A 65-year-old female was the driver involved in a front-impact car versus tree crash. The impact occurred slightly to the left of the car_s centerline, with a 15Ï20" intrusion of the tree into the engine compartment, displacing the front bumper, grille and engine. The steering wheel was bent, and because neither door could be opened, a rescue operation was conducted to remove the driver_s door with a hydraulic spreader to extricate the patient.
EMS providers arrived within four minutes of dispatch and found the restrained patient alone in the vehicle, complaining of severe chest pain and dypsnea. There was no chest wall asymmetry or paradoxical movement, and equal bilateral breath sounds were present. The patient was conscious and alert, recalling events and denying loss of consciousness. On exposure, no external life-threatening injuries were found. Initial vital signs: Pulse 124, respirations 24, BP 108/78 and 9% oxygen saturation on non-rebreather mask.
A secondary survey revealed minor epistaxis with nasal bone tenderness and edema, but no bony deformity and no other evidence of head or facial injury.
An abrasion was noted over the left anterior lower neck consistent with seatbelt placement. The left medial clavicle was tender, and an erythematous mark extended from the left clavicle over the left anterior chest, sternum at the midline, and the right lower chest, also consistent with seatbelt placement. The sternum was markedly tender, but neither it nor the ribs were unstable. There was no visible external injury to the abdomen, which was soft and non-tender. The back was also non-tender with no deformity apparent along the spine. There was no external injury to the pelvis or extremities.
During the 14-minute extrication, the patient continued to experience severe anterior chest pain and increasing dypsnea. She became pale, diaphoretic and more tachycardic. Hypotension developed, with palpable BP dropping to 80 systolic at approximately minute 10 of the extrication. Because the patient was becoming unstable, rescuers expedited their efforts and decided to perform a rapid extrication maneuver once the door was removed. Approximately one minute prior to successful extrication, the patient developed agonal breathing and her carotid pulses were lost. Once the door was removed, the patient was moved onto a long backboard, CPR was performed, and the patient was intubated and transported to a Level 1 trauma center.
On arrival at the trauma center, resuscitation proceeded rapidly according to ATLS guidelines. A focused assessment sonogram for trauma (FAST) showed a pericardial tamponade. Surgeons performed an immediate thoracotomy and pericardiotomy, which revealed a right atrial rupture (see photo). Resuscitative efforts failed to return organized heart activity, and the patient died.
As many as 20% of all prehospital fatalities are caused by blunt injury to the heart.1 Blunt cardiac injury (BCI) is a spectrum of injuries ranging from asymptomatic myocardial contusion to cardiac chamber rupture and death. Mechanisms by which BCI may occur include motor vehicle crashes (MVCs), falls from heights, direct blows to the chest and explosions. The most common mechanism of BCI is an MVC. Due to the tremendous force generated in these events, BCI often occurs in conjunction with other injuries, particularly to the chest.2 Although the majority of BCIs are associated with other significant injuries to the chest, occasionally an isolated direct blow to the chest may cause ventricularfibrillation and death, a condition termedcommotio cordis.3
Before BCI is diagnosed, other more likely sources of hemodynamic instability must be ruled out. These include, but are not limited to, hemorrhage, hypoxia and tension pneumothorax. Once these other causes of shock have been triaged, patients suspected of cardiogenic shock as a result of BCI should be treated in the field with fluid resuscitation and immediately transported to a trauma center.
Rupture of a cardiac chamber, coronary artery or intrapericardial portion of a great vessel leads to cardiogenic shock from pericardial tamponade and rapid death. Cardiac rupture is associated with a 60Ï100% mortality rate in the literature.4 There are case reports of patients surviving blunt cardiac rupture, but it appears to occur more commonly when the disrupted cardiac structure is a low-pressure structure, such as the atria or coronary sinus.
A clinically significant myocardial contusion may manifest as arrhythmia or hypotension. Depending on the severity, this may lead to decreased cardiac output. The coronary arteries may be damaged during BCI, leading to myocardial infarction and the associated sequelae. Valves may also be damaged, leading to acute or delayed cardiac failure.5
BCI is difficult to diagnose without the aid of echocardiography. Although this diagnostic capability isn_t available in the field,EMS providers are often the first to assess patients with possible BCI and have a unique opportunity to suggest this injury pattern. Thus, prehospital providers should inspect the scene of the injury and surrounding circumstances, as well as conduct a thorough physical exam.
Patients may complain of chest pain, shortness of breath or palpitations. Vital signs may be completely normal with minor contusions, or demonstrate tachycardia, arrhythmia or hypotension in more severe forms of injury. Although physical examination is non-specific, sternal tenderness or ecchymoses may be found. On auscultation, the finding of a murmur, rub or muffled heart sounds should raise suspicion of BCI, but these findings aren_t typically present. Because BCI is often associated with other injuries to the thorax, subcutaneous emphysema, flail chest and bony crepitus secondary to rib fractures may be present.6
Pericardiocentesis may be attemptedby qualified providers as a temporizing maneuver for patients in extremis where the other etiologies of shock have been triaged and cardiac tamponade secondary to BCIis suspected.JEMS
William F. Whalen, MS, EMT-P, is a physician assistant student atArcadiaUniversity and has been a paramedic inPennsylvania since 1979. He can be reached firstname.lastname@example.org.
Daniel N. Holena, MD, is a fellow in trauma and surgical critical care at theUniversity ofPennsylvania. he can be reached atDaniel.Holena@uphs.upenn.edu.
John P. Pryor, MD, FACS, is a trauma surgeon and the trauma program director at theUniversity ofPennsylvania. He can be reached atJohn.Pryor@uphs.upenn.edu.
- Pretre R, Chilcott M: ˙Blunt trauma to the heart and great vessels.ÓNew England Journal of Medicine. 336(9):626Ï632, 1997.
- DeMuth Jr WE, Baue AE, Odom Jr JA: ˙Contusions of the heart.ÓJournal of Trauma. 7(3):443Ï455, 1967.
- Wisner DH, Reed WH, Riddick RS: ˙Suspected myocardial contusion: Triage and indications for monitoring.ÓAnnals of Surgery. 212(1):82Ï86, 1990.
- Valani R, Mikrogianakis A,Goldman RD: ˙Cardiac concussion (commotio cordis).ÓCanadian Journal of Emergency Medicine. 6(6):428Ï430, 2004.
- Shorr RM, Crittenden M, Indeck M, et al: ˙Blunt thoracic trauma: Analysis of 515 patients.ÓAnnals of Surgery. 206(2):200Ï205, 1987.
- Martin SK, Shatney CH, Sherck JP, et al: ˙Blunt trauma patients with prehospital pulseless electrical activity (PEA): Poor ending assured.ÓJournal of Trauma. 53(5):876Ï880, 2002.