In a 28-year-old man with paroxysmal sympathetic hyperactivity after anoxic brain injury, non-sedating agents like propranolol and gabapentin were preferred to allow neurological prognostication.
Case Report (n=1)
This case highlights the clinical challenge of managing paroxysmal sympathetic hyperactivity following anoxic brain injury from cardiac arrest while avoiding sedation to preserve the integrity of neurological prognostication.
Abstract Introduction Paroxysmal sympathetic hyperactivity (PSH) is a rare phenomenon that occurs more commonly after traumatic brain injury (TBI), however it can also occur with anoxic brain injury. Key features include tachycardia, hypertension, tachypnea, hyperthermia, diaphoresis, and agitation which occurs due to a loss of inhibitory control over sympathetic activity in the brain. This case highlights a discord between management and required diagnosis in a patient with significant brain injury. Description We present a 28-year-old man with history of polysubstance abuse who presented voluntarily due to an accidental overdose on suspected opioids and cocaine. Upon arrival in the ED, the patient was initially awake and alert, however he rapidly declined. A blue substance was noted throughout his nares. He suffered cardiac arrest secondary to ventricular tachycardia. ROSC was obtained within eight minutes. He was admitted to the ICU and noted to have seizure-like activity with upper extremity posturing, tachypnea, tachycardia, and diaphoresis. Repeat EEGs were negative for seizure. Lumbar puncture was negative. Initial MRI brain was pertinent for T2/FLAIR hyperintensities in bilateral basal ganglia, concerning for hypoxic ischemic injury. The patient continued to have persistent episodes of dystonic posturing and sympathetic overactivity that our team was unable to manage due to instructions to avoid sedative medications for neuroprognostication. Follow-up CT indicated a loss of gray-white differentiation with effacement of cortical sulci in bilateral parietotemporal and occipital regions were noted, consistent with progression of hypoxic injury. Discussion The purpose of this case is to highlight management strategies that can be utilized to control sympathetic outflow while complying with neurological evaluation requirements. A variety of agents are used to manage PSH, including beta-blockers, benzodiazepines, and alpha-2 agonists. Propranolol is most often used, showing decreased mortality in TBI patients. In our patient, we were limited by its use due to bronchospasm. Clonidine and dexmedetomidine are alpha-2 agonists that have shown efficacy in reducing PSH frequency, severity, and duration with minimal adverse effects and while accelerating overall symptom remission. Baclofen can be used for temperature and posturing symptoms, while morphine is used for abortive therapy in acute episodes. In our case, non-sedating agents such as propranolol and gabapentin are preferred, while dexmedetomidine and even baclofen may be alternatives. Opioids and benzodiazepines should be used cautiously. The optimal approach is to prioritize non-sedating agents, titrate carefully, and minimize external triggers to control PSH episodes while preserving the integrity of neurological prognostication. This abstract is funded by: None
Ali et al. (Fri,) conducted a case report in Paroxysmal sympathetic hyperactivity following anoxic brain injury (n=1). Non-sedating agents (propranolol, gabapentin) was evaluated. In a 28-year-old man with paroxysmal sympathetic hyperactivity after anoxic brain injury, non-sedating agents like propranolol and gabapentin were preferred to allow neurological prognostication.