutritional deficiencies, inflammation, and the rate of weight loss in the development of this neuropathy, although the true cause is likely to be multifactorial in nature.

  Clinical Manifestations and Diagnosis Top

Patients with early or partial peroneal neuropathy complain of weakness in the muscles that dorsiflex the foot and toe, and muscles that evert the foot. Complete paralysis leads to foot drop and the characteristic high-stepping gait. Occasionally, there is sensory loss in the distribution of the peroneal nerve, namely the anterolateral surface of the lower leg and dorsum of the foot and toes. The knee and ankle reflexes should be normal, if not a more proximal lesion should be considered such as a plexus lesion, a sciatic nerve lesion, or L5 radiculopathy with involvement of the adjacent S1 root. When these symptoms are present, there is usually local tenderness over the nerve and a positive Tinel's sign at the fibular head and neck (tapping over these areas produce dysesthesia in the lateral calf and foot). A simple straight leg raise test is useful to exclude other proximal lesions. Examination of the contralateral leg should be done to allow for comparison.

A thorough history should be taken to identify the benign causes of compression such as leg crossing or other postural habits that repetitively compress the nerve. In such patients, the treatment usually is supportive and extensive investigations are not necessary. However, persistent or worsening symptoms are suggestive of progressive peroneal neuropathy and thus warrant further imaging-based investigations. [30]

Imaging aids in ruling out other causes of foot drop that may be missed in this group of patients. Plain radiographs of the knee and ankle are obtained to rule out concurrent fractures, arthritis, or mass lesions that may be compressing the nerve. Other imaging modalities such as ultrasound, computed tomography (CT) scan, and magnetic resonance imaging (MRI) are adjuncts that can further delineate the structure of the nerve. However, in patients with a history of bariatric surgery, ultrasound is the suggested initial imaging of choice due to its cost effectiveness and relative accessibility compared to both CT scan and MRI. [31] Meylaerts et al. [31] studied the sonographic characteristics of the common peroneal nerve in patients with foot drop after weight loss and discovered that a higher body mass index was associated with a thicker and more hyperechoic peroneal nerve. As adipose tissue has a higher echogenicity than normal nerve and muscle, this finding implies that there is more fat covering the peroneal nerve. Pathologic peroneal nerves have spots of hypoechoic areas, representing loss of protective adipose tissue and presence of intraneural edema. These findings are consistent with the early published reports that foot drop develops as a result of the loss of protective subcutaneous fat around the nerve after excessive weight loss.

Electrophysiological studies measure the motor conduction of the common peroneal nerve using bipolar stimulation applied to the nerve at the ankle and neck of the fibula. Such studies are not routinely required but are of value in assessing prognosis and detecting early signs of recovery. [32] Patients that have a conduction block with little or no axonal damage often recover in a few weeks, while patients with severe axonal damage neuropathies can take several months to recover.

  Treatment Options Top

The prognosis after foot drop is generally good as long as there is timely recognition and prompt treatment. In compressive peripheral peroneal neuropathy, recovery can be expected within 3 months provided the cause of compression is avoided. Education and supervision regarding appropriate diet and exercise are mandatory to prevent rapid weight loss and the associated complications of malnutrition. Patients should be advised against leg crossing and other postures that may cause nerve compression. Additionally, a thorough systems review during each visit will aid in early identification of neurologic complications caused by micronutrient deficiency. Emphasis on compliance to follow-up visits, vitamin and mineral intake, and periodic blood investigations for surveillance of micronutrient deficiencies is recommended.

For patients with symptoms that persist beyond 3 weeks in addition to confirmed complete conduction block of the peroneal nerve at the level of the fibula, an operation to repair or graft the nerve is necessary. In cases where the nerve is beyond repair, patients will benefit from foot stabilization using an ankle-foot orthoses, such as an L-shaped lightweight molded plastic brace or the use of customized shoes fitted with spring-loaded brace. The adjustable spring at the ankle hinge provides passive dorsiflexion preventing foot drop and equines limp. [33]

  Conclusion Top

The etiology of peroneal nerve palsy after bariatric surgery is multifactorial, with most sources in consensus with regard to the role of rapid weight loss and the associated effects of malnutrition. With early identification and prompt treatment, patients have a good prognosis and can be managed supportively.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

American Medical Association. Council on Scientific Affairs Report 4. Recognition of obesity as a Disease. Chicago, IL: Annual Meeting of the House of Delegates; 2013. Available from: http://www.npr.org/documents/2013/jun/ama-resolution-obesity.pdf. [Last accessed on 2016 Jul 20].  Back to cited text no. 1
World Health Organization. Obesity and overweight. World Health Organisation; 2014. Fact sheet N°311. Available from: http://www.who.int/mediacentre/factsheets/fs311/en/. [Last accessed on 2016 Jun 20].  Back to cited text no. 2
Dixon JB, Zimmet P, Alberti KG, Rubino F. International Diabetes Federation Position Statement on Bariatric Surgery. Belgium: Chaussée de La Hulpe; 2011. p. 2-3.  Back to cited text no. 3
Schauer PR, Kashyap SR, Wolski K, Brethauer SA, Kirwan JP, Pothier CE, et al. Bariatric surgery versus intensive medical therapy in obese patients with diabetes. N Engl J Med 2012;366:1567-76.  Back to cited text no. 4
Sjöström L. Review of the key results from the Swedish obese subjects (SOS) trial - A prospective controlled intervention study of bariatric surgery. J Intern Med 2013;273:219-34.  Back to cited text no. 5
Huang CS, Farraye FA. Complications following bariatric surgery. Tech Gastrointest Endosc 2006;8:54-65.  Back to cited text no. 6
Clark N. Neuropathy following bariatric surgery. Semin Neurol 2010;30:433-5.  Back to cited text no. 7
Koffman BM, Greenfield LJ, Ali II, Pirzada NA. Neurologic complications after surgery for obesity. Muscle Nerve 2006;33:166-76.  Back to cited text no. 8
Woltman HW. Crossing the legs as a factor in the production of peroneal palsy. JAMA 1929;93:670-2.  Back to cited text no. 9
Sprofkin BE. Peroneal paralysis - A hazard of weight reduction. JAMA 1958:102;82-7.  Back to cited text no. 10
Cruz-Martinez A, Arpa J, Palau F. Peroneal neuropathy after weight loss. J Peripher Nerv Syst 2000;5:101-5.  Back to cited text no. 11
Weyns FJ, Beckers F, Vanormelingen L, Vandersteen M, Niville E. Foot drop as a complication of weight loss after bariatric surgery: Is it preventable? Obes Surg 2007;17:1209-12.  Back to cited text no. 12
Thaisetthawatkul P, Collazo-Clavell ML, Sarr MG, Norell JE, Dyck PJ. A controlled study of peripheral neuropathy after bariatric surgery. Neurology 2004;63:1462-70.  Back to cited text no. 13
Denny-Brown D. Neurological conditions resulting from prolonged and severe dietary restriction; case reports in prisoners-of-war, and general review. Medicine 1947;26:41-113.  Back to cited text no. 14
Sherman DG, Easton JD. Dieting and peroneal nerve palsy. JAMA 1977;238:230-1.  Back to cited text no. 15
Smith BR, Schauer P, Nguyen NT. Surgical approaches to the treatment of obesity: Bariatric surgery. Med Clin North Am 2011;95:1009-30.  Back to cited text no. 16
Shankar P, Boylan M, Sriram K. Micronutrient deficiencies after bariatric surgery. Nutrition 2010;26:1031-7.  Back to cited text no. 17
Malinowski SS. Nutritional and metabolic complications of bariatric surgery. Am J Med Sci 2006;331:219-25.  Back to cited text no. 18
Towbin A, Inge TH, Garcia VF, Roehrig HR, Clements RH, Harmon CM, et al. Beriberi after gastric bypass surgery in adolescence. J Pediatr 2004;145:263-7.  Back to cited text no. 19
Chaudhry V, Umapathi T, Ravich WJ. Neuromuscular diseases and disorders of the alimentary system. Muscle Nerve 2002;25:768-84.  Back to cited text no. 20
Rhode BM, Tamin H, Gilfix BM, Sampalis JS, Nohr C, MacLean LD. Treatment of Vitamin B12 deficiency after gastric surgery for severe obesity. Obes Surg 1995;5:154-158.  Back to cited text no. 21
Davies DJ, Baxter JM, Baxter JN. Nutritional deficiencies after bariatric surgery. Obes Surg 2007;17:1150-8.  Back to cited text no. 22
Loh Y, Watson WD, Verma A, Chang ST, Stocker DJ, Labutta RJ. Acute Wernicke′s encephalopathy following bariatric surgery: Clinical course and MRI correlation. Obes Surg 2004;14:129-32.  Back to cited text no. 23
Ellis JM, Azuma J, Watanabe T, Fokers K, Lowell JR, Hurst GA, et al. Survey and new data on treatment with pyridoxine of patients having a clinical syndrome including the carpal tunnel and other defects. Res Commun Chem Pathol Pharmacol 1977;17:165-77.  Back to cited text no. 24
Folkers K, Ellis J, Watanabe T, Saji S, Kaji M. Biochemical evidence for a deficiency of Vitamin B6 in the carpal tunnel syndrome based on a crossover clinical study. Proc Natl Acad Sci U S A 1978;75:3410-2.  Back to cited text no. 25
Boylan LM, Sugerman HJ, Driskell JA. Vitamin E, Vitamin B-6, Vitamin B-12, and folate status of gastric bypass surgery patients. J Am Diet Assoc 1988;88:579-85.  Back to cited text no. 26
Kushner R. Managing the obese patient after bariatric surgery: A case report of severe malnutrition and review of the literature. JPEN J Parenter Enteral Nutr 2000;24:126-32.  Back to cited text no. 27
Tondapu P, Provost D, Adams-Huet B, Sims T, Chang C, Sakhaee K. Comparison of the absorption of calcium carbonate and calcium citrate after Roux-en-Y gastric bypass. Obes Surg 2009;19:1256-61.  Back to cited text no. 28
Flanagan EP, Leep Hunderfund AN, Kumar N, Murray JA, Krecke KN, Katz BS, et al. Clinical reasoning: A 55-year-old man with weight loss, ataxia, and foot drop. Neurology 2014;82:e214-9.  Back to cited text no. 29
Stewart JD. Foot drop: Where, why and what to do? Pract Neurol 2008;8:158-69.  Back to cited text no. 30
Meylaerts L, Cardinaels E, Vandevenne J, Velghe B, Gelin G, Vanormelingen L, et al. Peroneal neuropathy after weight loss: A high-resolution ultrasonographic characterization of the common peroneal nerve. Skeletal Radiol 2011;40:1557-62.  Back to cited text no. 31
Berry H, Richardson PM. Common peroneal nerve palsy: A clinical and electrophysiological review. J Neurol Neurosurg Psychiatry 1976;39:1162-71.  Back to cited text no. 32
Brashear R, Raney B. Handbook of Orthopaedic Surgery. 10 th ed. St. Louis, Toronto: The C.V. Mosby Company; 1986. p. 231-2, 326-7.  Back to cited text no. 33


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