Acute Stress Disorder

Clinical picture

• The presentation blends intrusion, negative mood, dissociation, avoidance, and arousal without requiring symptoms from every category.
• Dissociative features are prominent early: emotional numbing, reduced awareness of surroundings, derealization, and dissociative amnesia.
• Sleep disturbance, hypervigilance, exaggerated startle, and irritable or aggressive behavior appear within days of the index event.
• Patients most often surface in emergency departments, trauma centers, and primary care rather than in mental health settings.
• Functional collapse can be abrupt, with inability to work, drive, sleep alone, or return to the location where the trauma occurred.
• Many people recover spontaneously, so the diagnosis flags acute distress needing support rather than an inevitable path to PTSD.

Criteria snapshot

• Exposure to actual or threatened death, serious injury, or sexual violence, directly, as a witness, by learning of it, or through repeated occupational exposure.
• Requires at least nine symptoms drawn from five categories: intrusion, negative mood, dissociation, avoidance, and arousal.
• Duration is 3 days to 1 month after the trauma; beyond one month the presentation must be reassessed for posttraumatic stress disorder.
• Symptoms cause clinically significant distress or impairment and are not attributable to substances, medication, or traumatic brain injury.
• Unlike PTSD, no minimum count is required within any single cluster, which permits dissociation-heavy or arousal-heavy symptom profiles.

Neurobiology

• An acute noradrenergic and catecholamine surge at the time of trauma over-consolidates emotional memory and predicts later PTSD severity.
• Elevated heart rate in the first 24-48 hours after trauma is among the more replicated biological predictors of subsequent PTSD.
• A blunted cortisol response at the time of trauma is associated with failure to contain the sympathetic stress response afterward.
• Amygdala hyperreactivity with weak ventromedial prefrontal regulation is already measurable acutely, mirroring the chronic PTSD pattern.
• Peritraumatic dissociation appears to reflect prefrontal overmodulation of limbic arousal rather than the more typical underregulation.
• Prior trauma, female sex, low cortisol reactivity, and comorbid traumatic brain injury all raise the probability of progression to PTSD.

Psychology

• Acute fear conditioning to trauma cues is established within days, and avoidance that begins early blocks the natural course of extinction.
• Catastrophic appraisals of early symptoms as evidence of permanent damage strongly predict symptom persistence beyond one month.
• Peritraumatic dissociation impairs encoding and integration of the trauma memory, producing the fragmented recall seen later in PTSD.
• Perceived social support and validation during the first weeks are among the strongest modifiable protective factors against chronicity.
• Rumination about the event and about one's own conduct during it converts a time-limited stress reaction into a chronic disorder.

Differential & comorbidity

• Beyond one month the diagnosis becomes PTSD, while adjustment disorder applies when the stressor or the response falls short of criteria.
• Rule out concussion and traumatic brain injury, substance intoxication or withdrawal, and delirium in medically injured patients.
• Brief psychotic disorder with marked stressors, and normal acute stress reactions without impairment, are the key boundary conditions.
• Comorbid depression, panic attacks, and escalating alcohol use develop quickly after trauma and warrant direct, repeated screening.
• Assess suicide risk, means access, and ongoing interpersonal safety, especially after assault or intimate partner violence.

Pharmacologic treatment

• No medication is FDA-approved for acute stress disorder; pharmacotherapy targets specific symptoms rather than the syndrome itself.
• Avoid benzodiazepines in the acute period, since early use is associated with higher rather than lower rates of later PTSD.
• Short-term sleep support with trazodone 25-100 mg or prazosin 1-5 mg at bedtime for nightmares is a reasonable bridge.
• Do not use routine propranolol or hydrocortisone prophylaxis; trial evidence is inconsistent and neither is standard of care.
• Start an SSRI only when depression or panic is prominent, or when symptoms persist past one month and meet PTSD criteria.

Psychotherapy

• Trauma-focused CBT delivered over 5-6 sessions beginning about two weeks post-trauma reduces progression to PTSD.
• Do not use single-session psychological debriefing; critical incident stress debriefing shows no benefit and may increase symptoms.
• Psychological First Aid is the appropriate immediate intervention: safety, calming, connectedness, self-efficacy, and hope.
• Watchful waiting with structured follow-up at two and four weeks is appropriate for mild presentations that are already improving.
• Brief prolonged exposure started in the emergency department within hours of trauma reduced later PTSD in controlled trials.

Adjunct options

• Screen with the Acute Stress Disorder Scale or PCL-5 and repeat at one month to determine whether PTSD has emerged.
• Restore sleep, nutrition, and daily routine early, since sleep disruption in the first week predicts chronic symptom trajectories.
• Mobilize practical support including housing, finances, legal advocacy, and reconnection with family and community networks.
• Limit repeated media exposure to the event, which sustains physiologic arousal and reinforces intrusive imagery.
• Arrange definite scheduled follow-up rather than as-needed return, because most patients will not self-refer despite ongoing distress.

Clinical pearls

• Three days to one month is the window; past that, reassess for PTSD.
• Skip debriefing and skip benzodiazepines; both can worsen outcomes.
• Nine of fourteen symptoms, with no per-cluster minimum, unlike PTSD.