Paroxysmal sympathetic hyperactivity is a syndrome associated with brain trauma, stroke, encephalitis, and other forms of brain injury.
Results suggested that tracheostomy was independently associated with an increased incidence of PSH 1).
It is characterized by uncontrolled episodes of unbalanced sympathetic surges causing hyperthermia, diaphoresis, tachycardia, hypertension, tachypnea, and dystonic posturing.
Many treatment options are available, but only a few systemic studies of the efficacy of treatment algorithms exist. Treatments should focus on decreasing the frequency and intensity of episodes with regularly scheduled doses of medications, such as long-acting benzodiazepines, nonselective β-blockers, α2-agonists, morphine, baclofen, and gabapentin, usually in combination. Treatment of acute breakthrough episodes should focus on doses of as-needed morphine and short-acting benzodiazepines. A balance between control of symptoms without oversedation is the goal 2).
Patients who develop paroxysmal sympathetic hyperactivity have worse neurologic outcomes, longer hospital stays, and more complications. Despite the clear negative impact on outcome, consensus regarding diagnostic criteria, risk factors, pathophysiology, and treatment approaches is lacking. Recently, the importance of consensus regarding diagnostic criteria has been emphasized, and new theories of pathophysiology have been proposed 3).
A prospective observational study was done on patients, admitted in the intensive care unit, for treatment of severe TBI. The clinical characteristics and outcome of patients, with and without PSH, was compared. At the time of discharge, patients were assessed with the Disability Rating Scale (DRS), and at 6 months with the Glasgow Outcome Score Extended (GOSE).
The incidence of PSH was 8 % (29/343). Tachycardia, hypertension, and sweating were seen in all of the patients. Tachypnea was seen in 24 (82.8 %), hyperthermia in 28 (96.6 %), and posturing in 13 (44.8 %) patients. Thirteen (44.8 %) patients had all six symptoms of PSH. Follow-up data were available for 23 (79.3 %) patients. At the end of 6 months, 14 (60.9 %) patients had died, seven (30.4 %) were severely disabled, and two (8.7 %) were moderately disabled. There was a significant correlation of GOSE with the number of symptoms of PSH (Spearman's rho = 0.502, p = 0.015). The patients with PSH had significantly higher DRS scores at discharge, 25.3 vs. 19.9, p < 0.001; higher mortality at 6 months 60.9 vs. 30.4 %, p < 0.001; and higher proportions with unfavorable outcome.
Presence of PSH in patients with severe TBI was associated with prolonged hospital stay, poorer DRS at discharge, more deaths, and unfavorable outcome. The number of symptoms of PSH had a significant effect on outcome at 6 months 4).