The incidence and outcomes of hyperacute cardiovascular dysfunction following isolated traumatic brain injury: an observational cohort study.

Abstract

Background: The relationship between early cardiovascular dysfunction (CVD) in isolated traumatic brain injury (iTBI) and outcome has not been fully described. We aimed to (1) determine the prevalence and phenotype of CVD after iTBI in the hyper-acute phase and (2) compare treatment and outcomes in those with CVD vs non-CVD.

Methods: An observational cohort database study of severe iTBI patients (Head AIS 3+) at a level 1 trauma centre (2008-2019) and physician-led air ambulance service (2019-2020). CV dysfunction was defined as tachycardia or bradycardia, with hypotension. Physiology, laboratory results, 24-hour transfusion, and computer-topography (CT) findings were recorded. Outcomes were 28-day mortality and Glasgow Outcome Score (GOS).

Results: A total of 168 patients met inclusion criteria, average age 46 years (IQR 30-61), 77% male, median ISS 25 (IQR 17-29) with 51% Head AIS 5. Time from injury to pre-hospital assessment was 31 minutes (IQR 20-42) with 20% demonstrating CVD on initial observations. The CVD group were more shocked (lactate 6.1 (1.7-10.9) vs. 2.4 (1.4-3.3), P < 0.001) and coagulopathic (43% vs. 15%, P = 0.001). There was no difference in Head AIS or CT findings between groups, except frequency of hypoxic ischemic encephalopathy (HIE) (CVD: 21% vs. non-CVD: 1%, P < 0.001). 24-hour transfusion was higher in CVD patients: 3 (0-8) vs. 0 (0-0) units, P < 0.001. Mortality was greater in CVD vs non-CVD iTBI (61% vs. 31%, P = 0.002), but in patients with AIS 5 there was no difference ( P = 0.262). One-third of CVD survivors (13/33) were discharged home, and 4/18 patients with recorded GOS had good neurological outcome.

Conclusion: One in five patients with severe iTBI develop early CVD, associated with increased mortality, coagulopathy, and HIE. However, mortality and neurological outcome is highly variable in those with CVD across the iTBI severity spectrum. Further research is needed to define the pathophysiology and optimal treatment to improve outcomes for this subgroup of iTBI.