A 30-year-old man with history of alcohol use was found unresponsive with unknown down time in his hotel room by the hotel staff. While his initial Glasgow Coma Score (GCS) was 13 at the scene, his GCS rapidly declined after arriving in the trauma bay and was emergently intubated for airway protection. Neurological examination revealed a fixed and dilated pupil on the left side with GCS of 6T after a brief sedation interruption (Figure 1). Secondary trauma survey showed ecchymosis on the left chest, shoulder and knee. Computed tomography (CT) scan of the head showed a 19 mm left convexity acute subdural hematoma with 14 mm of midline shift as well as uncal herniation (Figure 2). CT scan of the chest showed small pneumomediastinum and mild left-sided pneumothorax. His toxicology screen was only positive for ethanol with a level of 45 mg/dL. TBI was assumed given the constellation of evidence including CT scan findings, external trauma to the left side of body and positive ethanol level on initial toxicology screen. The patient was taken emergently to the operating room for decompressive hemicraniectomy and hematoma evacuation. Intra-operative bronchoscopy and esophagogastroduodenoscopy did not reveal additional injuries to the bronchial trees or esophagus. Postoperatively, the patient was admitted to neurotrauma ICU for close monitoring and his GCS improved to 10T. On the post-trauma day (PTD) 1, the patient had a routine admission electrocardiogram (ECG) that showed non-specific T wave changes (Figure 3A) with a normal ejection fraction (EF) on transthoracic echocardiography (TTE). He was successfully extubated on PTD 2 with an improved GCS of 13 (E3V4M6).
On the early morning of PTD 3, the patient developed tachycardia and acute hypoxia. Chest X-ray demonstrated mild pulmonary edema bilaterally. ECG was obtained which revealed new QTc prolongation and T wave inversion (TWI) on the lateral leads (aVL, V5, and V6). (Figure 3B) His oxygen supplementation was escalated to high flow nasal canula at 45 liters per minute. Hypoxia was attributed to pulmonary edema secondary to aggressive fluid resuscitation following the injury. Subjectively, the patient denied any chest discomfort and thus the ECG changes were deemed to be non-specific. His respiratory status rapidly improved with diuresis, and supplemental oxygen was weaned off on the same day.
On the night of PTD4, the bedside nurse noted obvious TWI on the bedside monitor. That prompted a repeat ECG demonstrating a persistently prolonged QTc interval and worsening TWI on leads I, II, aVL, and V2-6. (Figure 3C) The patient continued to deny any chest discomfort or shortness of breath. Troponin I was obtained given these new ECG changes and returned mildly elevated at 0.63 ng/mL (normal range 0-0.1 ng/mL).
By the next morning, repeat ECG was unchanged while troponin I downtrended to 0.54 ng/mL and then to 0.36 ng/mL. Repeat TTE was performed and demonstrated left ventricular apical ballooning with an estimated EF of 26% (Supplementary Video 1). Clinically, the patient had no symptoms of heart failure. Cardiology consultation recommended the initiation of lisinopril and metoprolol for the management of TCM. For the remainder of his hospitalization, he was monitored in the telemetry unit until discharge to a rehabilitation facility. Follow-up TTE on PTD 20 revealed improvement in EF to 50-55%.