An unusual complication of polytrauma:

A patient with acetabulum fracture fixation develops Guillain-Barre Syndrome, precipitated by trauma/surgery – A case report

Senthilrajan Angamuthu*

Consultant Orthopaedic Surgeon, Kauvery Hospital, Salem, India



A rare instance of post-traumatic Guillain-Barré syndrome (GBS), an acute, autoimmune, inflammatory, demyelinating polyneuropathy affecting the peripheral nervous system and a potentially life-threatening cause of muscle weakness, is presented.

Case Presentation

A 56-year-old active male, working in the police department, came to the emergency department with a history of road traffic accident. He had a chest injury, blunt injury abdomen, and left hip injury.

On a primary survey, he had multiple rib fractures with haemo-pneumothorax, a stable liver contusion, left Acetabulum fracture-dislocation-posterior wall and posterior column fracture with displacement along with high Ischio-Pubic Rami Fracture. A big chunk of posterior wall fragment was displaced anterior to the femoral head just under the femoral neurovascular bundle and became an obstacle for closed reduction.


He was known to have Diabetes Mellitus, and was on medications; no history of any other systemic illness.

He was taken up for the emergency closed reduction of the Left hip joint. Unfortunately, we were not able to achieve the reduction due to acetabulum fracture and fragment interposition.

So, he was taken up for Left Acetabulum fracture fixation. Left acetabulum fracture was approached through the Posterior K-L Approach, displaced posterior column was derotated with the bone hook placed at the ischial spine and stabilized with posterior column plating; displaced posterior wall fragment was mobilized carefully, reduced, and fixed with lag screws.

He was mobilized out of bed and could sit on a chair by the third post-operative day. ICD drain was removed and he was discharged from the hospital on 8th postoperative day.

At the time of discharge, he was stable haemodynamically, without any new symptoms. He was on intravenous anti-coagulant when he was in the hospital and placed on oral anti-coagulant on discharge, for prevention of deep vein thrombosis and pulmonary thromboembolism.

Further evolution

On the 12th day, he presented to the emergency room with complaints of breathlessness for the previous two days which was getting worse.

On examination, he was dyspnoeic and tachypnoeic. He was in respiratory distress; his respiratory rate was more than 30 m-1 on room air. SpO2 was 82% on room air, and 98% with NIV support. Investigations indicated blood gas analysis showing respiratory alkalosis, with elevated total count and hyperkalemia. Emergency Pulmonary CT-Angiogram, done to rule out pulmonary thromboembolism (PTE), showed no evidence of PTE. CT-Brain was also done to rule out intracranial pathology and was normal.

He was admitted to the intensive care unit and maintained on NIV support. A sequence of onset of symptoms was inquired into again by reviewing the history. He said that he had right upper limb weakness after he was discharged from the hospital that was progressive and involved the other limbs. He also had gradual onset of breathing difficulty. We suspected at this stage that the cause could be neuro-muscular problems. CSF fluid analysis and Nerve Conduction Study (NCS) were done. NCS showed axonal and demyelinating form of GBS. Neurologist opinion was obtained and he was diagnosed to have demyelinating polyneuropathy – Guillain-Barré Syndrome (GBS), with trauma as a precipitating factor.

He was managed with team of doctors consisting of Orthopaedic surgeon, Neurologist, Neurosurgeon, Pulmonologist, Cardiologist, Intensivist and Nephrologist. He could not tolerate the NIV Support; he was intubated and ventilator support was given in view of progressive respiratory muscle weakness. Plasmapheresis was done on alternate days, along with other supportive medication and physiotherapy. Percutaneous Tracheostomy was done. After five cycles of plasmapheresis he showed signs of recovery; he was gradually weaned from ventilator supports, and the tracheostomy was closed. He was discharged with residual limb weakness- upper and lower limb power of 2/5.


He was advised to continue passive physiotherapy. He was reviewed frequently, and approximately after 12 weeks from the onset of initial symptoms, he had neurological recovery from 1/5 to 4/5 power and he was ambulant on his own without any aid.



Guillain-Barré syndrome (GBS) is an acute, autoimmune, inflammatory, demyelinating polyneuropathy affecting the peripheral nervous system. It causes symmetric ascending flaccid paralysis and areflexia. The annual incidence is 1 to 2 cases per 100,000; presentation varies from mild peripheral symptoms to fulminant GBS involving facial, bulbar, or respiratory musculature, leading to death.

Guillain-Barré syndrome may be preceded by infection, immunization, surgery, or trauma.

GBS has complicated COVID 19 and has also been reported after vaccination. COVID 19 Cross-reactivity of neural antigens with antibodies to infections such as Campylobacter jejuni, Mycoplasma pneumoniae, Haemophilus influenzae, cytomegalovirus, herpes simplex, and Epstein-Barr viruses are suspected.

Trauma to nervous tissue can also expose myelin to the body’s immune system, resulting in cross-reactivity and demyelination caused by the deposition of circulating antigen-antibody complexes in the blood vessels of peripheral nerves.

According to the literature review, GBS in our patient could be due to either polytrauma or major surgery as the patient doesn’t have any preceding symptoms of either respiratory or GI infection [1].

According to Xiaowen Li et al study the average time interval for the development of weakness in trauma patients suspecting GBS ranged from 8 to 14 days from trauma, and most of them had respiratory muscle weakness and respiratory failure [2].

Yang et al. retrospectively analysed 36 adult patients with GBS and found that the axonal subtype of GBS was proportionally higher in post-trauma patients, as seen in our patient [3].

The study conducted by Chuxin Huang et al discloses that the median age of the patients was 53years, and 72.1% of the patients were male. The median number of days between the trigger to the onset of GBS symptoms was 9. In their study 89.0% of patients developed post-injury/surgical GBS, the main locations of injury or surgeries preceding GBS were the spine and brain. They concluded that trauma and surgery both were the triggers for GBS rather than infective one, and this type of GBS was emerging and need to be studied in detail to reveal the possible pathomechanisms [4].

Hendawi et al reported a case of post pelvic fracture fixation GBS, they concluded that the possible cause for the trigger was hardware malposition damaging the neuronal structure myelin which could have precipitated the autoantibodies against the neural structures (5).

The study conducted by Lei Bao et al reported that Orthopaedic, gastrointestinal, and neurosurgery being the most common surgeries associated with post-surgical GBS, among these GBS was most common with orthopaedic procedures [6].

Jian Chen et al reported a severe form of GBS with orthopaedic procedure, respiratory muscles took 4 months to recover and extubation was performed 9 months later, even with combined immunotherapy and plasmapheresis, the patient was discharged from the hospital after 2 years with the power of both upper and lower limb was grade 2. They reported that the patient had recovered only grade 3 power in the upper limbs, and grade 2 power in the lower limbs at 5 years follow up [7,8].


In our case, the trauma and the surgical procedure both might have triggered it, but the patient doesn’t have any type of nerve damage during the perioperative period which is common with hip fracture-dislocation and acetabulum fracture fixation. We believe that the posterior column fracture pattern near the sciatic buttress and retraction of the sciatic nerve for surgical exposure might have produced subclinical nerve damage which could trigger the immune system which leads to GBS or trauma itself producing the acute inflammatory polyneuropathy.


In conclusion post-traumatic or post-surgical GBS, a potentially life-threatening cause of muscle weakness secondary to an inflammatory polyneuropathy, it should be diagnosed early with high suspicion and appropriate measures should be taken immediately as in such cases patients often have severe motor dysfunction, a high risk of respiratory failure and a poor prognosis.


  1. Willison HJ, Jacobs BC, van Doorn PA. Guillain-Barre syndrome. Lancet. 2016;388(10045):717-27.
  2. Li X, Xiao J, Y Ding, et al. Clinical and electrophysiological features of post-traumatic Guillain-Barré syndrome, BMC Neurol. 2017;17(1):142.
  3. Yang B, Lian Y, Liu Y, et al. A retrospective analysis of possible triggers of Guillain-Barre syndrome. J Neuroimmunol. 2016;293:17-21.
  4. Huang C, Zhang Y, Deng S, et al. Trauma-Related Guillain-Barré Syndrome: Systematic Review of an Emerging Concept. Neurol. 2020;11:588290.
  5. Hendawi T, Zavatsky JM. Guillain-Barré syndrome after pelvic fracture fixation: a rare cause of postoperative paralysis. Spine. 2015;40(6):E372-E374.
  6. Bao L, Chen X, Li Q, et al. Surgery and Guillain-Barré Syndrome: A Single Center Retrospective Study Focused on Clinical and Electrophysiological Subtypes Neuropsychiatr Dis Treat. 2020:16 969-974.
  7. Chen J, Jian-Xiong M, Cai-Hong Z, et al. Severe Guillain-Barré syndrome after surgery for multiple fractures: a rare case report with a 5-year follow-up and a brief review of the literature. BMC Musculoskeletal Disorders (2021) 22:8.
  8. Tile M, Helfet DL, Kellam JF. Text book of AO Trauma, Fractures of the pelvis and acetabulum. Principles and Method of Management – Fourth Edition. 2015.s

Dr. A. Senthilrajan

Consultant Orthopaedic Surgeon