Objective Prior studies have suggested that traumatic brain injury (TBI) may affect cardiac function. Our study aims were to determine the incidence, longitudinal course, and admission risk factors for systolic dysfunction in patients with moderate-severe TBI. Design Prospective cohort study Setting Level 1 trauma center Measurements Transthoracic echocardiogram (TTE) within 1 day and over the first week after moderate-severe TBI; TTE within 1 day after mild TBI (comparison group). Measurements and Main Results Systolic function was assessed by TTE, and systolic dysfunction was defined as fractional shortening (FS) < 25%. Multivariable Poisson regression models examined admission risk factors for systolic dysfunction. Systolic function in 32 patients with isolated moderate-severe TBI and 32 patients with isolated mild TBI (comparison group) was assessed with TTE. Seven (22%) moderate-severe TBI and 0 (0%) mild TBI patients had systolic dysfunction within the first day after injury (p<0.01). All patients with early systolic dysfunction recovered in one week. Younger age (RR 0.87, 95% CI 0.79 – 0.94, for one year increase in age) and lower admission GCS score (RR 0.34, 95% CI 0.20 – 0.58, for one unit increase in GCS) were independently associated with the development of systolic dysfunction among moderate-severe TBI patients. Conclusions Early systolic dysfunction can occur in previously healthy patients with moderate-severe TBI, and it is reversible over the first week of hospitalization. Younger age and lower admission GCS score are independently associated with the development of systolic dysfunction after moderate-severe TBI.
Background While systolic dysfunction has been observed following traumatic brain injury (TBI), the relationship between early hemodynamics and the development of systolic dysfunction has not been investigated. Our study aimed to determine the early hemodynamic profile that is associated with the development of systolic dysfunction after TBI. Methods We conducted a prospective cohort study among patients under 65 years old without cardiac comorbidities who sustained moderate-severe TBI. Transthoracic echocardiography was performed within the first day after TBI to assess for systolic dysfunction. Hourly systolic blood pressure (SBP), mean arterial pressure (MAP), heart rate, and confounding clinical variables (sedatives, fluid balance, vasopressors, and osmotherapy) were collected during the first 24 hours following admission. Multivariable linear mixed models assessed the early hemodynamic profile in patients who developed systolic dysfunction, compared to patients who did not develop systolic dysfunction. Results 32 patients were included, and 7 (22%) developed systolic dysfunction after TBI. Patients who developed systolic dysfunction experienced early elevation of SBP, MAP, and heart rate, compared to patients who did not develop systolic dysfunction (p<0.01 for all comparisons). Patients who developed systolic dysfunction experienced a greater rate of decrease in SBP [−10.2 mmHg (95% CI: −16.1, −4.2)] and MAP [−9.1 mmHg (95% CI: −13.9, −4.3)] over the first day of hospitalization, compared to patients who did not develop systolic dysfunction (p<0.01 for both comparisons). All sensitivity analyses revealed no substantial changes from the primary model. Conclusions Patients who develop systolic dysfunction following TBI have a distinctive hemodynamic profile, with early hypertension and tachycardia, followed by a decrease in blood pressure over the first day after TBI. This profile suggests an early maladaptive catecholamine-excess state as a potential underlying mechanism of TBI-induced systolic dysfunction.
Introduction:Abnormal electrocardiographic (ECG) findings can be seen in traumatic brain injury (TBI) patients. ECG may be an inexpensive tool to identify patients at high risk for developing cardiac dysfunction after TBI. The aim of this study was to examine abnormal ECG findings after isolated TBI and their association with true cardiac dysfunction, based on echocardiogram.Methods:Data from adult patients with isolated TBI between 2003 and 2010 was retrospectively examined. Inclusion criteria included the presence of a 12-lead ECG within 24 h of admission and a formal echocardiographic examination within 72 h of admission after TBI. Patients with preexisting cardiac disease were excluded. Baseline clinical characteristics, 12-lead ECG, and echocardiogram report were abstracted. Logistic regression was used to identify the relationship of specific ECG abnormalities with cardiac dysfunction.Results:We examined data from 59 patients with isolated TBI who underwent 12-lead ECG and echocardiographic evaluation. In this cohort, 13 (22%) patients had tachycardia (heart rate >100 bpm), 25 (42.4%) patients had a prolonged QTc, and 6 (10.2%) patients had morphologic end-repolarization abnormalities (MERA), with each having an association with abnormal echocardiographic findings: Odds ratios (and 95% confidence intervals) were 4.14 (1.02-17.05), 9.0 (1.74-46.65), and 5.63 (1.96-32.94), respectively. Ischemic-like ECG changes were not associated with echocardiographic abnormalities.Conclusions:Repolarization abnormalities (prolonged QTc and MERA), but not ischemic-like ECG changes, are associated with cardiac dysfunction after isolated TBI. 12-lead ECG may be an inexpensive screening tool to evaluate isolated TBI patients for cardiac dysfunction prior to more expensive or invasive studies.
To our knowledge, the present study is the largest study describing the use of serial TTE and its utilization in adult donors. The prevalence of cardiac dysfunction after adult brain death is high, but given enough time and support, many of these donors have improvement in cardiac function, ultimately leading to transplantation.
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