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| CASE REPORT |
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| Year : 2015 | Volume
: 3
| Issue : 1 | Page : 26-28 |
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Ataxia and weakness after sleeve gastrectomy
Rajish Sanjit Kumar Shil1, Ammar Fadhil Alomar2, Mohammad Rashid Farooqui3
1 Medical Student, Department of Internal Medicine, Ras-Al-Khaimah Medical and Health Sciences University, RAK College of Medical Sciences, Ras-Al-Khaimah, United Arab Emirates
2 Department of Neurology, Ibrahim Bin Hamad Obaidallah Hospital, Ras-Al Khaimah, United Arab Emirates
3 Department of Internal Medicine, Ras-Al-Khaimah Medical and Health Sciences University, RAK College of Medical Sciences, Ras-Al-Khaimah, United Arab Emirates
| Date of Web Publication | 12-Jun-2015 |
Correspondence Address:
Rajish Sanjit Kumar Shil
Ras-Al-Khaimah Medical and Health Sciences University, RAK College of Medical Sciences, Ras-Al-Khaimah
United Arab Emirates
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2347-2618.158698
The number of patients undergoing bariatric surgery increases every year, as obesity has become a major cause of several comorbidities. The frequency of complications associated with this procedure has been increasing. Here, we present a case of 32-year-old male with ataxia and peripheral polyneuropathy after a sleeve gastrectomy procedure, who went on to develop progressive weaknesses in the extremities within a duration of 8 months after surgery, and was admitted to hospital for neurological consultation and treatment. The case report highlights the symptoms that bariatric surgeons must detect and review the treatment. Keywords: Ataxia, bariatric surgery, gastrectomy
How to cite this article:
Shil RS, Alomar AF, Farooqui MR. Ataxia and weakness after sleeve gastrectomy. Saudi J Obesity 2015;3:26-8 |
| Introduction | |  |
Bariatric surgeries like Sleeve gastrectomy and Roux-en-Y gastric bypass reconfigure the gastrointestinal tract to achieve gastric restriction and malabsorption. This reconfiguration can result in nutritional and vitamin deficiencies if patients do not receive proper supplementation after surgery. [1]
Neurological complications after bariatric surgery are increasingly recognized and have been estimated to range from 4.6% to 16%, [2] since some cases are subclinical. These complications include peripheral neuropathy, myotonic syndrome, myelopathy, burning feet syndrome, lumbosacral plexopathy, and Wernicke-Korsakoff encephalopathy. [3],[4] Guillain-Barre syndrome has also been reported. [3],[5] It appears that nutritional deficiencies may play the most important role in the pathogenesis for such complications. [3],[4],[5],[6]
We are reporting a case of neurological disorder after sleeve gastrectomy procedure.
| Case report | | |
A 32-year-old male, with a history of morbid obesity (body mass index [BMI] - 102 kg/m 2 ), obstructive sleep apnea and eczema in the lower limbs, has undergone a bariatric procedure (sleeve gastrectomy), on January, 2014 in a hospital in Dubai, UAE. He did well postoperative and was discharged with oral multivitamins supplements. Two weeks postoperative, he developed generalized fatigability and imbalance on walking, which led to several falls and multiple bruises. He also developed nausea and loss of appetite along with these complaints. His condition continued to progress slowly to ataxia on standing and after 5 months of his surgery, he stopped taking multivitamins due to worsening nausea. With this condition, he gradually started to feel weakness in his lower limbs and needed support to do daily activities. His lower limb weakness progressed and then he developed weakness in the upper limbs. He also complained of feeling numbness in the lower limbs which started distally and progressed proximally up to the level of the knees. At the 8 th month after surgery, the weakness became so severe that he was bed-bound and 2 weeks later he was admitted via Emergency department in a tertiary care hospital in Ras-Al-Khaimah, UAE, on September, 2014. In the ED, he received STAT IM of Vitamin B complex (B1-B6-B12).
On admission, the patient was alert, conscious, oriented to time, place and person, with stable vital signs. His BMI was 55 kg/m 2 . His oral examination showed beefy red tongue and cracked lips. There were multiple bruises on the knees (attributed to previous falls), dark red discoloration and scaly skin at the lower aspects of both lower limbs (attributed to eczema). On neurological examination, his higher mental functions and cranial nerves were intact, except for bilateral rapid, fine, jerky, horizontal nystagmus, stage 3. On the upper limbs, power was of grade 4/5 according to the five-point scale of Medical Research Council of the Great Britain, there was areflexia bilaterally, and normal sensations. On the lower limbs, power was grade 0/5 distally and 2/5 at the hips, there was areflexia bilaterally and impaired sensation bilaterally from the level of the knee down including pain, fine touch, vibration, and proprioception. On finger nose testing, there were bilateral intentional tremors, and there was also dysdiadokokinesia.
The laboratory findings were within the normal range, including, complete blood count, serum electrolytes, renal functions, liver functions. Vitamin B12 level was not done on admission but was done later after starting treatment and was within normal limits. Vitamin B1 and E levels were also requested but were not available. Noncontrast computed tomography scan of the brain showed no abnormalities.
Electromyography (EMG) of the patient was reported as such, "severe sensory lesion in the both upper and lower limbs and while the motor fibers in the upper limbs show normal values, those in the lower limbs show fairly advanced axonal neuropathic process affecting the leg muscles including the tibialis anterior muscle which was also examined by needle sampling showing partial chronic denervation pattern and indeed the muscle has lost the majority of its axon. This concludes the picture of peripheral polyneuropathy caused by nutritional deficiencies."
According to the clinical setup, vitamin deficiency was suspected, and patient was admitted and started on Vitamin B complex (B1-B6-B12) intramuscular injection BD plus oral multivitamins tablets containing other vitamins as well. After 10 days of this treatment, the patient started complaining of pins and needles sensation on both upper and lower limbs for which he was started on pregabalin. Immediately after starting treatment, has improved, and his power became better within few days of treatment.
Three weeks posthospitalization, patient showed significant improvement, and his nystagmus disappeared, tongue changed back to normal, muscle power in upper limbs was 5/5, lower limbs muscle power was 3/5, could walk with support and sensations improved except for proprioception. His cerebellar functions improved as well. However, he stayed areflexic till discharge after weeks of admission. On discharge, he was advised to continue intensive physiotherapy and take multivitamins supplements.
| Discussion | | |
Bariatric surgery is now widely indicated in the treatment of morbid obesity. The rise of bariatric surgery brought along with it a variety of previously unreported complications. Neurologic or dry beriberi is usually seen in the setting of energy deprivation and inactivity, two conditions common after bariatric surgery. [7]
Our patient was suspected to have suffered from polyneuropathy due to multivitamin deficiencies, especially B1 and B12 vitamins. The symptoms of peripheral neuropathy, areflexia, nystagmus, ataxia are well-suggestive of B1 deficiency causing dry beriberi to this patient and this could be explained by significant improvement of the symptoms of the patient following initiation of multivitamin complex. Along with considering dry beriberi due to B1 deficiency, presence of nystagmus, ataxia, impaired finger nose coordination, dysdiadokokinesia, it shows that there is some element of Wernicke's encephalopathy in this patient, which is caused by B1 deficiency as well. The presence of beefy red tongue and its improvement following multivitamin supplements could be suggestive of niacin or folate deficiency causing the neuropathy to this patient.
Since, the patient presented with an acute illness of progressive severe weakness in the extremities within 2 weeks, Guillain-Barre syndrome was also considered for the diagnosis for which intravenous immunoglobulin (IVIG) must be administered. However, since the patient showed improvement on multivitamin supplements, and IVIG was not required for the patient, it excludes this diagnosis. Furthermore, there was no evidence of Guillain-Barre syndrome in the EMG findings, which is sufficient to exclude these diagnoses.
The unavailability of the Vitamin B1 and B12 levels before the initiation of the multivitamin therapy is our major weakness for the study. However, the B12 level to be in the higher level of normal, after 10 days of initiation of therapy, could be due to the IM injections of multivitamins. This high B12 level and patient still being areflexic with impaired proprioception, we could consider the diagnosis of B1 deficiency being the main cause of patient's neuropathy, although B12 deficient neuropathy is still not ruled out. Furthermore, the presence of cerebellar symptoms such as nystagmus, dysdiadokokinesia, and impaired finger nose coordination could also lead us toward the diagnosis of B1 deficiency neuropathy like dry Beri Beri or could be Wernicke's encephalopathy. Although there is the absence of mental confusion, ophthalmoplegia, it does not exclude the diagnosis of Wernicke's encephalopathy since this disease is diagnosed clinically and does not require the presence of the triad for considering the diagnosis. [8]
Alternatively, Vitamin E deficiency could also cause similar presentation as our patient here. Peripheral neuropathy due to Vitamin E deficiency is initially characterized by areflexia, with progression to an ataxic gait, and by decreased vibration and position sensations. Ophthalmoplegia, skeletal myopathy, and pigmented retinopathy may also be features of vitamin E deficiency. [9] Our patient was supplemented with oral multivitamins, which can treat this deficiency if present.
| Conclusion | | |
The patient in this report had sensorimotor axonal polyneuropathy as a complication sleeve gastrectomy procedure although these complications are not commonly seen after this procedure. This uncommon neurological complication might have been due to rapid weight loss and vitamin deficiency. We emphasize that morbid obesity needs to be managed in multidisciplinary teams and the patients should be educated for the importance of multivitamins especially Vitamin B, along with other vitamins (A, D, E, K) to be taken lifelong in any types of bariatric surgeries.
| Acknowledgments | | |
The authors would like to thank Dr. Mohammad Tawfik Ridha, Consultant Neurologist at Ibrahim Bin Hamad Obaidallah Hospital, Ras-Al-Khaimah, UAE, for his invaluable contributions and tireless efforts to complete this work successfully. Also, we would like to thank RAK Research and Ethics Committee (R.E.C) and RAKMHSU R.E.C for granting permission to complete the study.
Financial support and sponsorship
Nil.
Conflict of interest
There are no conflict of interest.
| References | | |
| 1. | Angstadt JD, Bodziner RA. Peripheral polyneuropathy from thiamine deficiency following laparoscopic Roux-en-Y gastric bypass. Obes Surg 2005;15:890-2.  |
| 2. | Feit H, Glasberg M, Ireton C, Rosenberg RN, Thal E. Peripheral neuropathy and starvation after gastric partitioning for morbid obesity. Ann Intern Med 1982;96:453-5. |
| 3. | 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. |
| 4. | Abarbanel JM, Berginer VM, Osimani A, Solomon H, Charuzi I. Neurologic complications after gastric restriction surgery for morbid obesity. Neurology 1987;37:196-200. |
| 5. | Halverson JD. Metabolic risk of obesity surgery and long-term followup. Ann J Clin Nutr 1992;55 Suppl: S602-5. |
| 6. | Mason EE. Starvation injury after gastric reduction for obesity. World J Surg 1998;22:1002-7. |
| 7. | Mahan LK, Escott-Stump S. Vitamins. In: Krause′s Food, Nutrition, and Diet Therapy. 11 th ed. Philadelphia: Saunders; 2004. p. 93-5. |
| 8. | Harper CG, Giles M, Finlay-Jones R. Clinical signs in the Wernicke-Korsakoff complex: A retrospective analysis of 131 cases diagnosed at necropsy. J Neurol Neurosurg Psychiatry 1986;49:341-5. |
| 9. | Russell RM, Suter PM. Vitamin and trace mineral deficiency and excess. Harrison′s Principles of Internal Medicine. 18 th ed., Vol. 1. USA: McGraw-Hilll; 2012. p. 594-605. |
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