TABLE 2514 Clues to Diagnosis of Blunt Cardiac Injury

BLUNT MYOCARDIAL INJURY Terminology There has been great confusion regarding the appropriate appellation for cardiac injuries related to blunt trauma. The terms cardiac (or myocardial) contusion, cardiac (or myocardial) concussion, blunt myocardial injury, and blunt cardiac injury have all been proposed. Certainly there is a spectrum of injuries to the heart for which the term blunt cardiac injury would be appropriate, if not very specific. Myocardial concussion, sometimes referred to as commotio cordis, suggests no obvious gross or microscopic pathology to explain the phenomenon. However, sudden death from dysrhythmia can occur. The initiating mechanism is usually from a sudden direct force to the chest, while an individual is participating in certain sports (e.g., karate, hockey, etc.). 23 The term myocardial contusion, although somewhat out of favor currently, may in fact have a pathologic definition (see below). The term blunt myocardial injury (BMI), a more encompassing term although not universally accepted, has come into vogue, since myocardial contusion rarely exists in the strictest sense but is often associated with other injuries (e.g., coronary artery thrombosis, infarction related to hypotension). Also, the underlying pathologic definition is less important than determining the cardiac risk profile of patients with blunt chest trauma.

Pathologic Changes The pathologic changes seen in the myocardium typically include subendocardial hemorrhage and a much larger area of focal myocardial edema, interstitial hemorrhage, and myocytolysis with infiltrates of polymorphonuclear leukocytes. The areas most frequently involved are (1) the anterior right ventricular wall, (2) the anterior interventricular septum, and (3) the anterior-apical left ventricle.

Additional myocardial injury may occur if there are concomitant intimal tears or compression from adjacent hemorrhage and edema. Indeed, some feel that much of the myocardial injury seen is due to redistribution of coronary blood flow. Very occasionally, transient hypotension may cause complete occlusion of a previously diseased coronary artery.

Usually there is complete clinical recovery with minimal residual scarring within 3 to 6 weeks of a myocardial contusion. However, in rare cases with severe transmural injury, a ventricular aneurysm may develop.

Physiologic Changes In addition to rhythm and conduction disturbances, some reduction in cardiac output can be found in most victims studied. The degree of cardiac depression is directly related to the mass of contused myocardium. Screening tests, such as the ECG and CPK-MB isoenzymes, usually do not accurately indicate the severity of the injury, nor are they predictive of major morbidity or mortality.

Although there seems to be a great concern about making the diagnosis, most patients with myocardial contusions have relatively little problem. However, occasionally there is a problem with an dysrhythmia, especially premature ventricular contractions (PVCs), atrial fibrillation, or a conduction defect, or there is clinical evidence of heart failure. Such problems are most apt to occur in patients with: (1) preexisting cardiac disease, (2) prolonged general anesthetics, or (3) hypotension because of other injuries.

Diagnosis Methods to diagnose myocardial injury have long been controversial. The variation in sensitivity reported for the various diagnostic tests has two origins. First, the tests require subjective interpretation. Second, there is no "gold standard" for comparison. Overall, significant BMI is an unlikely injury. A recent meta-analysis of studies of blunt cardiac trauma revealed that less than 3 percent of over 2200 patients in 25 prospective studies developed a cardiac complication (defined as requiring treatment or intervention). Most of these were ECG abnormalities (ventricular ectopy, superventricular dysrhythmias, symptomatic bradycardia). The most frequent cardiac rhythm finding, sinus tachycardia, was not considered, as it never required any specific treatment. ECG abnormalities requiring treatment were independently associated with a cardiac complications.24

Since diagnostic criteria (and even terminology) have not enjoyed universal or even general agreement, the focus has appropriately become predicting the likelihood of adverse events.

CLINICAL FEATURES Any patient involved in a motor vehicle accident involving speeds exceeding 35 mph and having any chest symptoms or signs should be suspected of having a BMI. Rarely, a patient with BMI will have angina-like pain that is not relieved by nitroglycerin.

Tachycardia that is out of proportion to the degree of trauma or blood loss may be the first sign of a BMI. Occasionally, an irregular rhythm due to atrial fibrillation or multiple premature atrial or ventricular contractions may be noted. Differentiation from an acute myocardial infarction in older individuals may be difficult in the ED.

RADIOLOGIC EXAMINATION The chest x-ray has its greatest value in the recognition of associated injuries. The closest x-ray correlates of BMI are pulmonary contusion or fractures of the first two ribs, the clavicles, or the sternum. Sternal fractures were thought to have been of importance, but, as noted above, when isolated, they are rarely associated with injury.78

Acute cardiac decompensation may be diagnosed by x-ray evidence of acute pulmonary edema (if the left ventricle is involved) associated with a normal-sized heart. Cardiac tamponade usually does not cause an enlarged cardiac silhouette, but a widened azygos vein is suggestive of this diagnosis.

ELECTROCARDIOGRAPHY As with other tests, the potential value of the ECG is controversial. Suggestions have ranged from a single ED-based ECG to 72 h of continuous ECG monitoring. A recent study of 71 patients with blunt chest trauma (not requiring admission to an intensive care unit) revealed that the initial ECG was predictive of subsequent clinically significant ECG events. Still, an initially normal ECG does not exclude the development of a clinically significant cardiac event, since, most abnormalities will develop within 24 h.25 The most frequent ECG abnormality is sinus tachycardia, although this finding does not suggest increased risk in and of itself. Significant ECG findings include injury pattern, tachydysrhythmias, ST-T wave abnormalities, and ectopy—particularly premature ventricular contractions.

One reasonable approach is to obtain an initial 12-lead ECG. If it is normal, then the patient must be monitored for 4 to 6 h. If there are no untoward events, patients can be safely discharged.26 (Some authorities advocate no further monitoring.) If the ECG is abnormal but there is no hemodynamic instability, the patient should be admitted to a monitored setting, with the 12-lead ECG repeated in 24 h. Some authorities suggest an intervening ECG at 6 and 12 h. Hemodynamic instability suggests an aggressive diagnostic approach (see below). If, at any time, the ECG is abnormal (or changed) or if there is ectopy or dysrhythmia, cardiac monitoring should be continued and a cardiology consult obtained.

CARDIAC ENZYMES Initially there was considerable controversy regarding the value of CPK-MB determination. Its certainly appeared that CPK-MB determinations were of questionable value and likely only to confuse, as they appeared to be of insufficient specificity and sensitivity. 27 Further, elevated MB fractions in this setting do not correlate with the clinical course.

Determination of cardiac troponins has shown promise28 (Fig 2.5.1-6.), has been advocated as a laboratory criterion, and has even been proposed as the "gold standard" for the diagnosis of BMI. These determinations have been shown to have greater specificity for myocardial injury than CK-MB or myoglobin. However, the issue at this time appears no clearer than it was for CK-MB. A recent study found that troponin T (TT) had a specificity of 91 percent in predicting clinically significant ECG changes among those with blunt thoracic trauma, but the sensitivity was only 27 percent.25 The authors concluded that TT determinations were useful. Using different criteria for the diagnosis of "myocardial contusion" (rather than untoward events), another study found very similar sensitivity (31 percent) and specificity (91 percent), minimally better than CK-MB.29 The authors of the latter study conclude that TT has no important diagnostic value. More recent work suggests the sequential TT and troponin I (TI) may improve predictability for adverse events and need for intensive monitoring. There is intensive work in this area, but—as with other diagnostic tests—lack of agreement on definition or other end points; in the case of troponin, appropriate cutoff values and the type of assay used will continue to veil its potential usefulness.

FIG. 251-6. Highest value of MBCK found (peak), peak MBCK to total CK ratio, and highest value of cTnI. Open circles indicate patients without cardiac contusion; solid circles indicate those with contusion. Heavy horizontal lines indicate upper reference limits for each parameter. (From Adams et al,28 reprinted with permission.)

ECHOCARDIOGRAPHY A recent detailed review concludes that echocardiography does not appear to be useful as a primary screening modality in the identification of patients likely to develop complications from myocardial injury.30 It may well be the most sensitive test, but observed wall motion abnormalities often resolve and are usually clinically insignificant. However, patients who do develop cardiac complications may benefit from echocardiographic evaluation. Thus, the current recommendation is to use echocardiography in selected patients who demonstrate cardiac dysrhythmias or dysfunction.31 While myocardial wall motion abnormalities may be present in stable patients with blunt chest trauma, this finding alone does not seem to predict the likelihood of a complication.

OTHER DIAGNOSTIC TESTS Technetium-labeled pyrophosphate scanning, thallium single-photon-emission computed tomography, and radionuclide angiography have all been controversially discussed in the literature. They do not appear to have any greater front-line diagnostic value than the diagnostic adjuncts already discussed.

Summary of Diagnostic Approach There is no consistent standard of care to advocate at this time. Certainly the trend toward identifying patients who require intensive monitoring or who are at higher risk for adverse events is better than trying to arrive at a diagnosis (BMI) that has poor clinical correlation. Certainly all patients should have a CXR. Any abnormalities found will help to stratify patients for risk and allow consideration of other diagnoses. All patients should have a 12-lead ECG and be initially monitored. A conservative practice would be to monitor all patients with significant chest wall trauma for up to 24 h, although, based on the current literature, 4- to 6-h of cardiac monitoring would be acceptable in patients who have been hemodynamically stable throughout. Patients with abnormal ECGs merit continued monitoring, serial 12-lead ECGs, and consideration for echocardiography. It is difficult to recommend outright the routine use of cardiac enzymes for screening purposes, although one cannot be faulted for considering cardiac troponin determination, particularly for delayed diagnosis. The reader is advised to stay abreast of this rapidly developing modality.

Patients with hemodynamic compromise at any time should not only be monitored in an intensive care unit setting, but also warrant echocardiography and a cardiac consultation for further diagnostic and therapeutic options.

Treatment Although some patients will require treatment of heart failure or rhythm or conduction disturbances, specific treatment interventions are seldom required. In general, blunt cardiac injuries cause death very rarely, as noted elsewhere, 24 and the incidence of clinically significant dysrhythmias or other cardiac complications is generally greatly overestimated.

Supplemental oxygen should be administered as needed to maintain the arterial P o2 above 80 mmHg, and analgesics should be given as needed to reduce excessive pain. Coronary vasodilators should not be used unless the patient has suspected preexisting coronary artery disease. Cardiac dysrhythmias should be diagnosed early and treated appropriately. Prophylactic treatment of dysrhythmias is not indicated. Low cardiac output or hypotension should be treated with fluids or inotropic agents as indicated.

In the absence of dysrhythmias or hemodynamic instability, patients with BMI can safely undergo surgical procedures if the pulmonary artery wedge pressure and cardiac output are closely monitored.

If the patient remains in a low-output state despite adequate fluid resuscitation, inotropic support, and correction of any mechanical problems such as tamponade, use of an intraaortic balloon counterpulsation device should be considered.

There is some question as to whether patients with a myocardial contusion and an intramural thrombus seen on two-dimensional echocardiography should have prophylactic anticoagulation if not otherwise contraindicated. In limited studies, patients with echocardiographically proven right ventricular thrombi did not develop subsequent systemic or pulmonary embolization. Furthermore, anticoagulation is contraindicated in most cases of multiple trauma because of the potential for severe hemorrhage.

OTHER BLUNT CARDIAC INJURIES Cardiac rupture is the most frequent finding at autopsy in patients dying at the scene, and up to 90 percent with this injury die at the scene. Among those who reach the hospital, a few arrive seemingly stable. Most of these patients will deteriorate suddenly and resuscitation will most likely be unsuccessful. The diagnosis is suggested when shock is out of proportion to the degree of recognized injury despite attempts at hemorrhage control and volume repletion. Immediate thoracotomy and surgical repair is the only hope for a successful outcome.

Septal defects are rare but may be evident when a systolic murmur is heard and an infarct pattern is seen on the ECG. An ultrasound exam may also prove helpful. The diagnosis can be suspected when hypoxemia is severe with a normal CXR. Patients with atrial septal defects are unlikely to survive.

Rupture of the aortic valve is the most common valvular lesion found in patients who survive nonpenetrating cardiac injury. Patients with bioprosthetic heart valves are particularly likely to have traumatic valve injury. The next most frequent blunt valvular injury is laceration of a papillary muscle or the chordae tendineae of the mitral valve. The prognosis for rupture of a mitral papillary muscle or a mitral valve leaflet is grave, and death usually occurs within a few days after injury.

Direct injury to the coronary arteries from blunt chest trauma occurs very rarely, but if it causes pericardial tamponade or intrathoracic bleeding, immediate operation is required. Coronary artery thrombosis is also rare but has been reported. Coronary artery spasm does not appear to occur.

The incidence of major cardiac injury from blunt trauma resulting in cardiac tamponade or acute hemopericardium at autopsy has been reported to be about 6 percent. Hemopericardium or pericardial effusion with or without frank tamponade can occur without any evidence of blunt cardiac injury. This may develop acutely or may be delayed for more than a week. As with other causes of pericardial effusion, the rate of fluid accumulation is the main determinant of its hemodynamic consequences. In some instances, only echocardiography or autopsy provides the diagnosis. Small posttraumatic pericardial effusions can be seen with many cardiac injuries following blunt chest trauma but are usually of little or no consequence. They generally remain asymptomatic and resolve without any therapy. In rare instances, a patient may develop late constrictive pericarditis, occasionally with extensive calcification of the pericardium.

FOLLOW-UP It is important that patients with proven or suspected cardiac injury be closely observed, not only throughout their hospital stay but also later, for undiagnosed injuries or complications. One should look particularly for posttraumatic pericarditis, ventricular septal defect, valvular defects, and ventricular aneurysms.

POSTPERICARDIOTOMY SYNDROME Etiology and Pathogenesis The cause of the postpericardiotomy syndrome (PPCS) is still largely unknown, but it may be a delayed hypersensitivity reaction to the presence of damaged myocardium in the pericardial cavity. This damaged tissue can act as a foreign protein, inducing the production of autoantibodies against similar tissues. In fact, antimyocardial antibodies can be measured, and their serum concentration varies with the severity of the symptoms. Autogenous blood and lipids in the pericardium can also set up an inflammatory response that may be a contributing factor.

Diagnosis PPCS should be suspected in individuals who develop chest paint, fever, and pleural or pericardial effusions 2 to 4 weeks after cardiac trauma (or heart surgery). Patients may also have friction rubs, arthralgia, and pulmonary infiltrates. The blood count often shows a leukocytosis, and the ECG will often show ST-T wave changes consistent with pericarditis.

Treatment Treatment is primarily symptomatic. Salicylates and rest can often reduce symptoms dramatically within 12 to 24 h, but glucocorticoids are occasionally required. Rarely, drainage of pleural or pericardial fluid may be required to relieve symptoms or rule out other problems.

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