SciELO - Scientific Electronic Library Online

 
vol.58 issue3Anesthesia for blalock-taussig shunt and pacemaker placement in an adult patient with univentricular heart: case reportCritical reading of the statistical data in scientific studies author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.58 no.3 Campinas May/June 2008

http://dx.doi.org/10.1590/S0034-70942008000300008 

CLINICAL REPORT

 

Painful peripheral polyneuropathy after bariatric surgery. Case reports

 

Polineuropatía periférica dolorosa después de la cirugía bariátrica. Relato de casos

 

 

Miriam Seligman MenezesI; Kelly O. HaradaII; Glauco AlvarezIII

IProfessora-Associada, Doutora da UFSM
IIResidência Médica em Neurologia; Especialista em Eletroneuromiografia
IIIDoutor em Medicina pela UFRGS; Professor Adjunto do Departamento de Cirurgia da UFSM

Correspondence to

 

 


SUMMARY

BACKGROUND AND OBJECTIVES: The number of patients undergoing bariatric surgery increases every year, and the frequency of complications associated with this procedure has been increasing. The main complications reported are nutritional, metabolic, neurological, and psychological/psychiatric. Among the neurological complications, peripheral neuropathies are important due to their high incidence. The objective of this report was to stress the importance of this type of complication, in which the initial manifestation might be neuropathic pain followed or accompanied by motor involvement, and whose prognosis depends on early diagnosis and treatment.
CASE REPORTS: The case of three patients were reported, two females and one male, who underwent bariatric surgery (restrictive method – Roux-en-Y gastric bypass) and developed, postoperatively, peripheral neuropathy with neuropathic pain as the initial symptom, with posterior or concomitant motor involvement. Electroneuromyography demonstrated in all three cases a sensitive-motor axonal peripheral neuropathy. In two patients, the fibular nerves were severely affected. In common, they all had an important weight loss in a short period of time before developing neurological symptoms.
CONCLUSIONS: Neurological complications are one of the most feared complications of bariatric surgeries. Nutritional deficiencies secondary to the surgery are the most important factors in its pathogeny. Nutritional surveillance, avoidance of severe and fast weight loss, and nutritional supplements are fundamental to avoid complications, especially neurological complications.

Key Words: COMPLICATIONS: peripheral neuropathy; PAIN: neuropathic; SURGERY: bariatric.


RESUMEN

JUSTIFICATIVA Y OBJETIVOS: El número de pacientes sometidos a la cirugía bariátrica aumenta a cada año con el surgimiento cada vez más frecuente, de complicaciones relacionadas con este procedimiento. Las principales complicaciones relatadas son las complicaciones nutricionales, metabólicas, neurológicas y psicológicas/psiquiátricas. Entre las complicaciones neurológicas se destacan por su incidencia las neuropatías periféricas. El objetivo de estos relatos es destacar este tipo de complicación, que puede tener como manifestación inicial, un dolor tipo neuropático, con posterior o concomitante envolvimiento motor, y cuyo pronóstico depende del diagnóstico y del tratamiento precoces.
RELATO DE LOS CASOS: Relatamos los casos de tres pacientes, de los del sexo femenino y uno del sexo masculino, sometidos a cirugía bariátrica (método restrictivo - bypass gástrico en Y de Roux), que evolucionaron en el postoperatorio con un cuadro de neuropatía periférica cuyo síntoma inicial fue dolor neuropático, con posterior o concomitante envolvimiento motor. Las electro neuromiografías demostraron en los tres casos, una Polineuropatía periférica sensitivo-motora de estándar axonal. En de los pacientes hubo un comprometimiento intenso de los nervios fibulares. Todos tuvieron en común, antes de la manifestación de los síntomas neurológicos, una importante pérdida ponderal en un corto período de tiempo.
CONCLUSIONES: Las complicaciones neurológicas son una de las más temibles complicaciones de la cirugía bariátrica. Ningún otro factor es más importante en su patogenia que las deficiencias nutricionales provenientes de la cirugía. La vigilancia nutricional, evitando las pérdidas ponderales acentuadas y rápidas, y la reposición de suplementos son fundamentales para evitar las complicaciones, particularmente los cuadros neurológicos.


 

 

INTRODUCTION

The prevalence of obesity has been increasing, both in developed and developing countries. In Brazil, according to the Instituto Brasileiro de Geografia e Estatística (Brazilian Institute of Geography and Statistics – IBGE-2002/2003), 38.9 million people (40.6% of the adult population) are overweight. Of those, 10.5 million people have a body mass index (BMI) above 25 and are considered obese 1.

The benefits of the surgical treatment of obesity, in patients with morbid obesity (BMI > 40 kg.m-2) refractory to clinical management or in patients with BMI > 35 kg.m-2 with co-morbidities, are well known 2,3. It has been shown that this procedure is safe, but it is not devoid of complications. Among the most frequent complications one can mention nutritional imbalances, but neurological complications are more incapacitating and have a greater potential for the development of sequelae.

Several neurological complications have been described: encephalopathies, neuropathies, myelopathies, and myotonic syndrome 4-12. Peripheral neuropathies are the most frequent neurological complications, and can affect up to 16% of operated patients 8.

Thus, the objective of this report was to alert for the occurrence of peripheral neuropathies as frequent complications of bariatric surgeries, and to emphasize that prognosis depends on the time between the beginning of the symptoms and institution of treatment 9; thus, early identification of the complication, and the knowledge of its physiopathology and possible treatments are important.

 

CASE REPORTS

Case 1: A 27 years old female patient who underwent bariatric surgery (Roux-en-Y gastric bypass) in January 2006, without complications. Her preoperative body mass index (BMI) was 44 kg.m-2 (107 kg).

Two months after the surgery, after losing 24 kg, with BMI = 34 kg.m-2, she developed throbbing pain and burning in her limbs, with the posterior development of difficulty to walk. Symptoms worsened progressively, and, four months after the onset of symptoms, the patient needed support to walk and standing. The pain was much more severe in the lower limbs, and worse on the knees, increasing when the patient stood up. By this time, the patient had already lost 46 kg, presenting with a BMI of 25 kg.m-2.

The patient also developed symptoms of depression, and was taking 20 mg of fluoxetine a day, besides oral potassium supplements. Her past medical history was negative for co-morbidities.

Electroneuromyography was done to confirm the clinical suspicion of neuropathy; it showed the presence of sensitive-motor axonal peripheral polyneuropathy, with severe degeneration of the distal branches of the fibular nerves. The patient was treated with a tricyclic antidepressant (amytriptiline) and an anticonvulsant (carbamazepine) for pain control, nutritional orientation, and physical therapy.

Case 2: A 45 years old female patient, with morbid obesity refractory to clinical treatment, preoperative BMI 43.2 kg.m-2, without co-morbidities, underwent bariatric surgery (Roux-en-Y gastric bypass) in July 2006, without complications. She had a good evolution for approximately 30 days, when she developed frequent episodes of nausea and vomiting, with a weight loss of 38 kg in 62 days. After one month, vomiting decreased significantly, but she developed numbness, tingling, and pain (sharp) on her hands and feet, and generalized weakness, which worsened progressively, until she needed support to walk. She also complained of cramps and cold feet. Electromyography showed the presence of a sensitive-motor axonal peripheral polyneuropathy. At the time of the diagnosis, the patient had lost 40 kg (BMI = 28.9 kg.m-2).

To control her pain, a tricyclic antidepressant (amytriptiline) and an anticonvulsant (gabapentin) were administered. The patient also received nutritional orientation and physical therapy.

Case 3: A 50 years old male patient, who underwent bariatric surgery in October 2006, with a preoperative BMI of 55 kg.m-2, developed, four months after the surgery, difficulty to feed himself due to stomach pain, intolerance to solid foods, and episodes of vomiting. Approximately five months after the surgery, he developed pain, numbness, tingling, loss of muscular strength on both hands and subsequent compromise of the lower limbs, which worsened progressively, up to the point that he needed support to walk. Electroneuromyography showed sensitive-motor axonal peripheral polyneuropathy with severe axonal degeneration in the distal branches of the fibular nerves. By the time of the electroneuromyographic evaluation, the patient had a BMI of 38 kg.m-2 (loss of 50 kg in six months, but the weight loss was more significant the month before the beginning of the neurological symptoms). The patient was treated with gabapentin and amytriptiline, for pain control, and nutritional orientation and physical therapy.

All patients showed improvement of symptoms and were able to recover the ability to walk without support 60 days after beginning the treatment, but remained with some degree of distal motor and/or sensitive deficit.

A specific nutritional deficiency was not investigated in any of the cases described.

 

DISCUSSION

Peripheral neuropathies after bariatric surgery can present clinically through three distinctive patterns: predominantly sensitive polyneuropathy, mononeuropathies, and radiculoplexoneuropathy.

Predominantly sensitive peripheral polyneuropathies present with symmetrical sensitive symptoms, such as numbness, burning sensation, sharp pain, and tingling. Besides sensitive symptoms, some patients present distal motor weakness on hands and feet, and the manifestation of "drop foot" is relatively common. Cramps, autonomic symptoms (constipation, fainting, syncope, hypotension, impotency, and urinary urgency or incontinence), and involvement of cranial (double vision, difficulty to swallow) and trunk nerves may occur 8.

Several mononeuropathies have been described: neuropathy of the median nerve in the wrist (carpal tunnel syndrome), radial nerve neuropathy, sensitive neuropathy of the superficial radial nerve, neuropathy of the ulnar nerve on the elbow, great occipital nerve neuropathy, neuropathy of the fibular nerve on the head of the fibula, lateral femoral cutaneous neuropathy, and sciatic nerve neuropathy. The most frequent syndromes are carpal tunnel syndrome and paresthetic meralgia (neuropathy of the lateral femoral cutaneous nerve) 8,10. In general, mononeuropathies are asymmetric, but they can be symmetric, especially in cases of carpal tunnel syndrome.

Radiculoplexoneuropathies may affect both the lumbosacral and cervical regions. Initially, symptoms are asymmetric and, in general, remain unilateral. The first symptoms include severe pain (burning, sharp pain, shocks, or allodynia) and numbness, followed by weakness of the involved limb. Autonomic symptoms, and cranial nerves, trunk and central nervous system involvement are not seen in this group 8.

Those disorders have an acute, subacute, or chronic onset. It is considered acute when it starts up to a month after the surgery, subacute when it starts between one and three months after the surgery, and chronic when it starts more than three months after the surgery 8.

Most polyneuropathies have an insidious onset and chronic evolution, but they can be acute or subacute. Radiculoplexoneuropathies are always acute or subacute, and chronic cases have not been reported. Mononeuropathies can develop any time in the postoperative period.

The cases presented here manifested clinically as symmetrical peripheral polyneuropathy predominantly sensitive, with an important painful component at the beginning of symptoms (neuropathic pain – painful polyneuropathy). Two cases were subacute (beginning approximately two to three months after the surgery), and one was chronic (beginning five months after the surgery). Diagnosis was defined by clinical criteria (sensitive symptoms, weakness, loss of reflexes, etc.) and confirmed by electroneuromyography.

Electroneuromyography results demonstrated axonal compromise of sensitive and motor fibers, similar to the pattern described in the literature 8,9,11,13. In two cases, severe axonal degeneration of the fibular nerves, suggesting greater susceptibility of this nerve, was striking. Signs of demyelization (focal conduction slowing/blockade and/or abnormal temporal dispersion) were not seen.

Elias et al. 13 reported a case of a patient who developed mononeuropathy of the fibular nerves after bariatric surgery, and indicated that the weight loss favored the development of neuropathy. Besides, it is known that the presence of polyneuropathy is a risk factor for mononeuropathies in regions of pressure, such as the fibular nerve at the head of the fibula 14.

Accentuated weight loss, especially when it occurs rapidly, is the best defined risk factor for the development of peripheral neuropathies described by most authors 8-10, 13,15. However, other risk factors for the development of peripheral neuropathies have been described: low postoperative BMI, low serum levels of albumin and transferrin, prolonged postoperative gastrointestinal symptoms (nausea, vomiting, diarrhea), and the presence of postoperative complications requiring re-hospitalization, inadequate supplementation of vitamins and calcium, and lack of compliance with postoperative nutritional guidelines 8.

One patient developed symptoms when she had lost 38 kg, BMI 29.8 kg.m-2 (initial weight, 121 kg – BMI = 43.5 kg.m-2) over a two-month period, but she did not present significant weight loss posteriorly. The other patient had lost 24 kg, BMI 34 kg.m-2 (initial weight, 107 kg – BMI = 44 kg.m-2); however, she continued to lose weight and, at the time of the diagnosis, she had lost 46 kg and her BMI was 25 kg.m-2. The third case presented here also had a significant weight loss, and his BMI went from 55 kg.m-2 to 38 kg.m-2 (loss of 50 kg); most of the weight loss occurred during the month that preceded the beginning of neurological symptoms, and had a direct relationship with gastrointestinal symptoms of nausea and vomiting.

Thaisetthawatkul et al. 8 observed that the weight loss of 71 patients who underwent bariatric surgery and developed neuropathies was greater than in patients who did not develop neuropathies (mean 43 ± 24 kg compared with 33 ± 23 kg, p < 0.001). Besides, the maximal weight loss was much faster in the neuropathy group (mean 8 ± 4 months compared with 19 ± 13 months, p < 0.001). Those results suggest that the magnitude and maintenance of weight loss and the consequent nutritional deficiencies are crucial factors to trigger the development of neuropathies.

The risk factors mentioned are more commonly associated with polyneuropathies than with the other two groups of neuropathies (mononeuropathies and radiculoplexoneuropathies). The presence of prolonged nausea and vomiting was a risk factor related directly with the development of polyneuropathy, probably because it favors even more the development of nutritional deficiencies 7,8,10,11,16. Two patients had postoperative vomiting that led to a rapid weight loss.

It has been shown that factors such as basal age, weight, and BMI, length of hospitalization, presence of diabetes mellitus, blood glucose levels, glycosylated hemoglobin, cholesterol, and triglycerides are not related with the development of neuropathies 8.

As for the type of surgery, Thaisetthawatkul et al. 8 showed that there are no differences between the group that underwent gastric bypass (restrictive-disabsorptive procedure) or gastroplasty (exclusively restrictive), but the incidence of neuropathy was extremely high in patients who underwent jejunoileal bypass (exclusively disabsorptive).

It is believed that neurological complications are secondary to nutritional and metabolic disturbances caused by the surgery, such as deficiency of iron and zinc, protein malnutrition, and vitamin deficiency (coballmine-B12, thiamine-B1, niacin-B6, folic acid, and vitamins D, A, and E) 8,16,17. Fast weight loss after bariatric surgery has been associated with low serum concentrations of vitamin B12, thiamine, and folic acid and vitamin supplements can improve significantly the nutritional profile of those patients 17-19.

Deficiency of thiamine, in particular, has been deemed to cause polyneuropathy after bariatric surgery 20. Chang et al. 15 demonstrated the presence of vitamin deficiency in 40 out of 99 patients who developed peripheral neuropathy after bariatric surgery; 17 patients had deficiency of vitamin B12, 29 had of thiamine deficiency, and 6 had both deficiencies. However, Abarbanel et al. 10 observed that the response to supplements of vitamin B1 provides significantly improvement only in cases of Wernicke-Korsakoff encephalopathy and "burning feet syndrome".

However, some clinical studies failed to demonstrate the presence of specific nutritional deficiency, such as deficiency of vitamin B12, thiamine, or folic acid, in patients with polyneuropathies after bariatric surgery 8,10.

Inflammatory processes can also be involved on the pathogenesis of peripheral neuropathy. Thaisetthawatkul et al. 8 described the pathological results of sural nerve biopsies in five patients: prominent axonal degeneration, and abnormal number of mononuclear inflammatory cells involving the epineurium and endoneurium without vasculitis. Four out of five patients who underwent biopsies had acute or subacute onset of symptoms, which occurred within three months after the surgery. Those biopsies were done in patients with polyneuropathy and radiculoplexoneuropathy. However, the authors concluded that this finding does not decrease the importance of nutritional deficiency and cachexia on the pathophysiology of neuropathies. But they believe that the etiology of neuropathies is multifactorial and differs in each subgroup.

Therefore, the specific treatment of post-bariatric surgery polyneuropathies includes nutritional re-orientation and vitamin supplements, avoiding or reducing the progression of weight loss and in cases of proven vitamin deficiency supplementation of the specific vitamin.

Symptomatic treatment is aimed at controlling neuropathic pain. In the cases presented here, gabapentin, carbamazepine, nortryptiline, and amytriptiline were used. On the guidelines of the European Federation of Neurological Societies (EFNS), Atta et al. 21 recommend tricyclic antidepressants (amytriptiline and nortryptiline) and the anticonvulsant gabapentin as first choice drugs for the treatment of neuropathic pain secondary to polyneuropathies. In the cases presented here, patients were treated with an association of those drugs, with good clinical response. Motor physical therapy also has an important role in patient rehabilitation.

As for the prognosis, Chang et al. 15 reported that among 99 patients who developed peripheral neuropathies, only 9 out of 17 cases of vitamin B12 deficiency, 12 out of 29 cases of thiamine deficiency, and 3 out of 6 cases of those combined deficiencies presented complete resolution of their symptoms.

Alves et al. 9 described two cases of beriberi after bariatric surgery that were adequately treated with vitamin B1 supplementation. One of the patients had complete resolution of neurologic symptoms, but the other patient (longer time between the development of symptoms and beginning treatment) had persistent motor deficit, indicating that the probability of irreversible damage increases with increased time between development of symptoms and institution of treatment.

Although all patients presented here recovered the ability to walk without support, neither one of them had complete resolution of the neurological symptoms, remaining with some degree of distal sensitive and/or motor deficit.

If, on one hand, bariatric surgery in the treatment of morbid obesity reduces associated co-morbidities, on the other it creates a "new category" of patients subjected to several complications that challenge professionals involved in their care.

Neurological complications are among the most feared, due to the potential of irreversibility. No other factor is more important for its pathogeny then nutritional deficiencies caused by the surgery.

Therefore, nutritional vigilance, avoiding accentuated and fast weight loss, and vitamin supplements are fundamental to prevent the development of complications secondary to bariatric surgery, especially neurological involvement.

 

REFERENCES

01. IBGE - Pesquisa de Orçamentos Familiares - POF 2002-2003 - Análise da disponibilidade domiciliar de alimentos e do estado nutrional no Brasil. Disponível em: http://www.ibge.gov.br/ home/estatistica/populacao/condicaodevida/pof/2002analise/default.shtm.         [ Links ]

02. NIH Conference. Gastrointestinal surgery for severe obesity. Consensus Development Conference Panel. Ann Intern Med 1991;115:956-961.         [ Links ]

03. Snow V, Barry P, Fitterman N et al. – Pharmacologic and surgical management of obesity in primary care: a clinical practice guideline from the American College of Physicians. Ann Intern Med 2005; 142:525-531.         [ Links ]

04. Singh S, Kumar A – Wernicke encephalopathy after obesity surgery: a systematic review. Neurology, 2007;68:807-811.         [ Links ]

05. Machado FCN, Valério BCO, Morgulis RNF et al. – Acute axonal polyneuropathy with predominant proximal involvement. Arq Neuropsiquiatr, 2006;64:609-612.         [ Links ]

06. Harwood SC, Chodoroff G, Ellengerg MR – Gastric partitioning complicated by peripheral neuropathy with lumbosacral plexopathy. Arch Phys Med Rehabil, 1987:68:310-312.         [ Links ]

07. Maryniak O – Severe peripheral neuropathy following gastric bypass surgery for morbid obesity. Can Med Assoc J, 1984;131: 119-120.         [ Links ]

08. Thaisetthawatkul P, Collazo-Clavell ML, Sarr MG et al. – A controlled study of peripheral neuropathy after bariatric surgery. Neurology, 2004;63:1462-1470.         [ Links ]

09. Alves LFA, Gonçalves RM, Cordeiro GV et al. – Beribéri pós-bypass gástrico: uma complicação não tão rara. Relato de dois casos e revisão da literatura. Arq Bras Endocrinol Metab, 2006; 50:564-568.         [ Links ]

10. Abarbanel JM, Berginer VM, Osimani A et al. – Neurologic complications after gastric restriction surgery for morbid obesity. Neurology, 1987; 37:196-200.         [ Links ]

11. Feit H, Glasberg M, Ireton C et al. – Peripheral neuropathy and starvation after gastric partitioning for morbid obesity. Ann Intern Med 1982; 96:453-455.         [ Links ]

12. Berger JR – The neurological complications of bariatric surgery. Arch Neurol, 2004;61:1185-1189.         [ Links ]

13. Elias WJ, Pouratian N, Oskouian RJ et al. – Peroneal neuropathy following successful bariatric surgery – case report and review of the literature. J Neurosurg, 2006;105:631-635.         [ Links ]

14. Cruz-Martinez A, Arpa J, Palau F – Peroneal neuropathy after weight loss. J Peripher Nerv Syst, 2000; 5:101-105.         [ Links ]

15. Chang CG, Adams-Huet B, Provost DA – Acute post-gastric reduction surgery (APGARS) neuropathy. Obes Surg, 2004; 14:182-189.         [ Links ]

16. Fujioka K – Follow-up of nutritional and metabolic problems after bariatric surgery. Diabetes Care, 2005;28:481-484.         [ Links ]

17. Bloomberg RD, Fleishman A, Nalle JE et al. – Nutritional deficiencies following bariatric surgery: what have we learned? Obes Surg, 2005;15:145-154.         [ Links ]

18. Avinoah E, Ovnat A, Charuzi I – Nutritional status seven years after Roux-en-Y gastric bypass surgery. Surgery, 1992;111: 137-142.         [ Links ]

19. MacLean LD, Rhode BM, Shizgal HM – Nutrition following gastric operations for morbid obesity. Ann Surg, 1983; 198:347-355.         [ Links ]

20. Chaves LC, Faintuch J, Kahwage S et al. – A cluster of polyneuropathy and Wernicke-Korsakoff syndrome in a bariatric unit. Obes Surg, 2002;12:328-334.         [ Links ]

21. Attal N, Cruccu G, Haanpää M et al. – EFNS guidelines on pharmacological treatment of neuropathic pain. Eur J Neurol, 2006;13:1153-1169.         [ Links ]

 

 

Correspondence to:
Dra. Miriam Seligman Menezes
Rua Cel. Estácio Mariense de Lemos, 190
97020-150 Santa Maria, RS
E-mail: miriamsm@husm.ufsm.br

Submitted em 23 de outubro de 2007
Accepted para publicação em 18 de janeiro de 2008

 

 

* Received from Hospital Universitário da Universidade Federal de Santa Maria (UFSM), Santa Maria, RS