A 59-year-old previously healthy female presented to the emergency department with hypotension and tachycardia after a high-speed head-on motor vehicle collision. She was initially treated with tracheal intubation and fluid resuscitation. There was minimal output from a left-sided chest tube, a markedly widened mediastinum on chest radiograph, and a negative focused assessment with sonography for trauma (FAST) examination for intraperitoneal or pericardial fluid. She was intermittently hypotensive throughout her initial treatment period, and traumatic aortic disruption was suspected. However, a computed tomography scan revealed a large hemomediastinum and hemopericardium with no evidence of aortic or great vessel injury. She was transported directly to the operating room where transesophageal echocardiography (TEE) revealed a circumferential pericardial effusion (Fig. 1) with systolic right atrial (RA) and diastolic right ventricular (RV) collapse consistent with cardiac tamponade (Video 1, Supplemental Digital Content, http://links.lww.com/AA/B30). A discontinuity at the RV apex covered by clot was noted (Fig. 2; Video 2, Supplemental Digital Content, http://links.lww.com/AA/B31). However, no flow was seen between the RV and pericardial space by color Doppler; a contrast-enhanced examination was not performed. The examination of the aorta, valvular structures, and ventricular septum was unremarkable. After sternotomy and evacuation of mediastinal blood, an actively bleeding rupture in the RA base was noted and repaired by suturing. This rupture was not identified on TEE. Although initially it was not actively bleeding, a second rupture site in the RV apex was discovered after gentle clot removal. This was repaired with rapid ventricular pacing to provide a still surgical field. The patient recovered and was discharged 16 days later in good condition.
The presentation of cardiac injury in blunt trauma is broad and graded by the American Association for the Surgery of Trauma with blunt avulsion of the heart being the most severe manifestation.1 Blunt cardiac rupture is rare (0.045%–0.5% of blunt trauma), with a high mortality rate (60%–90%) even among initial survivors presenting to hospital.1 The RA and RV are more vulnerable to injury than the left atrium or left ventricle due to proximity to the sternum. They may also be injured by a “water-hammer effect” in which forceful impact to the abdomen causes increased hydrostatic venous pressure to be rapidly transmitted to the RA.1 Integrity of the pericardium determines whether a patient presents with cardiac tamponade (if intact) or a massive hemothorax (if disrupted).1
Limitation in acquiring adequate windows for transthoracic echocardiography in the setting of chest wall injury makes TEE a valuable tool in hemodynamic assessment. TEE is especially useful in the unstable patient because it can be performed in the trauma bay when transport for diagnostic imaging is hazardous. Several important traumatic etiologies of hypotension have been associated with echocardiographic findings, including cardiac rupture, myocardial contusion, thoracic aortic injury, valvular incompetence, or hypovolemia from hemorrhage (Table 1).1–5 Valvular insufficiency from papillary muscle or chordae tendinae rupture is a rare but well-documented complication, particularly of the tricuspid valve.5 Acute mitral or aortic valve regurgitation is also possible and may require more urgent management than acute tricuspid regurgitation.4,5 Traumatic aortic injury concurrent with cardiac rupture is common (20%–50%)1,4 and warrants careful examination because traumatic aortic injury may manifest differently from nontraumatic dissection. An intimal avulsion may form without the development of a false lumen, or a pseudo-aneurysm may form if both intimal and medial dissection occurs. Traumatic injury tends to produce a thicker, less mobile intraluminal flap than that typical of nontraumatic dissection. Complete transection of intima, media, and adventitia is a highly fatal injury and may be indicated by an expanding hematoma surrounding the transection site.3 Injury is most commonly located at the aortic isthmus but may also occur in the ascending aorta.
Although contrast-enhanced echocardiography was not performed in this case, it may aid in the diagnosis of cardiac rupture, particularly if the presentation is subacute as from myocardial infarction or due to iatrogenic causes.6 With cardiac rupture, extravasated microbubbles will be noted in the pericardial fluid. Given the high likelihood of right chamber injury in blunt trauma, agitated saline may be sufficient for this purpose although commercial IV contrast agents have been described for delineating left-sided rupture after myocardial infarction.6,7 Given the rarity of traumatic cardiac rupture, the use of contrast enhancement in this setting has not been described in the literature but may have aided in preoperative localization of the injury to the RA, which was not otherwise visualized on TEE.
This case illustrates several important features of cardiac rupture. Multichamber rupture is possible after a traumatic injury, particularly to the right-sided chambers. There may be a dynamic nature to such “low”-pressure lesions, which may thrombose and temporarily seal if small enough in size, but they are inherently unstable. Careful examination of each chamber is therefore mandatory. Cardiac tamponade may not be a presenting feature if pericardial disruption and decompression of blood into the mediastinal or pleural space occur. However, even if initial FAST examination result is negative, tamponade may still develop as clot formation obstructs these pathways. In this case, this may have been the reason for the discrepancies between the initial FAST examination and the later imaging. TEE is a useful early adjunct in trauma management in the setting of ongoing instability because it can reveal concurrent injuries and guide resuscitation efforts.
Clinician’s Key Teaching Points
By Nikolaos J. Skubas, MD, Donald Oxorn, MD, and Martin J. London, MD
- Any cardiac structure may be injured by blunt chest trauma. In particular, right-sided cardiac structures may be more susceptible due to their proximity to the sternum. An acute increase in venous pressure from abdominal trauma may also result in right-sided cardiac injury via a “water-hammer effect.” Depending on pericardial integrity, cardiac tamponade, or with loss of pleural integrity, hemothorax may develop.
- Hemodynamic instability in cases of blunt chest trauma is associated with a variety of echocardiographic features, such as regional or global ventricular dysfunction from myocardial contusion (most commonly the RV), valvular regurgitation from valvular rupture (most commonly the tricuspid valve), aortic wall discontinuity from aortic rupture or dissection, and pericardial effusion, cardiac tamponade, or hemothorax from cardiac rupture. TEE can rapidly identify the putative mechanism and help in the planning of treatment.
- In this case, a healthy woman injured in a motor vehicle accident presented with tachycardia and hypotension. Initial imaging with the FAST surface ultrasound protocol appeared negative for cardiac injury or pericardial effusion, and chest tube output was minimal despite a widened mediastinum by chest radiograph. However, a computed tomography scan revealed a large hemomediastinum and hemopericardium and she was taken to the operating room for chest exploration. A large pericardial effusion and cardiac tamponade physiology with systolic RA and diastolic RV collapse were imaged with TEE. In the transgastric long-axis view with rightward turn of the probe, discontinuity of the RV free wall that was covered by clot was detected.
Name: Rebecca Gerlach, MD.
Contribution: This author was a senior anesthesia resident assisting with the management of the current case. She participated in the preparation and revision of the current manuscript and can attest to the originality of the current information.
Attestation: Rebecca Gerlach approved the final version for submission to Anesthesia & Analgesia Echo Rounds.
Name: David Mark, MD, FRCPC.
Contribution: This author was an attending anesthesiologist responsible for the management of the current case. He assisted in preparation and revision of the current manuscript.
Attestation: David Mark approved the final version for submission to Anesthesia & Analgesia.
Name: Anujan Poologaindran, BScH.
Contribution: This author assisted with the revision of the current manuscript.
Attestation: Anujan Poologaindran approved the final version for submission to Anesthesia & Analgesia.
Name: Rob Tanzola, MD, FRCPC.
Contribution: This author was the attending anesthesiologist responsible for the management of the current case. He participated in the preparation and revision of the current manuscript.
Attestation: Rob Tanzola can attest to the originality and integrity of the current information. He also approved the final version for submission to A & A and is the archival author.
This manuscript was handled by: Martin J. London, MD.
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