|
 
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| REVIEW ARTICLE |
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| Year : 2016 | Volume
: 1
| Issue : 1 | Page : 9-12 |
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Peroneal palsy after bariatric surgery
CAC Zhen1, T Bautista2, A Shabbir2
1 Department of Surgery, National University Hospital, University of Manchester, Singapore
2 Department of Surgery, National University Hospital, Singapore
| Date of Web Publication | 25-Oct-2016 |
Correspondence Address:
A Shabbir
NUHS Tower Block, Level 8, 1E Kent Ridge Road, Singapore 119228
Singapore
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2542-4629.193039
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 |
| Introduction | |  |
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 | | |
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 | | |
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 | | |
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 | | |
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
Nil
Conflicts of interest
There are no conflicts of interest.
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