When is it safe to start venous thromboembolism prophylaxis after blunt solid organ injury? A prospective American Association for the Surgery of Trauma multi-institutional trial.

BACKGROUND: The optimal time to initiate venous thromboembolism (VTE) chemoprophylaxis (VTEp) after blunt solid organ injury remains controversial, as VTE mitigation must be balanced against bleeding promulgation. Evidence from primarily small, retrospective, single-center work suggests that VTEp ≤48 hours is safe and effective. This study was undertaken to validate this clinical practice. METHODS: Blunt trauma patients presenting to 19 participating trauma centers in North America were screened over a 1-year study period beginning between August 1 and October 1, 2021. Inclusions were age older than 15 years; ≥1 liver, spleen, or kidney injury; and initial nonoperative management. Exclusions were transfers, emergency department death, pregnancy, and concomitant bleeding disorder/anticoagulation/antiplatelet medication. A priori power calculation stipulated the need for 1,158 patients. Time of VTEp initiation defined study groups: Early (≤48 hours of admission) versus Late (>48 hours). Bivariate and multivariable analyses compared outcomes. RESULTS: In total, 1,173 patients satisfied the study criteria with 571 liver (49%), 557 spleen (47%), and 277 kidney injuries (24%). The median patient age was 34 years (interquartile range, 25-49 years), and 67% (n = 780) were male. The median Injury Severity Score was 22 (interquartile range, 14-29) with Abbreviated Injury Scale Abdomen score of 3 (interquartile range, 2-3), and the median American Association for the Surgery of Trauma grade of solid organ injury was 2 (interquartile range, 2-3). Early VTEp patients (n = 838 [74%]) had significantly lower rates of VTE (n = 28 [3%] vs. n = 21 [7%], p = 0.008), comparable rates of nonoperative management failure (n = 21 [3%] vs. n = 12 [4%], p = 0.228), and lower rates of post-VTEp blood transfusion (n = 145 [17%] vs. n = 71 [23%], p = 0.024) when compared with Late VTEp patients (n = 301 [26%]). Late VTEp was independently associated with VTE (odd ratio, 2.251; p = 0.046). CONCLUSION: Early initiation of VTEp was associated with significantly reduced rates of VTE with no increase in bleeding complications. Venous thromboembolism chemoprophylaxis initiation ≤48 hours is therefore safe and effective and should be the standard of care for patients with blunt solid organ injury. LEVEL OF EVIDENCE: Therapeutic and Care Management; Level III.

A Rare Mechanism of Inhalation Injury: Direct Thermal Damage to the Lower Airway.

In patients with inhalation injury associated with major burns, the primary mechanism of tissue harm depends on the location within the respiratory tract. Proximal to the trachea, the upper respiratory tract epithelium is classically injured via direct thermal injury. Such injury occurs due to the inhalation of high-temperature air. These upper airway structures and the tracheobronchial tree's dense vasculature protect the lower airways and lung parenchyma from direct thermal damage. The lower respiratory tract epithelium and lung parenchyma typically become injured secondary to the cytotoxic effects of chemical irritants inhaled in smoke as well as delayed inflammatory host responses. This paper documents a rare case in which a patient demonstrated evidence of direct thermal injury to the lower respiratory tract epithelium. A 26-year-old Caucasian male presented to the emergency room with 66% total body surface area thermal burns and grade 4 inhalation injury after a kitchen fire. Instead of visualizing carbonaceous deposits in the bronchi, a finding common in inhalation injury, initial bronchoscopy revealed bronchial mucosa carpeted with hundreds of bullae. Despite the maximum grade of inhalation injury per the abbreviated injury score and a 100% chance of mortality predicted with the revised Baux score, as well as a clinical course complicated by pneumonia development, bacteremia, and polymicrobial external wound infection, this patient survived. This dissonance between his expected and observed clinical outcome suggests that the applicability of current inhalation injury classification systems depends on the precise mechanism of injury to the respiratory tract. The flaws of these grading scales and prognostic indicators may be rooted in their failure to account for other pathophysiologic processes involved in inhalation injury. It may be necessary to develop new grading and prognostic systems for inhalation injury that acknowledge and better account for unusual pathophysiologic mechanisms of tissue damage.