Case Presentation: FC is a 67-year-old female with prior history of diabetes, hypertension, and hyperlipidemia. She was initially admitted for three days of watery diarrhea. During her hospitalization, she suddenly suffered PEA arrest, and received CPR and ACLS algorithm for 26minutes before achieving ROSC. Patient was subsequently intubated. Her post-arrest neurologic exam was notable for fixed dilated pupils, absent cough and gag reflexes, and inability to move limbs. Urgent CT head imaging was concerning for anoxic brain injury. Neurology was consulted who recommended further MRI evaluation, notable for scattered areas of acute infarct suggestive of new onset strokes. Based on MRI read by radiology and neurology, the strokes were not large enough to cause lower extremity deficits. The etiology of her PEA arrest remained unclear despite extensive workup.On serial exams, patient was noted to have minimal reflexes on lower extremities and normal reflexes on upper extremities, which progressed to decreased reflexes on upper extremities as well. MRI lumbar spine showed degenerative disease without cord signal abnormalities. Given initial symptoms of diarrhea with worsening ascending areflexia, there was concern for Guillain-Barre syndrome (GBS). While technically limited, EMG showed diffusely absent motor and sensory nerve conduction responses without significant lumbar radiculopathy. A lumbar puncture showed xanthochromia, RBC 18, 0 PMNs, glucose 128 (high), protein 66 (high). Patient was started on empiric IVIG. By day3 of IVIG therapy, patient was able to track with eyes and follow simple commands, when previously she was completely unresponsive. In subsequent days, she became able to pull her own breaths on pressure support, with steadily improving tidal volumes. Given this response, the etiology of the patient’s PEA arrest was most likely diaphragmatic paralysis from undiagnosed GBS, leading to apnea, and with treatment she was able to regain some of her inherent diaphragmatic function.
Discussion: GBS is a rare bacterial illness stemming most commonly from Campylobacter, where clinical manifestations include bloody diarrhea and fevers, though watery diarrhea has also been reported. Viral infections and vaccinations can also lead to GBS via molecular mimicry as with bacterial infections. Untreated advanced cases of GBS often lead to ascending areflexia, with most fatal consequences involving diaphragmatic paralysis, with mortality rates around 12.1%. Treatment involves IVIG and plasmapheresis. For patients with acute cardiac arrest, other differentials such as pulmonary emboli, major cardiac event, septic shock, or acute strokes may be possible. In this case, given patient had such marked improvement with IVIG, there was likely a component of GBS that contributed to her initial acute hemodynamic change.
Conclusions: With this case, the importance of physical examination skills is highlighted, as it elucidated the underlying GBS etiology. This led to a significant change in patient’s management course and overall clinical status.