Silent ST elevation: unmasking blunt cardiac injury: a case report
Article information
Abstract
Blunt cardiac injury is a rare but serious complication of thoracic trauma. We present the case of a 22-year-old male pedestrian involved in a road traffic accident (pedestrian vs. four‑wheeler) who was found to have ST‑segment elevation on electrocardiography during trauma evaluation. Despite being hemodynamically stable and lacking clinical signs or symptoms of cardiac injury, his electrocardiography showed ST elevations in the inferior leads. This case underscores the importance of vigilant cardiac monitoring in polytrauma patients, in whom blunt cardiac injury may be easily overlooked.
INTRODUCTION
Blunt cardiac injury (BCI) is a spectrum of conditions ranging from myocardial contusion to cardiac rupture, most often resulting from high‑velocity blunt trauma [1]. Its diagnosis is challenging because clinical signs tend to be subtle or non‑specific. Although changes on electrocardiography (ECG) without underlying structural damage—particularly ST‑segment elevation—are uncommon in trauma patients, they require careful evaluation. We report a young man who developed ST‑segment elevation after a road traffic accident and was managed conservatively with serial ECG monitoring.
CASE REPORT
A previously healthy 22‑year‑old male pedestrian was struck at high speed by a four‑wheeler. On arrival at the emergency department, the Advanced Trauma Life Support primary survey was unremarkable. Physical examination revealed only minor abrasions over the left chest, with no palpable bony crepitus. Extended focused assessment with sonography in trauma (eFAST) was negative, excluding significant intraperitoneal hemorrhage or hemothorax. However, an adjunct ECG showed ST‑segment elevation in leads II, III, and aVF without reciprocal changes (Fig. 1).
Electrocardiography on presentation showing ST elevation in leads II, III, and aVF without reciprocal changes. HR, heart rate; bpm, beats per minute; VPB, ventricular premature beats.
The patient was hemodynamically stable, with no active chest pain. Six hours after injury, blood tests revealed a troponin I level of 72.95 ng/L (normal, <14 ng/L), raising suspicion for myocardial injury. Because transesophageal echocardiography was unavailable emergently, a transthoracic echocardiogram was performed and demonstrated normal ventricular function without regional wall motion abnormalities or pericardial effusion.
During the secondary survey, a type 3C open fracture of the right tibia and fibula was identified, necessitating orthopedic intervention. Cardiothoracic and vascular surgery and orthopedic teams were consulted. In the absence of chest pain or hemodynamic instability, the cardiothoracic and vascular surgery team recommended serial ECG monitoring with reevaluation if the patient’s condition deteriorated.
The patient was admitted to the intensive care unit under continuous cardiac telemetry. Serial ECGs, repeated 4 hours apart, consistently showed persistent but nonevolving ST‑segment elevation (Fig. 2). Laboratory parameters remained within normal limits (Table 1). He remained hemodynamically stable without chest pain. Troponin I levels trended downward over time (Table 2), and follow‑up echocardiograms were unremarkable. The orthopedic team performed surgical fixation of the right leg fracture, after which the patient’s postoperative course was uneventful. He was discharged without significant long‑term complications.
Serial electrocardiography after 4 hours showing no significant change in the ST elevation pattern. HR, heart rate; bpm, beats per minute.
Lab parameters
Serial troponin levels after trauma
Ethics statement
Written informed consent for publication of the research details and clinical images was obtained from the patient.
DISCUSSION
BCI is often underdiagnosed but may have life‑threatening consequences. It arises through several mechanisms: direct chest impact is most common—especially when the heart is full at end‑diastole—while indirect forces such as bidirectional compression and rapid deceleration can also cause structural damage or conduction disturbances. Owing to their anterior position, the right atrium and ventricle are most frequently injured. Lethal injuries include chamber rupture (64%), tears at the cavoatrial junction (33%), and coronary artery dissection or rupture. Commotio cordis—seen in young athletes—causes sudden cardiac arrest from ventricular fibrillation despite the absence of structural damage.
Survivors of BCI often sustain milder injuries, such as intramural hematomas that typically resolve within 4 to 12 weeks but can provoke transient conduction disturbances. More severe cases include papillary muscle rupture, leading to valvular regurgitation, and septal damage, which may progress from contusion to necrosis and delayed rupture, underscoring the need for early detection. Common arrhythmias include sinus tachycardia, premature contractions, and atrial fibrillation. In trauma patients, tachycardia initially suggests hemorrhage; BCI should be considered only after bleeding has been excluded [1].
Blunt cardiac injuries are classified by the American Association for the Surgery of Trauma into five grades according to severity [2]. Our patient most likely had a grade II injury, as indicated by ST‑segment elevations and elevated troponin I, yet he remained hemodynamically stable. The ECG pattern—namely, ST elevation in leads II, III, and aVF without reciprocal changes—suggested either right coronary artery involvement or myocardial contusion [3]. Given the normal echocardiogram and absence of regional wall motion abnormalities or pericardial effusion, conservative management was appropriate.
Emergency department diagnosis
Diagnosing BCI in the emergency department is challenging when overt clinical symptoms are absent [4]. Primary diagnostic tools include ECG, cardiac biomarkers (e.g., troponin), and echocardiography [5,6].
ECG abnormalities—such as tachyarrhythmias, bundle branch blocks, and nonspecific ST changes—are common in BCI [7]. However, ST‑segment elevation, as seen in our patient, is rare and mandates exclusion of coronary artery injury [3,8]. Differentiating trauma‑induced ECG changes from ischemic ECG patterns is crucial, especially in patients without prior cardiac history.
Recent studies highlight high‑sensitivity troponin assays and serial ECGs as valuable for distinguishing BCI from other etiologies [7,9]; nonetheless, troponin elevations lack specificity and may occur with renal failure or extreme exertion [9]. Serial troponin measurements at 0, 4, and 8 hours have demonstrated 100% sensitivity for diagnosing BCI.
Echocardiography is essential for excluding structural injuries such as septal defects or pericardial effusion. If hemodynamic instability or echocardiographic abnormalities arise, advanced imaging—such as transesophageal echocardiography or cardiac computed tomography (CT)—should be considered [10,11].
Management of BCI
Management depends on injury severity and hemodynamic status. Unnecessary surgery in stable patients with equivocal findings can worsen outcomes. Advances in diagnostics and minimally invasive techniques enable precise monitoring and treatment. While chest x‑ray, ECG, and bedside ultrasound remain routine, high‑yield modalities—such as CT imaging, cardiac biomarkers, and transesophageal echocardiography—provide clearer assessment. Clinical judgment, supported by prompt resuscitation, remains paramount [10].
For patients with isolated ECG changes and elevated troponins without instability, conservative management, involving serial ECGs, troponin monitoring, and 24 to 48 hours of observation, is usually sufficient [2,4,5].
In our case, elevated troponin levels, which are well‑established markers of myocardial injury, supported the BCI diagnosis. No standardized thresholds exist for proceeding to coronary angiography or surgery in stable BCI patients with troponin elevation and ST‑segment changes; thus, clinical judgment and multidisciplinary collaboration are essential [12].
This case emphasizes the importance of a multidisciplinary team—including trauma surgeons, cardiologists, and orthopedic specialists—when managing complex trauma patients. Patients with clinically or radiographically confirmed structural cardiac injuries require prompt cardiology evaluation to determine appropriate interventions, such as coronary angiography for assessing blood flow and identifying lesions needing revascularization [2,10,11]. Early detection and continuous monitoring of BCI are critical to prevent delayed complications, including arrhythmias or myocardial rupture. In stable patients with ECG changes, guidelines recommend continuous telemetry, serial troponin measurements, and echocardiography, as implemented in our case [12].
Follow-up and long-term considerations
Prospective studies on blunt thoracic injuries have shown no significant long‑term complications necessitating routine cardiac follow‑up [13]. Because BCI may be initially difficult to detect, it is now categorized by its sequelae: complex arrhythmias, coronary artery injury, heart failure, free‑wall rupture, septal rupture, and minor enzyme or ECG abnormalities [14].
Conclusions
In trauma patients presenting with ST‑segment elevation—even without classic signs or symptoms of cardiac injury—a high index of suspicion for BCI is essential. Early recognition and vigilant monitoring, including cardiac biomarkers and serial ECGs, guide management decisions and improve outcomes. Familiarity with BCI grading helps clinicians assess severity and select appropriate interventions.
Notes
Author contributions
Conceptualization: VD, AAM, AU; Investigation: VD, SR; Visualization: AAM; Writing–original draft: VD; Writing–review & editing: AAM, SR, AU. All authors read and approved the final manuscript.
Conflicts of interest
The authors have no conflicts of interest to declare.
Funding
The authors received no financial support for this study.
Data availability
Data sharing is not applicable as no new data were created or analyzed in this study.