Peripheral polyneuropathy after bariatric surgery for morbid obesity

INTRODUCTION

The prevalence of obesity has been increasing, both in developed and developing countries. In Taiwan, according to the Department of Health, Executive Yuan, R.O.C. (Nutrition and Health Survey, 2005-2008), 51% of the adult male population and 36% of the adult female population are overweight or obese.

The impact of obesity on society is huge because of its associated morbidity and mortality. The absence of effective conservative treatment, combined with the development of laparoscopic surgery, has led to a significant increase in the amount of bariatric surgery. The common laparoscopic techniques are gastric bending, sleeve gastrectomy, gastric bypass, and biliopancreatic surgery. However, the surgical procedures may have some complications occasionally.[1] Neurological complications, including peripheral neuropathy, myotonic syndrome, myelopathy, burning feet syndrome, meralgia paresthetica, lumbosacral plexopathy, and Wernicke-Korsakoff encephalopathy, are increasingly recognized.[2] Peripheral neuropathies are the most frequent neurological complications, and can affect up to 16% of operated patients.[2] Nutritional deficiencies may play an important role in pathogenesis.[3] The objective of this report is to highlight the symptoms of this type of complication, and to emphasize that prognosis depends on the time between the beginning of the symptoms and institution of treatment.

CASE REPORT

A 24-year-old woman underwent a successful laparoscopic gastric bypass on June 2008 for super morbid obesity (body weight 166 kg, body mass index 61.7). She did not subsequently take vitamin supplements. She developed frequent episodes of vomiting and abdominal pain. The differential diagnoses of symptoms include nutritional deficit and internal hernia. In the following 4 months, she lost 32 kg, her weight falling from 166 to 134 kg. Approximately 5 months after the surgery, she noticed muscle weakness in her lower limbs and experienced difficulty in walking and standing. The symptoms worsened progressively and she developed generalized weakness and ultimately became bed-ridden. Five weeks later, she was transferred to the rehabilitation unit of our hospital. She could not move her ankles and feet, and the strength of her hips was only grade 2 according to the five-point scale of Medical Research Council of the Great Britain. The strength of the upper limbs was grade 3 in proximal arms and grade 1 in distal hands. Foot drop and wrist drop developed and there was marked distal limb muscle atrophy [Figures 1 and 2]. The laboratory findings were within normal ranges, including complete blood cell counts, creatinine kinase, liver function, renal function, vitamin B₁₂, thyroid stimulating hormone (TSH), and serum electrolyte levels. Magnetic resonance imaging (MRI) of the cervical spine without contrast enhancement was normal [Figure 3]. Electromyography was done to confirm the clinical suspicion of neuropathy; it showed the presence of sensorimotor axonal polyneuropathy. According to the clinical presentation, thiamine deficiency was suspected – also called neuropathic beriberi. Two months after she had become bed-ridden, intravenous replacement therapy with vitamin B complex was started: 1 ml of B-complex was given once daily (containing 100 mg of thiamine, 5 mg of riboflavin, 5 mg of pyridoxine, 50 mg of nicotinamide, and 5 mg of sodium pantothenate). She experienced mild improvement during her hospitalization.

Figure 1

Bilateral wrist drop and finger drop, the inability to extend the wrist and finger upwards when the hand is palm down, in the patient with peripheral neuropathy after bariatric surgery for morbid obesity

Figure 2

Bilaterally foot drop and marked distal limb muscle atrophy were found in the patient with peripheral neuropathy after bariatric surgery for morbid obesity. This patient could not sit up, someone behind push her forward

Figure 3

Sagittal T2-weighted MR images of cervical spine showed no compression on the spinal cord

DISCUSSION

The amount of bariatric surgery (BS) is rapidly growing as the prevalence of obesity increasing.[4] Following bariatric surgery, neurological complications have recently gained attention. Well-reported neurologic complications of bariatric surgery include peripheral neuropathy (PN), burning feet syndrome, meralgia paresthetica, myotonic syndrome, myelopathy, Wernicke–Korsakoff encephalopathy, and lumbosacral plexopathy.[2]

Peripheral neuropathy is the most commonly described neurological complication. One controlled retrospective study identified 16% of patients with peripheral neuropathy.[2]

Thaisetthawatkul et al described three distinct clinical patterns of PN after BS: sensory – predominant polyneuropathy, mononeuropathy, and radiculoplexus neuropathy.[2] Sensory-predominant polyneuropathies present with symmetric sensory symptoms and signs, and some have distal motor weakness involving the hands and feet; the manifestation of “drop foot” is relatively common. The mononeuropathy group has asymmetric involvement at the common sites of entrapment such as median neuropathy at the wrists in most of the patients. Radiculoplexus neuropathy may affect both the lumbosacral and cervical regions. The symptoms begin asymmetrically and remain unilateral in almost all patients.

It is believed that nutritional deficiencies may play the most important role in the pathogenesis.[3] Deficiency of thiamine, in particular, has been deemed to cause polyneuropathy after bariatric surgery.[5–6] Chang et al demonstrated the presence of vitamin deficiency in 40 out of 99 patients who developed peripheral neuropathy after bariatric surgery; 17 patients had vitamin B₁₂ deficiency, 29 had thiamine deficiency, and 6 had both deficiencies.[7] However, it has not been established whether the development of PN after BS for morbid obesity may be attributed to a specific vitamin deficiency.[8]

A controlled study of peripheral neuropathy after bariatric surgery identified risk factors for development of PN.[2] Risk factors included rate and absolute amount of weight loss, prolonged gastrointestinal symptoms, not attending a nutritional clinic after BS, reduced serum albumin and transferrin after BS, postoperative surgical complications requiring hospitalization, and having a jejunoileal bypass.

In our patient, the rapid weight loss in addition to the fact that the patient did not take vitamin supplements probably contributed to the development of PN. Diagnosis of PN was defined by clinical symptoms and confirmed by electroneuromyography. The neuropathy is a sensory–motor polyneuropathy most prominent distally. It is usually symmetrical and characterized by weakness, dysesthesia, and cutaneous hyperesthesia. The prevailing pathologic change is axonal degeneration.[9]

Alves et al described two cases of beriberi after bariatric surgery that were adequately treated with vitamin B₁ supplements.[10] One of the patients had complete resolution of the neurologic symptoms, but the other patient (with a longer time between the development of symptoms and beginning of treatment) had persistent motor deficit. The probability of irreversible damage increases with increased time between development of symptoms and initiation of vitamin treatment. In our patient, the poor response to treatment might be associated with the delay in treatment.

CONCLUSION

The patient in this report had sensorimotor axonal polyneuropathy as a complication of bariatric surgery. This uncommon neurological complication might have been due to rapid weight loss and vitamin deficiency. Morbid obesity management is multidisciplinary teams management and the patients should be educated for the importance of multivitamins especially iron, calcium, vitamin D, vitamin B mainly B₁₂ and the thiamin, to be taken life long mainly in any bariatric surgery include malabsorption effect as gastric bypass or biliopancreatic division.