Stress Disorders Following Traumatic Injury: Assessment and Treatment Considerations

Brett D. Thombs, PhD, James A. Fauerbach, PhD, and Una D. McCann, MD

Dr. Thombs is a postdoctoral fellow, Dr. Fauerbach is associate professor, and Dr. McCann is associate professor in the Department of Psychiatry and Behavioral Sciences at the Johns Hopkins School of Medicine in Baltimore, Maryland.

Disclosure: Drs. Thombs and Fauerbach do not have any affiliations or financial interests in a commercial organization that might pose a conflict of interest.Dr. McCann receives grant and/or research support from the National Institute on Drug Abuse and is on the speaker’s bureaus of Bristol-Myers Squibb and Pfizer.

Funding/support:This work was supported by a grant from the United States Department of Education National Institute on Disability and Rehabilitation Research (grant no. H133A020101) awarded to Dr. Fauerbach.

Please direct all correspondence to: Brett D. Thombs, PhD, Johns Hopkins Burn Center, Bayview Medical Center, 4940 Eastern Ave, Baltimore, MD 21224;
Tel: 410-550-5298; Fax: 410-550-8161; E-mail: [email protected].

Abstract

Traumatic injury is a relatively common occurrence, with approximately 40 million injury-related visits to emergency departments in the United States per year. Psychiatric complications of physical injury are a public health concern. Approximately 12% to 16% of survivors of traumatic injury are diagnosed with acute stress disorder (ASD), and 30% to 36% warrant a diagnosis of posttraumatic stress disorder (PTSD) 12 months after the traumatic event. Phenomena related to injury, such as blood loss, pain, administration of narcotic analgesics, and traumatic brain injury, as well as high rates of premorbid psychiatric and substance abuse and/or dependence disorders, often overlap with stress-related symptoms of psychological origin. This complicates the assessment of dissociative processes required for the diagnosis of ASD, as well as the three core PTSD symptom clusters (re-experiencing of the trauma, avoidance and numbing, and hyperarousal). This article reviews specific aspects of stress disorders in the context of traumatic injury, with a focus on aspects of assessment. Psychopharmacologic and behavioral treatment recommendations are also reviewed.

Introduction

In 2002, there were approximately 40 million physical-injury–related visits to emergency departments in the United States, equivalent to approximately 13.8 visits per 100 persons in the population and more than one third of all admissions to emergency departments.¹ An estimated 7% of these visits are for injuries severe enough to require inpatient hospitalization. The high prevalence of physical injury, along with advances in trauma care that have resulted in greater numbers of individuals surviving traumatic injury,² underscore why psychiatric complications of physical injury are a major public health concern.³

The diagnosis of posttraumatic stress disorder (PTSD) first appeared in the diagnostic nosology in 1980 with the publication of the Diagnostic and Statistical Manual of Mental Disorders, Third Edition (DSM-III).⁴ The diagnosis has evolved somewhat since then: currently, a diagnosis of PTSD requires that an individual has “experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others” and reacted with “intense fear, helplessness, or horror.”⁵ Additionally, symptoms from three primary clusters (re-experiencing of traumatic event, avoidance and numbing, and persistent hyperarousal) must be present for ³1 month. At least one symptom is required from the re-experiencing symptom cluster, along with three or more from the avoidance/numbing cluster, and two or more hyperarousal symptoms.

Acute stress disorder (ASD) was added to the diagnostic nomenclature in the DSM-IV,⁵ to address stress symptomatology occurring within the first month and for the purported capacity to predict future PTSD in traumatized individuals.⁶ The diagnostic criteria have been criticized, however, due to their initial lack of empirical grounding and emphasis on dissociative symptoms.^7,8 Like PTSD, a diagnosis of ASD requires that an individual has “experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others” and reacted with “intense fear, helplessness, or horror.”⁵ Three or more dissociative symptoms are also required in addition to one or more symptoms from each of the three PTSD symptom clusters. Symptoms must last for ³2 days, but £4 weeks for a diagnosis of ASD.

Medical and psychological characteristics inherent to severe physical injury and its sequelae present unique challenges in understanding, assessing, and treating physical-injury–induced ASD and PTSD. Numerous symptom presentations may be associated with either physical or psychological pathology, such as those related to blood loss, pain, the administration of narcotic analgesics, or traumatic brain injury (TBI). However, there is a lack of reliable methods for clearly distinguishing between them. These complications are a limiting factor in understanding the prevalence, natural history, and comorbidities of stress disorders in injured populations and in providing accurate and effective assessment and treatment services.

Prevalence, Course, and Comorbidity

There is substantial variability in estimates of the prevalence of stress disorders following traumatic injury. Some of this is due to the difficulty in accurately differentiating physical and psychological phenomena.^9,10 Additionally, among other biases in population characteristics, disparity in type of accident and range of injury severity likely impact prevalence estimates. Some studies¹¹ have included patients who sought medical attention in an emergency department with no admission criterion for study inclusion, others included only those who were admitted to the hospital,^12,13 and others excluded the most severely injured patients who needed intensive care hospitalization.¹⁴ At the other end of the spectrum, there are studies that have only included severely injured patients who received intensive care.^15-17

Some research has employed structured clinical interviews, and other research has relied upon self-report questionnaires. Structural interviews provide a more accurate assessment of symptoms, including delineation of trauma-related origin, and tend to result in lower prevalence estimates than self-report measures.¹⁰ Nonetheless, even studies with seemingly similar populations have reported different prevalence rates.

Only a few studies have reported the prevalence of ASD in physically injured populations. These studies have tended to be relatively consistent, with most rates in the 12% to 16% range for motor vehicle accident survivors with minor TBI,¹⁸ motor vehicle accident survivors without TBI,¹⁹ inpatient survivors of industrial accidents and burn injuries,¹⁶ and hospitalized injury survivors of mixed etiology.¹³ Fuglsang and colleagues²⁰ reported a rate of only 6% prevalence, but this may have been influenced by the timing of the assessment. Another study²¹ of patients admitted to a level-1 trauma service with mixed injury etiologies reported an ASD prevalence rate of only 1%. This study, however, assessed current rather than peritraumatic dissociation and excluded current intravenous (IV) drug users, which may have impacted the prevalence (given the known relationship between substance abuse, premorbid mental health, and ASD and/or PTSD).^22-26 Of note, the two studies with the lowest rates^20,21 used the Clinician-Administered PTSD Scale (CAPS), which is a more stringent method than either assessment by self-report or with the Acute Stress Disorder Inventory, which was used in the other studies.

In a recent review, O’Donnell and colleagues¹⁰ reported prevalence rates of 18% to 42% for PTSD assessed 1–6 months postinjury.^{11,14,18,27,28} Studies with rates <30% did not require that patients be admitted to the hospital for their injuries¹¹ or excluded patients needing intensive care services.¹⁴ Rates at 12 months ranged from 2% to 36%, but most were in the 30% to 36% range.^12,22,29 Studies reporting lower rates excluded patients with “any sign of psychological problems,”²⁴ patients who were IV drug users,²¹ or patients who needed intensive care for their injuries.¹⁴ Note that the large range of prevalence rates across studies is likely related to many factors beyond those discussed here. Studies that have reported prevalence tend to be small, and larger epidemiological studies are needed.

Typically, untreated symptoms of posttraumatic stress tend to lessen over time for the majority of individuals. For example, in a study¹⁴ of motor vehicle accident survivors who sought emergency department services but who did not need intensive care services, only 50% of patients with a DSM-IV diagnosis of PTSD 3 months after the accident still qualified at 12 months.Similarly, in a group of mixed trauma survivors from an emergency department setting,¹¹ 30% were diagnosed with PTSD at 1 month and only 18% at 4 months. This is not always the case, however. Even after discharge from the hospital, survivors of severe physical injuries, such as burn injuries, continue to face a variety of stressors to their well-being, including pain, disfigurement, and functional limitations that may dampen the normal downward trend in posttraumatic stress symptomatology.^17,30,31 Fauerbach and colleagues²⁶ provide a good reference that addresses burn-related phenomena in the context of symptoms of PTSD.

A diagnosis of ASD after an injury has been shown to be a good predictor of a PTSD diagnosis.¹⁸ Severely injured trauma survivors, however, frequently do not endorse the dissociative symptoms that form the core of the ASD diagnosis, resulting in low rates of ASD compared to subsequent PTSD rates in the same populations.³² In fact, many individuals who are not diagnosed with ASD later develop PTSD.³² It has been suggested that reducing the number of required dissociative symptoms and increasing the symptom threshold for the other three symptom clusters may improve diagnostic utility.¹⁸ Injury severity in itself is not predictive of PTSD diagnosis or severity,¹⁰ although this may relate to how injury severity is measured.

Psychiatric comorbidity is the norm rather than the exception with PTSD, and depression and substance abuse disorders are the most common comorbidities. Large community samples^10,33,34 have found that between 80% and 85% of individuals diagnosed with PTSD also met criteria for at least one other psychiatric disorder, with general anxiety disorder, phobias, substance abuse, and major depressive disorder (MDD) the most common. In injured populations, the prevalence of comorbid MDD has been reported to be between 43% and 59%.^11,12,21,35 Substance abuse is also prominent, both premorbidly and comorbidly. For example, in a sample of 269 randomly selected injury survivors at two level-1 trauma centers, over half of acute-care inpatients exhibited high levels of posttraumatic stress and alcohol abuse and/or dependence.²³ In another similar sample of 101 traumatic injury survivors,³ 46% of individuals who screened positive for PTSD had a positive toxicology screen for alcohol, cocaine, or amphetamine upon admission. In addition to comorbidities, disorders such as simple phobias or depression may develop subsequent to trauma without a diagnosis of PTSD.³⁶

Assessment

Numerous validated self-report and structured interview tools are available to aid in the assessment of ASD and PTSD. For ASD, the Acute Stress Disorder Scale³⁷ and the ASDI³⁸ are 19-item self-report and clinician-administered questionnaires, respectively. Both are based on the DSM-IV diagnostic criteria for ASD, and published data are available for both on utility in predicting individuals who meet diagnostic criterion. The Stanford Acute Stress Reaction Questionnaire³⁹ is a self-report questionnaire that is also frequently employed to detect acute posttraumatic stress symptomatology. There is no published data, however, on its capacity to correctly predict individuals who meet diagnostic criteria.

For PTSD, the CAPS⁴⁰ is a widely used structured clinician-administered interview instrument. Commonly utilized self-report measures include the Posttraumatic Stress Diagnostic Scale,⁴¹ the Davidson Trauma Scale,⁴² and the civilian version of the Posttraumatic Stress Disorder Checklist,⁴³ all of which correspond to DSM-IV diagnostic criteria. Self-report questionnaires are likely to be particularly vulnerable to confounding psychological symptoms with injury-related symptoms.¹⁰ However, injury and treatment-related factors, such as blood loss, TBI, pain, administration of narcotic analgesics, injury-related functional limitations, and the hospital environment, can complicate diagnosis of stress-related disorders even when assessed by a structured interview or clinician diagnosis. Reviews by Bryant^44,45 discuss the mechanisms through which PTSD may develop in patients with TBI despite amnesia for the injury event, as well as assessment issues related to TBI and PTSD.

In assessing and diagnosing ASD and PTSD, symptoms with potential injury-related etiologies can be problematic in the identification of dissociation-related phenomena, as well as in ascertaining manifestations of the three core PTSD symptom clusters (re-experiencing, avoidance and numbing, and persistent hyperarousal). As such, assessment should take place once the patient is medically stable,²¹ and evaluations of patients with cognitive deficits related to TBI may need to include corroborative information rather than relying solely on spontaneous reporting by the patient.⁴⁴

Pain, the administration of narcotics, TBI, and intoxication at the time of injury can produce symptoms that mimic dissociation and underscore the need for a conservative approach to the diagnosis of dissociative phenomenon, particularly in the hospital.²¹ All five dissociative symptoms in the DSM-IV criteria for ASD (ie, emotional numbing, reduced awareness, depersonalization, derealization, and amnesia) are also consistent with TBI or the administration of narcotics.^21,45 For example, the high rate of alcohol and other substance intoxication at time of injury^3,21,45-49 renders questions about memory for the trauma potentially misleading in terms of the assessment of ASD. Adaptations to increase the validity of assessment procedures include asking about posttraumatic or current symptoms of dissociation rather than dissociative symptoms that may have occurred “while experiencing or after experiencing”⁵ the traumatic injury, as well as not assessing for symptoms until patients have discontinued the use of IV narcotics for ³24 hours.²¹ It should be noted, however, that two recent studies^21,50 did not find significant relationships between narcotic administration and dissociative symptoms.

In addition to dissociation-like phenomena, TBI may produce intrusive, recurrent images⁴⁴ as a result of frontal-lobe pathology⁵¹ or Capgras syndrome⁵² that can be mistaken for re-experiencing phenomena of a psychogenic nature. Furthermore, normal response to traumatic injury may produce a degree of ruminative thought related to the implications of the injury that should be carefully differentiated from intrusive memories related to posttraumatic stress phenomena.²¹

Apparent avoidance behaviors in the context of acute injury may occur for a number of reasons, not all of them posttraumatic stress-related per se. The restrictions and relative safety of the hospital setting may markedly reduce the patient’s need and/or ability to approach potentially unsettling stimuli. In this setting, imaginary exposure to potential stressors, such as asking a patient with a burn injury to imagine cooking, can provide an indication of the degree of trauma-related avoidance that may be expected upon discharge. Care should also be taken to separate depressive phenomenon, such as lack of motivation, lack of energy, and inability to carry out activities due to physical limitations from apprehension-based avoidance.

Finally, injured patients with substantial disfigurement may exhibit avoidant behavior that overlaps with trauma-related avoidance. The distinctiveness or similarity of avoidance patterns rooted in traumatic memory and those related to disfigurement is currently not clear. There is evidence that patients with visible cosmetic disfigurement from burn injuries who were diagnosed with PTSD tend to endorse the avoidance and emotional numbing symptom cluster most frequently and that visible burn injury is predictive of PTSD.^53,54 The difficulties most frequently reported by individuals with acquired disfigurements relate to negative self-perceptions and difficulties with social interactions,^55,56 and social anxiety has been identified as a central difficulty facing individuals with visible disfigurement.⁵⁷

Hyperarousal (ie, sleep disturbance, concentration difficulty, hypervigilance, and irritability) is the other core feature of PTSD. Reports of concentration deficits, irritability, sleep disturbance, and agitation, however, may be related to concomitant physical injury (eg, TBI). Additionally, sleep difficulties may be related to pain⁵⁸ or noise in the intensive care unit.⁵⁹

Treatment

Early Intervention of PTSD and ASD

Both pharmacologic and cognitive-behavioral therapy (CBT) have shown efficacy in the treatment of stress reactions to trauma. Single-session debriefing intervention methods⁶⁰ have been widely used in the acute posttrauma stage. Evidence from randomized clinical trials, however, does not justify the use of debriefing, and it may actually do harm in some cases.^61-65 There is evidence, on the other hand, that brief (ie, 4–5 sessions)^66,67 and longer (ie, £12 sessions)⁶⁸ CBT is efficacious in preventing the subsequent development of PTSD in samples of accident survivors diagnosed with ASD. In addition, a stepped collaborative care intervention that includes case management, motivational interviews, and pharmacotherapy and/or CBT has been effective in addressing both alcohol abuse and the development of PTSD.⁶⁹

Recommendations for pharmacologic treatment of early acute stress reactions close to the time of injury focus on the management of acute and distressful physiological stressors, such as pain and sleep disturbance. The use of traditional benzodiazepines to address sleep difficulties is cautioned against, however, due to the development of tolerance to the hypnotic effects of benzodiazepines with continued use, withdrawal symptoms of insomnia and anxiety following discontinuation after protracted use, interactions with alcohol, and a lack of demonstrated efficacy in the treatment of depression and PTSD.⁶¹ In fact, patients with acute stress responses who were administered benzodiazepines beginning approximately 1 week posttrauma had higher rates of PTSD diagnoses at 6 months compared to a control group.⁷⁰ A short course of a nonbenzodiazepine sedative-hypnotic⁶¹ or treatment with trazodone⁷¹ have been recommended to address acute sleep difficulties. Sleep hygiene and cognitive-behavioral approaches may also be successful for managing sleep disturbance.⁷²

Two small studies^73,74 have tested the effects of a 7–10-day course of the a-adrenergic blocker propranolol (beginning in the emergency department within hours of a traumatic event) on the development of PTSD. Both studies reported that acute posttraumatic administration of propranolol may have a preventative effect as determined by PTSD diagnoses at 6 months. Acute administration of propranolol, however, is highly experimental and not recommended practice.

Treatment of PTSD

Selective serotonin reuptake inhibitors (SSRIs) are the standard first-line psychopharmacologic treatment for PTSD due to demonstrated efficacy, relatively low risk in overdose, and efficacy in treatment of comorbid conditions such as MDD. Sertraline and paroxetine are approved by the Food and Drug Administration for PTSD, with evidence of efficacy from multiple clinical trials. Fluoxetine also has been shown to be effective in published trials.⁷² However, due to the natural reduction in symptoms after the initial reaction that occurs for most patients, physicians “should note an accumulation of symptoms after acute presentation, a lack of improvement or deterioration in the clinical picture, and the persistence or emergence of disability during a 3–4-week observation period” prior to beginning a course of SSRIs.⁶¹

Treatment should begin with low doses and should be increased gradually to indicated and tolerated dosage with consideration of switching to a different SSRI or either venlafaxine or mirtazapine if there is no response after 8 weeks of the therapeutic dose.⁷¹ Responders should continue on medication for ³1 year as required by the course of the symptoms.⁶¹ Some evidence has also been shown for tricyclic antidepressants, but their side-effect profile makes them a less desirable option.⁷²

Either psychopharmacology or CBT⁷⁵ may be sufficient as a single treatment mode for patients with mild-to-moderate symptoms, although a combined approach is recommended for more severe cases. Psychological treatment is also recommended for patients who do not respond to psychopharmacologic treatment. CBT is the only psychological treatment with demonstrated efficacy, and generally requires referral to a clinician trained in these techniques.⁶¹ Standard CBT, which consists of exposure therapy, cognitive restructuring, and relaxation and anxiety management techniques, has demonstrated efficacy for physically-injured populations.^61,76

Conclusion

The literature indicates that survivors of severe physical injury experience psychiatric sequelae similar to that found in other trauma survivor groups. However, unique aspects of physical injury—both medical and psychological—add complexity to the accurate assessment and efficacious treatment of stress disorders in patients with significant physical injuries. Phenomena related to injury, such as blood loss, pain, administration of narcotic analgesics, and TBI, as well as high rates of premorbid psychiatric and substance abuse and/or dependence disorders in physically traumatized populations, frequently overlap with symptoms of psychogenic origin (including dissociation, re-experiencing, avoidance and numbing, and hyperarousal). These factors also add complexity to pharmacologic and behavioral treatments. Nonetheless, as with other traumatized populations, the evidence supports the use of SSRIs and CBT as first-line treatment approaches. PP

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