Acute stress disorder overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Acute stress disorder from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

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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]

Overview

Acute stress disorder is defined as the development of characteristic symptoms lasting from 3 days to 1 month following exposure to one or more traumatic events.[1] The exact pathogenesis of acute stress disorder is not fully understood. It is thought that acute stress disorder is caused by either sympathetic nervous system, both directly and indirectly through the release od adrenaline and to a lesser extent noradrenaline from the medulla of the adrenal glands, or hypothalamic-pituitary-adrenal axis.[2] Acute stress disorder may be caused by either experiencing, witnessing, or being confronted with one or more traumatic events.[3][4][5][6] The point prevalence of acute stress disorder (ASD) following trauma exposure has been estimated at between 5 and 20 percent. Females are more commonly affected with acute stress disorder than males.[7][8][9][10][11][12] Common risk factors in the development of acute stress disorder are temperamental, environment, and genetic and physiological.[13][14][15][16][17] If left untreated, 50% of patients with acute stress disorder may progress to develop post traumatic stress disorder. Common complications of acute stress disorder include interference with sleep, energy levels, and capacity to attend to tasks, generalized withdrawal, and progression to post traumatic stress disorder. Prognosis is generally good, and the majority of individuals experiencing acute stress disorder recover completely. If the disorder lasts more than 4 weeks, a significant percentage will develop posttraumatic stress disorder (PTSD). The diagnosis of acute stress disorder is based on the DSM-5 diagnostic criteria, which include criterion A i.e the exposure to actual or threatened death, serious injury, or sexual violation in one (or more) of the following ways such as directly experiencing the traumatic event(s), witnessing, in person, the event(s) as it occurred to others, learning that the event(s) occured to a close family member or close friend, and experiencing repeated or extreme exposure to aversive details of the traumatic event(s), criterion B i.e presence of nine (or more) of the symptoms from any of the five categories of intrusion, negative mood, dissociation, avoidance, and arousal, beginning or worsening after the traumatic event(s) occurred, criterion C i.e duration of the disturbance (symptoms in Criterion B) is 3 days to 1 month after trauma exposure, criterion D i.e the disturbance causes clinically significant distress or impairment in social, occupational,or other important areas of functioning, and criterion E i.e the disturbance is not attributable to the physiological effects of a substance (e.g., medication or alcohol) or another medical condition (e.g., mild traumatic brain injury) and is not better explained by brief psychotic disorder.[18] Symptoms of acute stress disorder include dissociative symptoms, symptoms of reexperiencing the traumatic event, avoidence symptoms, symptoms of anxiety or increased arousal, symptoms of distress, chaotic and impulsive behavior, and post-concussive symptoms. The optimal therapy for acute stress disorder includes cognitive-behavioral therapy and pharmacotherapy. The mainstay of therapy for acute stress disorder is cognitive-behavioral therapy.[19][20][21][22][23][24] Pharmacologic medical therapies for acute stress disorder include beta blockers, alpha adrenergic agents, benzodiazepines and/or SSRIs.

Historical Perspective

Acute stress disorder was originally made known during world wars 1 and 2, where soldiers exhibited signs of stress up to 1 month after a traumatic event.[25]

Classification

There is no classification system established for acute stress disorder.

Pathophysiology

The exact pathogenesis of acute stress disorder is not fully understood. It is thought that acute stress disorder is caused by either sympathetic nervous system, both directly and indirectly through the release of adrenaline and to a lesser extent noradrenaline from the medulla of the adrenal glands, or hypothalamic-pituitary-adrenal axis.[2]

Causes

Acute stress disorder may be caused by either experiencing, witnessing, or being confronted with one or more traumatic events.[26][27][28][29]

Differential Diagnosis

Acute stress disorder must be differentiated from other diseases that closely mimic a range of acute stress disorder symptoms, including depersonalization, derealization, reduced awareness, and dissociative amnesia or from disorders that doesn't meet criteria for acute stress disorder such as post traumatic stress disorder, obsessive-compulsive disorder, anxiety disorders, depression, dissociative disorders, panic disorder, adjustment disorder, effects of analgesic medications, medical conditions involving coma or impaired awareness, effects of substance abuse, traumatic brain injury (TBI), exacerbation of a preexisting mental condition, brief psychotic episode, and psychotic disorders.

Epidemiology and Demographics

The point prevalence of acute stress disorder (ASD) following trauma exposure has been estimated at between 5 and 20 percent. Females are more commonly affected with acute stress disorder than males.[7][8][9][10][11][30]

Risk Factors

Common risk factors in the development of acute stress disorder are temperamental, environment, and genetic and physiological.[13][14][15][16][17]

Screening

According to the United States Preventive Services Task Force, screening for acute stress disorder is not recommended.[31]

Natural History, Complications, and Prognosis

If left untreated, 50% of patients with acute stress disorder may progress to develop post traumatic stress disorder. Common complications of acute stress disorder include interference with sleep, energy levels, and capacity to attend to tasks, generalized withdrawal, and progression to post traumatic stress disorder. Prognosis is generally good, and the majority of individuals experiencing acute stress disorder recover completely. If the disorder lasts more than 4 weeks, a significant percentage will develop posttraumatic stress disorder (PTSD). Of individuals who have cognitive-behavioral therapy (CBT) shortly after frightening events, only about 10% to 20% develop PTSD.

Diagnosis

Diagnostic Criteria

The diagnosis of acute stress disorder is based on the DSM-5 diagnostic criteria, which include criterion A i.e the exposure to actual or threatened death, serious injury, or sexual violation in one (or more) of the following ways such as directly experiencing the traumatic event(s), witnessing, in person, the event(s) as it occured to others, learning that the event(s) occured toa close family member or close friend, and experiencing repeated or extreme exposure to aversive details of the traumatic event(s), criterion B i.e presence of nine (or more) of the symptoms from any of the five categories of intrusion, negative mood, dissociation, avoidance, and arousal, beginning or worsening after the traumatic event(s) occurred, criterion C i.e duration of the disturbance (symptoms in Criterion B) is 3 days to 1 month after trauma exposure, criterion D i.e the disturbance causes clinically significant distress or impairment in social, occupational,or other important areas of functioning, and criterion E i.e the disturbance is not attributable to the physiological effects of a substance (e.g., medication or alcohol) or another medical condition (e.g.,mild traumatic brain injury) and is not better explained by brief psychotic disorder.[18]

History and Symptoms

Symptoms of acute stress disorder include dissociative symptoms, symptoms of reexperiencing the traumatic event, avoidence symptoms, symptoms of anxiety or increased arousal, symptoms of distress, chaotic and impulsive behavior, and post-concussive symptoms.

Physical Examination

Patients with acute stress disorder usually appear disheveled and unclean and may show the effects of dehydration and failure to care for themselves. Mental status examination of patients with acute stress disorder is usually remarkable for anxious, sad, irritable, apathetic, emotionally labile, angry, or calm, individuals may feel helpless, be confused, be in a state of disbelief, have markedly impaired concentration, have lowered self-esteem, or be driven to search for the deceased, patients may have visual or auditory hallucinations that the deceased person is present; feelings of unreality, flashbacks, numbness, and denial may occur, confusion in combination with preoccupation with those they have lost may be present that impair an individuals’ judgment and insight, and suicidal thoughts occur in as many as approximately 54% of survivors and may continue up to 6 months after the death; thoughts or plans of homicide may be present.

Laboratory Findings

There are no diagnostic lab findings associated with acute stress disorder.

Chest X Ray

There are no chest x ray findings associated with acute stress disorder.

CT

There are no CT scan findings associated with acute stress disorder.

MRI

There are no MRI findings associated with acute stress disorder.

Other Imaging Findings

There are no other imaging findings associated with acute stress disorder.

Other Diagnostic Studies

There are no other diagnostic studies associated with acute stress disorder.

Treatment

Medical Therapy

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

Psychotherapy

The optimal therapy for acute stress disorder includes cognitive-behavioral therapy and pharmacotherapy. The mainstay of therapy for acute stress disorder is cognitive-behavioral therapy.[19][20][21][22][23][24]

Primary Prevention

Effective measures for the primary prevention of acute stress disorder include getting medical treatment with a few hours of experiencing a traumatic event and counseling and preparation training in military personnel.

Secondary Prevention

There are no secondary preventive measures available for acute stress disorder.

References

  1. Bryant RA, Friedman MJ, Spiegel D, Ursano R, Strain J (2011). "A review of acute stress disorder in DSM-5". Depress Anxiety. 28 (9): 802–17. doi:10.1002/da.20737. PMID 21910186.
  2. 2.0 2.1 Acute stress disorder. Wikipedia(2015) https://en.wikipedia.org/wiki/Acute_stress_reaction Accessed on january 4, 2016
  3. Bryant, Richard A., et al. "A review of acute stress disorder in DSM‐5." Depression and anxiety 28.9 (2011): 802-817.
  4. Classen, Catherine, et al. "Acute stress disorder as a predictor of posttraumatic stress symptoms." American Journal of Psychiatry (1998).
  5. Elklit, Ask, and Dorte M. Christiansen. "ASD and PTSD in rape victims." Journal of Interpersonal Violence (2010).
  6. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
  7. 7.0 7.1 Holeva, Vassiliki; Tarrier, Nicholas; Wells, Adrian (2001). "Prevalence and predictors of acute stress disorder and PTSD following road traffic accidents: Thought control strategies and social support". Behavior Therapy. 32 (1): 65–83. doi:10.1016/S0005-7894(01)80044-7. ISSN 0005-7894.
  8. 8.0 8.1 Harvey AG, Bryant RA (1998). "The relationship between acute stress disorder and posttraumatic stress disorder: a prospective evaluation of motor vehicle accident survivors". J Consult Clin Psychol. 66 (3): 507–12. PMID 9642889.
  9. 9.0 9.1 Brewin CR, Andrews B, Rose S, Kirk M (1999). "Acute stress disorder and posttraumatic stress disorder in victims of violent crime". Am J Psychiatry. 156 (3): 360–6. doi:10.1176/ajp.156.3.360. PMID 10080549.
  10. 10.0 10.1 Creamer, Mark; Manning, Carolyn (1998). "Acute Stress Disorder Following an Industrial Accident". Australian Psychologist. 33 (2): 125–129. doi:10.1080/00050069808257393. ISSN 0005-0067.
  11. 11.0 11.1 Harvey AG, Bryant RA (1999). "Acute stress disorder across trauma populations". J Nerv Ment Dis. 187 (7): 443–6. PMID 10426466.
  12. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
  13. 13.0 13.1 Harvey AG, Bryant RA (1999). "Predictors of acute stress following motor vehicle accidents". J Trauma Stress. 12 (3): 519–25. doi:10.1023/A:1024723205259. PMID 10467559.
  14. 14.0 14.1 Harvey AG, Bryant RA (1998). "Predictors of acute stress following mild traumatic brain injury". Brain Inj. 12 (2): 147–54. PMID 9492962.
  15. 15.0 15.1 Barton KA, Blanchard EB, Hickling EJ (1996). "Antecedents and consequences of acute stress disorder among motor vehicle accident victims". Behav Res Ther. 34 (10): 805–13. PMID 8952123.
  16. 16.0 16.1 Guthrie RM, Bryant RA (2005). "Auditory startle response in firefighters before and after trauma exposure". Am J Psychiatry. 162 (2): 283–90. doi:10.1176/appi.ajp.162.2.283. PMID 15677592.
  17. 17.0 17.1 Blatchley FR, Donovan BT (1976). "Progesterone secretion during pregnancy and pseudopregnancy in the ferret". J Reprod Fertil. 46 (2): 455–6. PMID 1255579.
  18. 18.0 18.1 Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association. 2013. ISBN 0890425558.
  19. 19.0 19.1 Bryant RA, Harvey AG, Dang ST, Sackville T, Basten C (1998). "Treatment of acute stress disorder: a comparison of cognitive-behavioral therapy and supportive counseling". J Consult Clin Psychol. 66 (5): 862–6. PMID 9803707.
  20. 20.0 20.1 Bryant RA, Moulds ML, Guthrie RM, Nixon RD (2005). "The additive benefit of hypnosis and cognitive-behavioral therapy in treating acute stress disorder". J Consult Clin Psychol. 73 (2): 334–40. doi:10.1037/0022-006X.73.2.334. PMID 15796641. Review in: Evid Based Ment Health. 2005 Nov;8(4):109
  21. 21.0 21.1 Bryant RA, Moulds ML, Nixon RD, Mastrodomenico J, Felmingham K, Hopwood S (2006). "Hypnotherapy and cognitive behaviour therapy of acute stress disorder: a 3-year follow-up". Behav Res Ther. 44 (9): 1331–5. doi:10.1016/j.brat.2005.04.007. PMID 16368074.
  22. 22.0 22.1 Bryant RA, Moulds ML, Nixon RV (2003). "Cognitive behaviour therapy of acute stress disorder: a four-year follow-up". Behav Res Ther. 41 (4): 489–94. PMID 12643970.
  23. 23.0 23.1 Foa EB, Hearst-Ikeda D, Perry KJ (1995). "Evaluation of a brief cognitive-behavioral program for the prevention of chronic PTSD in recent assault victims". J Consult Clin Psychol. 63 (6): 948–55. PMID 8543717.
  24. 24.0 24.1 Scheeringa MS (2007). "CBT treatment of PTSD within the first month". Am J Psychiatry. 164 (8): 1267, author reply 1267-8. doi:10.1176/appi.ajp.2007.07030406r. PMID 17671292.
  25. Bryant, Richard (2000). Acute stress disorder : a handbook of theory, assessment, and treatment. Washington, DC: American Psychological Association. ISBN 978-1-55798-612-2.
  26. Bryant, Richard A., et al. "A review of acute stress disorder in DSM‐5." Depression and anxiety 28.9 (2011): 802-817.
  27. Classen, Catherine, et al. "Acute stress disorder as a predictor of posttraumatic stress symptoms." American Journal of Psychiatry (1998).
  28. Elklit, Ask, and Dorte M. Christiansen. "ASD and PTSD in rape victims." Journal of Interpersonal Violence (2010).
  29. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
  30. Diagnostic and statistical manual of mental disorders : DSM-5. Washington, D.C: American Psychiatric Association, 2013. Print.
  31. http://www.uspreventiveservicestaskforce.org/BrowseRec/Search?s=acute+stress+disorder Accessed on February 13, 2016.



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