Any massive crushing force applied to the anterior chest can cause bursting lacerations of the pericardium. These lacerations are almost invariably associated with injury to the heart or major blood vessels. The heart, protected in front by the sternum and ribs, is suspended in the pericardial sac by the aorta, pulmonary artery, and vena cava. The front or anterior surface of the heart is formed chiefly by the right ventricle and, to a lesser extent, the left ventricle. Traumatic injuries of the heart are caused by severe direct violence to the anterior chest. The nature of the injuries depends on the severity of the localized violence, whether the impact is inflicted while the heart is filled with blood, and whether the force applied is sufficient to compress or crush the heart between the sternum and vertebral column. Injuries to the heart are usually associated with injury to other structures of the chest. Blunt chest trauma is frequently caused by automobile accidents. The driver sustains this trauma when the chest forcibly strikes the steering wheel, the front-seat passenger when the chest strikes the dashboard. Air bags, and a lap belt combined with a good shoulder belt or harness can prevent or minimize this injury.
A localized force applied directly to the chest might be sufficient to cause a contusion of the anterior wall of either ventricle or the interventricular septum. Hemorrhage can occur in the conduction system with resultant arrhythmias.4 Grossly, recent contusions appear as dark red, hemorrhagic areas. They must not be confUsed with an acute myocardial infarct. If the localized impact drives the heart against the vertebral column, a contusion of the posterior wall of either ventricle or the interventricular septum could result. A posterior cardiac contusion must not be confused with postmortem lividity, a change frequently found on the posterior ventricular surfaces of the heart. Microscopic study of the antemortem contusion will reveal localized interstitial hemorrhage and injured myocardial fibers. With cellular injury, there are EKG changes and release of cellular enzymes (e.g., troponin). Primary trauma to the heart must, but cannot always, be differentiated from iatrogenic injury due to CPR, open cardiac massage, or intracardiac injections, especially if resuscitation is prolonged. The contused myocardium usually heals without any sequelae or residual injury. Rarely, it may undergo necrosis with rupture into the pericardial sac several days after the injury. It may also heal with fibrotic replacement of the contused myocardium and, rarely, form an aneurysm. Killen et al. reported a case of a posttraumatic pseudo-aneurysm of the left ventricle.5 They collected 12 more cases from a review of the literature. Complications were arrhythmia, cardiac failure, and embolism.
Lacerations of the heart occur primarily when a very severe crushing force is applied to the anterior chest. They can involve one or more areas of the heart, that is, atria, interatrial septum, ventricles, interventricular septum, papillary muscles, chordae tendinae, or cardiac valves. Cardiac lacerations infrequently occur as isolated injuries (Figure 5.1). Most often, they occur with other severe chest injuries. Rapid cardiac failure occurs whenever a cardiac valve, chordae tendinae, or papillary muscle is lacerated. Bolooki et al., while reporting two cases of ventricular septal defects produced by penetrating chest injuries, noted that defects caused by blunt trauma have been reported more frequently in the literature than defects from penetrating trauma.6
In 1971, Simson described the chin-sternum-heart syndrome.7 This syndrome is known to occur in parachutists wearing protective helmets when there is incomplete deployment or partial failure of a parachute. The pattern of cardiac injury, multiple atrial, endocardial and myocardial lacerations, is associated with sternal compression by the chin with laceration of the chin. One of the authors (DJD) has encountered a similar syndrome in individuals who have fallen down stairs, sustaining severe flexion injury to the neck. There is injury to the chin, compression or fracture of the sternum, cardiac injury, and cervical spine fracture with injury to the spinal cord. In some cases of blunt trauma to the chest, the ribs are fractured, with the fractured ends puncturing the heart.
If the pericardial sac is not torn, a laceration of the heart will result in rapid death due to cardiac tamponade. As little as 150 mL of blood can cause death. The resultant increase in the intrapericardial pressure due to cardiac tamponade interferes with the entry of blood into the right heart and produces
mechanical interference with the contractility of the ventricular myocardium. If the pericardial sac is lacerated, bleeding will occur into the pleural cavities.
On rare occasions, blunt force trauma to the anterior chest causes direct injury to a coronary artery, almost invariably the left anterior descending branch. Atherosclerotic vessels are more susceptible to trauma. Injury to coronary arteries can produce coronary occlusion from an intraluminal thrombus, hemorrhage into an atherosclerotic plaque, intimal laceration or a traumatic dissecting aneurysm.8,9 Because of its medicolegal implication, the diagnosis of traumatic coronary thrombosis must be made with caution. Objective evidence supportive of this diagnosis is:
• Injury to the chest wall and/or heart (fracture of the sternum and/or ribs overlying the thrombosed coronary artery, and/or injury to the myocardium adjacent to the thrombosed coronary artery)
• An incomplete tear of the wall of the thrombosed coronary artery, especially if survival is greater than 8-12 h and a myocardial infarction is present
• Finding the age of the infarct, when observed microscopically, to be consistent with the time interval between alleged coronary artery injury and death
In addition, serial electrocardiograph studies and cardiac enzyme determinations consistent with the time interval from trauma to testing support the hypothesis of injury to a coronary artery. It must not be forgotten, however, that posttraumatic coronary artery thrombosis may occur not as a primary complication of trauma but secondary to shock and intravascular stasis of blood, factors that are conducive to thrombus formation in victims with coronary atherosclerosis.
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