Acute Stress Disorder (ASD) was first outlined in 1994 at the diagnostic and statistical manual of mental disorders, Fourth Edition (DSM-IV) as a new diagnosis. The reasoning for adding this diagnosis was to provide healthcare services to patients that had acute traumas but were not covered by insurance due to its early stage. Secondly, it was hoped to predict PTSD development in acute trauma patients so early interventions could be initiated.
ASD explains acute stress reactions (ASRs) that occur in no less than three days and no more than four weeks. In contrast, ASRs that continue for a more extended period than four weeks can meet the criteria for post-traumatic stress disorder (PTSD). ASD was defined in an attempt to describe ASRs that were missed or treated as adjustment disorders. DSM-5 no longer requires dissociative symptoms for the diagnosis of ASD while still including it as a diagnostic criterion.
With the introduction of the DSM-5 in 2013, multiple changes were made to the diagnostic criteria. ASD was moved from the anxiety disorders bucket to a newly created bucket (i.e., trauma and stressor-related disorders) to distinguish further it's characteristics. Unlike DSM-IV, in DSM-V, dissociative symptoms are no longer a requirement for the diagnosis of ASD.
The etiology, epidemiology, pathophysiology, history and physical examination, evaluation, treatment, and side effects, prognosis, differential diagnosis, patient education, and enhancing outcomes of the Acute Stress Disorder will be discussed here.
According to the survey-based studies, twenty to ninety percent of the general population is exposed to one or more extreme stressful events in their life. Although a large number is exposed, only 1.3 to 11.2 percent of ASD developed long term symptomatic disease (such as PTSD).
There is limited evidence on risk factors for developing ASD after a traumatic event. However, the risk factors for PTSD could also be applied to ASD due to its close resemblance. Based on the two metanalyses performed by Ozer et al. and Brewin et al., Sareen J. categorized risk factors in three buckets:
ASD was initially added to the DSM-IV, 20 years ago, but there is limited data on its prevalence, especially in the general population. While ASD is a separate diagnosis compared to PTSD, but the difference is limited to the duration of ASR symptoms, making ASD prevalence measurement, more complicated. ASD prevalence is highly variable based on the study and nature of the trauma. The prevalence rates of ASD were reported < 1-week post-injury at 24.0–24.6% and 1–2 weeks post-injury at 11.7% to 40.6%.
Furthermore, there have been some epidemiologic studies on specific populations. In a meta-analysis performed by Wenjie Dai et al. in 2018 on the prevalence of ASD among road traffic accidents, showed a pooled prevalence of 15.81% (95% CI: 8.27-25.14%). Thirteen studies in eight countries pooled a total of 2989 accident patients. The results show the significance of early ASR symptoms in surveillance and therapy. ASD prevalence in emergency room encounters among children (7-17 years) exposed to trauma was 14.2 in two weeks. The prevalence of PTSD at nine weeks was 9.6 percent. In the postpartum cross-sectional study, mothers having preterm babies had significantly higher ASD than term babies ( 14.9 % versus 0%, 95% CI: 2.16;617.61, OR: 36.5).
The exact reason why most people recover after a traumatic event but few develop ASD remains unknown. Various models developed to explain the response to traumatic events. The majority of them are related to "fear conditioning." It is a form of Pavlovian learning that when a traumatic stimulus (e.g., explosion) occurs together with a neutral stimulus (e.g., smell) or context (e.g., night time), in the future encounters of the neutral stimulus or context, the brain, and the body exhibits the same fear responses (even in the absence of the traumatic stimulus).
Most healthy people adapt to fear conditioning by extinction learning- a gradual reduction in response to the traumatic stimulus. If this mechanism fails, the patient continues to re-experience fearful symptoms of the initial traumatic event.
Functional magnetic resonance imaging (fMRI) scans of the PTSD patients have shown hypoactivity of the frontal cortex and hyperactivity of the temporal cortex, demonstrating the possibility of a correlation between PTSD and neural functioning. A more recent study showed hyperactivation of the superior prefrontal and cingulate cortex and medial posterior precuneus.
ASD is a psychiatric disorder but still can have physiological manifestations (such as tachycardia) and abnormal fMRI's. However, no validated laboratory or radiographic test exists. The diagnosis is clinical and is based on history and physical examination. Careful behavior observation and careful listening to the patient's narrative is of immense value. Many patients are unable to fully reflect their feelings and history in the initial evaluation session and will require additional visits.
There are validated and quick psychometric questionnaires available that can be used to evaluate ASD children and adults. Child stress reaction checklist (CSDC), for example, measures symptoms of ASD and PTSD that can be completed in ten minutes. CSDC can be used for children 2 to 18 years old. for adults, there is a questionnaire which is designed explicitly for ASD (i.e., acute stress disorder scale).
General measures- discussed at the "deterrence and patient education" section.
Psychotherapy- Treatment of choice for ASD is a unique form of cognitive-behavioral therapy (CBT) called trauma-focused CBT. CBT can reduce the risk of further developing PTSD. This evidence-based practice can be delivered via the internet, in-person, or by phone. It focuses on increasing knowledge on trauma psychology, symptom management skills, identifying and disputing cognitive distortions, and exposure therapy. Exposure therapy is a CBT method that involves controlled patient exposure to the traumatic source to relieve the trauma memory mimicking fear extinction (discussed in the pathophysiology section). Exposure therapy is the standard of care for ASD (and PTSD). A transient worsening of the symptoms can appear, but it is not more common than other intervention methods. Debriefing-which involves asking the patient to explain in detail, the trauma and their feeling about it in the first 72 hours is widely available. studies have not shown the efficacy of debriefing in preventing the development of PTSD, and debriefing is discouraged from routine administration to ASD patients. Crisis intervention method with encouraging patients to avoid maladaptive coping behaviors (such as drinking alcohol)
Pharmacotherapy- Currently, there is no high-quality evidence for a pharmacotherapeutic agent for the treatment of ASD. SSRIs and propranolol were trialed to prevent or treat ASD but were showed little evidence on efficacy. Evidence for ASD pharmacotherapy is minimal, and most of the recommendations come from the research on PTSD. Due to similarities between ASD and PTSD and having more RCTs on PTSD, we will review pharmacotherapies for PTSD, which can be applied to ASD. PTSD Pharmacotherapy has been more effective in reducing mood symptoms, compared to recurrent memories and avoidance:
Other treatments- There is Evidence that ECT is beneficial for PTSD patients with concurrent depression with the ability to reduce symptoms for both conditions. It is suggested that one known side effect of ECT (i.e., memory disruption) could be used to help patients with severe PTSD. Clinical trials on mood stabilizers (such as topiramate and tiagabine) are limited in number and quality. Treatment arms were no better than the placebo or had limited effect size. There are cases reports that lamotrigine and/or gabapentin were effective treatments for PTSD patient nightmares and flashbacks, but more evidence is required to support these medications.
Symptom specific treatments:
PTSD psychotherapy is the first-line treatment for PTSD/ASD but is not shown to be very efficacious. Lack of effective therapies continues to make PTSD a chronic illness. Therefore there is an immediate need to explore new compounds and approaches. One promising approach is the use of psychedelics such as ketamine, psilocybin, and 3,4-methylenedioxymethamphetamine (MDMA) in the treatment of PTSD. In recent years, FDA has approved breakthrough therapy designations for both MDMA and psilocybin for the treatment of PTSD and depression. One MDMA-assisted psychotherapy study is set to get the FDA's approval by 2022.
For patients with ASD, first-line management would be of trauma-focused cognitive behavioral therapy, as oral therapies have found to be of limited benefit. Most of the studies on pharmacological treatment have focused on secondary prevention for PTSD rather than focusing on ASD. However, oral medications have found to be effective in PTSD.
Selective serotonin reuptake inhibitors (SSRIs)- SSRIs such as sertraline, paroxetine, and fluoxetine have been used for the treatment of PTSD. FDA has only approved sertraline and paroxetine.
two examples of the SSRI pharmacotherapy are provided below:
Serotonin-norepinephrine reuptake inhibitors (SNRIs) - Venlafaxine (Effexor) extended-release has shown to be effective in PTSD treatment. The extended-release oral form can be started at 37.5 mg once a day. The maximum dose is 300 mg once daily. Dose increases should be based on patient toleration and clinical improvement with no more than 75 mg/day increase in intervals of four or more days.
Second-generation antipsychotics (SGAs)- Two antipsychotics with the most clinical evidence are listed, below:
Alpha-1 selective adrenergic blockers- Prazosin is an antihypertensive medication and works by blocking specific receptors on the vascular smooth muscle. It is thought that prazosin and its metabolites can reduce the overactivation of the sympathetic system in ASD and PTSD. Prazosin can be used as monotherapy or augmentation with an SRI to minimize sleep disturbances mainly.
SRI side effects - SRIs can cause long QT-syndrome, SIADH, hyponatremia, suicide ideation (especially in children), seizures, increased risk of bleeding, sexual dysfunction, gastrointestinal symptoms (such as nausea, vomiting, and diarrhea) and serotonin syndrome. SRIs Should be prescribed by a professional and per guidelines.
Sexual dysfunction in the form of decreased libido delayed ejaculation, and anorgasmia is common (25% to 73%) among women and men taking SSRIs. Less than 10 percent of patients with sexual dysfunction due to SRIs therapy will improve after continued use of the SRI, and it is suggested to the first wait for up to 8 weeks for improvement. In the case of persistence, careful dose reduction can be tried. If the patient is still symptomatic for sexual side effects and has only partially responded to an SRI, it can be switched to another SRI. augmentation with bupropion can be tried if the patient has had a good response to the SRI. Please note that sexual dysfunction management recommendations are based on the research of depression treatment and not PTSD and ASD treatment.
SRIs should not be disconnected abruptly. This is to mitigate withdrawal symptoms.
SRIs can cause mania in patients with bipolar disorder and should not be used in patients with a history of bipolar disorder. In the case of mania, SRI should be discontinued, and appropriate bipolar disease therapy initiated. Sleep quality improved in 4 weeks.
SGA side effects - SGAs can cause long QT syndrome (all SGAs), metabolic syndrome (olanzapine, clozapine), anticholinergic symptoms, and extrapyramidal symptoms (EPS). EPS is less common with SGAs but still can occur:
Risperidone can cause hyperprolactinemia. Clozapine can cause dose-related seizures and dangerous neutropenia. Regularly Monitor neutrophil counts, before and during the treatment.
Prazosin side effects - prazosin can cause first dose orthostatic hypotension, dizziness, fatigue, and headache. Use with caution in patients with hepatic function impairment.
According to one recent study, later development of PTSD is strongly associated with ASD. It also showed that an abnormal fMRI is associated with subsequent PTSD severity. According to the DSM-5, PTSD remission occurs within three months in approximately half of the patients. It is recommended to continue pharmacotherapy for more than six months to one year to lessen the risk of relapse. The majority of the patients who developed PTSD recover within the next few years with a steep decline in the first year. At least one-third of the PTSD patients remain symptomatic for more than two years and are at risk of substance abuse.
ASD patients are 24 times more likely to die from a suicide attempt compared to those without ASD. one study found that all-cause mortality for patients with a stress disorder diagnosis two times more than those without.
Avoidance of many conditions that remind the patient of the traumatic event may continue to persist after the initial incident. For example, a car accident patient might avoid driving a car. The patient might lose her/his job due to abstinence from work or poor work performance. Resulting financial hardships can lead to homelessness in some cases. Social relationships can be limited and lead to break-ups with significant others, which would make the patient's emotional life, even more complicated.
Acute stress can lead to various psychiatric problems:
While dealing with patients with acute stress disorder, it is important to take note of the following:
Interprofessional communication and social services- ASD patients are twenty-four times more likely to die from suicide and have two times more risk of all-cause mortality compared to the general population. ASD can lead to chronic PTSD, which is a debilitating psychiatric disorder. PTSD can significantly affect a patient's quality of life. Due to these risks, management of a traumatic event requires an interdisciplinary work that can involve physicians in various disciplines (such as emergency medicine, psychiatry, orthopedics, and neurosurgery), psychologists, nurses, and social workers.
Interprofessional work can be achieved by respecting the roles of each team member and efficient communication. It is of significant importance due to the affordable care act, which calls for improved care coordination. One example would be social services. Trauma patients require regular followups and most likely require social assistance. social workers provide mental health services, referral services, care coordination, and followup in the case of complex mental and substance use disorders.
Patient education- Education plays an important role in the management of stress disorders. The patient needs to know that most people will have a strong emotional response, which will resolve in a few days to a week in most cases and will not be chronic. The patients should be advised to avoid scenarios that remind them of the event (such as watching TV shows with a similar theme), spend time with family, and have patience. The patient should be able to actively participate in the treatment planning, therapy options, and significant side effects of therapies.
|||Bryant RA,Friedman MJ,Spiegel D,Ursano R,Strain J, A review of acute stress disorder in DSM-5. Depression and anxiety. 2011 Sep; [PubMed PMID: 21910186]|
|||Bryant RA, The Current Evidence for Acute Stress Disorder. Current psychiatry reports. 2018 Oct 13; [PubMed PMID: 30315408]|
|||Bryant RA, Acute stress disorder as a predictor of posttraumatic stress disorder: a systematic review. The Journal of clinical psychiatry. 2011 Feb; [PubMed PMID: 21208593]|
|||Koopman C,Classen C,Cardeña E,Spiegel D, When disaster strikes, acute stress disorder may follow. Journal of traumatic stress. 1995 Jan; [PubMed PMID: 7712057]|
|||Dai W,Liu A,Kaminga AC,Deng J,Lai Z,Yang J,Wen SW, Prevalence of acute stress disorder among road traffic accident survivors: a meta-analysis. BMC psychiatry. 2018 Jun 13; [PubMed PMID: 29895273]|
|||Perrin M,Vandeleur CL,Castelao E,Rothen S,Glaus J,Vollenweider P,Preisig M, Determinants of the development of post-traumatic stress disorder, in the general population. Social psychiatry and psychiatric epidemiology. 2014 Mar; [PubMed PMID: 24022753]|
|||Sareen J, Posttraumatic stress disorder in adults: impact, comorbidity, risk factors, and treatment. Canadian journal of psychiatry. Revue canadienne de psychiatrie. 2014 Sep; [PubMed PMID: 25565692]|
|||Ozer EJ,Best SR,Lipsey TL,Weiss DS, Predictors of posttraumatic stress disorder and symptoms in adults: a meta-analysis. Psychological bulletin. 2003 Jan; [PubMed PMID: 12555794]|
|||Brewin CR,Andrews B,Valentine JD, Meta-analysis of risk factors for posttraumatic stress disorder in trauma-exposed adults. Journal of consulting and clinical psychology. 2000 Oct; [PubMed PMID: 11068961]|
|||Ophuis RH,Olij BF,Polinder S,Haagsma JA, Prevalence of post-traumatic stress disorder, acute stress disorder and depression following violence related injury treated at the emergency department: a systematic review. BMC psychiatry. 2018 Sep 25 [PubMed PMID: 30253782]|
|||Meiser-Stedman R,McKinnon A,Dixon C,Boyle A,Smith P,Dalgleish T, Acute stress disorder and the transition to posttraumatic stress disorder in children and adolescents: Prevalence, course, prognosis, diagnostic suitability, and risk markers. Depression and anxiety. 2017 Apr; [PubMed PMID: 28135019]|
|||Helle N,Barkmann C,Ehrhardt S,Bindt C, Postpartum posttraumatic and acute stress in mothers and fathers of infants with very low birth weight: Cross-sectional results from a controlled multicenter cohort study. Journal of affective disorders. 2018 Aug 1; [PubMed PMID: 29679899]|
|||Johnson LR,McGuire J,Lazarus R,Palmer AA, Pavlovian fear memory circuits and phenotype models of PTSD. Neuropharmacology. 2012 Feb; [PubMed PMID: 21782833]|
|||Geuze E,Vermetten E,Ruf M,de Kloet CS,Westenberg HG, Neural correlates of associative learning and memory in veterans with posttraumatic stress disorder. Journal of psychiatric research. 2008 Jul; [PubMed PMID: 17698081]|
|||Cwik JC,Sartory G,Nuyken M,Schürholt B,Seitz RJ, Posterior and prefrontal contributions to the development posttraumatic stress disorder symptom severity: an fMRI study of symptom provocation in acute stress disorder. European archives of psychiatry and clinical neuroscience. 2017 Sep; [PubMed PMID: 27455992]|
|||Regier DA,Kuhl EA,Kupfer DJ, The DSM-5: Classification and criteria changes. World psychiatry : official journal of the World Psychiatric Association (WPA). 2013 Jun; [PubMed PMID: 23737408]|
|||Cardeña E,Carlson E, Acute stress disorder revisited. Annual review of clinical psychology. 2011; [PubMed PMID: 21275643]|
|||Saxe G,Chawla N,Stoddard F,Kassam-Adams N,Courtney D,Cunningham K,Lopez C,Hall E,Sheridan R,King D,King L, Child Stress Disorders Checklist: a measure of ASD and PTSD in children. Journal of the American Academy of Child and Adolescent Psychiatry. 2003 Aug; [PubMed PMID: 12874500]|
|||Bryant RA,Moulds ML,Guthrie RM, Acute Stress Disorder Scale: a self-report measure of acute stress disorder. Psychological assessment. 2000 Mar; [PubMed PMID: 10752364]|
|||Kliem S,Kröger C, Prevention of chronic PTSD with early cognitive behavioral therapy. A meta-analysis using mixed-effects modeling. Behaviour research and therapy. 2013 Nov; [PubMed PMID: 24077120]|
|||Aulagnier M,Verger P,Rouillon F, [Efficiency of psychological debriefing in preventing post-traumatic stress disorders]. Revue d'epidemiologie et de sante publique. 2004 Feb; [PubMed PMID: 15107694]|
|||Shalev AY,Ankri Y,Israeli-Shalev Y,Peleg T,Adessky R,Freedman S, Prevention of posttraumatic stress disorder by early treatment: results from the Jerusalem Trauma Outreach And Prevention study. Archives of general psychiatry. 2012 Feb; [PubMed PMID: 21969418]|
|||Steenen SA,van Wijk AJ,van der Heijden GJ,van Westrhenen R,de Lange J,de Jongh A, Propranolol for the treatment of anxiety disorders: Systematic review and meta-analysis. Journal of psychopharmacology (Oxford, England). 2016 Feb; [PubMed PMID: 26487439]|
|||Ipser JC,Stein DJ, Evidence-based pharmacotherapy of post-traumatic stress disorder (PTSD). The international journal of neuropsychopharmacology. 2012 Jul; [PubMed PMID: 21798109]|
|||Bisson JI,Baker A,Dekker W,Hoskins MD, Evidence-based prescribing for post-traumatic stress disorder. The British journal of psychiatry : the journal of mental science. 2020 Mar; [PubMed PMID: 32345407]|
|||Villarreal G,Hamner MB,Cañive JM,Robert S,Calais LA,Durklaski V,Zhai Y,Qualls C, Efficacy of Quetiapine Monotherapy in Posttraumatic Stress Disorder: A Randomized, Placebo-Controlled Trial. The American journal of psychiatry. 2016 Dec 1; [PubMed PMID: 27418378]|
|||Guina J,Rossetter SR,DeRHODES BJ,Nahhas RW,Welton RS, Benzodiazepines for PTSD: A Systematic Review and Meta-Analysis. Journal of psychiatric practice. 2015 Jul; [PubMed PMID: 26164054]|
|||Argolo FC,Cavalcanti-Ribeiro P,Netto LR,Quarantini LC, Prevention of posttraumatic stress disorder with propranolol: A meta-analytic review. Journal of psychosomatic research. 2015 Aug; [PubMed PMID: 25972056]|
|||Kellner CH,Romanella SM, ECT as a Novel Treatment for PTSD. The journal of ECT. 2019 Jun; [PubMed PMID: 30113991]|
|||Davidson JR,Brady K,Mellman TA,Stein MB,Pollack MH, The efficacy and tolerability of tiagabine in adult patients with post-traumatic stress disorder. Journal of clinical psychopharmacology. 2007 Feb; [PubMed PMID: 17224720]|
|||Ralevski E,Olivera-Figueroa LA,Petrakis I, PTSD and comorbid AUD: a review of pharmacological and alternative treatment options. Substance abuse and rehabilitation. 2014; [PubMed PMID: 24648794]|
|||Kishimoto A,Goto Y,Hashimoto K, Post-traumatic Stress Disorder Symptoms in a Female Patient Following Repeated Teasing: Treatment with Gabapentin and Lamotrigine and the Possible Role of Sensitization. Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology. 2014 Dec; [PubMed PMID: 25598830]|
|||Lipinska G,Baldwin DS,Thomas KG, Pharmacology for sleep disturbance in PTSD. Human psychopharmacology. 2016 Mar [PubMed PMID: 26856810]|
|||Krediet E,Bostoen T,Breeksema J,van Schagen A,Passie T,Vermetten E, Reviewing the Potential of Psychedelics for the Treatment of PTSD. The international journal of neuropsychopharmacology. 2020 Mar 14; [PubMed PMID: 32170326]|
|||Howlett JR,Stein MB, Prevention of Trauma and Stressor-Related Disorders: A Review. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2016 Jan [PubMed PMID: 26315508]|
|||Davidson J,Baldwin D,Stein DJ,Kuper E,Benattia I,Ahmed S,Pedersen R,Musgnung J, Treatment of posttraumatic stress disorder with venlafaxine extended release: a 6-month randomized controlled trial. Archives of general psychiatry. 2006 Oct; [PubMed PMID: 17015818]|
|||Krystal JH,Rosenheck RA,Cramer JA,Vessicchio JC,Jones KM,Vertrees JE,Horney RA,Huang GD,Stock C, Adjunctive risperidone treatment for antidepressant-resistant symptoms of chronic military service-related PTSD: a randomized trial. JAMA. 2011 Aug 3; [PubMed PMID: 21813427]|
|||Reist C,Streja E,Tang CC,Shapiro B,Mintz J,Hollifield M, Prazosin for treatment of post-traumatic stress disorder: a systematic review and meta-analysis. CNS spectrums. 2020 May 4; [PubMed PMID: 32362287]|
|||Higgins A,Nash M,Lynch AM, Antidepressant-associated sexual dysfunction: impact, effects, and treatment. Drug, healthcare and patient safety. 2010; [PubMed PMID: 21701626]|
|||Bala A,Nguyen HMT,Hellstrom WJG, Post-SSRI Sexual Dysfunction: A Literature Review. Sexual medicine reviews. 2018 Jan; [PubMed PMID: 28778697]|
|||Horowitz MA,Taylor D, Tapering of SSRI treatment to mitigate withdrawal symptoms. The lancet. Psychiatry. 2019 Jun; [PubMed PMID: 30850328]|
|||Davis LL,Frazier EC,Williford RB,Newell JM, Long-term pharmacotherapy for post-traumatic stress disorder. CNS drugs. 2006; [PubMed PMID: 16734498]|
|||Gradus JL,Antonsen S,Svensson E,Lash TL,Resick PA,Hansen JG, Trauma, comorbidity, and mortality following diagnoses of severe stress and adjustment disorders: a nationwide cohort study. American journal of epidemiology. 2015 Sep 1; [PubMed PMID: 26243737]|
|||Nash WP,Watson PJ, Review of VA/DOD Clinical Practice Guideline on management of acute stress and interventions to prevent posttraumatic stress disorder. Journal of rehabilitation research and development. 2012; [PubMed PMID: 23015576]|
|||Gradus JL,Qin P,Lincoln AK,Miller M,Lawler E,Sørensen HT,Lash TL, Acute stress reaction and completed suicide. International journal of epidemiology. 2010 Dec; [PubMed PMID: 20624822]|
|||Courtenay M,Nancarrow S,Dawson D, Interprofessional teamwork in the trauma setting: a scoping review. Human resources for health. 2013 Nov 5; [PubMed PMID: 24188523]|