In the ED we often provide first line care for patients as the result of traumatic events.  Beyond attending to clinically apparent injuries, pain, and distress, we would be in a position to apply prophylactic treatment to attempt to prevent PTSD, a debilitating sequela of trauma, if such treatment were to exist and founded in good science.

Does such pharmacologic treatment exist?

Note: Cognitive behavioral therapy after trauma has been shown to attenuate development of PTSD and associated symptoms.

Below lie many oversimplifications and likely misinterpretations of clinical psychology, neuroscience, and PTSD.  Proceed with caution.



Results from an exposure to traumatic event; with subsequent re-experience, avoidance and hyperarousal phenomena that cause clinical distress and impact daily functioning.

Lifetime incidence 10% in men, 5% in women.



There are many factors related to the development of PTSD, including patient characteristics, history, social support system, and type of trauma, but these are not predictive.  Multiple mechanisms are proposed to describe the development of PTSD; including cognitive attribution (how people perceive and make sense of the causes of the event, and their subsequent cognitive and behavioral responses to this interpretation), negative memory re-consolidation (patient repetitively accessing and dysfunctionally emboldening traumatic memories), and various models of neuroendocrine, neurosignalling, and other neurobiological dysfunction.


Pharmacologic Targets:

1)      Hypothalamic-pituitary-adrenal axis.

Disturbance of cortical secretion in the HPA axis studied in septic shock, and subsequent placebo controlled trials studies in septic shock survivors suggest that administration of hydrocortisone was protective against development of PTSD.  The prevailing theory is that stress doses of steroids decreases the extreme sympathetic tone of and response to shock, as well as the need for exogenous vasopressors, which decreases the overall hyperadrenergic milieu in which memories of critical illness are encoded.

2)      The amygdala, which is involved in fear, mood, and memories, contains beta adrenergic receptors that are activated by norepinephrine in stress response, and likely is involved in the initial neurobiological/psychological adaptation to a traumatic experience that subsequently becomes maladaptive.  Administration of betablocker propranolol is theorized and somewhat demonstrated to reduce development of PTSD, vividness of intrusive memory recall, and arousal symptoms.  This mechanism seems related to the above cortical dysfunction model.



A Cochrane review in 2014 was performed to investigate pharmacologic prevention of PTSD after trauma.  Generally, primary outcomes were the incidence of PTSD in at 3 months using standardized scales or interviews.  Secondary outcomes were degree of symptomatology, scales of depression, anxiety, functional impairment, and medication side effects.

The studies included participants recruited in Emergency departments, trauma centers, ICUs, surgical inpatient services, and mental health facilities.

Study protocols for hydrocortisone included single dose, such as 100mg IV bolus 1 – 5 hours after the exposure, a 3 day IV taper in post-cardiac surgery patients, bolus and continuous infusion in septic patients, or 40mg PO in a 16 day taper.

Protocols for propranolol generally used 10 to 14 days of 40mg PO QID.



9 trials randomized, placebo controlled trials

345 patients total.



4 trials studied hydrocortisone:

165 patients.

The review demonstrated a significant “moderate” effect in preventing PTSD (RR: 0.17 [95% CI 0.05 to 0.56] p=0.004).



3 trials

118 patients

RR 0.62 (95% CI 0.24-1.59) p=0.32


Cochrane conclusion:

“There is moderate quality evidence of hydrocortisone for the prevention of PTSD development in adults.  No evidence to support efficacy of propranolol, escitalopram, temazepam, and gabapentin in preventing PTSD onset. “   Further, the review authors do not believe there is sufficient evidence to recommend a medication as therapy at this point.


My conclusion:

An important, interesting, and complicated subject, with current data suggesting that hydrocortisone (after further trials) has potential as prophylactic therapy after trauma to prevent PTSD.







Amos T, Stein DJ, Ipser JC. Pharmacological interventions for preventing post-traumatic stress disorder (PTSD). Cochrane Database Syst Rev. 2014 Jul 8;7


Kar N. Cognitive behavioral therapy for the treatment of post-traumatic stress disorder: a review. Neuropsychiatr Dis Treat. 2011;7:167-81.


Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey. Archives of General Psychiatry 1995;52(12):1048–60


Pitman RK, Sanders KM, Zusman RM, Healy AR, Cheema F, Lasko NB, et al.Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biological Psychiatry 2002;51:189–92.


Schelling G, Briegal J, Roozendaal B, Stoll C, Rothenhausler H-B, Kapfhammer HP. The effect of stress doses of hydrocortisone during septic shock on post traumatic stress disorder in survivors. Biological Psychiatry 2001;50:978–85.



May 2024