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Neurological complications are frequently recognized with weight reduction surgeries for morbid obesity. The spectrum of peripheral neuropathies complicating the weight loss surgery is wide, and among them, the acute axonal peripheral neuropathy resembling Guillain-Barre syndrome is rare and only less than a dozen cases are reported. We present three cases, which after bariatric surgery developed acute polyneuropathy that rapidly progressed over 4 weeks from the onset. All patients responded to aggressive parenteral Vitamin B1 and B12 replacement therapy. These cases highlight the fact that bariatric surgery although is a promising option to treat morbid obesity; it is certainly not devoid of potential neurological complications due to micronutrient deficiencies. Delay in the diagnosis of acute polyneuropathy may worsen its long-term sequelae. A multidisciplinary team management with careful nutritional monitoring at regular interval is crucial in all patients for early recognition and intervention to avoid these complications after bariatric surgery.
Obesity significantly increases the risk for ischemic heart disease, hypertension, stroke, diabetes mellitus, dyslipidemia, and even depression. It is determined by calculating the body mass index (BMI) defined as the weight in kilograms divided by height in meters squared (kg/m2). A BMI ranging between 25 and 29.9 is considered overweight, >30 is regarded as obese, and >40 (or ≥35 in the presence of co-morbidities) is morbidly or severely obese. Saudi Arabia's statistics suggest that 72.5% of Saudis are either overweight or obese. Bariatric surgeries are being used widely to manage morbid obesity to improve the quality of life and obesity-related premature deaths. With a rising prevalence of morbid obesity, the numbers of bariatric surgeries are also increasing, resulting in more neurological complications are appearing in the limelight due to micronutrient (vitamins and essential minerals) deficiencies. Laparoscopic sleeve gastrectomy (LSG) is the popular modality and in Saudi is most common weight reduction procedure (88%) being performed. The estimated incidence of neurologic complications secondary to nutritional deficiencies is up to 16% per year. Peripheral neuropathies complicating weight loss surgeries are uncommon, and among them, the acute axonal polyneuropathies resembling Guillain-Barre syndrome (GBS) are very rare and less than a dozen cases are reported in different English literature.[1,2,3,4,5] Our aim in presenting this case series is to identify the patients that presented with acute polyneuropathy following weight loss surgery, and to recognize the factors contributing to it and to highlight the fact that bariatric surgery although is an efficient and promising option to treat morbid obesity, it is certainly not devoid of potential and serious postsurgical neurological complications due to micronutrient deficiencies.
A 21-year-old female, with BMI of 58 kg/m2, underwent an uneventful LSG and discharged on oral multivitamin and mineral supplements. Four weeks after surgery, she developed recurrent vomiting with significant weight loss (almost 28 kg). Two weeks later, she developed paresthesia and pain in both lower limbs distally with walking difficulty, which progressively worsened and involved both upper arms in the next 3 weeks. Upon admission, her examination showed normal higher mental functions, intact cranial nerves, distal and proximal muscle weakness (power of-4/5) in all four limbs with generalized areflexia, sensory loss in gloves and stocking distribution, and impaired proprioception. Her serum folic acid level was 1.5 ng/ml (range 3.1–20.5) and Vitamin B12 level was 514 pg/ml (range 187–883). Serum level for Vitamin B1, B6, and E was not available in our laboratory. Nerve conduction study (NCS) showed diffuse sensory motor axonal peripheral neuropathy [Figure 1a]. Considering postbariatric acute polyneuropathy due to nutritional deficiency, she was started IM Vitamin B12 and intravenous (IV) Vitamin B1 along with oral folic acid and Vitamin E supplementation. Over the next 3–4 weeks, the patient's sensory symptoms of paresthesia and pain completely disappeared, and she started walking with minimal support. She also developed symptoms of generalized anxiety disorder after surgery and responded well to an antidepressant.
A 25-year-old young female with BMI of 41 kg/m2 had undergone an uneventful LSG. One month postsurgery, she developed recurrent vomiting with decreased food intake. She presented in ED after 3 months of surgery with 4 weeks history of paresthesia and weakness in both lower extremities that progressively increased to the extent that the patient became chair bound. Neurological examination revealed −4/5 power distally in the upper limbs and 3/5 in the lower limbs (more distally) with generalized areflexia, distal sensory loss, and impaired proprioception in all extremities. Her corrected serum calcium level was 8 (range 8.5–10.5), and Vitamin B12 level was within normal range. NCS showed diffuse sensory motor axonal peripheral neuropathy [Figure 1b]. She was empirically treated with parenteral Vitamin B12 and B1 with oral folic acid and Vitamin E, D, and calcium. During her hospital stay, she also developed recurrent episodes of generalized body stiffness with the loss of consciousness (serial ictal electroencephalography did not reveal epileptiform activity, and patient's episodes were labeled as pseudoseizures) and depressive illness (received antidepressants). This patient remained hospitalized for 6 weeks. In her latest follow-up 4 months after the discharge from the hospital, she was able to walk with little support.
A 23 years-old-female, had mini gastric bypass surgery for morbid obesity (BMI 46 kg/m2). Six weeks after surgery, she developed recurrent vomiting and abdominal pain and 2 weeks later developed pain and numbness in both feet that gradually progressed to an inability to walk and stand for the next 1 month. Her neurological examination showed weakness in all four limbs (−4/5 and 3/5 in the upper and lower limbs, respectively, more distally) with absent deep tendon reflexes (DTRs), sensory loss, and impaired proprioception all over. There was severe serum Vitamin B12 deficiency (80 pg/ml) and reduced folic acid (2.0). She was found to have Vitamin D deficiency with normal serum calcium levels. NCS showed severe axonal sensory-motor axonal peripheral neuropathy with florid active denervation in the lower limb muscles [Figure-1c]. Nutritional deficiencies were replenished by parenteral Vitamins B1 and B12 and oral folic acid, Vitamin E and D therapy. She showed gradual improvement in the next 6–8 weeks. Her outpatient follow-up after 4 months from her onset of symptoms showed a power of 5/5 all over with normal DTRs and sensory examination.
With the rising prevalence of morbid obesity, the numbers of bariatric surgical procedures (BSP) are also increasing, thus resulting in more neurological complications to be recognized. 20%–30% individuals who are obese already have preexisting micronutrient deficiency such as Vitamins B1, B12, D, folate, and copper before surgery, that gets worse after surgery because of altered diet, reduced absorption, persistent vomiting, and loss of gastric acid and intrinsic factor.[5,6] Because of this reason, it is recommended to do a routine nutritional assessment before surgery. 5%–30% of patients reported to have low thiamine levels in serum before bariatric surgery. Because all surgeries were done in other hospitals, and patients’ available record did not mention as well, so the contribution of preexisting nutritional deficiency before bariatric surgery as a risk factor was unknown in our patients. Neurological complications are evident at 3–20 months after BSP and can involve nerves, spinal cord, and brain [Table 1].
Vitamin B12 (cyanocobalamin) has its important role in myelin synthesis, and Vitamin B1 (thiamine) plays a central role in cerebral glucose metabolism. Because thiamine is not produced by the human body, its deficiency can occur rapidly within 2–3 weeks in patients undergoing BSP. Postoperatively, all our patients were prescribed recommended oral nutritional supplements containing mainly Vitamin B1, B12, D, E, K, folic acid, calcium, iron, and copper. They were apparently compliant and tolerating the supplements until they developed recurrent vomiting.
LSG is a safer procedure with a reduced rate of complications; however, it also limits the production of intrinsic factor, therefore, leading to Vitamin B12 deficiency. Two of our patients underwent LSG and developed acute polyneuropathy, rapidly progressed over 4 weeks from onset. Tabbara et al. in their series of 592 patients who underwent sleeve gastrectomy, reported only seven (1.18%) patients who developed neuropathy over 3–12 months. Becker et al. identified risk factors that may lead to the development of neurological complications such as prolonged vomiting and magnitude of weight loss. One of our patients showed a very fast drop in her weight, almost 28 kg within a month postsurgery, while recurrent and persistent vomiting with loss of appetite were seen in our all patients before developing neurological manifestations. Landais has described rapidly progressing acute axonal polyneuropathy (polyradiculoneuropathy) associated with thiamine deficiency that developed as early as 6 weeks of bariatric surgery with normal cerebrospinal fluid (CSF) proteins. In our patients, CSF analysis was not done and Vitamin B1 level was not available (our major limitations of this study) while two of our patients showed normal serum levels of Vitamin B12 because they received parenteral Vitamin B complex (B1, B6, B12) before arriving our hospital. The duration of neurological illness from onset to peak was 4 weeks that clinically resembled GBS, for which IV immunoglobulin should be considered. However, because Vitamin B1 and B12 deficiencies are the most common cause of postbariatric surgery polyneuropathy, patients were treated with aggressive parenteral multivitamin replacement, and they responded to this therapy. All our patients were treated with recommended vitamins regimen (intramuscular Vitamin B12 1000 μg daily for 1 week, then 1000 μg weekly, IV Vitamin B1 500 mg daily for 3 days followed by 100 mg/day, oral folic acid 5 mg/day).[3,8]
We concluded that early identification of neurological symptoms and intervention may help reduce the occurrence of these complications. Furthermore, it is crucial to approach a well-organized multidisciplinary team management, including proper presurgical patient counseling and stating the potential nutritional deficiencies that could lead to serious complications. Therefore, careful nutritional care and monitoring at 6 weeks, then at 3, 6, and 12 months and yearly after that should be anticipated. Counseling to avoid rapid and excessive weight loss, adequately treating recurrent vomiting and regular follow-ups with a registered dietitian can play an important role in preventing acute polyneuropathy. Lifelong oral multivitamin and mineral supplementations, especially Vitamin B1, B12, and Vitamin D with calcium are highly recommended after PBS. It should be emphasized that the “one-size-fit-all” approach should not be adopted for every patient; supplementation should be tailored according to each individual based on regular blood chemistry results. It is also recommended that one should not wait for the blood test results demonstrating vitamin deficiency in postbariatric patients with moderate-to-severe acute polyneuropathy; parenteral vitamin therapy (Vitamin B12 and B1) should be started expeditiously to reduce the risk of disease progression and irreversibility.
There are no conflicts of interest.