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Injury mortality was classically described with a trimodal distribution, with immediate deaths at the scene, early deaths due to hemorrhage, and late deaths from organ failure. We hypothesized that the development of trauma systems has improved prehospital care, early resuscitation, and critical care and altered this pattern. This population-based study of all trauma deaths in an urban county with a mature trauma system reviewed data for 678 patients (median age, 33 years; 81% male; 43% gunshot, 20% motor vehicle crashes). Deaths were classified as immediate (scene), early (in hospital, ≤4 hours from injury), or late (>4 hours after injury). Multinomial regression was used to identify independent predictors of immediate and early versus late deaths, adjusted for age, gender, race, intention, mechanism, toxicology, and cause of death. Results showed 416 (61%) immediate, 199 (29%) early, and 63 (10%) late deaths. Compared with the classical description, the percentage of immediate deaths remained unchanged, and early deaths occurred much earlier (median 52 vs 120 minutes). However, unlike the classic trimodal distribution, the late peak was greatly diminished. Intentional injuries, alcohol intoxication, asphyxia, and injuries to the head and chest were independent predictors of immediate death. Alcohol intoxication and injuries to the chest were predictors of early death, while pelvic fractures and blunt assaults were associated with late deaths. In conclusion, trauma deaths now have a predominantly bimodal distribution. Near elimination of the late peak likely represents advancements in resuscitation and critical care that have reduced organ failure. Further reductions in mortality will likely come from prevention of intentional injuries and injuries associated with alcohol intoxication.

Return to work may be easily monitored as a surrogate of long-term functional outcome for benchmarking and performance improvement of trauma systems. We hypothesized that employment rates among survivors of traumatic brain injury (TBI) decrease following injury and remain depressed for an extended period of time. Data were obtained from a statewide surveillance system of 3522 TBI patients (aged >15 years) who were discharged alive from acute care hospitals and followed yearly using telephone interviews (1996–1999). The study population consisted of patients with severe TBI (head abbreviated injury score 3, 4, or 5) and complete follow-up for 3 years postinjury (n= 572). Patients were mostly young males (43 ± 19 years, 65% male) with blunt TBI (92%). The preinjury employment rate was 67%, which declined to 52% (P< 0.001) in the first year and slowly rose in subsequent years but never reached the preinjury level (54% in year 2, P< 0.001; 57% in year 3, P= 0.001). Increasing severity of TBI was associated with a lower employment rate. Patients who remained employed worked the same number of hours as they did before the injury (47.8 ± 10.5 hours). Female employment rates rose similar to rates for males. However, women who were employed full-time before TBI were more likely to work part-time after TBI than men (50% vs 24%, P< 0.001). In conclusion, survivors of severe injury do not attain preinjury employment levels for several years. Once validated in other studies, postinjury employment may be used as an indicator to monitor functional outcomes in trauma registries.

Background: Intracranial hemorrhage (ICH) is a serious complication of warfarin therapy. Plasma infusion is the current standard of care in the US, even though most guidelines recommend prothrombin complex concentrate (PCC) as the preferred therapy; PCC has several advantages over plasma including no ABO blood type requirement, no lengthy thawing and infusion process, and a very small volume of virally inactivated pure vitamin K-dependent factors (VKDF) content that causes neither volume overload nor TRALI. Ideal PCC should contain adequate amounts of all VKDF (4-factor). As our group reported at the 2006 ASH meeting, PCC currently available in the USA have a very low FVII content (hence called a 3-factor PCC), often resulting in an incomplete correction of supratherapeutic INR. PCC is, therefore, often supplemented with 1–2 units of plasma to provide FVII; however, many elderly patients on warfarin do not tolerate an additional fluid volume and there is an urgency to correct coagulopathy in ICH. Recombinant FVIIa (rFVIIa) has been used to reverse warfarin effect with variable success. An experimental model has shown that rFVIIa corrects PT/INR in vitro but fails to correct bleeding because it does not address FII and X deficiencies critical for thrombin generation in vivo when compared with PCC. Therefore, we developed a trauma coumadin protocol (TCP) for urgent warfarin reversal for ICH, which includes both PCC and a low dose rFVIIa. Methods: TCP was approved by the Blood Utilization Review Committee of the Parkland Memorial Hospital and consists of administration of 4000 IU PCC (Profilnine, Grifols) and 1.2 mg rFVIIa; 5 mg intravenous Vit K1 is also administered daily for 3 days. PCC contains FII no more than 150 units, FX no more than100 units, and FVII no more than 35 units for each 100 units of FIX. Pre- and post-TCP VKDF were measured when possible (Table 2). We compared 19 patients treated with TCP with a 12 patient-non-TCP control group (warfarin-ICH) treated either with plasma alone (n=3) or plasma plus PCC (n=9). We will also compare (software delay) the 2 groups for extension of hematoma volume; the radiologist will be blinded to the therapy. Results: The TCP group included 12 females and 7 males aged 46–87 years (median 64). The control group included 4 females and 8 males aged 53–89 years (median 73). TCP patients had significantly faster as well as complete correction of PT/INR as compared to the controls. (Table-1). Post-TCP CT scans showed stable hematomas. 1/19 TCP patients with pituitary adenoma had pre-TCP INR of 7.2 and post-TCP INR of 0.9. He developed thrombotic stroke and acute myocardial infarction 2 days later; he was discharged home. The patient received 2.4 mg of rFVIIa because initially the dose of rVIIa was stratified based on INR (1.2 mg for INR 5.0 or less and 2.4 mg for INR greater than 5.0). . Examination of post-treatment FVII levels (Table-2) led us to modify TCP rFVIIa dose to a 1.2 mg, irrespective of INR. Conclusion: TCP rapidly and effectively corrects warfarin-associated coagulopathy in patients with ICH. Because thrombotic complications remain a concern, 4-factor PCC should further be evaluated. Table 1. Test results Time relative to TCP treatment TCP group n=19 Control group n=12 p value INR Mean ± SD (range) Pre 3.1±2.0 (1.4–5.1) 3.2 ±1.6 (1.4–7.2) 0.991 Post 1.1±0.3 (0.9–2.0) 1.4 ±0.3 (0.9–2.0) 0.003 PT Mean ± SD (range) Pre 28.1±17.3 (13.5–65.1) 28.9±14.0 (13.7–62.6) 0.887 Post 10.7±2.2 (9.3–18.1) 13.8±2.8 (9.3–18.3) 0.002 PTT Mean ± SD (range) Pre 36.0±10.3 (21.8–59.8) 38.2 ±11.5 (25.4–60.6) 0.591 Post 24.7±4.2 (19.5–32.2) 27.8±4.5 (22.8–30.9) 0.058 Time from TCP to INR correction (min) Mean ± SD (range) 145.4±107 (22–329) 267±76 (83–697) 0.023 Median 111 240 Table 2. Test results INR PT PTT FII FVII FIX FX Pretreatment Mean ± SD (range) 3.3±2.0 (1.5–7.4) 29.6±17.3 (14.4.–65.1) 35.7±9.9 (30.1–54.7) 54±41 (6–117) 23 ±12 (6–37) 57 ±28 (17–96) 44 ±30 (5–74) Posttreatment Mean ± SD (range) 1.1±0.4 (0.9–2.0) 11.0±3.0 (9.4–18.1) 25.9±4.1 (19.5–32.2) 148±84 (27–323) 394±141 (114–600) 97±22 (58–130) 144±54 (89–268)