Joanne Mouthaan1, Marit Sijbrandij2, Johannes B Reitsma3, Jan S K Luitse4, J Carel Goslings5, Berthold P R Gersons6, Miranda Olff7. 1. Department of Psychiatry, Academic Medical Center, University of Amsterdam, Meibergdreef 5, 1105 AZ Amsterdam, The Netherlands; Department of Clinical Psychology, Institute of Psychology, Leiden University, Wassenaarseweg 52, 2333 AK Leiden, The Netherlands. Electronic address: j.mouthaan@fsw.leidenuniv.nl. 2. Department of Clinical Psychology, VU University, Van der Boechorststraat 1, 1081 BT Amsterdam, The Netherlands; EMGO Institute for Health and Care Research, Van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands. Electronic address: e.m.sijbrandij@vu.nl. 3. Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands; Julius Center for Health Sciences and Primary Care, University Medical Center, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands. Electronic address: j.b.reitsma-2@umcutrecht.nl. 4. Trauma Unit, Department of Surgery, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. Electronic address: j.s.luitse@amc.uva.nl. 5. Trauma Unit, Department of Surgery, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. Electronic address: j.c.goslings@amc.uva.nl. 6. Department of Psychiatry, Academic Medical Center, University of Amsterdam, Meibergdreef 5, 1105 AZ Amsterdam, The Netherlands; Arq Psychotrauma Expert Group, Nienoord 5, 1112 XE Diemen, The Netherlands. Electronic address: b.gersons@arq.org. 7. Department of Psychiatry, Academic Medical Center, University of Amsterdam, Meibergdreef 5, 1105 AZ Amsterdam, The Netherlands; Arq Psychotrauma Expert Group, Nienoord 5, 1112 XE Diemen, The Netherlands. Electronic address: m.olff@amc.uva.nl.
Abstract
OBJECTIVE: Pharmacological intervention during traumatic memory consolidation has been suggested to prevent posttraumatic stress disorder (PTSD). The aim of this study was to examine the association between prescription of early pharmacotherapy and the risk of developing PTSD symptoms following traumatic injury. METHOD: The use of opiate analgesics, beta-adrenergic blockers, corticosteroids and benzodiazepines within 48 h postinjury was documented based on hospital charts for 629 Level 1 trauma center patients. PTSD symptoms were assessed using structured clinical interviews. Primary outcome was 6-week PTSD symptoms. Secondary outcomes were PTSD diagnoses at 6 weeks and during 1 year posttrauma. RESULTS: Linear regression analyses showed that opiate administration within 48 h was negatively associated with PTSD symptoms at 6 weeks (β=-0.14, P=.009) after controlling for demographic and injury-related characteristics and concurrent pharmacotherapy. Fewer patients with opiates had a PTSD diagnosis at 6 weeks (P=.047) and during 1 year posttrauma (P=.013) than patients with none of the specified pharmacotherapies. Low prescription frequency of beta-blockers (3.8%), corticosteroids (2.2%) and benzodiazepines (7.8%) precluded further examination of their role in the development of PTSD symptoms because of limited statistical power. CONCLUSIONS: This study suggests a possible beneficial influence of opiate administration within 48 h posttrauma on the development of PTSD symptoms. Future studies may evaluate the effectiveness of inhospital opiate analgesics compared to placebo in preventing PTSD and may focus on the mechanisms underlying the effect of opiates in preventing PTSD.
OBJECTIVE: Pharmacological intervention during traumatic memory consolidation has been suggested to prevent posttraumatic stress disorder (PTSD). The aim of this study was to examine the association between prescription of early pharmacotherapy and the risk of developing PTSD symptoms following traumatic injury. METHOD: The use of opiate analgesics, beta-adrenergic blockers, corticosteroids and benzodiazepines within 48 h postinjury was documented based on hospital charts for 629 Level 1 trauma center patients. PTSD symptoms were assessed using structured clinical interviews. Primary outcome was 6-week PTSD symptoms. Secondary outcomes were PTSD diagnoses at 6 weeks and during 1 year posttrauma. RESULTS: Linear regression analyses showed that opiate administration within 48 h was negatively associated with PTSD symptoms at 6 weeks (β=-0.14, P=.009) after controlling for demographic and injury-related characteristics and concurrent pharmacotherapy. Fewer patients with opiates had a PTSD diagnosis at 6 weeks (P=.047) and during 1 year posttrauma (P=.013) than patients with none of the specified pharmacotherapies. Low prescription frequency of beta-blockers (3.8%), corticosteroids (2.2%) and benzodiazepines (7.8%) precluded further examination of their role in the development of PTSD symptoms because of limited statistical power. CONCLUSIONS: This study suggests a possible beneficial influence of opiate administration within 48 h posttrauma on the development of PTSD symptoms. Future studies may evaluate the effectiveness of inhospital opiate analgesics compared to placebo in preventing PTSD and may focus on the mechanisms underlying the effect of opiates in preventing PTSD.
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