Printed in the USA * Copyright 0 1990 Pergamon Press plc
The Journal of Emergency Medicine, Vol. 6, pp. 617-623, 1990
Contmversles in Trauma Management
BLUNT TRAUMA TO THE HEART: THE PATHOPHYSIOLOGY OF INJURY Jason G. Nirgiotis,
MD,
Rolando Colon,
MD,
and Michael S. Sweeney,
MD
Division of Cardiothoracic Surgery, Department of Surgery, University of Texas Medical School at Houston, Houston, Texas Reprint address: Jason G. Nirgiotis, MD, The Department of Surgery, The University of Texas Medical School at Houston, 6431 Fannin, Suite 4020, Houston, TX 77030
0 Abstract - Blunt iduties to the heart are common and potentially lethal. These injuries often go undetected while more obvious problems are treated. A cardiac htjury should be suspected in any patient who sustains severe chest trauma. The spectrum of cardiac trauma ranges from injuries with no actual ceihdar damage (myocardial concussion) to cardiac chamber rupture. The pathophysiology, diagnosis, and treatment of these injuries are discussed.
the heart, roots of the great vessels, trachea and proximal bronchi, and the thoracic aorta and esophagus. It is protected by the sternum anteriorly and the thoracic vertebrae posteriorly. Although enclosed within bony structures, the mediastinal viscera are subjected to acute compressive forces or lacerations after direct blows or an impact associated with sudden deceleration. The damage inflicted to the heart by blunt trauma can be structural, functional, or both. The extent of this damage is proportional to the magnitude of deceleration or impact, the duration of exposure to these forces, and the rate of time change (3). Blunt cardiac trauma is produced by direct blows to the precordium with or without sternal or rib fractures, acute compression between the sternum and vertebrae, laceration following fracture of the sternum or ribs, and indirect forces following acute compression of the lower body (4). These forces can induce major changes in vasomotor tone and perfusion distributions of the coronary vasculature. Using radioactivity labeled microspheres in a swine model, Liedtke et al showed that the mean percentage epicardial blood flow in the impact zone increased significantly as compared with pretrauma values (5). Conversely, mean percentage endocardial flow decreased progressively and significantly from pretrauma levels. This redistribution of small vessel blood flow results in a picture similar to that of early myocardial ischemia and hypoxia. This can result in ischemia or necrosis of an area of myocardium with subsequent dysrhythmia, aneurysm formation, or rupture.
?? Keywords - blunt trauma; cardiac trauma; myocardial concussion; myocardial contusion; cardiac chamber rupture INTRODUCTION Blunt cardiac injury remains a major cause of morbidity and mortality in blunt trauma. It may be the mechanism of death in as many as 16% of fatal motor vehicle accidents (l), and its incidence may be as high as 76% in patients with severe bodily trauma (2). In the initial management of patients with blunt trauma, attention is focused on injuries to the head, extremities, lungs, and abdominal viscera. As a result, cardiac injury is the most common unsuspected visceral injury following blunt trauma (3). MECHANISMS
OF INJURY
CARDIAC
IN BLUNT
TRAUMA
The thoracic cage provides an anatomical bony protection for its underlying viscera. The mediastinum contains
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Controversies in Trauma Management provides a forum for the discussion of current and controversial issues in the management of trauma. This section is coordinated by William H. Campbell, MD, FRCPC, of University of Florida Health Science Center-Jacksonville. Jacksonville. Florida.
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Jason G. Nirgiotis, Roland0 Colon, Michael S. Sweeney
In general, blunt cardiac injury is not immediately fatal unless an acute life-threatening dysrhythmia or cardiac rupture occurs (6). The most common fatal dysrhythmia demonstrated in experimental models of blunt cardiac injury is ventricular fibrillation (7). Although the animal is able to support life, in other experiments with blunt cardiac injury, there is significant impairment of left ventricular function (8). In one study, cardiac output decreased 40% in animals that survived as long as one hour (9). Recovery to normal cardiac function in surviving animals took 2 to 3 weeks. This impairment can be more significant when an elevated pulmonary vascular resistance is present, a situation that occurs frequently in combined cardiopulmonary blunt trauma (10,ll). In the presence of elevated blood alcohol levels, the deleterious effects of injury on myocardial function are amplified. In animals pretreated with alcohol, an otherwise nonlethal cardiac contusion produces electromechanical dissociation (EMD) and a high mortality (12). In studies in dogs, alcohol causes significant reductions in cardiac index and elevations in total peripheral resistance (13,14). When subjected to cardiac trauma with blood alcohol levels of 60 mg%, 120 mg%, and 180 mg%, these animals have mortality rates related primarily to EMD of 17%, 50%, and 71%, respectively. Since trauma alone has been shown to cause significant reductions in both systemic arterial pressure and cardiac index that do not evoke peripheral reflex compensation (15), one mechanism for the excitation+ontraction decoupling that causes EMD may be that alcohol diminishes the sensitivity of cardiac reflexes even further through its potent depressant action on the central nervous system (14). In addition, alcohol has been shown to be a myocardial depressant, and rats given intraperitoneal alcohol demonstrate significant uncoupling of oxidative phosphorylation in cardiac mitochondria (16). The range of blunt cardiac injury can be subdivided into several distinct pathologic entities. These include myocardial concussion, myocardial contusion, cardiac chamber rupture, and other blunt cardiac injuries (coronary artery occlusion and rupture of valves, chordae tendinae, interventricular septum or pericardium).
MYOCARDIAL CONCUSSION Myocardial concussion, also known as commotio cordis, is relatively rare and was first described by Schlomka and Hinrichs in 1932 (17). They produced ventricular fibrillation in experimental animals by direct precordial trauma, yet at autopsy there were no morphologic changes in the myocardium. This lack of myocardial cellular damage, assessed both histopathologically and
chemically, is what distinguishes myocardial concussion from contusion (18). Despite no actual myocardial damage, a fatal ventricular arrhythmia may occur. This results from acute alterations in coronary blood flow, possibly from reflex coronary vasoconstriction and abnormal autonomic responses (19). Because there is no cellular damage, CPK isoenzymes are normal and diagnosis is dependent on ECG and clinical findings. The treatment of concussion is similar to the treatment of contusion, as is discussed in the next section.
MYOCARDIAL CONTUSION Myocardial contusion is estimated to occur in approximately 20% of patients who sustain nonpenetrating chest trauma (20,21). It is the most common lesion encountered in significant blunt cardiac trauma. The lesion is caused by a direct impact to the sternum, which results in a sudden reduction of the anteroposterior diameter of the mediastinum. The mechanism of impact is usually a deceleration injury, as in a motor vehicle accident or a fall, or a direct blow with a blunt object. The right ventricle is most commonly affected because of its position immediately behind the sternum. By definition, myocardial contusion results in structural damage similar to that found in acute myocardial infarction. Grossly, the zone of contusion appears as an area of myocardial hemorrhage with extravasation of red blood cells between the muscle fibers. The superficial changes may reflect only a small portion of the underlying structural damage (20). Microscopically, there is cell necrosis and fragmentation, with an infiltrate of polymorphonuclear leukocytes (3). The transition zone between contusion and normal myocardium tends to be more abrupt than that seen in ischemic myocardial I infarction. In postmortem studies on dogs following blunt chest trauma, Chiu and coworkers report large collections of contrast material in the terminal branches of vessels in the area of damaged myocardium (6,22). Morphologic examination shows that these collections are actually newly formed dilated vascular channels or giant capillary-sinusoids. Within 72 hours after injury, a second type of histologic vascular pattern appears consisting of small new vessels in granulation tissue. These vascular changes persist in the myocardium examined 7 days after injury. These new vessels are similar to the dilated collateral vessels found in response to the stimulus of cardiac hypoxia described in the review of circulation to the myocardium by Mautz (23). The opening of these arteriovenous commumcations results in a fall in distal
Blunt Trauma to the Heart
coronary resistance and an increase in flow to the area of injury. This preferential overperfusion of the epicardial layers of myocardium at the expense of subendocardial perfusion is similar to that occurring in the early evolutional phase of myocardial ischemia (5). An adynamic zone is formed from this healing of myocardial contusion with patchy scar interspersed with normal myocardium. This may be the result of injury and repair in the presence of normal or enhanced circulation. Depending on the severity of the injury, these areas may go on to full thickness necrosis, although usually they remain as an area of patchy, irregular fibrosis (18). These adynamic areas can become the focus of ventricular dysrhythmias, or may remain as an area of weakness susceptible to the development of a ventricular aneurysm (24). In a study of coronary angiography in dogs following blunt cardiac trauma, it was shown that injuries to the epicardial vessels occurred in all animals (25). Injury was limited mostly to the branches of the left anterior descending and right coronary arteries, sparing the left circumflex artery, which was posterior to the site of impact. These injuries become angiographically evident between 3 hours and 3 days after impact and usually are completely resolved after 2 to 5 weeks. Further studies showed that dogs subjected to blunt cardiac impact have depressed hemodynamic measurements (left ventricular end-diastolic pressure, left ventricular positive and negative rates of charige of pressure, and left ventricular ejection fraction) at 3 hours after impact and recover gradually to near normal levels at 2 to 5 weeks after trauma (26). Recovery of left ventricular performance occurs in spite of residual patchy scarring in the region of impact. Studies on the hemodynamic adaptation to acute myocardial contusion have demonstrated that patients with defects of right ventricular (RV) wall motion defined by gated cardiac scintigraphy have significantly lower RV ejection fractions and evidence of RV systolic dysfunction (higher RV end-systolic volume) than those patients with normal ventricular wall motion (10). However, RV stroke work and RV pump function are similar between the groups due to a larger RV preload (higher RV end-diastolic volume) in the contused patients. The right ventricle’s adaptation by the Frank-Starling mechanism may help account for the fact that most patients with myocardial contusion do not have any clinical hemodynamic instability. The optimal method for diagnosing myocardial contusion is a subject of debate, and multiple diagnostic modalities have been suggested. From a clinical standpoint, the diagnosis should be suspected in any patient who has sustained blunt chest trauma in which the mechanism for cardiac injury is present. Patients with
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associated thoracic trauma such as sternal fractures, multiple rib fractures, chest wall contusions, pulmonary contusion, or signs of a mediastinal hematoma, should also undergo evaluation for possible cardiac injury. In one study of patients with traumatic thoracic aortic rupture, it was found that 8 of 13 (62%) patients had an associated cardiac contusion (27). Precordial chest pain, similar to the ischemic pain of angina or acute myocardial infarction, can be the presenting symptom. The most common sign associated with myocardial contusion is sinus tachycardia, but this finding is not helpful in the traumatized patient (18,20). The most commonly accepted criteria for the diagnosis of myocardial contusion are CPK-MB fractions greater than 5% coupled with ECG abnormalities. An electrocardiogram can be obtained rapidly in the emergency department and may show multiple types of supraventricular and ventricular dysrhythmias. Besides sinus tachycardia, there may be premature atria1 and ventricular contractions, or right bundle branch block (18). Irritability of the myocardium in the absence of acidosis or electrolyte imbalance is an important sign of myocardial contusion. A CPK-MB level of over 5% of the total CPK indicates that there has been some damage to myocardial tissue and is predictive for actual structural damage (28,29). The CPK-MB fraction reaches its highest level at approximately 24 hours and returns to normal within 72 hours after injury. False elevations of CPK-MB levels can occur following crush injuries or severe tongue injuries in head and neck trauma (18). Two-dimensional echocardiography has emerged as a useful tool in the evaluation of patients with blunt cardiac trauma (30). Morphologic and dynamic sequelae are readily detected non-invasively. An abnormal echocardiogram can show right and left ventricular dyskinesia secondary to myocardial contusion, as well as segmental areas of abnormal wall motion. It is also useful to detect pericardial effusions, ruptured valves, ruptured ventricular septum, and the development of posttraumatic ventricular aneurysms, a late sequela of myocardial contusion (31,32). In King and colleagues’ study, 47% of patients with positive isoenzymes had detectable echocardiographic abnormalities (33). Other studies have been used to diagnose myocardial contusion with variable success. Radionuclide ventricular angiography with intravenous technetium-99m was studied by Harley et al in a high risk group of trauma patients (34). Although 75% of the first-pass tests were abnormal, only 23% of these patients had abnormal ECGs, and none had positive CPK-MB fractions. Thus, it appears that this test is more sensitive at detecting myocardial dysfunction when there is no actual cellular damage, that is, in myocardial concussion. Go et al
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screened eight patients for contusion with nuclear technetium pyrophosphate scans and found two positive results (35). This examination is not very sensitive and is not used routinely (36). Bodin and coworkers demonstrated 38 of 55 patients with blunt chest trauma to have positive thallium 201 myocardial scintigraphy, all of whom also had dysrhythmias or ECG abnormalities (37). From a review of the literature it is evident that the optimal methods of diagnosis and management of myocardial contusion have not been agreed upon. It would seem prudent that any patient with a history and clinical evidence of severe blunt thoracic trauma be screened for myocardial injury. At our institution and others, these patients are screened with an initial 1Zlead ECG and continuous cardiac monitoring for 24 hours (38,39,40). An initial screening ECG is useful, since patients at risk for complications may be identified by ECG abnormalities that are present on arrival to the emergency department (41). In addition, CPK with isoenzymes are checked every 6 to 8 hours after injury for 24 hours (39,42,43). Some authors have claimed that CPK-MB fractions are not a useful screening test for myocardial contusion. In a retrospective study, Keller et al find no relationship between the MB fraction and either ECG signs of myocardial contusion or MUGA scan abnormalities (44). Mooney and coworkers suggest that there is no actual myocardial damage and that the myocardium is only mechanically “stunned” since they find no correlation between contusion diagnosed by first-pass radionuclide angiography and either ECG changes or MB fractions (45). This theory contradicts the previously reported experimental and clinical data that shows myocardial damage at a cellular level both chemically and histopathologically ( 18,20,25,28). In an experimental animal model, Baxter et al demonstrate that increasing amounts of force result in increasing degrees of contusion with increasing electrical instability and irreversible myocyte damage reflected by cardiac enzyme release (46). Clinically, Healy and coworkers conclude that “high-risk” patients can be identified by the height of the CPK-MB fractions (47). In their review of 342 patients they find a strong correlation between CPK-MB elevation and the development of cardiac complications, with a 100% incidence of complications when the CPK-MB levels were > 200 mcgL. If both the ECG and CPK-MB fractions are normal during the initial 24 hours, myocardial injury can be excluded (48). If either the ECG or CPK-MB fractions are abnormal, or dysrhythmias occur, an echocardiogram is performed (33,38,39). Some groups have suggested that an echocardiogram be performed as a screening examination on all patients suspected of having a myocardial injury (40). The echocardiogram is performed at
Jason G. Nirgiotis, Roland0 Colon, Michael S. Sweeney
the bedside within 48 hours of admission. As mentioned earlier, myocardial contusion is defined by myocardial cellular damage, assessed either histopathologically or chemically (CPK-MB fractions) ( 18). If the ECG is abnormal or dysrhythmias occur, but both the CPK-MB fractions and the echocardiogram are normal, this is considered a severe myocardial concussion, since there is no evidence of cellular damage. These patients receive continuous cardiac monitoring for 24 hours and a repeat 1Zlead ECG in 24 hours. If there is no progression of abnormalities, no further workup or hospitalization is needed (43). If the CPK-MB fractions are positive but the echocardiogram is normal, the patient is classified as a mild myocardial contusion (42). If the echocardiogram is positive, this is classified as a severe myocardial contusion. All patients with a diagnosis of contusion should be admitted to the hospital for continuous cardiac monitoring in an intermediate care unit for 48 to 72 hours or until their CPK-MB fractions return to normal (38,39). As with myocardial infarction, bedrest is essential, and dysrhythmias should be treated appropriately (39). While in the hospital, repeated physical examinations (and echocardiograms if the initial one was abnormal) can help detect some complications associated with myocardial contusion. The appearance of a new murmur will point to the presence of a ruptured intraventricular septum, valve leaflet, or chordae tendinae. Friction rubs can be the result of traumatic pericarditis, which is usually self-limiting. Some reports have suggested the development of atherosclerotic heart disease as a delayed complication of myocardial contusion (6,49). Emergency operations for associated injuries should be undertaken, and inotropic support instituted as needed (50). In a study on the risks of anesthesia, evidence of myocardial contusion by 2-D echocardiogram correlate with an increased incidence of hemodynamic instability (hypotension with increased CVP, dysrhythmia) both before and after anesthesia (51). However, with proper pharmacologic and fluid treatment, these patients have no additional morbidity or mortality, and had no cardiac symptoms at a followup of 10 months. A pulmonary artery catheter can be useful in the diagnosis and treatment of hemodynamic instability in these patients. In the presence of cardiogenic shock unresponsive to medical support, an intra-aortic balloon pump device can be helpful (50). The degree of cardiac impairment caused by a myocardial contusion is directly dependent on the amount of myocardium that is damaged. Experimental data suggests that death occurs within minutes to hours if greater than 50% of the ventricular mass is contused (52). However, if the damaged area is limited, myocardial contusion carries a low morbidity and mortality.
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Blunt Trauma to the Heart
BLUNT CARDIAC RUPTURE Cardiac rupture following blunt trauma is ram. Only 0.5% (14 of 2,751) of all patients with blunt trauma during a 6-year period reviewed by Fischer’s group had recognized blunt cardiac rupture (53). Nonpenetrating myocardial rupture is the result of a sudden forceful compression of the heart between the sternum and vertebra resulting in direct injury, or a sudden increase in intracardiac pressures following acute compression of the lower body (cave-in injuries). In the original studies of Bright and Beck, each of the four cardiac chambers were injured with equal frequency (4). However, a later review of all survivors shows the distribution of injuries to be as follows: right atrium 50%, left atrium 24%, right ventricle 17%, and left ventricle 9% (54). Maximal burst energy by compressive forces is probably achieved when direct pressure is applied while the atrioventricular valves are closed in end diastole or late systole. Ventricular rupture is most often caused by precordial impaction and probably results from forceful compression of the heart during end-diastole when the ventricle is maximally filled (53). Conversely, it appears that atria1 rupture results primarily from rapid deceleration. The atria rupture at the junction of the atria and the insertion of the vena cava or pulmonary veins (53). When atria1 rupture is caused by compressive forces, it most likely occurs when the heart is compressed during late systole with the mitral and tricuspid valves closed (54). Death is usually the result of tamponade or exsanguination . Patients with blunt cardiac rupture always present with hypotension, and usually have an elevated central venous pressure. Cyanosis of the upper body is an associated sign that is frequently misinterpreted (54). This may be caused by compression of the segment of the superior vena cava within the pericardium, or by compression of the vessels of the upper mediastinum by a mediastinal hematoma. The diagnosis should be assumed in patients who sustain blunt chest trauma and arrive at the emergency department with signs of cardiac tamponade. There is no time for complex diagnostic procedures, and decompressive pericardiocentesis should be immediately performed. This allows for a major temporary improvement in hemodynamics and the patient is then promptly transported to the operating room for definitive repair. If the patient loses vital signs during transport from the scene or shortly after arrival to the hospital, emergency department thoracotomy is indicated. When surgical intervention can be performed in the operating room, a median stemotomy is the incision of choice. Repair of atria1 perforations is by simple suture techniques after control with a vascular clamp. Ventric-
ular ruptures are controlled with digital compression and repaired with individually pledgeted nonabsorbable sutures. While in the operating room, the left mediastinal pleura should be inspected for the presence of a mediastinal hematoma or other evidence of aortic transection seen in 20% of patients with blunt cardiac rupture (55). Morbidity and mortality from blunt rupture of the heart remains high, with most patients dying prior to transport to an emergency department (56). In an autopsy series, only 6.5% (23 of 353) of patients with traumatic cardiac rupture survived for more than 30 minutes following injury (57). Survival rates for patients who reach the hospital alive range from 70% (55) to 50% (53), to 15% (58). OTHER BLUNT CARDIAC INJURIES Rupture of the pericardium from blunt trauma is infrequent and usually associated with cardiac injury (59). Rarely, however, an isolated lesion occurs resulting in hemiation of the heart through the pericardial defect. Munchow et al reported two cases of patients successfully resuscitated from cardiac arrest caused by hemiation of the heart (60). In patients who develop congestive heart failure or persistent murmurs after severe blunt trauma, rupture of the cardiac valves or ventricular septum should be suspected. These injuries are most easily diagnosed by echocardiogram. If an injury is found, angiography and elective repair may then be performed. The interventricular septum is most susceptible to rupture if the trauma occurs during late diastole or early systole (61). Injury of the cardiac valves may be from indirect violent compressive force applied to the abdomen and legs, or from direct trauma to the chest (62). Damage to the aortic valve, the most vulnerable to blunt trauma, ranges from laceration or detachment of the cusps from the aortic annulus, to rupture of the annulus (3). Rupture of the chordae tendinae and papillary muscles are the most common mitral valve injuries. These are most likely to occur if the blow occurs when the left ventricle is distended during diastole (63). Valvular incompetence is usually produced by rupture of a valve leaflet or detachment of a commissural attachment. Numerous successful operative repairs of these injuries have been reported (3). Mural thrombosis with subsequent thromboembolism is a potentially lethal complication of blunt cardiac trauma (64). Patients who develop signs of either arterial or pulmonary embolism after blunt chest trauma should be evaluated with a 2-D echocardiogram to rule out an intracardiac mural thrombus (65). If a thrombus is present, the patient should be anticoagulated, if not otherwise contraindicated.
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Thrombosis of the coronary arteries from blunt trauma is a rare, but potentially lethal injury (66,67). An exact cause and effect relationship between trauma and coronary occlusion has been difficult to prove partly because of the presence of preexisting atherosclerosis. There have been several reports of occlusion in previously healthy teenagers (68). Treatment is similar to that with other forms of myocardial ischemia from coronary artery disease.
CONCLUSION Blunt chest trauma remains a common injury. A wide range of injuries to the heart may result from this type of trauma. An appropriate search for cardiac injury should be made in any patient sustaining blunt trauma to the chest so that diagnosis and treatment can be promptly initiated.
REFERENCES 1. Lienoff HD. Acute coronary thrombosis in industry: direct nonpenetrating injury with report of injury. Arch Intern Med. 1942;70: 33-9. 2. Sigler LH. Traumatic injury of the heart - incidence of its occurmnce in forty-two cases of severe accidental bodily injury. Am Heart J. 1945;30:459-78. 3. Liedtke AJ, DeMutb WE. Non-penetrating cardiac injuries: collective review. Am Heart J. 1973;86:687-97. 4. Bright EF. Beck CS. Non-penetrating wounds of the heart: clinical and experimental studies. Am Heart J. 1935;10:293-321. 5. Liedtke AJ, Allen RP, Nellis SH. Effects of blunt cardiac trauma on coronary vasomotion, reperfusion, myocardial mechanics, and metabolism. J Trauma. 1980;20:777-85. 6. Doty DB, Anderson AE, Rose EF, Go RT, Chiu CL, Ehrenhaft JL. Cardiac trauma: clinical and experimental correlations of myocardial contusion. AM Surg. 1974;180:452-9. 7. Viano DC, Artinian CG. Myocardial conduction system dysfunction from thoracic impact. J Trauma. 1978;18:452-9. 8. Stein PD. Sabbah I-IN, Viano DC, Vostal JJ. Response of the heart to non-penetrating cardiac trauma. J Trauma. 1982;22:364-73. 9. Anderson AE, Doty DB. Cardiac trauma: an experimental model of isolated myocardial contusion. J Trauma. 1975;15:237-41. 10. Sutherland GR, Cheung HW, Holliday RL, Driedger AA, Sibbald WJ. Hemodynamic adaptation to acute myocardial contusion complicating blunt chest injury. Am J Cardiol. 1986;57:291-7. 11. Sutherland GR, Calvin JE, Driedger AA, Holliday RL, Sibbald WJ. Anatomic and cardiopulmonary responses to trauma with associated blunt chest injury. J Trauma. 1981;21:1-12. 12. Liedtke AJ, DeMuth WE. Effects of alcohol on cardiovascular performance after experimental nonpenetrating chest trauma. Am J Cardiol. 1975;35:243-50. 13. Desiderio MA. The potentiation of the response to blunt cardiac trauma by ethanol in dogs. J Trauma. 1986;26:467-73. 14. Desiderio MA. Effects of acute, oral ethanol on cardiovascular performance before and atter experimental blunt cardiac trauma. J Trauma. 1987;27:267-77. 15. DeGroot M, Prewitt RM. Right ventricular contusion: experimental pathophysiology and treatment in an open-chest canine preparation. J Trauma. 1984;24:721-7. 16. Nicholas GG, DeMuth WE. Blunt cardiac trauma: the effect of alcohol on survival and metabolic function. J Trauma. 1980;20: 58-60. 17. Schlomka G, Hinrichs A. Experimentelle Untersuchungen tiber den Einfluss stumpfer Brustkorbverletmngen auf das Elektrokardiogram. Z Gesamte Exp Med. 1932;81:43-61. 18. Tenzer ML. The spectrum of myocardial contusion: a review. J Trauma. 1985;25:620-7. 19. Frazer M. Commotio cordis, revisited. Am J Forensic Med Path. 1984;6:249-5 1. 20. Saunders CR, Doty DB. Myocardial contusion. Surg Gyn Obstet. 1977;144:595-603. 21. Jones JW, Hewitt RL, Drapanas T. Cardiac contusion: a capricious syndrome. AM Surg. 1975;181:567-71.
22. Chiu CL, Roelofs JD, Go RT, Doty DB, Rose EF, Christie JH. Coronary angiographic and scintigraphic findings on experimental cardiac contusion. Radiology. 1975;116:679-83. 23. Mautz FR. Anatomical and physiological considerations in the development of a collateral circulation to the myocardium. Dis Chest. 1957;31:265-85. 24. Stone DL, Fleming HA. Aneurysm of the left ventricle and left coronary artery after non-penetrating chest trauma. Br Heart J. 1983;50:495-7. 25. Sabbab I-IN, Mohyi J, Stein PD. Coronary arteriography in dogs following blunt cardiac trauma: a longitudinal assessment. Cathet Cardiovbiagn. 1988;15:155-63. 26. Sabbah I-IN. Movhi J. Hawkins ET. Stein PD. Loneitudinal evaluation of lefi ventricular performance in dogs f&owing nonpenetrating cardiac trauma. J Trauma. 1989;29:175-9. 27. Kram HB, Appel PL, Shoemaker WC. Increased incidence of cardiac contusion in patients with traumatic thoracic aortic rug me. Ann Surg. 1988;208:615-18. 28. Lindsey D, Navin T, Finley P. Transient elevation of serum activity of MB isoenzyme of CPK in drivers involved in automobile accidents. Chest. 1978;74:15-18. 29. Ravel R. Clinical laboratory manual. 4th ed. Chicago: Yearbook Medical Publishers; 1984:231. 30. Beggs CW, Helling TS, Evans LL, Hays LV, Kennedy FR, Crouse LJ. Early evaluation of cardiac injury by two-dimensional echocardiography in patients suffering blunt chest trauma. Ann Emerg Med. 1987;16:542-5. 31. Miller FA, Seward JB, Gersh BJ, Tajik AJ, Mucha P. Twodimensional echocardiographic findings in cardiac trauma. Am J Cardiol. 1982;50:1022-7. 32. Markiewicz W, Best LA, Burstein S, Peleg H. Echocardiographic evaluation after blunt trauma to the chest. Int J Cardiol. 1985;8: 269-74. 33. King RM, Mucha P Jr, Seward JB, Gersh BJ, Fame11 MB. Cardiac contusion: a new diagnostic approach utilizing two dimensional echocardiography. J Trauma. 1983;23:610-14. 34. Harley DP, Menz I, Miranda R, Nelson RJ. Myocardial dysfunction following blunt chest trauma. Arch Surg. 1983;118:1384-7. 35. Go RT, Doty DB, Chiu CL. A new method of diagnosing myocardial contusion in man by radionuclide imaging. Radiology. 1975;116:107-10. 36. Brantigan CD, Burdick D, Hopeman AR, Eiseman B. Evaluation of technetium scanning for myocardial contusion. J Trauma. 1978;18:460-3. 37. Bodin L, Rouby JJ, Viars P. Myocardial contusion in patients with blunt chest trauma as evaluated by thallium 201 myocardial scintigraphy. Chest. 1988;94:72-76. 38. Frazee RC, Mucha P, Fame11MB, Miller F. Objective evaluation of blunt cardiac trauma. J Trauma. 1986;26:510-20. 39. Sweeney MS, Lewis CTP, Murphy MC, Williams JP, Frazier OH. Cardiac surgical emergencies. Crit Care Clin. 1989;5:659-78. 40. Helling TS, Duke P, Beggs CW, Crouse LJ. A prospective evaluation of 68 patients suffering blunt chest trauma for evidence
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of cardiac injury. J Trauma. 1989;29:961-6. 41. Dubrow TJ, Mihalka J, Eisenhauer DM, et al. Myocardial contusion in the stable patient: what level of care is appropriate? Surgery. 1989;106:267-74. 42. Fabian TC, Mangiante EC, Patterson CR, Payne LW, Issacson ML. Myocardial contusion in blunt trauma: clinical characteristics, means of diagnosis, and implications for patient management. J Trauma. 1988;28:50-7. 43. Kudsk KA, Voeller GR, Mangiante EC, Fabian TC. Myocardial contusion: diagnosis and management. Contemp Surg. 1989;35: 11-16. assays in 44. Keller KD, Shatney CH. Creatinine phosphokinase-MB patients with suspected myocardial contusion: diagnostic test or test of diagnosis? J Trauma. 1988;28:58-63. 45. Mooney R, Niemann JT, Bessen HA, et al. Conventional and right precordial ECGs, creatine kinase, and radionuclide angiography in post-traumatic ventricular dysfunction. Ann Emerg Med. 1988;17: 890-4. 46. Baxter BT, Moore EE, Synhorst DP, Reiter MJ, Harken AH. Graded experimental myocardial contusion: impact on cardiac rhythm, coronary artery flow, ventricular function, and myocardial oxygen consumption. J Trauma. 1988;28:1411-17. 41. Healy MA, Brown R, Fleiszer D. Blunt cardiac injury: is this diagnosis necessary? J Trauma. 1990;30:137-46. 48. Baxter BT, Moore EE, Moore FA, McCroskey BL, Ammons LA. A plea for sensible management of myocardial contusion. Am J Surg. 1989;158:557-62. 49. Lasky I. Forensic aspects of traumatic non-penetrating heart disease. Med Sci Law. 1966;6:132-141. 50. Flancbaum L, Wright J, Siegel JH. Emergency surgery in patients with post-traumatic myocardial contusion. J Trauma. 1986;26: 795-803. 51. Eisenach JC, Nugent M, Miller FA, Mucha P Jr. Echocardiographic - _ evaluation of patients with blunt chest injury: correlation with perioperative hypotension. Anesthesiology. 1986;64:364-6. 52. Utlev JR. Dotv DB. Collins JC. Suaw EA. Wachtel C. Todd EP. Cardiac outpu;, coronary flow, ventricular fibrillation and survival following varying degrees of myocardial contusion. J Surg Res. 1976;20:53943. 53. Martin TD, Flynn TC, Rowlands BJ, Ward RE, Fischer RP. Blunt cardiac rupture. J Trauma. 1984;24:287-90.
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54. Leavitt BJ, Meyer JA, Morton JR, Clark DE, Herbert WE, Hiebert CA. Survival following non-penetrating traumatic rupture of cardiac chambers. Ann Thorac Surg. 1987;44:532-535. 55. Calhoon JH, Hoffman TH, Trinkle JK, Harman PK. Grover FL. Management of blunt rupture of the heart. J Trauma. 1986;26: 495-502. 56. Kulshrestha P, Das B, Iyer KS, et al. Cardiac injuries - a clinical and autopsy profile. J Trauma. 1990;30:203-207. 57. Parmley LF, Manion WC, Mattingly TW. Non-penetrating traumatic injury of the heart. Circulation. 1958;18:371-96. 58. Mattox KL, Von Koch L, Beall AC Jr, et al. Logistic and technical considerations in the treatment of the wounded heart. Circulation. 1975;(suppl I), 51;52:1210-14. 59. Boyd TF, Streider JW. Immediate surgery for traumatic heart disease. J Thorac Cardiovasc Surg. 1965;50:3-7. 60. Munchow OBG, Carter R, Vannix RS, Anderson FS. Cardiac arrest during ventricular hemiation: report of a case of two successful resuscitations. JAMA. 1960;173: 1350-l. 61. Inkley SR, Barry FM. Traumatic rupture of inter-ventricular septum proved by cardiac catheterization. Circulation. 1958;18: 91617. 62. Beck CS, Bright EF. Changes in the heart and pericardium brought about by compression of the legs and abdomen. J Thorac Surg. 1933;2:616-28. 63 Manzzucco A, Rizzoli G. Faggian G. et al. Acute mitral regurgitation after blunt chest trauma. Arch Intern Med. 1983;143: 2326-9. 64 Kertes P, Westlake G, Luxton M. Multiple peripheral emboli after cardiac trauma. Br Heart J. 1983;49:187-9. 65 Timberlake GA, McSwain NE. Thromboembolism as a complication of myocardial contusion: a new capricious syndrome. J Trauma. 1988;28:535-40. 66 Oren A, Bar-Schlomo B, Stem S. Acute coronary occlusion following blunt injury to the chest in the absence of coronary atherosclerosis. Am Heart J. 1976;92:501-5. 67 Jenkins JL, Nishimura A. Coronary artery obstruction inmyocardial infarction resulting from nonpenetrating chest trauma. Tex Med. 1975;71:78-83. 68. Stem T, Wolf RY, Reichart B, Harrington OB, Crosby VG. Coronary artery occlusion resulting from blunt trauma. JAMA. 1974;230:1308-9.