Surgeries carry a risk of complications. Polyneuropathies, including Guillain-Barré syndrome (GBS), are potential complications of bariatric surgery. The incidence of these conditions is expected to increase as these surgeries become increasingly popular. We present a case report of three patients who developed a polyneuropathy after bariatric surgery. GBS was diagnosed in each patient, with nutritional deficiencies being suspected as a contributing factor. All patients began a 5-day intravenous immunoglobulin course in addition to receiving rehabilitative support, multivitamins, intravenous thiamine, vitamin D (therapeutic dose), and selenium. The patients’ symptoms improved but did not completely resolve. GBS can be a complication of bariatric surgery. Although a clear cause-effect relationship cannot be established for the present cases, the cumulative literature on the subject suggests that it is important to include it as a potential risk when counseling patients for such surgeries.
The prevalence of obesity has been on the rise worldwide over the last few decades. Obesity is associated with clinical and biochemical changes in various body systems [
One evidence-based recommendation for those with morbid obesity is to undergo bariatric surgery. It is estimated that 15,000 bariatric operations are performed annually in Saudi Arabia [
Surgeries in general carry a risk for a variety of complications. Macro- and micronutritional deficiencies may occur in some patients after bariatric surgery and can result in serious neurological sequelae, [
A 20-year-old female with a body mass index (BMI) of 42 kg/m2, who met the National Institutes of Health criteria for bariatric surgery, underwent sleeve gastrectomy surgery in July 2016. She was discharged home without any complications. The initial 3-month postoperative period was uneventful without any nausea or vomiting. Net postoperative weight loss was 30 kg in 4 months. In early November 2016, she reported feeling flu-like symptoms (cough, sore throat, and runny nose) with a low-grade fever. Her upper respiratory symptoms improved, but 2 weeks later, symptoms rapidly progressed to bilateral ascending lower limb (LL) numbness reaching her waist. The numbness became progressively worse and she started to develop bilateral lower extremity weakness with recurrent falling attacks and severe leg pain. In addition, she developed choking attacks, hoarseness with on and off dysphagia, dyspnea, and constipation without urinary retention.
The neurologist’s evaluation showed reduced distal and proximal muscle power, diminished LL reflexes, and decreased pinprick sensation up to L1 bilaterally. In addition, big toe proprioception was impaired and the patient had a decreased sense of vibration up to the knee bilaterally. There was no involvement of the upper limbs (ULs), and the cerebellum and cranial nerves were intact.
Initial laboratory test results were unremarkable, including a thyroid function test and vitamin B12 levels (1186 pmol/L). A lumber puncture was performed and cerebrospinal fluid (CSF) revealed the following: white blood cell count (WBC) 1 cell/cubic mm, red blood cell count (RBC) 11 cell/cubic mm, protein level 0.31 g/L, glucose level 3.4 mol/L. CSF bacterial and fungal culture results were negative. Serologic tests showed normal complement and high immunoglobulin G (16.7 g\L) levels, as well as negative antinuclear antibody (ANA) results. Because of her progression in symptoms, the patient underwent further neurological workup. Magnetic resonance imaging (MRI) scan results for the spinal cord were normal except for a high-signal density on the L1 vertebral body. The results of nerve conduction study (NCS) was normal apart from the absence of F waves, and electromyography (EMG) testing showed axonal involvement. These findings were consistent with the axonal form of GBS.
The patient required intubation and was admitted to the intensive care unit (ICU), where she received intravenous immunoglobulin (IVIG) for 5 days. Nutritional supplements, including IV thiamine, vitamin B6, and vitamin B12, were given in addition to selenium. She continued rehabilitation and physical therapy. Her symptoms gradually improved, but she required the assistance of walkers before her symptoms completely resolved.
A 36-year-old female with diabetes mellitus, hypertension, and hypothyroidism underwent a cesarean section a few weeks prior to admission and a gastric sleeve procedure 1 year before that.
Two days before admission to hospital, the patient developed ascending numbness followed by weakness, which progressed over 2 days. It interfered with her movement, making her bed bound. She reported a 1-day history of subjective fever and diarrhea a week before the onset of symptoms, which subsided spontaneously. Weakness was not associated with double vision, shortness of breath, slurred speech, abnormal movement, or confusion. She did not have fever, diarrhea, or abdominal pain and did not have similar attacks previously.
She lost approximately 40 kg in 2 months; she did not receive any vitamin supplementation after surgery. The patient reported vomiting three to four times daily postoperatively until a month before her presentation.
Examination showed that the cranial nerves were intact with no motor or sensory abnormalities. Her UL and LL tone was normal. There was a symmetrical decrease in power in her ULs both proximally and distally. LL power was also decreased. Her reflexes were diminished but elicitable, but her plantar response was mute with various maneuvers. The sensory examination was unremarkable and her coordination was intact.
The patient was admitted to hospital as a case of postbariatric surgery myeloneuropathy or GBS. IVIG was given for a complete course of five continuous days. Thiamine loading and maintenance were given parentally. Vitamin B12 and D levels were within normal limits. She was discharged with persistent weakness to undergo rehabilitation. No MRI or NCS was done at admission.
She presented again with the same concern and was admitted to neurology inpatient services. An MRI scan of the entire spine was performed, which showed early dorsal spine spondylitic changes with small anterior osteophytes at the lower dorsal spine. An EMG/NCS was also done, showing pure motor neuropathy and myopathic changes at proximal muscle and a normal sensory picture, suggestive of acute motor axonal neuropathy for early Guillain-Barré syndrome.
She continued to receive vitamin supplementation and physiotherapy. Plasma exchange was discussed but declined by the family. She will require ongoing extensive neurorehabilitation at a dedicated center at King Faisal Specialist Hospital and Research Centre or King Fahad Medical City in Riyadh.
A 22-year-old Saudi female with a case of morbid obesity (initial BMI of 43 kg/m2 and final postoperative BMI of 34.6 kg/m2), who met the National Institute of Health criteria for bariatric surgery, underwent an elective laparoscopic gastric sleeve procedure on January 22, 2017. She was discharged home 1-day postoperatively without any complications.
A month after surgery, she developed gradual bilateral LL numbness described as a tingling sensation, followed by LL weakness that progressed to pain. In addition, she reported short-term memory impairment. Initially, she was unable to walk without support, which gradually progressed to a complete inability to walk. There was no UL involvement. The patient reported falling down numerous times because of dizziness; however, she did not lose consciousness or have any convulsions. She also reported hoarseness of speech but no other bulbar symptoms. The patient did not have urinary or bowel changes, nor did she have visual changes. Her family history was unremarkable.
The physical examination showed that she was pale, in pain, dehydrated but conscious, oriented and alert, hemodynamically stable, and afebrile. The motor examination revealed normal LL tone, a slight decrease in power with absent reflexes, and decreased sensation up to the knees. UL reflexes were decreased. Initial laboratory test results (complete blood count, erythrocyte sedimentation rate, and C-reactive protein) were normal. Nutritional assessment showed the following results: normal vitamin B12 (456
A lumber puncture revealed clear colorless CSF with a volume of 0.5 mL and the following results: WBC 3 cells/mm3, RBC 107 cells/mm3, glucose level 4 mmol/L, and protein level 0.80 g/L. CSF viral bacterial and fungal culture results were negative. Because of the progression of her symptoms, she underwent further neurological workup. An MRI study of the dorsal spine was unremarkable, except for EMG axonal involvement. These findings were consistent with GBS.
She did not require admission to ICU but received a course of IVIG (30 g daily), nutritional replacement, vitamin B complex, and vitamin D. She started physiotherapy and was discharged from hospital in good condition.
GBS is an inflammatory polyneuropathy that has a significant overlap in symptoms with nutritional polyneuropathies. It is an acute post-infectious autoimmune syndrome affecting the peripheral nerves and resulting in ascending symmetrical motor and sensory deficits. Patients present with ascending weakness. Cranial nerve deficits and respiratory muscle involvement occur in the later stages. Weeks prior to the onset of symptoms, patients may have a viral or bacterial infection,
Supportive care and specific therapy are the main components of managing GBS, with supportive care being the fundamental therapeutic route. The progression of neuropathy can be significantly threatening, thus giving rise to multiple complications that necessitate close monitoring, including respiratory compromise, cranial nerve dysfunction, and autonomic instability. Pain and psychological stress should not be neglected and must be managed as well as physical therapy. High-dose intravenous immunoglobulin or plasmapheresis (in severe cases) should be initiated after the diagnosis has been confirmed [
Review of literature: GBS case reports after bariatric surgeries.
Name and author | Year | Country | Study type | Treatment | Outcome |
---|---|---|---|---|---|
Guillain-Barré-like syndrome after bariatric surgery [ |
2015 | Russia | Case report | Vitamin B complex (milgamma), thiamine, pyridoxine, and ferrous sulfate | The neurological symptoms stabilized when treatment was initiated. Over the next several months, the symptoms gradually improved; he required the assistance of a walker for 6 months before his symptoms completely resolved. |
Guillain-Barré syndrome and postbariatric surgery polyneuropathies [ |
2009 | Washington, DC, USA | Case report | Gabapentin, physical therapy | Symptoms gradually improved; she required the assistance of a walker for 6 months before her symptoms completely resolved. |
Guillain-Barré syndrome (demyelinating) six weeks after bariatric surgery: a case report and literature review [ |
2015 | Karachi, Pakistan | Case report | Intravenous immunoglobulin (IVIG) and rehabilitation | She had complete recovery on follow-up. |
Weakness after gastric bypass [ |
2002 | Los Angeles and Kansas City, USA | Case series | First patient: plasmapheresis. Therapy was changed to intravenous immunoglobulin G (for 1 year) |
First patient: regained some strength in her legs but is confined to a wheelchair because of uncontrollable shaking and persistent weakness of her upper limb. |
Neurological complications of bariatric surgery [ |
2016 | Jeddah, Saudi Arabia | 451 patients who underwent bariatric surgery | Fourteen patients had full recovery from the neurological signs and symptoms; one patient died. | |
Acute axonal polyneuropathy with predominant proximal involvement: an uncommon neurological complication of bariatric surgery [ |
2006 | São Paulo, Brazil | Case report | Vitamin supplementation (B1 and B6 vitamin) and IVIG | Rapidly recovered proximal muscle strength. |
Neurological complications of bariatric surgery [ |
2014 | Abymes, France | Case series | First patient: IV thiamine replacement therapy, followed by intramuscular thiamine daily and physiotherapy |
First patient: after a few days of treatment, there was a slight improvement in gait disorders. She slowly but progressively improved after physiotherapy, and 6 months later, she had nearly completely recovered. |
Rare neurological complication of bariatric surgery: acute motor axonal neuropathy (AMAN), a severe motor axonal form of Guillain-Barré syndrome [ |
2014 | France | Case report | IVIG | Seven days after initiation of treatment, she was transferred to the rehabilitation department. |
All three of our cases presented with GBS-like symptoms. Their laboratory results and nutritional assessments were all normal, which ruled out nutritional deficiencies as a cause. Their EMG results and clinical findings were, however, consistent with GBS, and they improved with IVIG treatment. Such findings are consistent with a diagnosis of GBS. Chang et al. [
On the other hand, in their cross-sectional study, Algahtani et al. [
GBS is a potential delayed complication of bariatric surgery that warrants counseling preoperatively. The adverse effects of each postbariatric surgery polyneuropathy should be clearly explained to patients undergoing this type of procedure. A clear awareness program and follow-up schedules should be planned and practiced by the operating surgeon, dietician, and family physician.
Informed consent was obtained from all individual participants included in the case report.
The authors have nothing to disclose. This manuscript is not under consideration by any other journal. This article does not contain any studies with human participants or animals performed by any of the authors.
The authors declare that they have no conflict of interest.
All authors read and approved the final manuscript.