ABSTRACT
A recent large civilian randomized controlled trial on the use of tranexamic acid (TXA) for trauma reported important survival benefits. Subsequently, successful use of TXA for combat casualties in Afghanistan was also reported. As a result of these promising studies, there has been growing interest in the use of TXA for trauma. Potential adverse effects of TXA have also been reported. A US Department of Defense committee conducted a review and assessment of knowledge gaps and research requirements regarding the use of TXA for the treatment of casualties that have experienced traumatic hemorrhage. We present identified knowledge gaps and associated research priorities. We believe that important knowledge gaps exist and that a targeted, prioritized research effort will contribute to the refinement of practice guidelines over time.
Subject(s)
Antifibrinolytic Agents/therapeutic use , Hemorrhage/prevention & control , Tranexamic Acid/therapeutic use , Wounds and Injuries/drug therapy , Antifibrinolytic Agents/pharmacology , Humans , Postoperative Complications/chemically induced , Randomized Controlled Trials as Topic , Research , Risk Factors , Seizures/chemically induced , Thrombosis/chemically induced , Tranexamic Acid/pharmacology , Wounds and Injuries/surgeryABSTRACT
INTRODUCTION: This research investigated whether decompression sickness (DCS) risk or severity could be reduced using drug interventions that are easier to implement and equal to or more efficacious than recompression therapy. METHODS: Using a rat model of DCS, anti-inflammatory or anticoagulant drugs, including lidocaine, aspirin (ASA), methylprednisolone (MP), alpha-phenyl-N-butylnitrone (PBN), and transsodium crocetinate (TSC) were tested to determine their effect on incidence of DCS, death, and time of symptom onset. Each treatment group consisted of approximately 40 animals that received the drug and approximately 40 controls. Animals were exposed to one of five compression and decompression profiles with pressure ranging from 6.3 ATA (175 fsw) to 8.0 ATA (231 fsw); bottom time was either 60 or 90 min; and decompression rate was either 1.8 or 15 ATA x min(-1). Following decompression, the rats were observed for 30 min while walking on a wheel. DCS was defined as an ambulatory deficit or abnormal breathing. RESULTS: None of the drugs reached statistical significance for all DCS manifestations. Lidocaine post-dive and MP were the only treatments with marginally (P < 0.15) significant differences in DCS outcomes compared to controls. Lidocaine post-dive significantly decreased the incidence of neurological DCS from 73-51%. MP significantly extended the time of onset of death from DCS from 5.4 min to 7.1 min. DISCUSSION: Of the treatments investigated, lidocaine given post-dive has the best chance of success in adjuvant therapy of DCS. Future studies might investigate adjuvant drugs given in combination or during recompression.
