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Post Bariatric Surgery Neuropathy

Article · September 2017

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Zakia Yasawy Ali Hassan

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 Case Report

Post bariatric Surgery Acute Axonal Polyneuropathy: Doing

Your Best is Not Always Enough
Zakia Mohammad Yasawy, Ali Hassan
Department of Neurology, College of Medicine, University of Dammam, King Fahd Hospital of University, Al Khobar, Kingdom of Saudi Arabia

Abstract
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.

Keywords: Bariatric surgery, nutritional deficiency, obesity, polyneuropathy

Introduction Guillain‑Barre syndrome (GBS) are very rare and less than a

Obesity significantly increases the risk for ischemic heart
disease, hypertension, stroke, diabetes mellitus, dyslipidemia,
and even depression.[1] 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.[2] Bariatric
surgeries are being used widely to manage morbid obesity
to improve the quality of life and obesity‑related premature
deaths.[1] 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.[3] Laparoscopic sleeve gastrectomy  (LSG) is
the popular modality and in Saudi is most common weight
reduction procedure (88%) being performed.[2] The estimated
incidence of neurologic complications secondary to nutritional
deficiencies is up to 16% per year.[4] Peripheral neuropathies
complicating weight loss surgeries are uncommon, and
among them, the acute axonal polyneuropathies resembling
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dozen cases are reported in different English literature.[1‑5] 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.
Case Report
Case 1
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
Address for correspondence: Dr Ali Hassan,
Department of Neurology, College of Medicine, University of Dammam,
King Fahd Hospital of University, Al Khobar, Kingdom of Saudi Arabia.
E‑mail: ahrajput@uod.edu.sa
This is an open access article distributed under the terms of the Creative Commons
Attribution‑NonCommercial‑ShareAlike 3.0 License, which allows others to remix, tweak,
and build upon the work non‑commercially, as long as the author is credited and the
new creations are licensed under the identical terms.
For reprints contact: reprints@medknow.com

DOI: How to cite this article: Yasawy ZM, Hassan A. Post bariatric surgery acute
10.4103/aian.AIAN_24_17 axonal polyneuropathy: Doing your best is not always enough. Ann Indian
Acad Neurol 2017;20:309-12.

© 2006 - 2017 Annals of Indian Academy of Neurology | Published by Wolters Kluwer - Medknow 309
 Yasawy and Hassan: Postbariatric surgery acute polyneuropathy

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.
Case 2
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.
Case 3
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.
Discussion
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

a c

Figure 1: Electrodiagnostic studies showed significantly low compound muscle action potential amplitudes of Tibial (a‑case‑1) and Peroneal (b‑case‑2)
motor nerves with normal distal latency and conduction velocity, while the sign of active denervation in the form of positive sharp waves noted in
tibialis anterior muscle (c‑case‑3). These findings favor axonal neuropathic process
310 Annals of Indian Academy of Neurology  ¦  Volume 20  ¦  Issue 3  ¦  July-September 2017
 Yasawy and Hassan: Postbariatric surgery acute polyneuropathy
assessment before surgery. 5%–30% of patients reported to
have low thiamine levels in serum before bariatric surgery.[7]
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.[7] 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.[7] Two of our
patients underwent LSG and developed acute polyneuropathy,
rapidly progressed over 4 weeks from onset. Tabbara et al.[7] 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.[4] 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[5] 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
Table 1: Common neurological complications with
micronutrient deficiencies following bariatric surgery
Vitamins/nutrient deficiencies Neurological complications
Vitamin A Xerophthalmia, night blindness
Vitamin B1 (thiamine) WE, KS, acute
polyradiculoneuropathy
Vitamin B6 Polyneuropathy, myelopathy
Vitamin B9 (folate) Polyneuropathy, ON, restless leg
syndrome
Vitamin B12 (cyanocobalamin) Polyneuropathy, ON, depression,
dementia, myelopathy
Vitamin D Myopathy, osteomalacia
Vitamin E Peripheral neuropathy,
myopathy, myelopathy
Copper Polyneuropathy, ON,
myelopathy, myopathy
WE = Wernicke encephalopathy, KS = Korsakoff’s syndrome,
ON = Optic neuropathy
Annals of Indian Academy of Neurology  ¦  Volume 20  ¦  Issue 3  ¦  July-September 2017
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.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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 Yasawy and Hassan: Postbariatric surgery acute polyneuropathy

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312 Annals of Indian Academy of Neurology  ¦  Volume 20  ¦  Issue 3  ¦  July-September 2017

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