SciELO - Scientific Electronic Library Online

vol.28 número4Porcentaje de adiposidad y su relación con el índice de inmunorreactividad de los receptores hormonales en mujeres mexicanas con cáncer de mamaCirugía bariátrica en diabetes mellitus tipo 1: experiencia a largo plazo en dos casos índice de autoresíndice de materiabúsqueda de artículos
Home Pagelista alfabética de revistas  

Servicios Personalizados




Links relacionados

  • En proceso de indezaciónCitado por Google
  • No hay articulos similaresSimilares en SciELO
  • En proceso de indezaciónSimilares en Google


Nutrición Hospitalaria

versión On-line ISSN 1699-5198versión impresa ISSN 0212-1611

Nutr. Hosp. vol.28 no.4 Madrid jul./ago. 2013 



Peroneal palsy after bariatric surgery; is nerve decompresion always necessary?

Parálisis del nervio peroneo tras cirugía bariátrica; ¿La descompresión quirúrgica es siempre necesaria?



Ana M. Ramos-Leví1, Jordi A. Matías-Guiu2, Antonio Guerrero2, Andrés Sánchez-Pernaute3 and Miguel A. Rubio1

1Servicio de Endocrinología y Nutrición. Hospital Clínico San Carlos. IdISSC. Madrid.
2Servicio de Neurología. Hospital Clínico San Carlos. IdISSC. Madrid.
3Servicio de Cirugía General y Digestiva. Hospital Clínico San Carlos. IdISSC. Madrid. España.





We present two patients who underwent successful bariatric surgery and developed peroneal nerve palsy six months after the procedure. This is an unusual complication which determines a significant functional limitation, mainly because of foot drop, and its presence may be a hallmark of excessive and rapid weight loss. We discuss possible pathogenic mechanisms and therapeutic options, and we emphasize the important role of an adequate nutritional management, in order to avoid the need for a surgical nerve decompression.

Key words: Peroneal neuropathy. Bariatric surgery. Neurological complications. Foot drop.


Se presentan dos pacientes sometidos a cirugía bariátrica que desarrollaron una neuropatía del nervio peroneo común seis meses después de la intervención. Se trata de una complicación poco frecuente que supone una importante limitación funcional, y su aparición puede ser indicativa de una pérdida de peso demasiado rápida y excesiva. Se discute la patogenia y las posibles alternativas terapéuticas, y se destaca el papel esencial del correcto manejo nutricional, con el fin de evitar la necesidad de descompresión quirúrgica nerviosa.

Palabras clave: Parálisis peronea. Mononeuropatía peroneo. Cirugía bariátrica. Complicaciones neurológicas. Pie caído.

"BS": bariatric surgery;
"PN": peroneal neuropathy.
"BMI": body mass index;
"%WL": percentage weight loss;
"%EWL": percentage excess weight loss.



The rise in the number of patients undergoing bariatric surgery (BS) has led to an increase in the incidence and recognition of medical complications associated to weight loss and nutrient deficiency.1 Several reports have described alterations of the nervous system in 1.3-16% of cases, including both central and peripheral involvement, and, in the majority of cases, vitamin deficiency was the main causal mechanism.2-5

Among the complications affecting the peripheral nervous system after BS, peroneal neuropathy (PN) is unusual.2 We present two cases of PN, which developed shortly after successful BS. We suggest a causal association and propose treatment alternatives.


Case reports

Case 1

A 30 year-old woman, with a long-term history of obesity without associated comorbidities, underwent vertical gastric gastroplasty with a body mass index (BMI) of 43.6 kg/m2. She then followed a 4-week period of hyperproteic oral fluids and two months later, correct tolerance to solid diet was reached. Vitamin and mineral supplements were introduced starting at the immediate postoperative period. Weight and BMI during the first postoperative months decreased quickly (table I) due to body-image dissatisfaction and obsessive behavior, which led her to reduction in food intake below advised recommendations, to only 600800 kcal/day. Psychiatric evaluation evidenced an eating disorder not otherwise specified and subclinical anorexia nervosa, restrictive type. She was started on sertraline 100 mg/day and fluoxetine 5 mg/day. At 6-months' follow-up, she presented with right lower-limb paresthesias, foot drop, and frequent stumbling. Physical examination revealed hypoesthesia and inadequate extension of the right foot (strength 0/5), but reflexes were maintained. Laboratory data at this time were: total proteins 6.9 g/dL, serum albumin 4.3 g/dL, prealbumin 20.3 mg/dL, serum iron 108 ug/dL, folic acid 3.5 ng/mL (2-20), vitamin B12 220 pg/mL (120-900), zinc 72 ug/dL (60-150), selenium 92 ug/L (60-120), copper 112 ug/dL (70-140), vitamin 25-hydroxi-D 33 ng/ml (30-100), retinol 0.48 mg/L (0.43-0.67), ratio vitamin E/cholesterol 5.92 mg/g (5-12). Electromyogram evidenced focal right peroneal mononeuropathy at the fibular head. Diet was improved and routine oral vitamin and mineral supplementation was maintained. The patient reached 85 kg one year later, which has been her stable weight thereafter, and neurological symptoms disappeared since then.



Case 2

A 45-year-old man, obese since the age of 4, a 15-year history of medication controlled-hypertension and smoking-habit, underwent laparoscopic biliopancreatic diversion with duodenal switch with a BMI of 40.1 kg/m2, with no postoperative complications. Routine vitamin and mineral supplements were prescribed. At 6-months' follow-up, he achieved a complete diet, and blood pressure was controlled with only one drug. Progression of his postoperative weight is shown in table 1. Six months after BS, he presented with numbness of the right foot and steppage gait. He recalled a frequent habit of crossing his legs. Physical examination revealed normal reflexes and sensitivity, but diminished muscle strength (muscular balance in dorsal flexion of the foot 1/5). Laboratory data revealed normality of glucose and lipid metabolism parameters and no nutritional deficiencies, except for low 25-hydroxivitamin D: total proteins 7 g/dL, serum albumin 4.4 g/dl, serum iron 69 ug/dL, folic acid 17.7 ng/mL (220), vitamin B12 365 pg/mL (120-900), zinc 95 ug/dL (60-150), selenium 80 ug/L (60-120), copper 119 ug/dL (70-140), 25-OH-vitamin D 9.6 ng/ml (30-100), retinol 0.49 mg/L (0.43-0.67), ratio vitamin E/cholesterol 6.1 mg/g (5-12). Electromyogram evidenced loss of anterior tibial muscle neurons and decrease in conduction speed, which confirmed the suspicion of mononeuropathy of right peroneal nerve. Physical therapy was recommended and neurological symptoms disappeared completely six months later. Vitamin and mineral oral supplementation was maintained.



Up to 16% of patients can develop peripheral neurologic complications following BS, according to observational series.4-6 Peroneal neuropathy (PN), however, is unusual. In general, it may be present in up to 1015% of patients complaining of sensorimotor symptoms such as paresthesias and foot drop,7 but, in a large controlled study, PN was identified in only 2 of 435 patients after BS.2 In the two cases that we report, PN appeared approximately six months after the surgical procedure, when weight loss had been significantly greater, in comparison to age- and sex-matched controls in our center (table I). These have been the only two cases identified in our own series of almost 1,500 bariatric surgeries performed over a period of twenty years, though it is true that electromyography is not routinely carried out in the postoperative follow-up, and subclinical cases may have been missed out.

Clinical symptoms of PN comprise pain at the site of entrapment, occasional paresthesias, foot drop and a slapping gait, all of which determine a significant functional limitation8. Examination shows weakness of toe dorsiflexion and foot dorsiflexion and eversion, and sensory loss may affect the entire territory of the superficial peroneal nerve (that is, dorsal foot and lateral leg), or be limited to a partial location. It is important to confirm the diagnosis with electromyography, and to distinguish it from a L5 radiculopathy. The two possible etiologies, which are not mutually exclusive, that have been assumed to explain the development of this complication after BS are nutritional and vitamin deficiencies on one hand, and peroneal nerve compression due to fat-pad loss at the fibular head, on the other.7

The patients here reported presented with vitamin and mineral levels within the normal range using oral supplementation exclusively. Although we were not able to evaluate thiamine levels at that time, vitamin B1 was included among the prescribed supplements following BS in the immediate postoperative period.

The fact that neurological involvement was limited to the peroneal nerve, probably suggests that the main cause was extrinsic compression, since peroneal nerve is especially vulnerable to impingement because of its superficial location.8 Excessive weight loss could determine fat-pad loss at the fibular head, and would be one of the main responsible mechanisms contributing to nerve entrapment in this clinical setting. In case number 1, the rapid and disproportionate weight loss was caused by her restrictive behavior, as it has been previously described9. And in case number 2, the habit of crossing legs may have contributed to unleashing neurological symptoms, as it has also been described.3

Vitamin deficiency, on the other hand, would be less plausible; this would be more relevant in cases of polyneuropathy. Ischemic origin was reasonably ruled out due clinical presentation and normality of glucose and lipid metabolism parameters.

Management of mononeuropathies after BS has not been thoroughly evaluated; there is not enough evidence regarding the best treatment approach, and both vitamin supplementation and surgical decompression have been proposed. To our knowledge, the majority of case-series published have used the latter as the first option.3 However, we describe improvement of peroneal deficits in these patients using conservative and physical therapy. An adequate nutritional approach after BS has been associated to a lower rate of complications involving the peripheral nervous system.10 But additionally, the cases that we present suggest that a suitable nutritional control may probably be helpful as well for recovery of peripheral neurological symptoms already established, by keeping vitamin and mineral levels within a normal range and, more importantly, with an appropriate caloric intake.

We remark the importance of close follow-up of patients undergoing BS in order to avoid excessive weight loss. In case this happens, development of peripheral mononeuropathies may occur, regardless of the normality of mineral and vitamin levels. PN is not frequent, but it is truly invalidating, and may be a hallmark indicating that loss of weight is occurring too rapidly and in a disproportionate amount. Early detection and nutritional intervention may avoid the need for surgical nerve decompression.



1. Ocón Bretón J, Pérez Naranjo S, Gimeno Laborda S, Benito Ruesca P, García Hernández R. Effectiveness and complications of bariatric surgery in the treatment of morbid obesity. Nutr Hosp 2005; 20: 409-14.         [ Links ]

2. 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.         [ Links ]

3. Ellias WJ, Pouratian N, Oskouian RJ, Schirmer B, Burns T. Peroneal neuropathy following successful bariatric surgery. Case report and review of the literature. J Neurosurg 2006; 105: 631-5.         [ Links ]

4. Koffman BM, Greenfield LJ, Ali II, Pirzada NA. Neurologic complications after surgery for obesity. Muscle Nerve 2006; 33: 166-76.         [ Links ]

5. Juhasz-Pocsine K, Rudnicki SA, Archer RL, Harik SI. Neurologic complications of gastric bypass surgery for morbid surgery. Neurology 2007; 68: 1843-50.         [ Links ]

6. Berger JR. The neurological complications of bariatric surgery. Arch Neurol 2004; 61: 1185-9.         [ Links ]

7. 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.         [ Links ]

8. Dong Q, Jacobson JA, Jamadar DA, Gandikota G, Brandon C, Morag Y, Fessell DP, Kim SM. Entrapment neuropathies in the upper and lower limbs: anatomy and MRI features. Radiol Res Pract 2012; 2012: 230679.         [ Links ]

9. Sevinç TT, Kalaci A, Do ramaci Y, Yanat AN. Bilateral superficial peroneal nerve entrapment secondary to anorexia nervosa: a case report. J Brachial Plex Peripher Nerve Inj 2008; 3: 12.         [ Links ]

10. Thaisetthawatkul P, Collazo-Clavell ML, Sarr MG, Norell JE, Dyck PJ. Good nutritional control may prevent polyneuropathy after bariatric surgery. Muscle Nerve 2010; 42: 709-14.         [ Links ]



Ana Ma Ramos-Leví.
Servicio de Endocrinología y Nutrición.
Hospital Clínico San Carlos. IdISSC, Madrid.
C/ Prof. Martín Lagos s/n.
28040 Madrid. España.
E-mail: /

Recibido: 12-II-2013.
Aceptado: 13-IV-2013.

Creative Commons License Todo el contenido de esta revista, excepto dónde está identificado, está bajo una Licencia Creative Commons