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Journal club: Myocardial contusion
Journal Club: Myocardial Contusion RICHARD N. NELSON, MD, ROBERT BEHRENDT, DOUGLAS A. RUND, MD Ohio State University
College
of Medicine
Spectrum of myocardial contusion. Torres-Mirabal P, Gruenberg JC, Brown RS, et al. Am Surg 1982;48:383392. The authors studied 282 consecutive patients with blunt chest trauma who were admitted to a trauma service over a 26-month period. The first 56 patients, studied retrospectively, had discharge diagnoses of blunt chest trauma or myocardial contusion; the subsequent 226 patients were evaluated prospectively. The second group was included in the study population because their admission diagnosis included significant blunt chest trauma. They underwent electrocardiography (ECG), creatinine phosphokinase (CPK) determinations, and CPK-muscle brain (CPK-MB) isoenzyme studies on admission and twice daily for three days. Myocardial contusion was the diagnosis in 42 of the patients based on abnormal ECG (36 patients), elevated CPK (29 patients), or positive CPK-MB results (33 patients). Four of 56 (7%) of the patients in the retrospective group and 38 of 226 (17%) of the patients in the prospective group had their conditions diagnosed using these criteria. The investigators determined that the total incidence of myocardial contusion using these criteria was 15%. The most common ECG abnormalities were non-specific T-wave changes, inverted T-waves, and sinus tachycardia. Less frequent abnormalities were incomplete right bundle branch block, sinus bradycardia, left anterior hemiblock, left axis deviation, premature ventricular contractions, left ventricular strain, third degree atrio-ventricular (A-V) block, second degree A-V (Wenckebach) block, atria1 fibrillation, and atria1 flutter. The total CPK was elevated on admission in 35 of these patients, and subsequently became elevated in three patients. The CPK was not determined in three patients. The CPK-MB result was positive in 35 patients, negative in three patients, and not tested in two patients. In two patients, the CPK-MB result was considered falsely positive because total CPK was greater than 2,000 IU/l. Twenty-nine patients with an abnormal ECG and either increased total CPK or positive CPK-MB underwent right and left ventricular function studies following Swan-Ganz catheter placement.
From the Division of Emergency sity, Columbus, Ohio.
Medicine,
Ohio State Univer-
Address reprint requests to Dr. Rund: Division of Emergency Medicine, Rhodes Hall, University Hospitals, 450 W. 10th Ave., Columbus, OH 43210. 588
MD,
Twelve patients were considered hemodynamically stable and were not studied. One patient died intraoperatively shortly after admission. Eight patients had cardiac index determinations only. Three of these patients had cardiac indices less than 2.9 Ymin/m*. Twenty-one patients received a fluid challenge of 500’ ml of 5% plasmanate solution over 30 minutes to construct Starling curves. Six patients showed biventricular dysfunction. Six patients showed isolated right ventricular (RV) dysfunction, three patients had isolated left ventricular (LV) function, three patients had an upslope-peak-downslope function pattern, and three patients showed normal ventricular function curves. In addition, 22 patients underwent multiple gated acquisition (MUGA) scans. Results of 12 scans were normal, and those of 10 scans were abnormal. Six patients with normal scan results had abnormal ventricular function study results. Of the ten patients with abnormal scan results, one had a normal cardiac index, four had failing ventricular function. two had depressed cardiac indices, and three patients did not have cardiac indices determined. Seven of 42 patients (17%) suffered major morbidity or mortality. Biventricular dysfunction was present in three of these patients, left ventricular dysfunction was present in one, low cardiac index (c2.91 min/m*) was present in two patients, and no determinations were made on the one patient who died introperatively. The authors conclude that ECG, total CPK, and CPK-MB determinations are sensitive in detecting myocardial contusion following blunt chest trauma. However, these determinations are not predictive of major morbidity and mortality. Only direct hemodynamic measurement was found to be useful in identifying those patients at greatest risk.
Commentary Dr. Murk Smith: The main point of this article is to determine which patients with myocardial contusion are at greatest risk for developing serious complications. However, I cannot justify the author’s conclusion that only direct hemodynamic measurements and construction of Starling curves are useful in identifying those patients at greatest risk. Consider, for example, that ventricular function curves of 18 out of 21 patients were abnormal. However, ventricular function studies were done only on four of the seven patients with major morbidity and mortality. All four of these patients had abnormal re-
THE LITERATURE
sults. Therefore, the sensitivity of abnormal ventricular function curves for predicting major morbidity and mortality was 100% (4/4), but the specificity was only 22% (4/18). If we look at the same considerations for cardiac index, six of the patients with major morbidity and mortality had cardiac indices measured. Four of these six had cardiac indices of less than 2.9; two were greater than 2.9. In addition, one patient of the 29 who had cardiac index determinations was below 2.9, yet did not have major morbidity or mortality. Therefore, the sensitivity of cardiac index in predicting major morbidity and mortality was 4/6, or 67%. The specificity was 415 or 80%. We can consider results of MUGA scans in the same manner. Such MUGA scans were done in 22142 patients, and results were abnormal in ten. Of seven patients with major morbidity and mortality, only three underwent MUGA scans, and results of all three were abnormal. This gives a sensitivity of 100% (313) and a specificity of 30% (3/10). Therefore, both cardiac index and MUGA scans may have been as good as, or even better than, ventricular function curves in predicting major morbidity and mortality. However, the sampling methods used by the authors do not allow one to reach any conclusions. Myocardial contusion-Implications for patients with multiple traumatic injuries. Snow N, Richardson JD, Flint LM. Surgery 1982;92;744-750. The authors prospectively studied 300 consecutive patients with suspected blunt chest trauma who were admitted to a trauma service over an 18-month period. Of the 300 patients, 41 (14%) were diagnosed as having myocardial contusion based on an abnormal electrocardiogram (ECG) and/ or serial creatinine phosphokinase isoenzyme (CPK-MB) levels greater or equal to 5% of the total CPK activity. Of these patients, 30 (73%) showed external signs of chest trauma (contusions, abrasions, palpable crepitus, rib fractures, or visible flail segments). Twenty-seven patients (66%) had associated thoracic injuries (hemothorax, pneumothorax, rib fractures, flail chest, or pulmonary contusion), 37 patients (90%) incurred extrathoracic injuries, and 20 patients (49%) complained of non-specific chest pain. Of the 41 patients with a diagnosis of myocardial contusion, 34 (83%) had abnormalities on initial ECG, and two more patients subsequently developed ECG abnormalities. Such abnormalities included non-specific ST and T wave changes (50%), sinus tachycardia (47%), premature ventricular contractions (25%), ischemic changes (140/o), and some form of conduction block (31%). Thirty-four patients (83%) had CPK-MB greater than or equal to 5% of total CPK level. Of these, 27 had abnormal ECGs. Twenty-seven of the 41 patients required urgent surgery (19 of them within 24 hours of injury). There were no intraoperative deaths, although five patients experienced transient hypotension, and seven had dysrhythmias. Twenty-eight patients (68%) developed cardiac complica-
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tions. Of these, 23 had dysrhythmias
(11 of which were considered “life-threatening”), six experienced congestive heart failure, five had myocardial ischemia, five had pericarditis, and four experienced cardiogenic shock. Treatment modalities included pharmacological inotropic support (seven), electrical therapy for dysrhythmias (three), pacemaker (three), in&a-aortic balloon pump (three), and pericardial window (one). Three patients in this series died. No patient with negative ECG or CPK-MB results had a subsequent clinical course compatible with a serious cardiac contusion. Five of the seven patents with negative CPK-MB results developed serious dysrhythmias requiring intervention. Patients with myocardial contusion were released as soon as their ECG, CPK, and clinical status normalized. Followup showed no residual disability in most patients at four to six weeks. The authors conclude that patients with suspected blunt chest trauma should have serial ECGs and CPK-MB determinations performed if the history or objective findings suggest myocardial contusion. These patients should be monitored in an intensive care or telemetry unit. If, after 72 hours, ECGs and CPK-MB levels are normal and no cardiac problems develop, patients who are otherwise stable may be safely transferred to regular nursing units or home, if appropriate. However, because 68% of patients with myocardial contusion (as defined by the authors’ criteria) sustained significant cardiovascular sequelae, these patients should be carefully monitored. Finally, the authors observe that surgical intervention in patients with myocardial contusion can be safely undertaken with careful perioperative monitoring.
Commentary Dr. Murk Smith: Considering the conflicting results of other studies and the apparently low specificity of all noninvasive testing, I feel that the authors proposed a reasonable and prudent protocol for detecting significant myocardial contusion in patients with blunt chest trauma as well as for monitoring and discharging these patients. Furthermore, they suggest that emergency surgery in these patients may be performed safely, and may actually lessen factors that aggravate compromised cardiac function. It is interesting that the data of this study and that of Torres-Mirabal, both large series, were so similar. In this study, 14% of patients, as compared with 17% in the latter study, were diagnosed as having myocardial contusion. Of patients with myocardial contusion, 83% had ECG abnormalities in this study, as compared with 86% in the latter study. Finally, 83% of patients with myocardial contusion in both studies had elevations of CPK-MB levels. Dr. Richard Nelson: The authors have studied a large series of patients with suspected blunt chest injuries. In the process, they apparently identified a subgroup of patients at particular risk for developing cardiac complications because of cardiac contusion. However, I feel this study would have been improved 589
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by the inclusion of a control group, perhaps consisting of trauma patients without blunt chest injuries, but with similar trauma severity scores. I suspect many of these patients would nonetheless meet the author’s electrocardiographic criteria for cardiac contusion, because many would display ECG abnormalities such as sinus tachycardia and non-specific ST and T wave changes. Further, it would be interesting to see how many patients in the control group would show increased CPK-MB levels either because of direct skeletal muscle damage or indirect cardiac damage caused by shock and hypoxia. This article did not change my opinion that myocardial contusion is a very difficult diagnosis to make. Evaluation of noninvasive tests of cardiac damage in suspected cardiac contusion. Potkin RT, Werner JT, Tro-
baugh GB, et al. Circulation
1982;66:627-631.
The authors prospectively studied 100 patients admitted to the intensive care unit with a diagnosis of non-penetrating chest trauma and at least one of the following: severe chest pain, hemothorax, pneumothorax, or fractured rib, clavicle, or sternum. Noninvasive tests commonly used in diagnosing myocardial contusion were applied to these patients and subsequently evaluated. Tests evaluated were serial ECGs, total CPK, and CPK-MB isoenzymes, continuous Holter monitoring, and Tc-99m pyrophosphate scintigraphy. Fifteen patients in this series died, autopsies were performed on all of them, and the results were then used to determine the accuracy of the noninvasive tests in diagnosing cardiac contusion. Electrocardiograms were obtained on admission and daily for three days. The results were considered abnormal if there were any abnormalities of the ST-segment, T-wave. QT-interval, or atrioventricular or intraventricular conduction. Sinus tachycardia was not included as an abnormal rhythm as is done in many other studies. In addition to serial ECGs, all patients were monitored for dysrhythmias for 24 to 48 hours using continuous Holter monitoring. Cardiac enzymes, including CPK and CPK-MB, were determined for admission and repeated at 12 hours and then daily for three days. A CPK-MB greater than or equal to 2% of total CPK was considered abnormal. All patients received Tc-99m pyrophosphate scans on days one and three of their hospitalization. Using a scale of 0 to 4, 2-4 + discrete uptake was considered positive, 2 + diffuse uptake was equivocal, and 0- 1 + diffuse uptake was negative. Seventy percent of the patients had abnormal ECGs. The most common abnormalities were non-specific ST-T wave changes (SS/lOO or 58%). Intraventricular conduction defects occurred in 16/100 patients (16%), and 11 of these had transient right bundle branch block (RBBB). The remainder had left bundle branch block (two) and intraventicular conduction defect (three). No patient had new Q waves develop. Rhythm disturbances were seen in 73% of patients, 54% had unifocal premature ventricular contractions, and only 27% had complex dysrhythmias (at least Lown grade 3). ‘Iwo patients had transient atrioventricular block, and three pa590
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tients had ventricular tachycardia. Only seven patients received treatment for dysrhythmias, and no patient required temporary pacing. Total CPK ranged from 198 to 200,000 IU/l. The median CPK level was 1,985 IU/l. The CPK-MB fractions ranged from 0 to 1,400 IU/l with a median of 27 IU/l. Seventy-two patients had CPK-MB fractions greater than 6 IU/l, but only 27 had CPK-MB/CPK ratios of greater than 3%. Two patients had positive results on Tc-99m pyrophosphate scans. Five patients had equivocal results; results of the remaining 93 scans were negative. Autopsies were performed on all 15 patients who died. Five of these patients were found to have gross or histological evidence of cardiac contusion. Four of the five patients with necropsy-proven cardiac contusion had ECG changes. However, all ten patients without contusion also had ECG changes. One of the five patients with documented cardiac contusion at necropsy had transient RBBB. One patient had ventricular tachycardia but did not have evidence of cardiac contusion on necropsy. Only one of the five patients with documented cardiac contusion at autopsy had CPK-MBICPK greater than or equal to 2%. Also, six of ten patients without myocardial contusion had CPK-MB/CPK greater than 2%. None of the five patients with documented cardiac contusion had positive Tc-99m scans. The one patient with a positive scan who subsequently died also had ECG changes and CPK-MB/CPK greater than 2%; yet, the patient had no evidence of myocardial contusion at autopsy. The authors conclude that none of the 100 patients with non-penetrating chest trauma had clinically significant cardiac damage. Furthermore, noninvasive tests of cardiac damage, including CPK-MB, serial ECGs, Holter monitoring, and Tc-99m scans were non-specific and did not reflect clinically significant myocardial contusion.
Commentary Dr. Richard Nelson: If one accepts post-mortem evidence of myocardial contusion as a gold standard by which other diagnostic modalities are measured, this article has some disturbing implications. Not only are the usual methods for diagnosing cardiac contusion of no value, but, according to the authors’ data, a patient with blunt chest trauma who has a normal ECG, no dysrhythmias, normal CPK-MB/CPK ratio, and normal Tc-99m scan is as likely, or more likely to have myocardial contusion than those patients with abnormal results. The low degree of sensitivity and specificity of these tests is indeed surprising. It is of further interest to note that none of the patients died as a direct result of myocardial contusion. Six patients died from CNS injury, six from pneumonia, and three from ARDS. Two-dimensional echocardiographic findings in cardiac trauma. Miller FA, Senard JB, Gersh BJ, et al. Am J
Cardiol 1982;50: 1022- 1027. The authors studied seven patients with histories of significant blunt chest trauma. Six patients were studied be-
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tween two and seven days after the injury, and the seventh patient was referred for evaluation 11 months after injury. All patients had abnormal two-dimensional (2-D) echocardiographic results. The findings included generalized right ventricular dilatation (four patients), localized RV dilatation (three patients), localized myocardial thinning (three patients), segmental wall motion abnormalities (two patients), right and left ventricular thrombi (live patients), pericardial effusion (one patient), and tricuspid insufficiency and aneurysm of the right sinus of Valsalva (one patient). Other tests were ECG (abnormal in five of seven patients), chest radiograph (enlarged cardiac silhouette in two of seven patients), CPK-MB fractions (elevated in four of six patients), and cardiac physical examination (results abnormal in two of seven patients). Follow-up echocardiograms were done on six patients anywhere from seven days to three months after the initial study. Results of three follow-up examinations were normal, in two they were improved, and in one (done at seven days) results were unchanged. No patient in this series died. The authors conclude that two-dimensional echocardiography is a useful, noninvasive means to diagnose myocardial contusion and assess postraumatic cardiac function.
Commentary Dr. Greg Decker: The authors state that this article does not document the sensitivity or specificity of the 2-D echocardiogram in diagnosing cardiac contusion. A larger, prospective study with a control group is needed to determine the specificity of echocardiographic findings; also, double-blinding would help remove any bias in the cardiologist’s interpretation of the echo itself. From the data presented, patient management was affected little by echocardiographic results, with the possible exception of patients with intracavitary thrombi. Two of the five patients with thrombi received anticoagulative treatment, and three did not. Yet, all five patients did well. As the authors point out, whether anticoagulative treatment is needed in patients with thrombi requires further study. In conclusion, 2-D echocardiography may be a useful adjunct in evaluating patients with cardiac contusion. The mainstays in diagnosis, however, remain the same: ECG, cardiac examination, and cardiac enzymes . Dr. Richard Nelson: I agree with the authors and Dr. Decker that echocardiography shows promise as an aid in determining cardiac damage resulting from cardiac contusion. However, I disagree with the authors’ conclusion that echocardiography is useful for diagnosing cardiac contusion. One cannot determine just how the patients in this study were selected. I doubt if they were selected from a series of patients with blunt chest trauma, because there were no normal echocardiographic results. Thus one cannot draw any conclusions as to whether 2-D echo is a specific, or
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even sensitive test for diagnosing cardiac contusion. For this, one needs a larger, prospective series of patients with chest trauma, with and without cardiac contusion. Anatomic and cardiopulmonary responses to trauma with associated blunt chest injury. Sutherland GR, Calvin JE, Driedger AA, et al. J Trauma 1981;21:1-12. Twenty-five consecutive patients with severe multisystem injuries, including blunt chest trauma, were studied prospectively. Most patients (24) sustained their injuries in motor vehicle accidents; one patient was injured by a falling tree. All patients were stabilized hemodynamically before inclusion in the study. Fluid resuscitation, blood transfusions, and surgical procedures were performed as needed. Twelvelead ECGs were done on all patients shortly after admission, at the time of radionuclide angiographic study, and one day afterwards. Serum enzyme levels (lactate dehydrogenase [LDHI, serum glutamic oxaloacetic transaminase [SGOT], and CPK) were also measured. All patients were studied by radionuclide angiography within 48 hours of admission. The patients were injected with stannous pyrophosphate, and then with Tc-99m pertechnetate. Then, ECG-gated cardiac scintigraphy was performed, after which cardiac-wall motion and ventricular ejection fractions were determined. Eight patients also underwent Tc-99m pyrophosphate scanning 48 to 72 hours after admission. In addition, 17 of the 25 patients were monitored by Swan-Ganz triple-lumen catheter. Various cardiac function parameters were then measured. Seventeen of 25 patients (68%) (Group I) demonstrated right or left ventricular wall motion abnormalities on radionuclide angiography. Eight of 25 patients (32%) (Group II) had no wall motion abnormalities. Twelve patients showed solitary RV hypokinesis, two patients showed LV hypokinesis, and three patients showed biventricular hypokinesis. In addition, two patients showed ticuspid insufficiency. Right ventricular ejection fraction (RVEF) was significantly lower in patients in group 1 (27.2 ? 9.9%) than in those in Group 2 (46.5 ? 9.6%). Left ventricular ejection fraction (LVEF) was not significantly different between the two groups (52.2 * 13.5% for group 1; 58.9 2 12.2% for group 2). Patients in group 1 demonstrated an average of 1.4 ECG changes per patient, and patients in group 2 had 0.63 ECG changes per patient. Serum enzyme levels were elevated in all patients in both groups and were of no diagnostic value. Invasive hemodynamic studies showed no significant differences in heart rate, blood pressure, pulmonary arterial systolic, diastolic, and mean pressures, pulmonary capillary wedge pressure, central venous pressure, systemic vascular resistance, pulmonary vascular resistance, stroke volume index, and right and left ventricular stroke work index between the two groups. The Tc-99m pyrophosphate scintigraphs were not found to be sensitive for the diagnosis of myocardial contusion. Follow-up radionuclide angiography was obtained at two to 20 weeks in 13 of the 17 patients in 591
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Group 1. Twelve patients demonstrated improvement or resolution of abnormalities; one patient showed worsening. Five patients in Group 1 and one patient in Group 2 died. Myocardial contusion was confirmed at autopsy in four of the five patients in Group 1. There was no evidence of myocardial contusion found in the patient from group 2. Three of the patients in group 1 died following cardiac arrest. The other three patients died from sepsis. The authors conclude that focal defects in myocardial wall contractility constitute prima facie evidence of myocardial contusion. They further conclude that radionuclide angiography is an accurate means of diagnosing wall motion abnormalities, and hence myocardial contusion.
Commentary Dr. Howard Werman: This study seems to suffer from the same problems that plague the entire literature of myocardial contusion: there is no “gold standard” for the diagnosis of myocardial contusion. Hence, the specificity and sensitivity of ECG-gated radionuclide angiography cannot be determined. The authors demonstrate that the test is not infallible. In five patients who died and were thought to have myocardial contusion as demonstrated by ventricular wall dyskinesis, only four had evidence of contusion at autopsy. In addition, two of eight patients with complete or incomplete RBBB on initial ECG were not identified as having ventricular dyskinesis on nuclide scanning. This is one of the more commonly identified ECG abnormalities associated with myocardial contusion in other studies. Thus, false-positive and falsenegative values probably exist with this study. I disagree with their choice of a control group in this study. The authors suggest that the traumatic injuries are not significantly different in these groups. If one removes cranial and orthopedic injuries, which are more axial injuries, then patients in group 1 had 3.0 injuries per patient, and those in group 2 had only 2.4 injuries per patient. In addition, there is a relative lack of abdominal injuries in patients in group 2 (16 versus three). Thus, the two groups may not be comparable. Finally, myocardial contusion represents a spectrum of disease that includes localized myocardial necrosis, ventricular-wall dyskinesis, and dysrhythmias. The nuclide scan only identifies ventricular wall motion abnormalities in defining myocardial contusion. However, the authors attribute mortality in part to refractory cardiac dysrhythmias that developed in these patients. The ultimate question regrading nuclide scanning is whether this modality will affect outcome in this group of patients. It may be that this test will not influence management in patients with myocardial contusion any more than continuous ECG monitoring, as refractory dysrhythmias appear to be the most lethal complications of such injuries.
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Evaluation of technetium scanning for myocardial contusion. Brantigan CO, Burdick D, Hopeman AR, et al. J Trauma 1978;18:460-468. In this article the authors attempt to determine whether myocardial contusion can be accurately diagnosed by Tc99m pyrophosphate scanning. Twenty-nine patients with blunt, non-penetrating chest trauma of sufficient magnitude to cause myocardial contusion were evaluated with serial electrocardiograms, enzyme studies (including SGOT, LDH, and CPK isoenzymes), and the radionuclide scan. Each patient underwent scanning within five days of the injury, and all scans were classified as positive, negative, or equivocal. The scans were re-read and re-classified by the same radiologist at the conclusion of the study; the radiologist had no knowledge of his previous reading or the patient’s clinical course. The criterion for diagnosing myocardial contusion was ECG changes occurring immediately after the traumatic period that reverted to normal in the recovery period. Thirteen patients were thus diagnosed as having myocardial contusion; 15 patients had contusion excluded by ECG, and one patient was considered equivocal for the diagnosis. Measurements of CPK, LDH, and SGOT levels were not helpful in diagnosing myocardial contusion because of false enzyme concentration elevations caused by associated soft tissue trauma. The CPK-MB isoenzyme levels were not found to be elevated in any patient, although the number of patients tested for this was small. On initial reading, two of the ECG-positive groups’ scans were read as positive. The repeat reading failed to confirm one previously positive reading and added two scans later considered positive. Of the remaining fifteen scans in patients without ECG changes, one scan was initially read as positive, and two more positives were added at the final reading. In addition, an incidental finding was that of one patient with ECG changes who underwent emergency surgery for repair of a ruptured right atrium. Postoperative scanning failed to show the severely contused right ventricle viewed directly at surgery. The authors conclude that technetium-99m scanning is an unreliable method for diagnosing myocardial contusion.
Commentary Dr. Robert Behrendt: There are several problems with this study. The five-day lag period before obtaining the scan does not address the serious need for diagnosing myocardial contusion on an emergency basis to help guide subsequent therapy. Furthermore, five days may have been sufficient time to allow a potentially positive scan result to revert to normal. Second, the criterion for diagnosing myocardial contusion (i.e., ECG changes) has been shown in other studies to be non-specific and probably inadequate. Another commonly used diagnostic test, CPK-MB isoenzyme measurement, was considered unreliable even though levels were only measured in a few pa-
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tients. Finally, the scans themselves, and the interpretation of the scans, seemed inconsistent. Although I disagree with some of this study’s assumptions, I do agree with the authors’ conclusion that Technetium scanning has no proven place in the diagnosis of myocardial contusion. Dr. Douglas Rund: The pathological picture of myocardial contusion associated with blunt chest injury is typically described as subendocardial hemorrhage, myocardial edema, interstitial hemorrhage, and focal myocytolysis. The clinical diagnosis is traditionally made by noting ECG changes and CPK-MB changes associated with blunt chest trauma. The diagnosis re-
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quires that the patient be monitored in an appropriate setting. Electrocardiographic monitoring, and even hemodynamic monitoring for signs of failure, constitute treatment similar to that for myocardial infarction. The studies reported here raise doubts about both traditional diagnostic techniques and the pathological picture of myocardial contusion. As is often the case, clinical care of the patient with suspected myocardial contusion should proceed cautiously along currently accepted pathways until a study of suffkient scope and technical precision clarifies the current understanding of myocardial contusion.
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Spectrum of myocardial contusion. Torres-Mirabal P, Gruenberg JC, Brown RS, et al. Am Surg 1982;48:383392. The authors studied 282 consecutive patients with blunt chest trauma who were admitted to a trauma service over a 26-month period. The first 56 patients, studied retrospectively, had discharge diagnoses of blunt chest trauma or myocardial contusion; the subsequent 226 patients were evaluated prospectively. The second group was included in the study population because their admission diagnosis included significant blunt chest trauma. They underwent electrocardiography (ECG), creatinine phosphokinase (CPK) determinations, and CPK-muscle brain (CPK-MB) isoenzyme studies on admission and twice daily for three days. Myocardial contusion was the diagnosis in 42 of the patients based on abnormal ECG (36 patients), elevated CPK (29 patients), or positive CPK-MB results (33 patients). Four of 56 (7%) of the patients in the retrospective group and 38 of 226 (17%) of the patients in the prospective group had their conditions diagnosed using these criteria. The investigators determined that the total incidence of myocardial contusion using these criteria was 15%. The most common ECG abnormalities were non-specific T-wave changes, inverted T-waves, and sinus tachycardia. Less frequent abnormalities were incomplete right bundle branch block, sinus bradycardia, left anterior hemiblock, left axis deviation, premature ventricular contractions, left ventricular strain, third degree atrio-ventricular (A-V) block, second degree A-V (Wenckebach) block, atria1 fibrillation, and atria1 flutter. The total CPK was elevated on admission in 35 of these patients, and subsequently became elevated in three patients. The CPK was not determined in three patients. The CPK-MB result was positive in 35 patients, negative in three patients, and not tested in two patients. In two patients, the CPK-MB result was considered falsely positive because total CPK was greater than 2,000 IU/l. Twenty-nine patients with an abnormal ECG and either increased total CPK or positive CPK-MB underwent right and left ventricular function studies following Swan-Ganz catheter placement.
From the Division of Emergency sity, Columbus, Ohio.
Medicine,
Ohio State Univer-
Address reprint requests to Dr. Rund: Division of Emergency Medicine, Rhodes Hall, University Hospitals, 450 W. 10th Ave., Columbus, OH 43210. 588
MD,
Twelve patients were considered hemodynamically stable and were not studied. One patient died intraoperatively shortly after admission. Eight patients had cardiac index determinations only. Three of these patients had cardiac indices less than 2.9 Ymin/m*. Twenty-one patients received a fluid challenge of 500’ ml of 5% plasmanate solution over 30 minutes to construct Starling curves. Six patients showed biventricular dysfunction. Six patients showed isolated right ventricular (RV) dysfunction, three patients had isolated left ventricular (LV) function, three patients had an upslope-peak-downslope function pattern, and three patients showed normal ventricular function curves. In addition, 22 patients underwent multiple gated acquisition (MUGA) scans. Results of 12 scans were normal, and those of 10 scans were abnormal. Six patients with normal scan results had abnormal ventricular function study results. Of the ten patients with abnormal scan results, one had a normal cardiac index, four had failing ventricular function. two had depressed cardiac indices, and three patients did not have cardiac indices determined. Seven of 42 patients (17%) suffered major morbidity or mortality. Biventricular dysfunction was present in three of these patients, left ventricular dysfunction was present in one, low cardiac index (c2.91 min/m*) was present in two patients, and no determinations were made on the one patient who died introperatively. The authors conclude that ECG, total CPK, and CPK-MB determinations are sensitive in detecting myocardial contusion following blunt chest trauma. However, these determinations are not predictive of major morbidity and mortality. Only direct hemodynamic measurement was found to be useful in identifying those patients at greatest risk.
Commentary Dr. Murk Smith: The main point of this article is to determine which patients with myocardial contusion are at greatest risk for developing serious complications. However, I cannot justify the author’s conclusion that only direct hemodynamic measurements and construction of Starling curves are useful in identifying those patients at greatest risk. Consider, for example, that ventricular function curves of 18 out of 21 patients were abnormal. However, ventricular function studies were done only on four of the seven patients with major morbidity and mortality. All four of these patients had abnormal re-
THE LITERATURE
sults. Therefore, the sensitivity of abnormal ventricular function curves for predicting major morbidity and mortality was 100% (4/4), but the specificity was only 22% (4/18). If we look at the same considerations for cardiac index, six of the patients with major morbidity and mortality had cardiac indices measured. Four of these six had cardiac indices of less than 2.9; two were greater than 2.9. In addition, one patient of the 29 who had cardiac index determinations was below 2.9, yet did not have major morbidity or mortality. Therefore, the sensitivity of cardiac index in predicting major morbidity and mortality was 4/6, or 67%. The specificity was 415 or 80%. We can consider results of MUGA scans in the same manner. Such MUGA scans were done in 22142 patients, and results were abnormal in ten. Of seven patients with major morbidity and mortality, only three underwent MUGA scans, and results of all three were abnormal. This gives a sensitivity of 100% (313) and a specificity of 30% (3/10). Therefore, both cardiac index and MUGA scans may have been as good as, or even better than, ventricular function curves in predicting major morbidity and mortality. However, the sampling methods used by the authors do not allow one to reach any conclusions. Myocardial contusion-Implications for patients with multiple traumatic injuries. Snow N, Richardson JD, Flint LM. Surgery 1982;92;744-750. The authors prospectively studied 300 consecutive patients with suspected blunt chest trauma who were admitted to a trauma service over an 18-month period. Of the 300 patients, 41 (14%) were diagnosed as having myocardial contusion based on an abnormal electrocardiogram (ECG) and/ or serial creatinine phosphokinase isoenzyme (CPK-MB) levels greater or equal to 5% of the total CPK activity. Of these patients, 30 (73%) showed external signs of chest trauma (contusions, abrasions, palpable crepitus, rib fractures, or visible flail segments). Twenty-seven patients (66%) had associated thoracic injuries (hemothorax, pneumothorax, rib fractures, flail chest, or pulmonary contusion), 37 patients (90%) incurred extrathoracic injuries, and 20 patients (49%) complained of non-specific chest pain. Of the 41 patients with a diagnosis of myocardial contusion, 34 (83%) had abnormalities on initial ECG, and two more patients subsequently developed ECG abnormalities. Such abnormalities included non-specific ST and T wave changes (50%), sinus tachycardia (47%), premature ventricular contractions (25%), ischemic changes (140/o), and some form of conduction block (31%). Thirty-four patients (83%) had CPK-MB greater than or equal to 5% of total CPK level. Of these, 27 had abnormal ECGs. Twenty-seven of the 41 patients required urgent surgery (19 of them within 24 hours of injury). There were no intraoperative deaths, although five patients experienced transient hypotension, and seven had dysrhythmias. Twenty-eight patients (68%) developed cardiac complica-
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tions. Of these, 23 had dysrhythmias
(11 of which were considered “life-threatening”), six experienced congestive heart failure, five had myocardial ischemia, five had pericarditis, and four experienced cardiogenic shock. Treatment modalities included pharmacological inotropic support (seven), electrical therapy for dysrhythmias (three), pacemaker (three), in&a-aortic balloon pump (three), and pericardial window (one). Three patients in this series died. No patient with negative ECG or CPK-MB results had a subsequent clinical course compatible with a serious cardiac contusion. Five of the seven patents with negative CPK-MB results developed serious dysrhythmias requiring intervention. Patients with myocardial contusion were released as soon as their ECG, CPK, and clinical status normalized. Followup showed no residual disability in most patients at four to six weeks. The authors conclude that patients with suspected blunt chest trauma should have serial ECGs and CPK-MB determinations performed if the history or objective findings suggest myocardial contusion. These patients should be monitored in an intensive care or telemetry unit. If, after 72 hours, ECGs and CPK-MB levels are normal and no cardiac problems develop, patients who are otherwise stable may be safely transferred to regular nursing units or home, if appropriate. However, because 68% of patients with myocardial contusion (as defined by the authors’ criteria) sustained significant cardiovascular sequelae, these patients should be carefully monitored. Finally, the authors observe that surgical intervention in patients with myocardial contusion can be safely undertaken with careful perioperative monitoring.
Commentary Dr. Murk Smith: Considering the conflicting results of other studies and the apparently low specificity of all noninvasive testing, I feel that the authors proposed a reasonable and prudent protocol for detecting significant myocardial contusion in patients with blunt chest trauma as well as for monitoring and discharging these patients. Furthermore, they suggest that emergency surgery in these patients may be performed safely, and may actually lessen factors that aggravate compromised cardiac function. It is interesting that the data of this study and that of Torres-Mirabal, both large series, were so similar. In this study, 14% of patients, as compared with 17% in the latter study, were diagnosed as having myocardial contusion. Of patients with myocardial contusion, 83% had ECG abnormalities in this study, as compared with 86% in the latter study. Finally, 83% of patients with myocardial contusion in both studies had elevations of CPK-MB levels. Dr. Richard Nelson: The authors have studied a large series of patients with suspected blunt chest injuries. In the process, they apparently identified a subgroup of patients at particular risk for developing cardiac complications because of cardiac contusion. However, I feel this study would have been improved 589
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by the inclusion of a control group, perhaps consisting of trauma patients without blunt chest injuries, but with similar trauma severity scores. I suspect many of these patients would nonetheless meet the author’s electrocardiographic criteria for cardiac contusion, because many would display ECG abnormalities such as sinus tachycardia and non-specific ST and T wave changes. Further, it would be interesting to see how many patients in the control group would show increased CPK-MB levels either because of direct skeletal muscle damage or indirect cardiac damage caused by shock and hypoxia. This article did not change my opinion that myocardial contusion is a very difficult diagnosis to make. Evaluation of noninvasive tests of cardiac damage in suspected cardiac contusion. Potkin RT, Werner JT, Tro-
baugh GB, et al. Circulation
1982;66:627-631.
The authors prospectively studied 100 patients admitted to the intensive care unit with a diagnosis of non-penetrating chest trauma and at least one of the following: severe chest pain, hemothorax, pneumothorax, or fractured rib, clavicle, or sternum. Noninvasive tests commonly used in diagnosing myocardial contusion were applied to these patients and subsequently evaluated. Tests evaluated were serial ECGs, total CPK, and CPK-MB isoenzymes, continuous Holter monitoring, and Tc-99m pyrophosphate scintigraphy. Fifteen patients in this series died, autopsies were performed on all of them, and the results were then used to determine the accuracy of the noninvasive tests in diagnosing cardiac contusion. Electrocardiograms were obtained on admission and daily for three days. The results were considered abnormal if there were any abnormalities of the ST-segment, T-wave. QT-interval, or atrioventricular or intraventricular conduction. Sinus tachycardia was not included as an abnormal rhythm as is done in many other studies. In addition to serial ECGs, all patients were monitored for dysrhythmias for 24 to 48 hours using continuous Holter monitoring. Cardiac enzymes, including CPK and CPK-MB, were determined for admission and repeated at 12 hours and then daily for three days. A CPK-MB greater than or equal to 2% of total CPK was considered abnormal. All patients received Tc-99m pyrophosphate scans on days one and three of their hospitalization. Using a scale of 0 to 4, 2-4 + discrete uptake was considered positive, 2 + diffuse uptake was equivocal, and 0- 1 + diffuse uptake was negative. Seventy percent of the patients had abnormal ECGs. The most common abnormalities were non-specific ST-T wave changes (SS/lOO or 58%). Intraventricular conduction defects occurred in 16/100 patients (16%), and 11 of these had transient right bundle branch block (RBBB). The remainder had left bundle branch block (two) and intraventicular conduction defect (three). No patient had new Q waves develop. Rhythm disturbances were seen in 73% of patients, 54% had unifocal premature ventricular contractions, and only 27% had complex dysrhythmias (at least Lown grade 3). ‘Iwo patients had transient atrioventricular block, and three pa590
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tients had ventricular tachycardia. Only seven patients received treatment for dysrhythmias, and no patient required temporary pacing. Total CPK ranged from 198 to 200,000 IU/l. The median CPK level was 1,985 IU/l. The CPK-MB fractions ranged from 0 to 1,400 IU/l with a median of 27 IU/l. Seventy-two patients had CPK-MB fractions greater than 6 IU/l, but only 27 had CPK-MB/CPK ratios of greater than 3%. Two patients had positive results on Tc-99m pyrophosphate scans. Five patients had equivocal results; results of the remaining 93 scans were negative. Autopsies were performed on all 15 patients who died. Five of these patients were found to have gross or histological evidence of cardiac contusion. Four of the five patients with necropsy-proven cardiac contusion had ECG changes. However, all ten patients without contusion also had ECG changes. One of the five patients with documented cardiac contusion at necropsy had transient RBBB. One patient had ventricular tachycardia but did not have evidence of cardiac contusion on necropsy. Only one of the five patients with documented cardiac contusion at autopsy had CPK-MBICPK greater than or equal to 2%. Also, six of ten patients without myocardial contusion had CPK-MB/CPK greater than 2%. None of the five patients with documented cardiac contusion had positive Tc-99m scans. The one patient with a positive scan who subsequently died also had ECG changes and CPK-MB/CPK greater than 2%; yet, the patient had no evidence of myocardial contusion at autopsy. The authors conclude that none of the 100 patients with non-penetrating chest trauma had clinically significant cardiac damage. Furthermore, noninvasive tests of cardiac damage, including CPK-MB, serial ECGs, Holter monitoring, and Tc-99m scans were non-specific and did not reflect clinically significant myocardial contusion.
Commentary Dr. Richard Nelson: If one accepts post-mortem evidence of myocardial contusion as a gold standard by which other diagnostic modalities are measured, this article has some disturbing implications. Not only are the usual methods for diagnosing cardiac contusion of no value, but, according to the authors’ data, a patient with blunt chest trauma who has a normal ECG, no dysrhythmias, normal CPK-MB/CPK ratio, and normal Tc-99m scan is as likely, or more likely to have myocardial contusion than those patients with abnormal results. The low degree of sensitivity and specificity of these tests is indeed surprising. It is of further interest to note that none of the patients died as a direct result of myocardial contusion. Six patients died from CNS injury, six from pneumonia, and three from ARDS. Two-dimensional echocardiographic findings in cardiac trauma. Miller FA, Senard JB, Gersh BJ, et al. Am J
Cardiol 1982;50: 1022- 1027. The authors studied seven patients with histories of significant blunt chest trauma. Six patients were studied be-
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tween two and seven days after the injury, and the seventh patient was referred for evaluation 11 months after injury. All patients had abnormal two-dimensional (2-D) echocardiographic results. The findings included generalized right ventricular dilatation (four patients), localized RV dilatation (three patients), localized myocardial thinning (three patients), segmental wall motion abnormalities (two patients), right and left ventricular thrombi (live patients), pericardial effusion (one patient), and tricuspid insufficiency and aneurysm of the right sinus of Valsalva (one patient). Other tests were ECG (abnormal in five of seven patients), chest radiograph (enlarged cardiac silhouette in two of seven patients), CPK-MB fractions (elevated in four of six patients), and cardiac physical examination (results abnormal in two of seven patients). Follow-up echocardiograms were done on six patients anywhere from seven days to three months after the initial study. Results of three follow-up examinations were normal, in two they were improved, and in one (done at seven days) results were unchanged. No patient in this series died. The authors conclude that two-dimensional echocardiography is a useful, noninvasive means to diagnose myocardial contusion and assess postraumatic cardiac function.
Commentary Dr. Greg Decker: The authors state that this article does not document the sensitivity or specificity of the 2-D echocardiogram in diagnosing cardiac contusion. A larger, prospective study with a control group is needed to determine the specificity of echocardiographic findings; also, double-blinding would help remove any bias in the cardiologist’s interpretation of the echo itself. From the data presented, patient management was affected little by echocardiographic results, with the possible exception of patients with intracavitary thrombi. Two of the five patients with thrombi received anticoagulative treatment, and three did not. Yet, all five patients did well. As the authors point out, whether anticoagulative treatment is needed in patients with thrombi requires further study. In conclusion, 2-D echocardiography may be a useful adjunct in evaluating patients with cardiac contusion. The mainstays in diagnosis, however, remain the same: ECG, cardiac examination, and cardiac enzymes . Dr. Richard Nelson: I agree with the authors and Dr. Decker that echocardiography shows promise as an aid in determining cardiac damage resulting from cardiac contusion. However, I disagree with the authors’ conclusion that echocardiography is useful for diagnosing cardiac contusion. One cannot determine just how the patients in this study were selected. I doubt if they were selected from a series of patients with blunt chest trauma, because there were no normal echocardiographic results. Thus one cannot draw any conclusions as to whether 2-D echo is a specific, or
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even sensitive test for diagnosing cardiac contusion. For this, one needs a larger, prospective series of patients with chest trauma, with and without cardiac contusion. Anatomic and cardiopulmonary responses to trauma with associated blunt chest injury. Sutherland GR, Calvin JE, Driedger AA, et al. J Trauma 1981;21:1-12. Twenty-five consecutive patients with severe multisystem injuries, including blunt chest trauma, were studied prospectively. Most patients (24) sustained their injuries in motor vehicle accidents; one patient was injured by a falling tree. All patients were stabilized hemodynamically before inclusion in the study. Fluid resuscitation, blood transfusions, and surgical procedures were performed as needed. Twelvelead ECGs were done on all patients shortly after admission, at the time of radionuclide angiographic study, and one day afterwards. Serum enzyme levels (lactate dehydrogenase [LDHI, serum glutamic oxaloacetic transaminase [SGOT], and CPK) were also measured. All patients were studied by radionuclide angiography within 48 hours of admission. The patients were injected with stannous pyrophosphate, and then with Tc-99m pertechnetate. Then, ECG-gated cardiac scintigraphy was performed, after which cardiac-wall motion and ventricular ejection fractions were determined. Eight patients also underwent Tc-99m pyrophosphate scanning 48 to 72 hours after admission. In addition, 17 of the 25 patients were monitored by Swan-Ganz triple-lumen catheter. Various cardiac function parameters were then measured. Seventeen of 25 patients (68%) (Group I) demonstrated right or left ventricular wall motion abnormalities on radionuclide angiography. Eight of 25 patients (32%) (Group II) had no wall motion abnormalities. Twelve patients showed solitary RV hypokinesis, two patients showed LV hypokinesis, and three patients showed biventricular hypokinesis. In addition, two patients showed ticuspid insufficiency. Right ventricular ejection fraction (RVEF) was significantly lower in patients in group 1 (27.2 ? 9.9%) than in those in Group 2 (46.5 ? 9.6%). Left ventricular ejection fraction (LVEF) was not significantly different between the two groups (52.2 * 13.5% for group 1; 58.9 2 12.2% for group 2). Patients in group 1 demonstrated an average of 1.4 ECG changes per patient, and patients in group 2 had 0.63 ECG changes per patient. Serum enzyme levels were elevated in all patients in both groups and were of no diagnostic value. Invasive hemodynamic studies showed no significant differences in heart rate, blood pressure, pulmonary arterial systolic, diastolic, and mean pressures, pulmonary capillary wedge pressure, central venous pressure, systemic vascular resistance, pulmonary vascular resistance, stroke volume index, and right and left ventricular stroke work index between the two groups. The Tc-99m pyrophosphate scintigraphs were not found to be sensitive for the diagnosis of myocardial contusion. Follow-up radionuclide angiography was obtained at two to 20 weeks in 13 of the 17 patients in 591
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Group 1. Twelve patients demonstrated improvement or resolution of abnormalities; one patient showed worsening. Five patients in Group 1 and one patient in Group 2 died. Myocardial contusion was confirmed at autopsy in four of the five patients in Group 1. There was no evidence of myocardial contusion found in the patient from group 2. Three of the patients in group 1 died following cardiac arrest. The other three patients died from sepsis. The authors conclude that focal defects in myocardial wall contractility constitute prima facie evidence of myocardial contusion. They further conclude that radionuclide angiography is an accurate means of diagnosing wall motion abnormalities, and hence myocardial contusion.
Commentary Dr. Howard Werman: This study seems to suffer from the same problems that plague the entire literature of myocardial contusion: there is no “gold standard” for the diagnosis of myocardial contusion. Hence, the specificity and sensitivity of ECG-gated radionuclide angiography cannot be determined. The authors demonstrate that the test is not infallible. In five patients who died and were thought to have myocardial contusion as demonstrated by ventricular wall dyskinesis, only four had evidence of contusion at autopsy. In addition, two of eight patients with complete or incomplete RBBB on initial ECG were not identified as having ventricular dyskinesis on nuclide scanning. This is one of the more commonly identified ECG abnormalities associated with myocardial contusion in other studies. Thus, false-positive and falsenegative values probably exist with this study. I disagree with their choice of a control group in this study. The authors suggest that the traumatic injuries are not significantly different in these groups. If one removes cranial and orthopedic injuries, which are more axial injuries, then patients in group 1 had 3.0 injuries per patient, and those in group 2 had only 2.4 injuries per patient. In addition, there is a relative lack of abdominal injuries in patients in group 2 (16 versus three). Thus, the two groups may not be comparable. Finally, myocardial contusion represents a spectrum of disease that includes localized myocardial necrosis, ventricular-wall dyskinesis, and dysrhythmias. The nuclide scan only identifies ventricular wall motion abnormalities in defining myocardial contusion. However, the authors attribute mortality in part to refractory cardiac dysrhythmias that developed in these patients. The ultimate question regrading nuclide scanning is whether this modality will affect outcome in this group of patients. It may be that this test will not influence management in patients with myocardial contusion any more than continuous ECG monitoring, as refractory dysrhythmias appear to be the most lethal complications of such injuries.
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Evaluation of technetium scanning for myocardial contusion. Brantigan CO, Burdick D, Hopeman AR, et al. J Trauma 1978;18:460-468. In this article the authors attempt to determine whether myocardial contusion can be accurately diagnosed by Tc99m pyrophosphate scanning. Twenty-nine patients with blunt, non-penetrating chest trauma of sufficient magnitude to cause myocardial contusion were evaluated with serial electrocardiograms, enzyme studies (including SGOT, LDH, and CPK isoenzymes), and the radionuclide scan. Each patient underwent scanning within five days of the injury, and all scans were classified as positive, negative, or equivocal. The scans were re-read and re-classified by the same radiologist at the conclusion of the study; the radiologist had no knowledge of his previous reading or the patient’s clinical course. The criterion for diagnosing myocardial contusion was ECG changes occurring immediately after the traumatic period that reverted to normal in the recovery period. Thirteen patients were thus diagnosed as having myocardial contusion; 15 patients had contusion excluded by ECG, and one patient was considered equivocal for the diagnosis. Measurements of CPK, LDH, and SGOT levels were not helpful in diagnosing myocardial contusion because of false enzyme concentration elevations caused by associated soft tissue trauma. The CPK-MB isoenzyme levels were not found to be elevated in any patient, although the number of patients tested for this was small. On initial reading, two of the ECG-positive groups’ scans were read as positive. The repeat reading failed to confirm one previously positive reading and added two scans later considered positive. Of the remaining fifteen scans in patients without ECG changes, one scan was initially read as positive, and two more positives were added at the final reading. In addition, an incidental finding was that of one patient with ECG changes who underwent emergency surgery for repair of a ruptured right atrium. Postoperative scanning failed to show the severely contused right ventricle viewed directly at surgery. The authors conclude that technetium-99m scanning is an unreliable method for diagnosing myocardial contusion.
Commentary Dr. Robert Behrendt: There are several problems with this study. The five-day lag period before obtaining the scan does not address the serious need for diagnosing myocardial contusion on an emergency basis to help guide subsequent therapy. Furthermore, five days may have been sufficient time to allow a potentially positive scan result to revert to normal. Second, the criterion for diagnosing myocardial contusion (i.e., ECG changes) has been shown in other studies to be non-specific and probably inadequate. Another commonly used diagnostic test, CPK-MB isoenzyme measurement, was considered unreliable even though levels were only measured in a few pa-
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tients. Finally, the scans themselves, and the interpretation of the scans, seemed inconsistent. Although I disagree with some of this study’s assumptions, I do agree with the authors’ conclusion that Technetium scanning has no proven place in the diagnosis of myocardial contusion. Dr. Douglas Rund: The pathological picture of myocardial contusion associated with blunt chest injury is typically described as subendocardial hemorrhage, myocardial edema, interstitial hemorrhage, and focal myocytolysis. The clinical diagnosis is traditionally made by noting ECG changes and CPK-MB changes associated with blunt chest trauma. The diagnosis re-
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quires that the patient be monitored in an appropriate setting. Electrocardiographic monitoring, and even hemodynamic monitoring for signs of failure, constitute treatment similar to that for myocardial infarction. The studies reported here raise doubts about both traditional diagnostic techniques and the pathological picture of myocardial contusion. As is often the case, clinical care of the patient with suspected myocardial contusion should proceed cautiously along currently accepted pathways until a study of suffkient scope and technical precision clarifies the current understanding of myocardial contusion.
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