Variables that may leave a person susceptible to trauma before a trauma occurs may be physiological, biological, or environmental (i.e., previous trauma history). For example, heightened pre-trauma physiological responses to perceived danger cues have been linked to PTSD symptom severity. Pole et al. (2009) found that police cadets who exhibited higher pre-trauma fear potentiated startle and greater skin conductance to both high and low threat danger cues were more likely to develop PTSD and have greater PTSD symptom severity after a traumatic event. Monitoring pre-trauma physiological responses to aversive stimuli may help determine who may need immediate preventative treatment following a trauma. The prevalence of PTSD has also been linked to previous trauma history. This is found in patients who experience trauma in both adulthood and childhood (Binder et al., 2008). In a meta-analysis, Ozer, Best, Lipsey, and Weiss (2008) found that both child and adult trauma experiences significantly and equally increased the likelihood of developing PTSD after a current trauma.

Some genetic underpinnings have recently been discovered to correspond with the development of PTSD. Segman et al. (2005) showed that gene expression patterns in the immediate aftermath of a trauma were predictive of later development of PTSD. Koenen et al. (2005) was the first to show that FKBP5 gene alleles were associated with increased peritraumatic dissociation in children which has been linked to PTSD development (Saxe et al., 2005). Since then, a number of studies have looked at single nucleotide polymorphisms (SNPs) within the FKBPF gene and how they are related to symptoms of PTSD in children and adults. Binder et al. (2008) studied 8 SNPs within this gene and found that while the SNPs did not directly predict PTSD outcome or correlate with non-child abuse trauma, 4 of the 8 SNPs interacted with history of child abuse to predict adult PTSD symptoms. It was shown that children with these particular alleles experienced greater amounts of peritraumatic dissociation, which was related to higher rates of PTSD in adulthood. Xie et al. (2010) found a relationship between childhood trauma experience and later PTSD development. In this study, SNPs of the FKBP5 genotype moderated the effect of childhood trauma experience on risk for PTSD but only for African American participants. Recently published data (Ressler et al., 2011) shows a sex-specific gene predictor of PTSD. These data reveal that a single SNP in a putative estrogen response element within the PACAP-PACI receptor pathway predicts PTSD diagnosis and symptoms in females. This latter finding may help explain why PTSD occurs about twice as frequently in females as in males.

In addition to pre-trauma factors, some predictors of PTSD occur during the trauma. These factors can include trauma severity and type, duration and amount of trauma, and emotions felt during the trauma. In regards to trauma type, certain life-threatening experiences are more likely to lead to PTSD. Using data from the National Comorbidity Survey, Kessler, Sonnega, Bromet, Hughes, and Nelson (1995) found that PTSD is most common after combat exposure among men and rape among women. In a prospective study of rape victims, Rothbaum, Foa, Riggs, Murdock, and Walsh (1992) showed that 94 % of rape victims experience PTSD symptoms within the first 2 weeks of trauma, with natural recovery leading to rates of 47 % after 3 months. Furthermore, the 13.8 % prevalence of PTSD in military veterans from the wars in Iraq and Afghanistan (Tanielian & Jaycox, 2008) is twice that of the civilian population, 6.8 %, according to data from the most recent National Comorbidity Survey (Kessler et al., 2005). Motor vehicle crashes have been shown to have a higher PTSD rate than other traumas such as robbery or tragic death (Norris, 1992). While past data suggest that certain types of traumatic experiences put individuals at a higher risk for PTSD, they do not fully account for the variance in PTSD diagnoses and symptom severity. Thus, additional factors related to the trauma ought to be considered in predicting PTSD.

Other characteristics of traumatic events have been examined to better predict PTSD. Indicators of trauma severity such as subjective assessment of life threat have been implicated as consistent predictors of PTSD. Resnick, Kilpatrick, Best, and Kramer (1992) showed that individuals who thought they would be seriously injured or killed were more likely to develop PTSD. Furthermore, in a meta-analysis of studies on PTSD predictors, Ozer et al. (2008) found that perceived life threat was a systematic and consistent predictor of both PTSD diagnosis and symptoms. Duration of trauma exposure may also be linked to PTSD. For example, some research indicates that more deployments to a combat zone can increase the risk of PTSD (Tanielian & Jaycox, 2008). The continued stress in the recovery phase following a traumatic event may also exacerbate PTSD. After the September 11th attacks, for example, Galea et al. (2002) found that having lost one’s possessions during the course of the traumatic event was related to higher rates of PTSD. Finally, one’s initial response to the traumatic event may influence their likelihood of developing PTSD. Such appraisals often manifest themselves in how the patient experiences trauma, with two common reactions being peritraumatic emotionality (i.e., high levels of emotions during or immediately after the trauma) and peritraumatic dissociation (i.e., dissociative experiences during or immediately after the trauma). In their meta-analysis of PTSD predictor studies, Ozer et al. (2008) concluded that both emotionality and dissociation during or immediately after the trauma correspond to greater PTSD symptoms and rates of PTSD. Peritraumatic dissociation in particular was the strongest of seven statistically significant predictors of PTSD found by the meta-analysis; thus, especially when including emotionality, the psychological response one has during and immediately following a trauma appears to have a very strong relationship to his or her risk for developing PTSD. Noting responses of high emotionality or dissociative feelings may help identify individuals at a greater risk for eventually being diagnosed with PTSD. Ultimately, however, the typical response after a trauma suggests that PTSD symptoms dissipate over time, leaving a minority of trauma survivors with chronic PTSD (Bryant, 2003). Merely having reactions like dissociation and emotionality that are highly related to PTSD does not necessitate that an individual with such peri-traumatic responses will in fact develop chronic PTSD.

In many cases, the consequences that occur in the aftermath of trauma can indicate whether someone will later develop PTSD. One important aspect in the immediate aftermath of trauma is one’s perceived social support. From a meta-analysis of 11 studies, totaling 3,537 patients, Ozer et al. (2008) found an inverse relationship between social support and PTSD symptoms. Specifically, after the trauma had occurred, individuals who reported lower levels of social support tended to have either more PTSD symptoms or a higher rate of PTSD diagnosis. Furthermore, the strength of the relationship between social support and PTSD symptoms or diagnosis increased as the length of the study increased (Ozer et al., 2008). As more time elapses since the trauma occurred, social support appears to play a stronger role in abating the symptoms of PTSD. Similar results have been noted in studies of large-scale disasters such as the events on September 11th, as low social support was linked to a higher prevalence of PTSD (Galea et al., 2002). However, whether the passage of time allows for more people to provide social support to those with PTSD or whether social support is less important in the immediate aftermath of a trauma remains unclear.

Not only do external factors influence the course of PTSD, but one’s own personal responses to the traumatic event play an important role as well. Cognitive appraisals in particular are key predictors as Bryant (2003) notes that exaggerated, catastrophic appraisals in particular have been linked both directly to PTSD and to acute stress disorder (ASD), which often subsequently leads to or predicts PTSD. In addition to psychological factors, physiological indicators immediately following a trauma, such as heart rate (Bryant, Harvey, Guthrie, & Moulds, 2000; Shalev et al., 1998) and cortisol levels (Delahanty, Raimonde, & Spoonster, 2000; Resnick, Yehuda, Pitman, & Foy, 1995), have been shown to be predictors of subsequent PTSD development. However, at this stage of our knowledge, there have been no prospective studies validating any predictor in the immediate aftermath of trauma as specific and sensitive enough to determine who requires intervention and who will recover on their own.

Psychological debriefing (PD) is a term which refers to a number of different methods of crisis intervention, the most common of which is Critical Incident Stress Debriefing (CISD-Mitchell, 1983; Mitchell & Everly, 1996). CISD was developed as a crisis intervention to be implemented within 48 h of a trauma event. CISD intervention involves 7 phases. Phase 1, the introduction phase, consists of a description of the CISD process. Phase 2, the fact phase, involves the participant explaining what happened. Phase 3, the thought phase, is when participants convey their thoughts from the incident. In phase 4, the feeling phase, participants share their emotional reactions to the incident. Phase 5, the assessment phase, examines physical and psychological symptoms. Phase 6, the education phase, explains stress reactions and management. Finally, Phase 7, the reentry phase, sums up the debriefing and offers referrals for the participant. CISD is designed to be completed in 3–4 h and can be given individually or in a group session. The term CISD is often used interchangeably with PD in the literature. It should be noted that CISD is one form of PD and can be implemented in a number of different ways. CISD was created for emergency service personnel and offers an alternative to more time consuming psychotherapy. However, this model, as well as PD in general, has been heavily scrutinized in the literature for lacking sufficient support for its claim to be a prevention method for the development of PTSD. As a whole, debriefing literature reviews have determined the practice to be equivocal at best and harmful at worst (Litz, Gray, Bryant, & Adler, 2002; Rose, Bisson, Churchill, & Wessely, 2002). One randomized, controlled trial provided PD for individuals admitted to the hospital after a motor vehicle crash (MVC) (Mayou, Ehlers, & Hobbs, 2000). This method of PD included a review of the accident, addressed initial cognitive appraisals of the trauma, and discussed appropriate emotional expressions. Participant’s trauma intrusion and avoidance symptoms were measured using the impact of event scale (IES) at both a 4-month and 3-year follow-up. Results indicate that individuals who had high initial scores on the IES remained symptomatic if they received the intervention and recovered if they did not receive the intervention at follow-up. The authors suggest that PD may interfere with the natural recovery process and that individuals more likely to develop chronic PTSD may be harmed by a 1-h debriefing intervention. Due to these adverse findings and negative reviews, emphasis has been placed on conducting more methodologically rigorous studies of early intervention for PTSD.

The unpredictability of trauma events makes randomized-controlled trials of debriefing a difficult task. The developers of CISD have used this fact to maintain the credibility of debriefing based mainly on anecdotal accounts of the method (Everly, Flannery, & Mitchell, 2000). Multiple reviewers have condemned the methodology of research cited by CISD supporters (Devilly, Gist, & Cotton, 2006). A number of RCTs have been conducted which show a lack of support for the implementation of debriefing immediately following a trauma event. These studies are critiqued in depth in the Cochrane Review (Rose et al., 2002) which concludes that single session individual psychological debriefing is not useful as a preventative treatment for PTSD and in some cases (Bisson, Jenkins, Alexander, & Bannister, 1997) may lead to increased long-term PTSD symptoms. The Cochrane Review went as far as to suggest that “compulsory debriefing of victims of trauma should cease”. These negative reviews have led to a transformation of PD into a more encompassing model which utilizes group CISD as the main treatment model but also includes aspects of trauma support such as pre-incident planning, crisis assessment, and individual crisis intervention. This integrated model is known as Critical Incident Stress Management (CISM) and is described by its authors not as psychotherapy, but as a collection of support services for trauma victims (Everly et al., 2000). Supporters suggest that CISD provided within the CISM model is a more efficacious approach to PD. However, Devilly et al. (2006) determined that there is not enough empirical study to warrant this claim.

PD research has lacked specificity in terms of defined components of the treatment. Generally the term PD refers to an overarching crisis intervention strategy and it is necessary to parse out the specific aspects of the treatment in order to implement the treatment properly. In a randomized, controlled trial, Sijbrandij, Olff, Reitsma, Carlier, and Gersons (2006) analyzed two key aspects of PD based on the CISD protocol, psychoeducation, and emotional ventilation. In this study participants received the CISD treatment with the education phase excluded or with the emotional reaction phase excluded or they received no intervention. Results indicate that PTSD symptoms significantly reduced for all treatment groups with no differences between the two debriefing methods or no debriefing. In addition, individuals with early hyperarousal symptoms experienced an adverse effect of emotional debriefing in that these individuals had higher rates of PTSD at 6-month follow-up than the no debriefing group, further acknowledging that debriefing may be harmful for some people.

More recent reviews acknowledge that the lack of empirically supported research of PD is problematic and may be harmful to the emergency worker groups that utilize the practice most frequently (Suveg, 2007; Tuckey, 2007). These reviews suggest that it is necessary for groups which utilize PD to invest in the necessary scientifically sound research to prove the utility of PD or abandon the practice all together in favor of alternative evidence-based approaches.

In recent years, more attention has been given to pharmacological approaches in preventing PTSD. However, there are no currently recommended pharmacological treatments for early prevention of PTSD. A conceptual model of the pathogenesis of PTSD developed by Pitman and Delahanty (2005) suggests that the body’s release of stress hormones in response to traumatic events leads to over-consolidation of the traumatic memory and fear conditioning. Thus, pharmacological treatments that inhibit this stress response may prevent the subsequent development of PTSD. Research examining the use of medications such as benzodiazepines, however, has suggested that early administration of these drugs can actually worsen outcomes in recently traumatized individuals, as demonstrated by higher rates of PTSD compared to control conditions (Gelpin, Bonne, Peri, & Brandes, 1996; Mellman, Bustamante, David, & Fins, 2002).

Other medications such as morphine, ketamine, and propranolol are being explored for their impact on subsequent PTSD. Propranolol, for instance, is a beta-adrenergic antagonist that blocks the reuptake of norepinephrine and is often used to treat hypertension (Fletcher, Creamer, & Forbes, 2010). A recent study showed that administration of propranolol reduces neural reactivity in the amygdala, which supports the idea that propranolol may inhibit anxiety responses in trauma-exposed individuals (Hurlemann et al., 2010). In clinical studies, Pitman et al. (2002) conducted a double-blind, placebo-controlled pilot study examining the effectiveness of propranolol at preventing the development of PTSD. Results indicated that administering propranolol within 6 h of the traumatic event and continuing a 10-day course of propranolol led to a reduction in one measure of physiological reactions to trauma-related stimuli 3 months later (Pitman et al., 2002). Similar results were documented by Vaiva et al. (2003) in a nonrandomized study of trauma-exposed individuals, with early administration of propranolol leading to lower rates of PTSD 2 months later. However, another double-blind, randomized-controlled trial of propranolol administered within 48 h of trauma exposure failed to produce significant differences in PTSD rates compared to placebo (Stein, Kerridge, Dimsdale, & Hoyt, 2007). A recent randomized-controlled trial that administered a 19-day trial of up to 240 mg a day of propranolol found no differences in PTSD severity, diagnostic outcome, or physiological reactivity at 4 and 12 weeks post-trauma between propranolol and placebo (Hoge et al., 2012). Thus, results on propranolol as a preventative strategy have been inconsistent and are likely to be abandoned, especially in light of these recent Hoge et al. (2012) data.

Morphine use following traumatic injury has been examined for its potential in preventing PTSD, presumably due to its inhibiting effect of norepinephrine, although the mechanism of action of the PTSD reduction remains speculation (Fletcher et al., 2010). Bryant, Creamer, O’Donnell, Silove, and McFarlane (2009) conducted a naturalistic study of acute morphine administration following traumatic injury and found that patients with greater morphine doses reported less PTSD symptoms 3 months after the initial trauma. A review of medical records of military personnel who experienced combat injury in Iraq indicated that early morphine administration, regardless of dose, were associated with decreased rates of PTSD (Holbrook, Galarneau, Dye, Quinn, & Dougherty, 2010). Similar findings have been found in child trauma populations (Nixon et al., 2010; Saxe et al., 2001). While these studies point to the potential of morphine to prevent subsequent PTSD symptomatology, randomized-controlled trials are needed to further investigate the efficacy of morphine as a preventative strategy and to elucidate the mechanism of action. It is unlikely that physicians will adopt widespread administration of morphine to trauma survivors in the absence of severe physical injury.

Another pharmacological treatment that has been examined for its relationship to PTSD development is ketamine. Ketamine is an N-methyl-d-aspartate receptor antagonist that is often used in emergency settings as an anesthetic or sedative (Schonenberg, Reichwald, Domes, Badke, & Hautzinger, 2005). Schonenberg et al. (2005) found that ketamine use in accident victims was actually associated with elevated rates of PTSD. However, a study of military service members with burn injuries found that ketamine administration during surgery was associated with lower rates of PTSD (McGhee, Maani, Garza, Gaylord, & Black, 2008). These contradictory findings are perplexing and point to the need for further research.

In summary, the use of pharmacotherapy to prevent the development of PTSD in trauma-exposed individuals is an important area to explore, but research on potential medications such as morphine and ketamine is in the preliminary stages. Inconsistent results have been documented and few randomized-controlled trials have been conducted. The recent negative RCT with propranolol has effectively eliminated it as a preventative strategy (Hoge et al., 2012). Thus, more work is needed in this area to determine the efficacy of these or other pharmacological treatments as preventive strategies.

Besides debriefing approaches such as CISD, there are other brief interventions that have been developed and tested for their ability to reduce distress associated with traumatic events and to prevent the development of PTSD. For example, another intervention that utilizes a group-based debriefing model specifically with military populations is a program called Battlemind Psychological Debriefing. Three different versions of Battlemind Debriefing exist, including a version at postdeployment, event-driven debriefing (e.g., following a specific traumatic event), and time-driven debriefing that occurs in theater at regularly scheduled intervals (Adler, Bliese, et al. 2009; Adler, Castro, & McGurk, 2009). The intervention consists of five phases, including introducing the program, identifying specific events that may be causing difficulties for unit members, normalizing reactions to the event, identifying common problems to look for in themselves and their buddies (e.g., anger, sleep problems), and finally reinforcing certain training principles (Adler, Bliese, et al. 2009; Adler, Castro, & McGurk, 2009). Battlemind Psychological Debriefing is said to diverge from other forms of PD in its lack of emphasis on recounting the traumatic event, its focus on specific deployment-related issues, and its group application and delivery at regularly scheduled intervals during deployment (Adler, Bliese, et al. 2009; Adler, Castro, & McGurk, 2009). A recent study documented some preliminary support for this program compared to a stress education condition, with results suggesting that Battlemind Debriefing led to fewer PTSD and depression symptoms, especially among groups with high combat exposure (Adler, Bliese, et al. 2009; Adler, Castro, & McGurk, 2009). However, more research is needed to establish the efficacy of this intervention.

Other interventions have been developed as well. Gidron et al. (2001) created a memory-structuring intervention based on the theory that memories of traumatic events tend to be fragmented and that creating a more organized, chronological memory of the event can prevent the development of PTSD. The intervention consisted of phone contact with a therapist who would listen to the patient’s recounting of the traumatic memory and clarify details. The therapist would then read back a more organized and structured version of the traumatic memory, which would be repeated and practiced by the patient to facilitate processing. In a small pilot study utilizing a randomized-controlled design, results indicated that patients who received the memory-structuring intervention had lower PTSD symptoms 3 months later. However, a follow-up study found no overall group differences, although the intervention did appear effective at reducing PTSD symptoms specifically among women (Gidron et al., 2007). Given the small sample size utilized in both of these studies, these results should be considered preliminary with more research needed to interpret the results.

Another intervention developed specifically for survivors of sexual assault is a video-based treatment designed to precede a forensic rape exam. This brief 17-min video first provides information about the exam itself to prepare survivors for the procedure. Following this segment, the video goes on to provide psychoeducation about common reactions to rape and strategies to help limit avoidance and reduce anxiety (Resnick, Acierno, Holmes, Kilpatrick, & Jager, 1999). Results of a randomized study indicated preliminary support for reduced distress and marijuana abuse among women who watched the video compared to women who received standard care, with women with prior assaults appearing to benefit the most from the intervention (Resnick, Acierno, Kilpatrick, & Holmes, 2005). A more recent report on this intervention not only continued to identify significant benefits for women with a prior assault history but also documented a small increase in PTSD and anxiety at the 6-week follow-up among women with no prior assault history (Resnick et al., 2007). Further research on this video-based treatment is needed, but the potential of such a brief and easily disseminated intervention could be significant for trauma survivors and PTSD prevention.