INTRODUCTION

In 2010 nearly 2 million adults experienced nonfatal injuries requiring hospitalization, while millions more with traumatic injuries were treated in emergency departments (ED).1 The potential development of posttraumatic stress disorder (PTSD), characterized by core symptoms of re-experiencing, avoidance/numbing, and hyperarousal, exacerbates trauma’s aftermath. Approximately 6.8% of United States (U.S.) adults currently have PTSD, and 40% of them reported suicidal thoughts, while 19% attempted suicide.^2,3 People with PTSD often experience significant health conditions, such as hypertension, asthma, peptic ulcers, gastrointestinal problems, and increased use of medical services.⁴Thus, trauma and PTSD patients are vulnerable to future health problems and are in need of more preventive efforts.

Due to equivocal research findings, one of the most highly debated PTSD risk factors is peritraumatic dissociation (PD). PD is an experience of change in cognitive functioning and perception during or immediately after a trauma, characterized by derealization, numbing or detachment, depersonalization, reduced awareness of surroundings, and dissociative amnesia.^5,6 PD was the strongest predictor of subsequent PTSD symptoms in 2 meta-analyses of PTSD risk factors.^7,8 However, confounding variables were not properly accounted for, and a causal relationship could not be established. _9–12 Other studies found that PD did not significantly predict PTSD over persistent dissociation, subjective accident-related vulnerability, sociodemographic characteristics, and initial mental health problems.^13–15

Some researchers suggest that incorporating trauma history improves understanding of the relationship between PD and PTSD and identified a link between the 2, but others found that PD was unrelated to prior trauma.^7,13,16–18 Most prior studies assessed dissociation several weeks or months post trauma, making these data susceptible to recall bias.^11,15 Thus, there is a need to clarify the relationships between PD, prior trauma, and current PTSD symptoms by examining these 3 variables simultaneously and measuring PD more immediately post trauma. The present study examined the association between PD and PTSD with an improved methodology by assessing participants in an emergency setting. Specifically, PD was assessed within hours of a traumatic event, and PTSD symptoms were monitored over the course of 12 weeks. Furthermore, trauma history was obtained at the time of presentation in the ED, which should help to differentiate between current trauma exposure and past trauma experiences. We hypothesize that both PD and prior PTSD symptoms will predict PTSD symptoms at 4 and 12 weeks post-trauma.

METHODS

Participants

Participants (N=48) completed procedures as part of a randomized controlled study comparing early intervention for PTSD to an assessment-only control group in traumatized individuals presenting to the emergency department (ED).¹⁹ Eligible participants met DSM IV criteria A for PTSD, exposure to a traumatic event involving actual or threatened death and intense fear, helplessness, or horror, within the past 72 hours. Exclusion criteria included current or past psychosis, suicidal ideation, substance dependence, and a loss of consciousness for more than 5 minutes due to the trauma. We included only those participants randomly assigned to assessment in the current analyses.

Measures

PTSD Diagnostic Scale (PDS)²⁰. This self-report measure assesses prior trauma exposure and yields a DSM-IV PTSD diagnosis for a previous trauma and demonstrated excellent internal consistency in the present study (0.92). Our analyses used a continuous measure of total PTSD symptoms.

Immediate Stress Reaction Checklist (ISRC)²¹.

The ISRC is a 27-item questionnaire designed to examine individuals’ acute stress responses in the immediate aftermath of a traumatic event. For our analyses, a total score was calculated for PD based on the peritraumatic dissociation questions: numbing/detachment, reduced awareness, derealization, depersonalization. Internal consistency was acceptable (0.72).

PTSD Symptom Scale, Interview Version (PSS-I)²².

The PSS-I corresponds to the 17 DSM-IV PTSD symptoms and showed excellent internal consistency (0.90) in the present study. We used a continuous measure of total PTSD symptoms for our analyses.

Procedure

Participants were ED patients of a southeastern Level I trauma hospital. This inner-city ED is the largest trauma center in the state, sees over 100,000 patients annually, and serves a largely African-American and medically indigent population at risk for trauma. ED patients were randomized to receive either 3 sessions of exposure therapy or assessment only. At baseline, participants received interviewer-administered and self-report questionnaires, which included the PDS and the ISRC.^20,21 Patients were assessed again at 4-week and 12-week follow ups, with PTSD symptom levels measured using the PSS-I.²² This study was approved by the university institutional review board and the hospital research oversight committee.

Data Analysis

We used hierarchical linear regression to evaluate the association of PD and prior PTSD symptoms to PTSD symptoms at 4-week and 12-week follow up. We included covariates of gender, race, age, relationship status, and trauma type in the first step and controlled for in all models. In the second step, PD measured by the ISRC was included as a predictor of PTSD, as assessed by the PSS-I. Prior PTSD symptoms on the PDS were included in the third step.

RESULTS

Demographic variables are described in Table 1. Of the 48 participants, most were female (n=30, 62.5%) and African American (n =40, 82%). The remaining participants self identified as “white” (n=7, 16%) or “other” (n=1, 2%). 55% were single, 7% were married and 15% were cohabitating. Mean age was 34 years (SD=12). Trauma types included motor vehicle collisions (n=22, 46%), sexual assaults (n=11, 23%), nonsexual assaults (n=11, 23%) and other (n=4, 8%). Mean scores for symptom measures were as follows: 10.38 for PD (SD=4.81), 17.94 for PDS (SD=12.26), 24.69 for PSS 4-week (SD=11.14), and 21.83 for PSS 12-week (SD=12.31). Using PTSD symptoms from a prior trauma on the PDS, 19 (39.6%) of patients met criteria for chronic PTSD. At 4 week follow up, 25 (52.1%) patients met diagnostic criteria for current PTSD from the presenting trauma, while at 12-week follow up, 19 (45.25%) patients met diagnostic criteria for PTSD from the presenting trauma. The linear regression models (Table 2) indicate that PD was positively associated with PTSD symptoms at 4 weeks (β=0.29, p=0.04) , accounting for 17% of the overall variance. Prior PTSD symptoms were also significantly associated with PTSD symptoms at 4 weeks (β=0.35, p=0.02), accounting for 9% of the variance in PTSD symptoms above and beyond that of PD and demographics (R² change = 0.09, p = .019). At 12 weeks, prior PTSD symptoms (β=0.09, p=0.54) and PD (β=−0.02, p=0.91) were not significant. The overall variance accounted for in the final 4-week and 12-week models can be found in Table 2.

DISCUSSION

This study sought to parse the effect of past and current trauma reactions on PTSD symptom development. Because most people experience PTSD symptoms immediately following a traumatic event, while only a minority will develop PTSD, predictors, such as negative emotional reactions, are essential to understanding the disorder. We hypothesized that PD coupled with a history of PTSD symptoms would best represent this negative reaction, predicting later development of PTSD. The findings suggested that PD measured immediately after the trauma was associated with increased PTSD symptoms 1 month post-trauma. Past support for the association between PD and subsequent PTSD has been mixed, perhaps due to the often retrospective assessment of PD.¹⁵ Retrospective reports are prone to bias, especially when assessing unawareness or disengagement.²³ The current study overcame this limitation by assessing PD immediately after trauma (mean time from trauma to assessment = 11.06 hours). This improved methodology may help clarify the conflicting findings of prior studies.

Second, as hypothesized, prior PTSD symptoms influenced the development of PTSD 4 weeks post trauma (54% met criteria for PTSD from a prior trauma). This finding is consistent with research showing that both child and adult trauma experiences significantly increase the likelihood of developing PTSD upon exposure to an adult traumatic event.⁷ Research also indicates that maladaptive reactions to previous trauma are a greater predictor of subsequent PTSD outcome than trauma exposure frequency.²⁴ In line with this research, our measure of past PTSD pathology used DSM-IV symptom severity, not simply trauma exposure.

Our findings indicate that evaluating trauma victims for PD and past PTSD symptoms can help identify individuals likely to develop PTSD. This has implications for preventative care and can be used by first responders and emergency care clinicians. Although our findings cannot fully suggest that dissociative symptoms alone warrant an intervention, if this dissociation occurred during or immediately following a trauma and is coupled with a history of PTSD symptoms, early intervention, screening, and referrals to mental health resources may still be helpful. At the very least, these individuals should be monitored more closely.

LIMITATIONS

There were methodological limitations of this study. First, because individuals self reported PTSD symptoms from a past trauma immediately following a current trauma, their reports may be skewed by their reaction to the current trauma, perhaps explaining the large correlation between our past trauma variable and 4-week and 12-week PTSD symptoms. Notably, however, PD remained significantly associated with PTSD symptom outcome above and beyond the variance accounted for by symptoms related to a past trauma experience. Second, we assessed past PTSD symptoms retrospectively. Long-term prospective studies could more accurately assess symptoms from multiple traumas. Third, we lacked a control group in the initial analyses and therefore decided to conduct post-hoc case control analyses comparing patients who did and did not meet diagnostic criteria for PTSD at 4 weeks and 12 weeks. Results from an independent samples t-test indicated that at the 12-week time point, those patients who had PTSD did not differ on their past PTSD symptoms (t(42)=−2.00, p=0.051) or PD scores (t(47)=−1.69, p=0.10) from patients without PTSD. The only significant difference that emerged was their PTSD symptom scores at 4 weeks from the PSS-I (t(47)=−4.28, p=0.0), such that those who met diagnostic criteria for PTSD at 12 weeks reported greater PTSD symptoms at 4 weeks. To further investigate this, we conducted another independent samples t-test comparing patients with and without PTSD at the 4-week time point, when we could first diagnose PTSD. Results indicated significant differences on both prior PTSD symptoms and PD scores between groups. Specifically, patients with PTSD at 4 weeks reported significantly greater PD (t(53)=−3.49, p=0.0) and prior PTSD symptoms (t(48)=−3.18, p=0.0). Finally, while our immediate measure of PD is likely more accurate than those taken weeks or months post-trauma, self reporting a lack of awareness is intrinsically flawed. Future studies should develop and include objective measures of PD such as cognitive tasks or physiological reactions.

CONCLUSION

To our knowledge this is the first study to measure PD and other symptoms within hours of a trauma. We believe that the benefits of obtaining this data at such a crucial time point for the development of PTSD make a significant contribution to understanding the onset and course of PTSD. This study was conducted in an inner city ED that specializes in indigent care. Beyond continued exposure to trauma, this population is at risk for legal issues, injury, and inadequate social support. Our results indicate that PD and trauma history have a large impact on PTSD development for this vulnerable population.

Footnotes

Supervising Section Editor: Abigail Hankin, MD, MPH
Submission history: Submitted January 17, 2012; Revision received March 13, 2012; Accepted March 19, 2012
Reprints available through open access at http://escholarship.org/uc/uciem_westjem
DOI: 10.5811/westjem.2012.3.11777
Address for Correspondence: Cole Gregory Youngner, BA
Emory University School of Medicine, Atlanta, Georgia.
Email: cyoungner1a2n@gmail.com.
Conflicts of Interest: By the WestJEM article submission agreement, all authors are required to disclose all affiliations, funding sources and financial or management relationships that could be perceived as potential sources of bias. The authors disclosed none. This work was funded through CDC Grant 5 R49 CE001494 and NIH grant R34 MH083078.

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