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INTRODUCTION — Acute stress disorder (ASD) is characterized by acute stress reactions that may occur in the initial month after a person is exposed to a traumatic event. The disorder includes symptoms of intrusion, dissociation, negative mood, avoidance, and arousal. Some patients who experience ASD go on to experience posttraumatic stress disorder (PTSD), which is diagnosed only after four weeks following exposure to trauma.
Treatment for ASD is aimed at curtailing symptoms of acute stress responses and preventing their development into PTSD.
The treatment of ASD is discussed here. The epidemiology, pathogenesis, clinical manifestations, course, and diagnosis of ASD are discussed separately. The epidemiology, pathogenesis, clinical manifestations, course, diagnosis, and treatment of PTSD are also discussed separately. (See "Acute stress disorder in adults: Epidemiology, pathogenesis, clinical manifestations, course, and diagnosis" and "Posttraumatic stress disorder in adults: Epidemiology, pathophysiology, clinical manifestations, course, assessment, and diagnosis" and "Pharmacotherapy for posttraumatic stress disorder in adults" and "Psychotherapy for posttraumatic stress disorder in adults".)
OVERVIEW — First-line treatment for acute stress disorder (ASD) is trauma-focused cognitive-behavioral therapy (CBT), which has been shown to reduce the likelihood of subsequently developing PTSD. Short-term use of a benzodiazepine may be useful for reducing acute arousal and sleep disturbance. Treatment of acute stress disorder is also addressed in trials of interventions to prevent PTSD. (See "Pharmacotherapy for posttraumatic stress disorder in adults" and "Psychotherapy for posttraumatic stress disorder in adults", section on 'Prevention'.)
A proportion of people with ASD will adapt without formal intervention (between one half to one quarter of people with ASD) .
COGNITIVE-BEHAVIORAL THERAPY — Trauma-focused cognitive-behavioral therapy (CBT) for acute stress disorder (ASD) typically includes patient education, cognitive restructuring, and exposure.
Educating patients about posttraumatic reactions should aim to:
●Normalize the stress response
●Heighten expectancy of recovery
●Explain the stress responses in terms of conditioning models that require the patient to learn that reminders are no longer dangerous.
Cognitive restructuring is used to address maladaptive or unrealistic appraisals the patient may have about the trauma, his or her response to the event, and fears of potential future harm.
Trauma-focused CBT for ASD optimally includes both imaginal exposure and in vivo exposure. In imaginal exposure, the patient provides a detailed narrative of his or her traumatic experience in which the patient orally relives the traumatic experience with the therapist (usually for at least 30 minutes), with the intention of achieving extinction learning. By reliving the memory repeatedly, the patient can learn that the salient reminder of the trauma (eg, the memory) is no longer a threat and does not result in aversive outcomes. Based on a similar mechanism, in vivo exposure is conducted to ensure that the patient is not avoiding feared situations in their daily life, thereby consolidating the learning that reminders are no longer signaling threat.
Indications — For most patients with ASD, we recommend early intervention with trauma-focused CBT that includes exposure treatment. For some patients treated for ASD, including patients with the features below, it is necessary to delay exposure therapy for several months into the PTSD phase:
●Extreme avoidance or dissociative responses, because these presentations may indicate extreme stress responses that may be complicated by exposure
●A primary response of anger, because anger often does not respond optimally to exposure exercises and may respond better to cognitive therapy
●An acute grief response, because exposure therapy may complicate normal grieving
●Borderline or psychotic features, because these people require containment and exposure may complicate their presentation
●Significant suicidal risk, because these patients require suicide management
●Persisting PTSD responses to childhood trauma, because addressing childhood trauma weeks after a recent trauma may be excessively difficult
Administration — CBT is typically delivered at least two weeks after trauma exposure. This allows the individual additional time for transient symptoms to abate and for post-trauma stressors to ease. The commencement of therapy should be timed with respect for other stressful events stemming from the trauma. The patient may find it difficult to focus attention on therapy if distracted by trauma-related events or experiences, such as pain, surgery, legal proceedings, relocation, or other stressors.
CBT for ASD patients should typically be provided by a trained clinician over six weekly sessions of 60 to 90 minutes; additional sessions can be added if necessary. (See "Psychotherapy for posttraumatic stress disorder in adults", section on 'Exposure therapy'.)
Efficacy — In a meta-analysis of four trials of patients with ASD [2-5], treatment with trauma-focused CBT reduced ASD symptoms by the completion of treatment, and also reduced the proportion of participants who developed PTSD during the subsequent three to six months compared to supportive counseling (Relative Risk = 0.36 [95% CI 0.17 to 0.78]) .
A subsequent trial found exposure treatment to be more effective than cognitive restructuring or a waitlist control . The trial randomly assigned 90 individuals who experienced trauma and met diagnostic criteria for ASD to receive imaginal and in vivo exposure, cognitive restructuring, or to a waitlist control group. After six weeks of treatment, fewer patients in the exposure group met diagnostic criteria for PTSD as compared to those in the cognitive restructuring or waitlist groups. At six months, patients in the exposure group remained less likely to meet PTSD criteria, and were 2.8 times more likely to achieve remission of their initial symptoms than patients in the waitlist group.
PHARMACOTHERAPY — Clinical trials have not yielded sufficient evidence to determine the efficacy of medications for acutely traumatized individuals or those diagnosed with ASD; however, based on our clinical experience, we suggest short-term benzodiazepine treatment of patients with ASD and intense anxiety, agitation, or sleep disturbance in the immediate period following the traumatic event. As an example, clonazepam 0.5 to 2 mg/day in divided doses can be used.
Benzodiazepines — Small, nonrandomized trials of benzodiazepine treatment suggest that benzodiazepines may be helpful for acute anxiety, agitation, or sleep disturbance in the immediate period following the traumatic event in patients with ASD. Prolonged use may be detrimental to adaptation leading to higher rates of PTSD.
●A small, uncontrolled trial described benzodiazepine treatment of four patients, within one to three weeks of trauma exposure, who had ASD symptoms that included disturbed sleep . Temazepam 30 mg was administered orally at bedtime for five days, followed by two days at 15 mg. The patients experienced improved sleep and reduced ASD symptoms.
●A trial compared 13 individuals treated with a benzodiazepine within one week of trauma exposure to 13 individuals with comparable trauma exposure who did not receive a benzodiazepine; participants in the two groups were pair matched for gender and symptom severity . Ten patients were treated with clonazepam (mean dose 2.7 mg/day), and three were treated with alprazolam (mean dose 2.5 mg/day). Participants in the two groups did not experience mean differences in PTSD severity ratings at one or six months. Nine participants in the benzodiazepine group compared to three controls met PTSD diagnostic criteria at six months.
Other medications — Other medications have been studied in varied populations (including individuals experiencing a traumatic event, acutely traumatized, or diagnosed with ASD) with the objective of preventing the subsequent development of PTSD. These trials, limited by small sample sizes and yielding inconclusive findings, are inadequate to recommend the use of these medications for treatment of ASD symptoms.
Antidepressants — Two randomized trials found mixed results for imipramine in the treatment of children with ASD following severe burns. Negative results were also seen for fluoxetine in one of the trials.
●A trial of 25 children, age 2 to 19, who met ASD criteria following severe burns, compared treatment with imipramine to chloral hydrate . After daily treatment for seven days, patients were more likely to respond in the imipramine group compared to chloral hydrate (83 versus 38 percent).
●A trial of 60 children, age 4 to 18, with ASD symptoms following severe burns, compared imipramine, fluoxetine, and placebo . Following daily treatment for one week, a statistically significant difference in response was not seen among the three groups (60 and 72 versus 55 percent).
Propranolol — Propranolol has been tested in the immediate aftermath of trauma exposure, with the hypothesis that reducing noradrenergic activation would result in reduced conditioning of the trauma memories and prevent the development of PTSD. Although positive results were initially seen in an uncontrolled trial  and in subsequent testing of fear conditioning , the only randomized trial examining the development of PTSD symptoms was negative . Negative results were also seen for gabapentin in that trial.
●41 patients with ASD symptoms following a traumatic event were randomly assigned a 10-day course of propranolol or placebo . The results reported a trend toward limiting subsequent fear conditioning in the propranolol group.
●48 patients who experienced an acute physical injury and were admitted to a surgical trauma center were randomly assigned to receive 14 days of treatment with propranolol, gabapentin, or placebo . Neither medication showed a benefit compared to placebo in PTSD or depressive symptoms at one, four, or eight months postinjury.
Morphine — Several uncontrolled studies have noted that morphine (which reduces norepinephrine), used for pain control in the initial 48 hours after trauma exposure, is linked to reduced subsequent PTSD symptoms, although the relationship between morphine and the development of PTSD has not been tested in randomized trials. They may point to the importance of pain management in preventing PTSD .
●A retrospective study of 696 US military personnel who experienced physical trauma compared the rate of morphine use during early trauma care between those who subsequently developed PTSD and those who did not. Subjects with PTSD were less likely to have received morphine (OR 0.48, 95% CI 0.34 to 0.68) .
●A study of 155 consecutive hospital admissions of patients after traumatic injury showed that those who developed PTSD had received lower doses of morphine than those who had not developed PTSD .
●A dose-related association between morphine use and subsequent development of PTSD was observed in an earlier analysis of 24 children who received inpatient medical care for treatment of acute burns .
SUMMARY AND RECOMMENDATIONS
●For patients with ASD, we suggest first-line treatment with trauma-focused cognitive-behavioral therapy that includes exposure over supportive therapy or cognitive restructuring alone (Grade 2B). (See 'Cognitive-behavioral therapy' above.)
•Although early intervention is indicated in most patients with ASD, some patients may benefit from a delay in starting exposure therapy (eg, patients who are suicidal, acutely grieving, or have experienced extreme avoidance or dissociation in response to the trauma) so that urgent problems can be addressed through appropriate strategies, such as suicide management. (See 'Indications' above.)
•CBT is typically provided in an individual format in five to six weekly, 60 to 90 minute sessions. (See 'Administration' above.)
●We suggest short-term benzodiazepine treatment of patients with ASD and intense anxiety or agitation, or sleep disturbance, in the immediate period following the traumatic event (Grade 2C). As an example, clonazepam 0.5 to 2 mg/day can be used in divided doses. Prolonged treatment with a benzodiazepine beyond two weeks may be detrimental to adaptation, leading to higher rates of PTSD. (See 'Pharmacotherapy' above.)
- Bryant RA. Acute stress disorder as a predictor of posttraumatic stress disorder: a systematic review. J Clin Psychiatry 2011; 72:233.
- Bryant RA, Harvey AG, Dang ST, et al. Treatment of acute stress disorder: a comparison of cognitive-behavioral therapy and supportive counseling. J Consult Clin Psychol 1998; 66:862.
- Bryant RA, Sackville T, Dang ST, et al. Treating acute stress disorder: an evaluation of cognitive behavior therapy and supportive counseling techniques. Am J Psychiatry 1999; 156:1780.
- Bryant RA, Moulds M, Guthrie R, Nixon RD. Treating acute stress disorder following mild traumatic brain injury. Am J Psychiatry 2003; 160:585.
- Bryant RA, Moulds ML, Nixon RD, et al. Hypnotherapy and cognitive behaviour therapy of acute stress disorder: a 3-year follow-up. Behav Res Ther 2006; 44:1331.
- Kornør H, Winje D, Ekeberg Ø, et al. Early trauma-focused cognitive-behavioural therapy to prevent chronic post-traumatic stress disorder and related symptoms: a systematic review and meta-analysis. BMC Psychiatry 2008; 8:81.
- Bryant RA, Mastrodomenico J, Felmingham KL, et al. Treatment of acute stress disorder: a randomized controlled trial. Arch Gen Psychiatry 2008; 65:659.
- Mellman TA, Byers PM, Augenstein JS. Pilot evaluation of hypnotic medication during acute traumatic stress response. J Trauma Stress 1998; 11:563.
- Gelpin E, Bonne O, Peri T, et al. Treatment of recent trauma survivors with benzodiazepines: a prospective study. J Clin Psychiatry 1996; 57:390.
- Robert R, Blakeney PE, Villarreal C, et al. Imipramine treatment in pediatric burn patients with symptoms of acute stress disorder: a pilot study. J Am Acad Child Adolesc Psychiatry 1999; 38:873.
- Robert R, Tcheung WJ, Rosenberg L, et al. Treating thermally injured children suffering symptoms of acute stress with imipramine and fluoxetine: a randomized, double-blind study. Burns 2008; 34:919.
- Vaiva G, Ducrocq F, Jezequel K, et al. Immediate treatment with propranolol decreases posttraumatic stress disorder two months after trauma. Biol Psychiatry 2003; 54:947.
- Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol Psychiatry 2002; 51:189.
- Stein MB, Kerridge C, Dimsdale JE, Hoyt DB. Pharmacotherapy to prevent PTSD: Results from a randomized controlled proof-of-concept trial in physically injured patients. J Trauma Stress 2007; 20:923.
- Norman SB, Stein MB, Dimsdale JE, Hoyt DB. Pain in the aftermath of trauma is a risk factor for post-traumatic stress disorder. Psychol Med 2008; 38:533.
- Holbrook TL, Galarneau MR, Dye JL, et al. Morphine use after combat injury in Iraq and post-traumatic stress disorder. N Engl J Med 2010; 362:110.
- Bryant RA, Creamer M, O'Donnell M, et al. A study of the protective function of acute morphine administration on subsequent posttraumatic stress disorder. Biol Psychiatry 2009; 65:438.
- Saxe G, Stoddard F, Courtney D, et al. Relationship between acute morphine and the course of PTSD in children with burns. J Am Acad Child Adolesc Psychiatry 2001; 40:915.