(915) A Case of Paroxysmal Sympathetic Hyperactivity Status Post Traumatic Brain Injury

Introduction: Paroxysmal sympathetic hyperactivity (PSH) is a severe complication of traumatic brain injury (TBI) and is characterized by six core symptoms, such as hyperthermia, hypertension, tachycardia, tachypnea, diaphoresis, and posturing. The prevalence of PSH following a TBI is nearly 33%, and is associated with poor outcomes including longer hospital stays and worse Glascow Outcome Scale scores. While there is currently no gold standard for the pharmacologic management of PSH, individual drugs and combinations of drugs are chosen based on clinician preference and whether the indication is for prevention or for treatment of a PSH episode.

Description: An 18 year old male presented to our hospital with significant head trauma following a motor vehicle accident. On admission, he had a glascow coma scale (GCS) of 4. His CT head findings are as follows: multiple intra-axial hemorrhage in left frontal and parietal lobes, bilateral subdural hemorrhage, left parafalcine hemorrhage, subarachnoid hemorrhage, intraventricular hemorrhage, extensive skull fractures, and pneumocephalus. Surgery was contraindicated, so his course was driven by aggressive medical management. Days 1 through 18 consisted of mannitol and hypertonic saline, multiple continuous sedative agents, antibiotics, desmopressin, a pentobarbital-induced coma, and insertion of a tracheostomy. On day 19, this patient became hypertensive, tachycardic, tachypneic, hyperthermic, and diaphoretic. Given high suspicion of PSH, he was initiated on clonidine 0.1mg PO TID as well as propranolol 20mg PO TID. By day 22, vitals had stabilized. He discharged to a neurological rehabilitation center on day 26.

Discussion: An increasing amount of literature and case reports outline the treatment and prevention of PSH, but there remains no standard guidelines. Propranolol, a non-selective and highly lipophilic beta-blocker, at doses of 20-80 mg every 4-8 hours, inhibits peripheral catecholamine activity and blocks CNS receptors. Clonidine, an alpha-2 agonist, at doses of 0.1-0.3 mg every 6-8 hours, down-regulates the sympathetic activity that is augmented in PSH. In combination, clonidine and propranolol are among the recommended agents for treatment of PSH, as long as bradycardia and hypotension are not of concern.