The aim of this study was to examine cardiac dysfunction during the first 2 weeks after isolated traumatic brain injury and its association with in-hospital mortality.
Level 1 regional trauma center.
Adult patients with severe traumatic brain injury.
After institutional review board approval, data from adult patients with isolated traumatic brain injury who underwent echocardiography during the first 2 weeks after traumatic brain injury between 2003 and 2010 were examined. Patients with preexisting cardiac disease were excluded. Clinical characteristics and echocardiogram reports were abstracted. Cardiac dysfunction was defined as left ventricular ejection fraction less than 50% or presence of regional wall motion abnormality.
We examined data from 139 patients with isolated traumatic brain injury who underwent echocardiographic evaluation. Patients were 58 ± 20 years old, 66% were male patients, and 62.6% had subdural hematoma; admission Glasgow Coma Scale score was 3 ± 1 (3–15) and head Abbreviated Injury Scale was 4 ± 1 (2–5). Of this cohort, 22.3% had abnormal echocardiogram: reduced left ventricular ejection fraction was documented in 12% (left ventricular ejection fraction, 43% ± 8%) and 17.5% of patients had a regional wall motion abnormality. Hospital day 1 was the most common day of echocardiographic exam. Abnormal echocardiogram was independently associated with all cause in-hospital mortality (9.6 [2.3–40.2]; p = 0.002).
Cardiac dysfunction in the setting of isolated traumatic brain injury occurs and is associated with increased in-hospital mortality. This finding raises the question as to whether there are uncharted opportunities for a more timely recognition of cardiac dysfunction and subsequent optimization of the hemodynamic management of these patients.
1Departments of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA.
2Department of Neurological Surgery, University of Washington, Seattle, WA.
3Department of Pediatrics, University of Washington, Seattle, WA.
4Department of Radiology, University of Washington, Seattle, WA.
* See also p. 213.
Supported, in part, by grant 3R01NS072308-03from National Institute of Neurological Diseases and Stroke.
Drs. Krishnamoorthy and Vavilala received funding support from the National Institutes of Health. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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