Article

Morphine Use after Combat Injury in Iraq and Post-Traumatic Stress Disorder

Naval Health Research Center, San Diego, CA 92106-3521, USA.
New England Journal of Medicine (Impact Factor: 55.87). 01/2010; 362(2):110-7. DOI: 10.1056/NEJMoa0903326
Source: PubMed

ABSTRACT

Post-traumatic stress disorder (PTSD) is a common adverse mental health outcome among seriously injured civilians and military personnel who are survivors of trauma. Pharmacotherapy in the aftermath of serious physical injury or exposure to traumatic events may be effective for the secondary prevention of PTSD.
We identified 696 injured U.S. military personnel without serious traumatic brain injury from the Navy-Marine Corps Combat Trauma Registry Expeditionary Medical Encounter Database. Complete data on medications administered were available for all personnel selected. The diagnosis of PTSD was obtained from the Career History Archival Medical and Personnel System and verified in a review of medical records.
Among the 696 patients studied, 243 received a diagnosis of PTSD and 453 did not. The use of morphine during early resuscitation and trauma care was significantly associated with a lower risk of PTSD after injury. Among the patients in whom PTSD developed, 61% received morphine; among those in whom PTSD did not develop, 76% received morphine (odds ratio, 0.47; P<0.001). This association remained significant after adjustment for injury severity, age, mechanism of injury, status with respect to amputation, and selected injury-related clinical factors.
Our findings suggest that the use of morphine during trauma care may reduce the risk of subsequent development of PTSD after serious injury.

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    • "Observational studies of hospital patients also suggested a possible beneficial effect of morphine administration within 48 h after trauma exposure to survivors who experience pain, reducing the likelihood of a PTSD outcome[71,72]. A similar result was reported retrospectively in 696 military personnel with severe combat injury, in which not having PTSD was associated with higher likelihood of having received morphine—as per participants' medical charts[73]. Given the retrospective nature of most studies, more research is needed to separate a specific effect of morphine from a generic 'analgesic' effect. "
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    ABSTRACT: Post-traumatic stress disorder (PTSD) is a frequent, tenacious, and disabling consequence of traumatic events. The disorder’s identifiable onset and early symptoms provide opportunities for early detection and prevention. Empirical findings and theoretical models have outlined specific risk factors and pathogenic processes leading to PTSD. Controlled studies have shown that theory-driven preventive interventions, such as cognitive behavioral therapy (CBT), or stress hormone-targeted pharmacological interventions, are efficacious in selected samples of survivors. However, the effectiveness of early clinical interventions remains unknown, and results obtained in aggregates (large groups) overlook individual heterogeneity in PTSD pathogenesis. We review current evidence of PTSD prevention and outline the need to improve the disorder’s early detection and intervention in individual-specific paths to chronic PTSD.
    Full-text · Article · Feb 2016 · Current Psychiatry Reports
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    • "These CRF/opioid interactions adjust the activity and reactivity of LC neurons so that level of arousal and processing of sensory stimuli are optimized to facilitate adaptive behavioral responses to stressors. The protective effects of opioids are apparent in the many studies documenting that morphine administration shortly after a single traumatic event reduces the incidence of PTSD (Bryant et al., 2009; Holbrook et al., 2010). "
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    ABSTRACT: The stress response is characterized by the coordinated engagement of central and peripheral neural systems in response to life-threatening challenges. It has been conserved through evolution and is essential for survival. However, the frequent or continual elicitation of the stress response by repeated or chronic stress, respectively, results in the dysfunction of stress response circuits, ultimately leading to stress-related pathology. In an effort to best respond to stressors, yet at the same time maintain homeostasis and avoid dysfunction, stress response systems are finely balanced and co-regulated by neuromodulators that exert opposing effects. These opposing systems serve to restrain certain stress response systems and promote recovery. However, the engagement of opposing systems comes with the cost of alternate dysfunctions. This review describes, as an example of this dynamic, how endogenous opioids function to oppose the effects of the major stress neuromediator, corticotropin-releasing hormone, and promote recovery from a stress response and how these actions can both protect and be hazardous to health.
    Full-text · Article · May 2015 · F1000 Prime Reports
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    • "Pharmacotherapy Study Timepoints IRR 95% CI p n PTSD or ASD / N total * Risk of bias Intervention Control SG AC BA ITT Total † Delahanty et al ( 2013 ) 29 Hoge et al ( 2012 ) 30 Holbrook et al ( 2010 ) 36 Kobayashi et al ( 2011 ) 37 Nugent et al ( 2010 ) 31 Pitman et al ( 2002 ) 9 Schelling et al ( 2001 ) 34 Schelling et al ( 2004 , 2006 ) 12 , 23 Sharp et al ( 2010 ) 35 Stein et al ( 2007 ) 32 Stein et al ( 2007 ) 32 Tarsitani et al ( 2012 ) 38 Vaiva et al ( 2003 ) 39 Weis et al ( 2006 ) 33 Zohar et al ( 2011 ) 18 Overall ( I 2 =0 , 95% CI 0 – 54 ) Hydrocortisone β blocker Morphine Albuterol β blocker β blocker Hydrocortisone Hydrocortisone β blocker β blocker Gabapentin β blocker β blocker Hydrocortisone Hydrocortisone 2 2 1 2 1 2 1 1 1 1 1 1 1 1 2 0·37 1·30 0·63 0·21 3·46 0·64 0·17 0·85 1·56 1·00 0·80 0·46 0·24 0·33 0·20 0·65 0·03 – 3·96 0·34 – 4·97 0·52 – 0·77 0·01 – 3·36 0·15 – 77·86 0·10 – 4·27 0·03 – 1·17 0·19 – 3·78 0·69 – 3·50 0·27 – 3·66 0·18 – 3·59 0·16 – 1·33 0·03 – 1·92 0·04 – 2·83 0·02 – 2·30 0·55 – 0·78 0·41 0·70 0·00 0·27 0·43 0·65 0·07 0·83 0·29 1·00 0·77 0·15 0·18 0·31 0·19 0·00 2 / 24 5 / 21 147 / 493 0 / 23 1 / 12 2 / 11 1 / 9 3 / 26 10 / 127 3 / 12 2 / 10 4 / 33 1 / 11 1 / 14 1 / 9 3 / 27 5 / 20 96 / 203 27 / 232 0 / 14 6 / 20 7 / 11 3 / 22 12 / 237 4 / 16 4 / 16 10 / 38 3 / 8 3 / 14 3 / 8 "
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    ABSTRACT: Background An increasing number of studies have investigated the pharmacological prevention of post-traumatic stress disorder (PTSD) and acute stress disorder (ASD). This is the first systematic review to examine the effects of pharmacotherapies (eg, β blockers, hydrocortisone, and selective serotonin re-uptake inhibitors) given within the first month after a traumatic or aversive event to prevent PTSD or ASD compared with no pharmacotherapy or placebo control. Methods A systematic literature search in PubMed, PsycINFO, Embase, and the Cochrane database of randomised trials was done. Studies included randomised controlled trials, controlled clinical trials, and cohort studies; their overall quality was low to moderate. We computed the pooled incidence risk ratio (IRR): the risk of incidence of PTSD or ASD in the pharmacotherapy groups relative to the incidence of PTSD or ASD in the control groups. Additionally, we computed Hedges' g effect sizes for PTSD or ASD continuous outcomes. Findings 15 studies met inclusion criteria (1765 individuals). Pharmacotherapy was more effective in preventing PTSD or ASD than placebo or no intervention (14 studies, 1705 individuals, IRR 0·65, 95% CI 0·55–0·78; number needed to treat 11·36), although no effect was found when only randomised controlled trials were included (ten studies, 300 individuals, IRR 0·69, 95% CI 0·40–1·21). Hydrocortisone showed a large effect in reducing the risk of PTSD (five studies, 164 individuals, IRR 0·38, 95% CI 0·16–0·92). Interpretation No firm evidence was found for the efficacy of all early pharmacotherapies in the prevention of PTSD or ASD, but hydrocortisone reduced the risk of developing PTSD. The small number of studies and their limited methodological quality cast uncertainty about the effects. Funding None.
    Full-text · Article · Apr 2015 · The Lancet Psychiatry
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