B25-23 Epidemiology, Trauma Kinetics, Neuroimaging Predictors, and Ventilatory Factors in Severe Traumatic Brain Injury Under Invasive Mechanical Ventilation: A Retrospective Intensive Care Unit Cohort From Ecuador

Abstract Rationale Severe traumatic brain injury (TBI; Glasgow Coma Scale ≤ 8) drives intensive care unit (ICU) mortality in Latin America, yet granular data on trauma type, kinetics, neuroimaging, and ventilation remain scarce. We quantified these domains and early prognostic signals in a single-center cohort from Ecuador. Methods Retrospective cohort of adults with severe TBI admitted to the ICU (March 2019-March 2020). Inclusion required invasive mechanical ventilation (IMV) within 24 hours. Variables: demographics; trauma type (road-traffic accident RTA, fall, assault); trauma kinetics (direct impact vs crash/collision); baseline CT (sulcal and basal cistern effacement, midline shift, contusion, intraparenchymal hemorrhage, subdural hematoma, subarachnoid hemorrhage, skull fracture) categorized with Marshall, Rotterdam, and Stockholm frameworks; severity scores (APACHE II, SAPS II); admission arterial blood gas; ventilatory parameters including baseline exhaled tidal volume (VTe) indexed to predicted body weight on ICU arrival; outcomes (in-hospital mortality, ICU length of stay, ventilator days). Chi-square, and Pearson correlations were used; p 0.05 significant. The sample size was the census of all eligible ICU admissions. Results Ninety-five patients were included; men 82.1%; mean age 46.6 ± 20.5 years; in-hospital mortality 43.2%. Trauma type: RTA 70.9%, falls 26.6%, assault 2.5% (Figure 1B). Trauma kinetics: direct impact 63.3%, crash 36.7% (Figure 1C). CT findings: sulcal effacement 86.3%, basal cistern effacement (significant predictor p = 0.007), midline shift 38.9%, skull fracture 32.6% (Figure 1D). Mortality correlated with basal cistern and sulcal effacement, but not midline shift. Severity scores discriminated outcomes: SAPS II (p = 0.0017), APACHE II (p = 0.0016) with r = 0.781. Admission pH (p = 0.040) and baseline VTe (p = 0.0019) were associated with mortality, while ventilator days and ICU stay were not (Figure 1A). Conclusions In this RTA-dominant cohort, early loss of intracranial compliance—reflected by basal cistern and sulcal effacement—and systemic derangement (higher APACHE II/SAPS II, acidemia) were stronger mortality signals than age or midline shift. Findings support neuroprotective ventilation (VTe 4-8 mL/kg PBW; avoid prophylactic hyperventilation), early hyperosmolar therapy when basal cistern/sulcal effacement is present, and prompt shock control to reverse acidemia. This abstract is funded by: No funding