No Resuscitative Thoracotomy? When to Stop Chest Compressions After Prehospital Traumatic Cardiac Arrest.

INTRODUCTION: Although indications and outcomes for trauma patients who require resuscitative thoracotomies are well studied, little is known about how prehospital chest compressions support survival in patients who do not meet criteria for subsequent resuscitative thoracotomy. METHODS: Data from a single institutional retrospective review of trauma patients who required prehospital chest compressions from 1/2015 to 12/2020 were collected. Patients who underwent compressions only were compared to those who underwent subsequent resuscitative thoracotomy. The primary outcome was in-hospital mortality. RESULTS: Fifty-two patients were identified, 22 of whom underwent compressions only and 30 of whom went on to undergo thoracotomy. Patients who underwent compressions only were more likely to be female (36% vs 10%, P = .04), older (mean 46 vs 35 years, P = .04), and to experience blunt trauma (78% vs 43%, P = .01). Injury severity score was similar between the cohorts (mean 18 vs 28, P = .11). One patient in the compressions only cohort had a REBOA placed compared to two in the thoracotomy cohort (1.9% vs 3.67%, P > .99). Return of spontaneous circulation (ROSC) was achieved in 17% of the compressions only cohort compared to 45% of the thoracotomy cohort (P = .03). In-hospital mortality in the compressions only cohort was 100%, whereas in-hospital mortality in the thoracotomy cohort was 94% (P = .50), with a mean of zero survival days in both groups (P = .33). CONCLUSION: Prehospital chest compressions without thoracotomy were uniformly fatal, even if transient ROSC was obtained. Our findings support termination of chest compressions for those trauma patients who do not meet criteria for resuscitative thoracotomy.

Early Propranolol Is Associated With Lower Risk of Venous Thromboembolism After Traumatic Brain Injury.

BACKGROUND: Traumatic brain injury (TBI) results in an elaborate systemic cascade of secondary injury elicited in part by an intrinsic catecholamine response, which ultimately leads to changes in inflammation and coagulopathy. Attenuation of this catecholamine response with agents such as propranolol confers a survival advantage. The related impact of propranolol on venous thromboembolism (VTE) after TBI is largely unknown. STUDY DESIGN: A single institution retrospective review was conducted of all TBI patients requiring intensive care unit (ICU) admission with an injury severity scale (ISS) ≥ 25 from January 2013 to May 2015. Patients who received at least one dose of propranolol within 24 hours of admission (PROP) were compared to patients who did not receive any doses of propranolol (NPROP) during their hospitalization. RESULTS: Of the 131 patients analyzed, 31 (23.7%) patients received propranolol. The PROP cohort was more severely injured overall (ISS 29 vs 26.5, P = .02). While unadjusted VTE rates were similar (16.1% vs 19.0%, P = .72), the adjusted VTE rate was lower in the PROP cohort (AOR 0.20 (95% CI 0.04-0.97), adjusted P-value < .05). CONCLUSION: Propranolol use in TBI patients who have sustained critical injuries may mitigate the risk of VTE. The mechanism by which this outcome is achieved requires further investigation.

Characterizing the delays in adequate thromboprophylaxis after TBI.

BACKGROUND: We sought to compare enoxaparin dosing for venous thromboembolism (VTE) prophylaxis in trauma patients with and without traumatic brain injury (TBI) to better understand the time and dose required to reach target anti-Xa levels. Our hypothesis was that patients with TBI have significant delays in the initiation of adequate pharmacological prophylaxis and require a higher enoxaparin dose than currently recommended. METHODS: The medical records of trauma patients who received enoxaparin dosing based on anti-Xa trough levels between August 2014 and October 2016 were reviewed. Patients were included if their anti-Xa trough level reached the target range (0.1 IU/mL to 0.2 IU/mL). RESULTS: A total of 163 patients had anti-Xa levels within the target range of which 41 (25.2%) had TBI. Patients with TBI had longer delays before initiating enoxaparin (7.5 days vs. 1.5 days after admission, p<0.01) and were more likely to receive unfractionated heparin prior to enoxaparin (46.3% vs. 11.5%, p<0.01). Anti-Xa levels reached the target range later in patients with TBI (11 days vs. 5 days after admission, p<0.01). Enoxaparin 40 mg two times per day was the median dose required to reach the target anti-Xa levels for both cohorts. VTE rates were higher among patients with TBI (22.0% vs. 9.0%, p=0.03). Four patients (9.8%) had progression of their intracranial hemorrhage prior to receiving enoxaparin, although none progressed during enoxaparin administration. CONCLUSION: Among patients with TBI who reached target anti-Xa levels, 11 days after admission were required to reach a median enoxaparin dose of 40 mg two times per day. Unfractionated heparin was used as pharmacological prophylaxis in about half of these patients. The delay in reaching the target anti-Xa levels and the use of unfractionated heparin likely contribute to the higher VTE rate in patients with TBI. LEVEL OF EVIDENCE: Level III, therapeutic.

Appendectomy: a risk factor for colectomy in patients with Clostridium difficile.

BACKGROUND: The appendix, considered an intestinal microbiota reservoir, may be protective against the risk of fulminant Clostridium difficile infection. METHODS: Retrospective analysis was performed in patients with C. difficile infection at St. Francis Medical Center from 2007 to 2011. Outcome of infection and history of appendectomy were compared. Statistical analysis was by chi-square and multivariate logistic regression. RESULTS: In total, 507 patients were hospitalized for C. difficile. Of 388 patients with intact appendix, 20 (5.2%) developed fulminant infection and required colectomy, whereas of 119 patients with previous appendectomy, 13 (10.9%) required colectomy. An increased severity of disease, indicated by increased rate of colectomy, occurred for the group with a history of appendectomy (P = .03). Age and sex were adjusted by multivariant regression (P = .05). CONCLUSIONS: Appendectomy may be a risk factor for increased severity of C. difficile infection. Although the mechanism is unknown, further studies are warranted.