Posttraumatic Cardiac Contrecoup (original) (raw)
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World Journal of Surgery, 1999
A prospective study was carried out to analyze the evolution of patients who survived penetrating cardiac trauma. A total of 642 patients were evaluated. A 1-year follow-up, which included physical examinations, electrocardiography, echocardiography and stress tests, was completed in 192 patients. Data processing included calculation of average and percentage values. At follow-up, 90% of patients were asymptomatic at 2 days after surgery, with normal cardiac monitoring; baseline and control ECGs showed myocardial infarction in 9.1% of patients. Baseline ECGs showed pericarditis as well in 27% of patients and repolarization changes in 35.2%. The latter became normal within 1 to 6 months after the trauma. All (100%) of the patients had a functional status I stress test, and 56% had a normal echocardiography. In conclusion, the epidemiologic behavior of penetrating cardiac trauma is identical to that of general trauma. ECG is useful during the postsurgery period for diagnosis of traumatic myocardial infarction. Likewise, the stress test is useful in patients with myocardial infarction and echocardiography in the presence of either myocardial infarction or any symptom suggesting anatomic or functional alterations of the heart.
Annals of Emergency Medicine, 1988
Right ventricular infarction due to ischemic heart disease can be diagnosed by a right precordial electrogram or by first-pass radionuclide angiography (FPRNA). Prior FPRNA studies have shown that cardiac dysfunction after blunt chest trauma (myocardial contusion) is most often due to right ventricular dysfunction. We hypothesized that right ventricular dysfunction due to ischemic heart disease and myocardial contusion should produce similar ECG changes due to myocyte disruption. The purpose of our study was to evaluate the diagnostic value of the right precordial electrogram in suspected cardiac contusion. Thirty-five patients with suspected myocardial contusion based on mechanism of injury~clinical findings and no history of clinical heart disease were enrolled prospectively All patients had conventional ECG, right precordial electrogram, and FPRNA studies. Twenty patients had normal cardiac scans (group 1); percentage of myocardial creatine kinase (CK-MB) was measured in 12 of these patients and was less than 5% in 11. Fifteen patients had abnormal cardiac scans (wall motion abnormality and~or decreased right ventricular ejection fraction) (mean, 34% +-7%
Blunt cardiac injury: a 10 year institutional review
Injury, 1997
A 10 year review of all blunt cardiac injuries (N = 70) at a single trauma institution was conducted. The majority of patients were diagnosed on the basis of elevated myocardial band fraction qf creatine kinase (CK-MB), ST/T wave changes or arrhythmias. The presence of CK-MB elevation was not predictive qf arrhythmias, cardiac complications, inotrope requirement, or mortality. The presence of ECG abnormalities or arrhythmias was also not predictive of inotrope requirement or mortality. Cardiac complications requiring treatment occurred in 26per cent (N=18) qf patients. Patients requiring inotropes (N=12, 17 per cent) had higher Injury Severity Scores (ISS), longer times from injury to emergency, and higher mortality rates, than those not requiring them. Patients who died (N=IO) had a higher ISS, lower Revised Trauma Score, and a more frequent need for inotropes. Only three deaths were directly attributable to the cardiac injury. Myocardial contusion is an i~qury often qf little clinical importance. Patients present with injuries qfl little or no consequence', severe injuries where the diagnosis is readily apparent, or as a confounding variable in a multiply i~qured patient. Early use of transthoracic echocardiography is advocated.
Journal of Surgical Research, 1976
Myocardial injury is a frequent cause of death after blunt chest trauma. Death may occur immediately from rupture of valves or myocardium [7]. Immediate or delayed death due to ventricular fibrillation has been demonstrated experimentally and clinically [2, 3, 81. Depression of cardiac output has been shown following myocardial contusion without valve dysfunction [2]. Although cardiac function has been related to the amount of myocardium damaged following infarction, no such relationship has been demonstrated with contused myocardium [4,61. The importance of coronary flow changes in cardiac dysfunction accompanying contusion has been suggested by reports of coronary occlusion accompanying closed chest trauma [9]. Other studies suggest that flow to contused myocardium is increased [2].