We present a case of post-traumatic neurological deficit due to Guillain-Barre syndrome. This case is the first presentation described to the best of our knowledge.
A 37 year-old male was admitted to the ICU after a motor vehicle collision where he was found head trapped underneath the car, agitated and confused. Glasgow Coma Scale (GCS) at the scene was 13. At admission the patient was agitated, with multiple superficial abrasions over scalp and forehead and swelling over the right temporal region. Remainder of the initial physical examination was normal. The admission computed tomography (CT) revealed a C6 spinous process fracture without spinal cord compression. Head CT was normal. The blood toxicology screen was positive for opiates. Patient was admitted for observation to the surgical ICU. The past medical history was significant for hypertension, depression, recent upper respiratory infection, chronic back pain and a L4-5 laminectomy. Thirty-six hours following the admission, the patient complained of “tingling” sensation and weakness in his lower extremities, progressively involving the upper extremities and difficulty breathing. The patient was stridorous, hypertensive with new onset atrial fibrillation. He was emergently intubated, and lorazepam, metoprolol, nitroprusside, and methylprednisolone were started. On repeat physical examination, he was able to open his eyes spontaneously, with a new right facial droop. The pupils were equal bilaterally. The cough and gag reflexes were weak. The patient was unable to move extremities. There was no rectal tone. The deep tendon reflexes were absent in four extremities. He was still able to communicate with his facial muscles. The patient underwent a repeat head and neck CT showing no evidence of cord compression. Magnetic resonance imaging (MRI) of the head and neck were also normal. The magnetic resonance angiography (MRA) was normal except for an occluded right vertebral artery. A lumbar puncture was performed. The Lyme and Campylobacter serologies were negative. Lumbar puncture (LP) results were abnormal (4 WBC, 4 RBC, protein 65mg/dl, glucose 105) suggestive of a non-bacterial inflammatory process. The electromyography (EMG) showed severe, generalized sensorimotor polyneuropathy with both axonal and demyelinating features. Based on the clinical findings, ascending nature, EMG and LP results, Guillain-Barre syndrome(GBS) was diagnosed. The patient underwent exchange plasmapheresis for 5 consecutive days with significant improvement and was discharged to a rehabilitation center 10 days after admission with improved motor strength in all extremities.
GBS is an idiopathic acute inflammatory demyelinating polyneuropathy with progressive muscle weakness, areflexia, and with spontaneous remission. The incidence is 0.6-2.4/100.000 population. Both sexes and all ages are affected. Demyelination in GBS is believed to be immunologically mediated. It has been reported following infections (URI, GI infections, Camphylobacter, Lyme disease, H. influenza, Cytomegalovirus, HSV), vaccinations, epidural anesthesia, thrombolytic agents, and systemic diseases (e.g. Hodgkin’s, SLE, and Sarcoidosis). In our patient, the presentation was unusual; it is possible that a previous URI was the initial culprit, which caused impaired motor functions leading to the MVC, hospitalization and delayed respiratory distress. Or the trauma was the sole reason for the presentation of GBS. If trauma is the sole reason, this case is one of the few in the literature. Regardless of the cause, we want to stress the importance of having a wide spectrum of differential diagnosis in post-traumatic neurologic deficits.
This case presents an unusual manifestation of GBS in the setting of post-traumatic neurologic deficit. The intensivists should keep this diagnosis as part of their differential diagnosis in patients with post-traumaic neurologic deficits.
A.R. Barakat, None.