In this issue, Fani and colleagues provide in the overview article and case presentations a comprehensive and helpful review of 2 common and disabling conditions: acute stress disorder (ASD) and posttraumatic stress disorder (PTSD).
It has been estimated that PTSD affects about 7.7 million adults in the United States.1 Because ASD is a newer diagnosis, information about the disorder is still forthcoming. The percentage of trauma survivors in whom ASD develops has varied in different reports from 6% to 33%.2,3 However, these percentages may change as measures for ASD become more uniform among researchers.4
In the wake of the terrorist attacks on September 11, 2001, and the subsequent global war on terrorism, there is increasing public awareness of both the complexity and the far-reaching consequences of ASD and PTSD.5,6 High rates of psychological trauma occurred after the attacks and have persisted. It has been estimated that PTSD has developed or will develop in almost one third of those directly witnessing the September 11 attacks.7 The tragedy of recent natural disasters has also brought these traumatic conditions into sharper relief.8 In light of these events and other traumas, including motor vehicle accidents, workplace accidents, and violent assaults, one can expect that persons will present to the ED with symptoms characteristic of a stress-related condition or with recurrence or complications of PTSD.
In their overview article, Fani and colleagues provide us with the core symptoms of both ASD and PTSD, and they enumerate the time course of symptoms for considering each diagnosis. ASD extends beyond 48 hours, occurs within 4 weeks of an event, and lasts a maximum of 4 weeks. On the other hand, a diagnosis of PTSD requires an 8-week duration of persistent symptoms. These distinctions can be useful to the ED physician, although they may be somewhat artificial. For example, in a study of traumatic responses among survivors of rape, 94% of persons met the clinical criteria for PTSD (excluding the time requirement) 1 week after the incident.9 However, at 3 months, only 15% met the criteria for PTSD; this percentage rose to 25% 9 months after the rape.
When a patient presents to the ED with symptoms of stress after a traumatic event, an important aspect of the examination is to determine whether a patient is at risk for the development of PTSD. Factors to consider during the ED assessment include the severity of the reaction to the initial traumatic event, the presence of a preexisting psychiatric condition, the presence of a family history of psychiatric illness, and the extent of social support.10 These factors, which can be readily assessed in the ED, not only can help predict which patients may be at risk for a stress disorder but also may help identify which patients to refer for ongoing psychiatric care after the ED visit.
When examining patients who present to the ED with stress-related symptoms, clinicians must be particularly vigilant for the host of psychiatric comorbidities that can accompany a stress disorder. Most obvious among these are other anxiety disorders, depression, and substance use disorders. Comorbid depression substantially complicates PTSD management and increases the risk of suicidal behavior. It is also evident that after experiencing a traumatic event, persons often self-medicate with alcohol or drugs; the ED clinician must assiduously assess for use/misuse/abuse of drugs and alcohol in all patients who present with stress symptoms related to trauma.
The cases presented by Fani and associates indicate the complexity of clinical scenarios that the ED physician will face. Case 3 illustrates how patients may present with apparent medical symptoms (eg, shortness of breath, headache) that dominate the clinical picture. The symptoms of PTSD may only become manifest on more detailed inquiry. Unfortunately, a challenge for ED physicians is that they often are working under time constraints or lack the opportunity to probe for such symptoms through a complete history taking to delineate the chronology of events.
Case 1 raises an interesting question: can PTSD develop in someone who has a head injury and cannot remember what happened to him or her? The answer is yes; amnesia does not always "protect" a person from the later development of PTSD. This has obvious clinical (and medicolegal) import. In addition, this phenomenon may reflect the variability of neurobiologic responses and their impact on memory formation following a traumatic incident. J. Douglas Bremner, MD, is a leading expert in this area, and his work on hippocampal structure in PTSD is groundbreaking.
The overview article provides a glimpse of the emergent neurobiology of anxiety disorders, including PTSD. As the article highlights, brain neurotrophins (most notably brain-derived neurotrophic factor [BDNF]) may play a critical role in mobilizing the brain's response to a traumatic event. In a recent article, Berton and colleagues11 described a series of experiments using transgenic mice that implicate BDNF in the pathophysiology of anxiety disorders. Moreover, von Bohlen und Halbach and colleagues12 demonstrated trophic effects of BDNF among dendritic spines in the hippocampus. This line of inquiry is of interest in PTSD, since the concepts of brain plasticity and human resilience are germane to our appreciation of how persons cope with stress.
MANAGING STRESS DISORDERS
Fani and colleagues offer particularly useful insights into the pharmacologic management of ASD and PTSD. They highlight the important study by Pitman and associates,13 which showed that giving propranolol prophylactically to patients with acute stress symptoms to avert the later onset of PTSD was not effective. They also mention another study that showed that the use of alprazolam in patients with acute stress may negatively impact the development of PTSD.14
What should the ED clinician do? As in many instances, use of medications to manage ASD or PTSD should be judicious and time-limited--hence the importance of prompt evaluation and aftercare by the psychiatric service soon after the patient is discharged from the ED. Fani and colleagues make the distinction that medications may have a particular role in targeting distinct symptoms. The short-term use of a benzodiazepine or a nonbenzodiazepine hypnotic to regain a healthy sleep pattern is an obvious example.
The pharmacologic management of patients with chronic PTSD who present to the ED with PTSD exacerbation is more complicated (and again is likely to be even more difficult because of comorbidities). There is emergent information that second-generation antipsychotics (SGAs) may have some beneficial effects in PTSD. However, use of SGAs for this indication has not been approved by the FDA. Furthermore, SGAs are associated with serious adverse effects, particularly when patients take these medications as maintenance therapy.15
Fani and colleagues suggest that use of opiate antagonists may be a promising future strategy, with much interest in the potential of corticotropin-releasing factor antagonists. These approaches seem to make sense given our emerging understanding of the neurobiology of stress and PTSD. At present, however, selective serotonin reuptake inhibitors remain the mainstay of treatment and are a class of drugs with which ED physicians generally have had experience.
Fani and colleagues throw a curveball in their discussion of the literature that suggests a limited role for psychological therapies. Clearly, desensitization therapy is established for PTSD, but this is not a particularly relevant strategy in the ED. Stress debriefing (which comes in myriad forms) is a common and empirically validated approach. In a meta-analysis of psychological therapies for patients with PTSD, more than half of the patients improved with treatment.16 However, most patients with established PTSD continue to experience at least some symptoms.
ASD and PTSD, although difficult to manage in the ED, are important to ED physicians nonetheless. Increasingly, EDs at academic medical centers are collaborating with the US Department of Defense and with other agencies in disaster-preparedness programs and in civilian responses to mock terrorist attacks. Recognition and management of ASD and PTSD are important aspects of these programs; both disorders reveal our vulnerabilities.
The ED physician is usually the first or one of the first medical personnel to respond to a patient in crisis. It would seem logical to conclude that the manner in which that physician responds may be an important variable in the patient's longer-term outcome. *
REFERENCES1. Kessler RC, Chiu WT, Demler O, et al. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication [published correction appears in Arch Gen Psychiatry. 2005;62:709]. Arch Gen Psychiatry. 2005;62:617-627.2. Creamer M, Manning C. Acute stress disorder following an industrial accident. Australian Psychologist. 1998;33:125-129.3. Classen C, Koopman C, Hales R, Spiegel D. Acute stress disorder as a predictor of posttraumatic stress symptoms. Am J Psychiatry. 1998;155:620-624. 4. Gibson LE. National Center for PTSD. Acute stress disorder. Available at: http://www.ncptsd.va.gov/facts/specific/fs_asd.html. Accessed July 24, 2006.5. Hoge CW, Auchterlonie JL, Milliken CS. Mental health problems, use of mental health services, and attrition from military service after returning from deployment to Iraq or Afghanistan. JAMA. 2006;295:1023-1032.6. Starkman MN. The terrorist attacks of September 11, 2001, as psychological toxin: increase in suicide attempts. J Nerv Ment Dis. 2006;194:547-550.7. Yehuda R. Post-traumatic stress disorder. N Engl J Med. 2002;346:108-114.8. Neuner F, Schauer E, Catani C, et al. Post-tsunami stress: a study of posttraumatic stress disorder in children living in three severely affected regions in Sri Lanka. J Trauma Stress. 2006;19:339-347.9. Foa EB, Rothbaum BO, Riggs DG, Murdock TB. Treatment of posttraumatic stress disorder in rape victims: a comparison between cognitive-behavioral procedures and counseling. J Consult Clin Psychol. 1991;59:715-723.10. Vieweg WV, Julius DA, Fernandez A, et al. Posttraumatic stress disorder: clinical features, pathophysiology, and treatment. Am J Med. 2006;119:383-390.11. Berton O, McClung CA, Dileone RJ, et al. Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress. Science. 2006;311:864-868.12. von Bohlen und Halbach O, Krause S, Medina D, et al. Regional- and age-dependent reduction in trkB receptor expression in the hippocampus is associated with altered spine morphologies. Biol Psychiatry. 2006;59:793-800.13. Pitman RK, Sanders KM, Zusman RM, et al. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol Psychiatry. 2002; 51:189-192.14. Gelpin E, Bonne O, Peri T, et al. Treatment of recent trauma survivors with benzodiazepines: a prospective study. J Clin Psychiatry. 1996;57:390-394.15. Buckley PF. Broader therapeutic uses of atypical antipsychotic medications. Biol Psychiatry. 2001;50:912-924.16. Bradley R, Greene J, Russ E, et al. A multidimensional meta-analysis of psychotherapy for PTSD [published correction appears in Am J Psychiatry. 2005; 162:832]. Am J Psychiatry. 2005;162:214-227.