Acute stress disorder medical therapy

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Acute stress disorder Microchapters


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]


Pharmacologic medical therapies for acute stress disorder include beta blockers, alpha adrenergic agents, benzodiazepines and/or SSRIs.

Medical Therapy


Basic principles of intervention after emotional trauma include the following:

Reduce stress by all possible means
Ensure that survivors have a safe environment
Promote contact with loved ones and other sources of support
Support self-esteem; help patients understand that their reaction to the trauma is a normal reaction to an abnormal situation, not a sign of weakness or psychopathology
Help survivors focus on immediate needs, such as rest, food, shelter, social supports, or a sense of belonging to a community
Promote coping mechanisms
Help patients reframe any destructive cognitions
Administer medication (eg, beta-blockers, alpha agonists, benzodiazepines, or nonactivating selective serotonin reuptake inhibitors [SSRIs]), if needed, to decrease arousal
Avoid increasing stress - Avoid prompting discussion of issues that cannot be resolved; avoid abreaction in groups and the resulting contagion effect; respect defenses, and do not force reality on people who cannot handle it yet; keep in mind that debriefing may be harmful
Discuss the experience with patients who want to talk about it, and avoid pressuring those who do not wish to discuss it
Identify persons at high risk - Screen for physical causes of psychiatric problems (eg, dehydration, head trauma, infection, metabolic abnormality, or toxins)
Have faith in the normal healing processes


Medications to decrease arousal and insomnia have a long-term impact on acute stress disorder

Alpha adrenergic agents and beta blockers limit hyperarousal. An atypical neuroleptic or mood stabilizer may be needed for an extreme aggression, agitation, dissociation, or psychosis
SSRIs may be helpful in dealing with the symptoms such as depression, anxiety, withdrawal, and avoidance and can be effective in longer-term treatment
Benzodiazepines, can be helpful in the initial stages, by there ability to limit hyperarousal and ability to foster sleep; however, continuous administration of benzodiazepines may interfere with readaptation and grieving. Longer-acting agents are beneficial when follow-up treatment is in short supply and medication is administered at the emergency site
Comorbid conditions such as attention deficit hyperactivity disorder (ADHD) should be treated. Reduction in atleast one disabling symptom such as insomnia or hyperarousal may have a powerful positive impact on the individual’s ability to re-compensate.

The mechanism of action and common features of various pharmacological agents that may be helpful in acute stress disorder is shown below in a tabular form:

Drug class Drug Action Examples Features
Beta-Adrenergic blocking agents Beta blockers inhibit inotropic, chronotropic, and vasodilatory responses to beta adrenergic stimulation Propranolol Propranolol may be useful for the treatment of hyperarousal
Selective Serotonin Reuptake Inhibtors Escitalopram Escitalopram i sthe S-enantiomer of citalopram

Escitalopram has a faster onset of depression relief, usually 1-2 weeks in comparison with other antidepressants

Sertraline Sertraline selectively inhibits presynaptic serotonin reuptake with minimal or no effect on the reuptake of norepinephrine or dopamine
Citalopram Citalopram enhances serotonin activity through selective reuptake inhibition at the neuronal membrane

Citalopram is the least activating of the SSRIs and is particularly useful in acute stress disorder The incidence of adverse effects especially sexual is less with citalopram than with other SSRIs

  • Benzodiazepines bind to specific receptors on the gamma amino- butyric acid (GABA) receptor complex, thereby increasing the affinity of (GABA) for its receptor
  • They also increase the frequency of chlorine channel opening in response to GABA binding
  • GABA receptors are chlorine channels that mediate postsynaptic inhibition, resulting in postsynaptic neuron hyperpolarization
  • They have sedative-hypnotic and anxiolytic effect
Clonazepam Clonazepam is a long-acting benzodiazepine that increases presynaptic GABA inhibtion and reduces the monosynaptic and polysynaptic reflexes
Diazepam Diazepam depresses all levels of the CNS such as limbic and reticular formations, by increasing activity of GABA
Lorazepam Lorazepam is a sedative-hypnotic with short onset of effect and a relatively long half-life

By increasing the action of GABA, lorazepam may depress all levels of the CNS, including limbic and reticular formations It is important to monitor the patient's blood pressure after administering a dose and to adjust the dose as necessary

Alpha Adrenergic Receptors Clonidine Clonidine affects alpha1, alpha2, and alpha3-adrenergic receptors

It is frequently given to children but is not approved by the US Food and Drug Administration (FDA) for any psychiatric uses in children It is available in tablets and in transdermal skin patches

Guanfacine Guanfacine has an action similar to that of clonidine but has a longer half-life and is less sedating

It is more selective alpha agonist, affecting only alpha2-adrenergic receptors Guanfacine is not recommended for children younger than 12 years

Antihistamines Older, sedating antihistamines such as diphenhydramine are often prescribed as sedatives because of their CNS- depressing properties Diphenhydramine Diphenhydramine is available as nonprescription preparations containing 25 mg of diphenhydramine in liquid, chewable, and capsule forms


  1. Famularo R, Kinscherff R, Fenton T (1988). "Propranolol treatment for childhood posttraumatic stress disorder, acute type. A pilot study". Am J Dis Child. 142 (11): 1244–7. PMID 3177336.
  2. Gelpin E, Bonne O, Peri T, Brandes D, Shalev AY (1996). "Treatment of recent trauma survivors with benzodiazepines: a prospective study". J Clin Psychiatry. 57 (9): 390–4. PMID 9746445.