[Experimental and clinical study on pulmonary contusions. I. Physiopathology of pulmonary contusion in the early stage and pathological changes].
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Intracerebral contusions can lead to regional ischemia caused by extensive release of excitotoxic aminoacids leading to increased cytotoxic brain edema and raised intracranial pressure. rCBF measurements might provide further information about the risk of ischemia within and around contusions. Therefore, the aim of the presented study was to compare the intra- and perilesional rCBF of hemorrhagic, non-hemorrhagic and mixed intracerebral contusions. In 44 patients, 60 stable Xenon-enhanced CT CBF-studies were performed (EtCO2 30 +/- 4 mmHg SD), initially 29 hours (39 studies) and subsequent 95 hours after injury (21 studies). All lesions were classified according to localization and lesion type using CT/MRI scans. The rCBF was calculated within and 1-cm adjacent to each lesion in CT-isodens brain. The rCBF within all contusions (n = 100) of 29 +/- 11 ml/100 g/min was significantly lower (p < 0.0001, Mann-Whitney U) compared to perilesional rCBF of 44 +/- 12 ml/100 g/min and intra/perilesional correlation was 0.4 (p < 0.0005). Hemorrhagic contusions showed an intra/perilesional rCBF of 31 +/- 11/44 +/- 13 ml/100 g/min (p < 0.005), non-hemorrhagic contusions 35 +/- 13/46 +/- 10 ml/100 g/min (p < 0.01). rCBF in mixed contusions (25 +/- 9/44 +/- 12 ml/100 g/min, p < 0.0001) was significantly lower compared to hemorrhagic and non-hemorrhagic contusions (p < 0.02). Intracontusional rCBF is significantly reduced to 29 +/- 11 ml/100 g/min but reduced below ischemic levels of 18 ml/100 g/min in only 16% of all contusions. Perilesional CBF in CT normal appearing brain closed to contusions is not critically reduced. Further differentiation of contusions demonstrates significantly lower rCBF in mixed contusions (defined by both hyper- and hypodense areas in the CT-scan) compared to hemorrhagic and non-hemorrhagic contusions. Mixed contusions may evolve from hemorrhagic contusions with secondary increased perilesional cytotoxic brain edema leading to reduced cerebral blood flow and altered brain metabolism. Therefore, the treatment of ICP might be individually modified by the measurement of intra- and pericontusional cerebral blood.
BACKGROUND: The objective of this study was to determine the individual and combined effects of pulmonary contusion and fat embolism on the hemodynamics and pulmonary pathophysiology in a canine model of acute traumatic pulmonary injury. METHODS: After a thoracotomy, twenty-one skeletally mature dogs were randomly assigned to one of three groups. Unilateral pulmonary contusion alone was produced in Group 1 (seven dogs); pulmonary contusion and fat embolism, in Group 2 (seven dogs); and fat embolism alone, in Group 3 (seven dogs). Pulmonary contusion was produced by standardized compression of the left lung with a piezoelectric force transducer. Fat embolism was produced by femoral and tibial reaming followed by pressurization of the intramedullary canals. Cardiac output, systolic blood pressure, peak airway pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, partial pressure of arterial oxygen, and partial pressure of carbon dioxide were monitored for all groups. From these data, several outcome parameters were calculated: total thoracic compliance, alveolar-arterial oxygen gradient, and ratio of partial pressure of arterial oxygen to fractional inspired oxygen concentration. All of the dogs were killed after eight hours, and tissue samples were obtained from the brain, kidneys, and lungs for histological analysis. Lung samples were assigned scores for pulmonary edema (the presence of fluid in the alveoli) and inflammation (the presence of neutrophils or hyaline membranes, or both). The percentage of the total area occupied by fat was determined. RESULTS: Pulmonary contusion alone caused a significant increase in the alveolar-arterial oxygen gradient but only after seven hours (p = 0.034). Fat embolism alone caused a significant transient decrease in systolic blood pressure (p = 0.001) and a significant transient increase in pulmonary arterial pressure (p = 0.01) and pulmonary capillary wedge pressure (p = 0.015). Fat embolism alone also caused a significant sustained decrease in the ratio of partial pressure of arterial oxygen to fractional inspired oxygen concentration (p = 0.0001) and a significant increase in the alveolar-arterial oxygen gradient (p = 0.0001). The combination of pulmonary contusion and fat embolism caused a significant transient increase in pulmonary capillary wedge pressure (p = 0.0013) as well as a significant sustained decrease in partial pressure of arterial oxygen (p = 0.0001) and a significant decrease in systolic blood pressure (p = 0.001) that lasted for an hour. Pulmonary contusion followed by fat embolism caused a significant increase in peak airway pressure (p = 0.015), alveolar-arterial oxygen gradient (p = 0.0001), and pulmonary arterial pressure (p = 0.01), and these effects persisted for five hours. Total thoracic compliance was decreased 6.4 percent by pulmonary contusion alone, 4.6 percent by fat embolism alone, and 23.5 percent by pulmonary contusion followed by fat embolism. The ratio of partial pressure of arterial oxygen to fractional inspired oxygen concentration was decreased 23.7 percent by pulmonary contusion alone, 52.3 percent by fat embolism alone, and 65.8 percent by pulmonary contusion followed by fat embolism. The mean pulmonary edema score was significantly higher with the combined injury than with either injury alone (p = 0.0001). None of the samples from the lungs demonstrated inflammation. Fat embolism combined with pulmonary contusion resulted in a significantly greater mean percentage of the area occupied by fat in the noncontused right lung than in the contused left lung (p = 0.001); however, no significant difference between the right and left lungs could be detected with fat embolism alone. The mean percentage of the glomerular and cerebral areas occupied by fat was greater with fat embolism combined with pulmonary contusion than with fat embolism alone (p = 0.0001 and p = 0.01, respectively). (ABSTRACT TRUNCATED)
OBJECTIVE: The aim of this study was to investigate the direct influence of lung contusion on pulmonary surfactant in multiple trauma patients. DESIGN: Prospective, nonrandomized study. SETTING: University hospital, trauma intensive care unit. PATIENTS: Eighteen multiple trauma patients with unilateral lung contusions and Injury Severity Scores >19 were studied prospectively. INTERVENTIONS: Bronchoalveolar lavage was performed daily until either day 7 or extubation. Samples from the side of lung contusion (n = 62) and the contralateral, uninjured side (n = 62) were obtained at the same time in 14 patients. Total phospholipids, total phospholipid classes, and surfactant apoprotein A were quantified. Additionally, surfactant function was measured with a pulsating bubble surfactometer in four patients. All data are presented as mean +/- SEM. Statistical analyses were performed using programs of SPSS for Windows 6.1.3 (SPSS Inc., Chicago, IL) (Student's t-test; p < .05). MEASUREMENTS AND MAIN RESULTS: Total phospholipids were significantly increased on the side of lung contusion (contusion side, 40+/-7 microg/mL; contralateral side, 21+/-3 microg/mL; p = .004). The percentage contents of phosphatidylcholine (contusion side, 87.1%+/-1.0%; contralateral side, 84.3%+/-1.0%; p = .04) and sphingomyelin (contusion side, 2.9%+/-0.3%; contralateral side, 1.9%+/-0.2%; p = .004) were significantly higher. In contrast, the percentage content of phosphatidylglycerol was significantly decreased (contusion side, 4.1%+/-0.1%; contralateral side, 6.9%+/-0.6%; p = .001). No alterations were found for the relative contents of phosphatidylethanolamine (contusion side, 2.4%+/-0.2%; contralateral side, 2.2%+/-0.2%; p = .47), phosphatidylinositol (contusion side, 3.5%+/-0.4%; contralateral side, 4.6%+/-0.5%; p = .06), and surfactant apoprotein A (contusion side, 7177+/-1404 ng/mL; contralateral side, 4513+/-787 ng/mL, p = .10). There was no statistical difference for minimal surface tension measured with the pulsating bubble surfactometer after 5 mins of oscillation (contusion side, 29.5+/-2.3 mN/m; contralateral side, 23.7+/-2.1 mN/m; p = .08). CONCLUSIONS: Direct damage of lung parenchyma by lung contusion alters the composition of surfactant. No additional changes in surfactant function were observed that would argue in favor of functional compensation.
BACKGROUND: Despite the predominance of superficial injuries after explosive blast exposure, major morbidity or mortality among immediate survivors is caused by delayed perforation of intestinal mural contusions. Previous studies have suggested that small bowel and colonic contusions larger than 10 mm in diameter are at high risk. This experimental study aimed to identify contusions at high risk of late perforation. METHODS: Histological features of injury were classified in 188 blast-induced intestinal contusions in 16 anaesthetized Large White pigs. RESULTS: Some 16 per cent of small bowel and 12 per cent of colonic contusions were at high risk of late perforation. Small bowel contusions larger than 15 mm in diameter had a worse histological grading than those smaller than 15 mm (chi 2 = 0.09, 2 d.f., P = 0.01). Contusions that extended over more than half the bowel circumference (chi 2 = 14.79, 2 d.f., P = 0.0006) and those affecting the mesenteric border (chi 2 = 7.5, 2 d.f., P = 0.024) were more severe injuries. Colonic contusions larger than 20 mm in diameter had a worse histological grading than smaller ones (chi 2 = 14.95, 2 d.f., P = 0.0006). Confluent, rather than diffuse, colonic contusions were more severe injuries (chi 2 = 6.37, 2 d.f., P = 0.04). CONCLUSION: Once identified at laparotomy, the number of small bowel contusions requiring excision may be reduced from 86 to 60 per cent; similarly, excision of colonic contusions can be reduced from 73 to 27 per cent if small bowel contusions smaller than 15 mm in diameter and colonic contusions of less than 20 mm are managed conservatively.
In order to elucidate the mechanisms of release of EAAs and their excitotoxicity in cerebral contusion, cortical contusion was produced in the rat parietal cortex, and the changes in extracellular levels of EAAs in the central and peripheral areas of contusion were investigated using microdialysis. The cortical contusion induced a rapid increase in dialysate concentration of glutamate ([Glu]d) from a baseline level of 4.6+/-2.8 microM to a maximum level of 36.3+/-12.8 microM. This elevation of glutamate was significantly attenuated by mild hypothermia (32 degrees C for 90 min, comprising 20 min before and 70 min after the injury induction) in the peripheral area of contusion (p < 0.01) but not in the central area. Histological evaluations revealed that the hypothermia reduced the necrosis volume of contusion to 38.3% of that in the normothermic control (p < 0.01). In situ administration of Co2+, an inhibitor of Co2+-dependent exocytotic release of EAAs from the nerve terminals, via the microdialysis system, also attenuated the [Glu]d elevation following cortical contusion, in the peripheral area of contusion (p < 0.01) but not in the central area. These findings indicate that cerebral contusion involves heterogeneous and complex mechanisms of EAA release into the extracellular space. The release of EAAs in the contusion core was nonsensitive to hypothermia and Co2+ administration, suggesting that such EAA release was related to primary disruption of the cell membrane or vascular wall by the physical force of the head trauma, resulting in leakage of EAAs from the metabolic pool in the cytosole or blood stream. In contrast, in the peripheral area, the effectiveness of hypothermia and Co2+ administration implied a presynaptic mechanism of EAA release, which consisted, at least in part, of Ca2+-dependent exocytotic EAA release from depolarized nerve terminals. The EAAs released in the contusion core may diffuse towards a peripheral direction and act on the postsynaptic receptors, causing neuronal depolarization. Such a diffusion-reaction process appears to induce additional release of EAAs from the depolarized nerve terminals. Hypothermia may block this diffusion-reaction process and eventually reduce the contusion volume.
In a group of 40 cerebral contusions with a different period of survival by histological and histochemical methods changes in the contusion foci and their surroundings were assessed. The authors compared their own findings with those of other authors. Their finding of leucostasis and incipient leucodiapedesis was found in cerebral contusions with 7 hours survival. A more marked incidence of leucocytes near the contusion was in cases with a survival of 30 hours. A readily apparent gliomensenchymal reaction near the contusion focus was found in patients who survived the injury for eight days. In the glial elements acid phosphatase and no-specific esterase activity was detected. In contusion of the frontal lobe with a 13-day survival considerable cellulization and increase in the amount of capillaries was found near the contusion focus. In survival of contusion of the frontal lobe for 28 days the glial elements with an acid phosphatase and non-specific esterase activity form a margin round the contusion focus. Even in contusion of the frontal lobe with 5-month survival numerous granular cells were found in the neighbouring area. The results obtained by the authors are not always consistent with those of others. The data of other authors frequently vary too. Therefore it is important to be careful about estimates of the age of cerebral contusions and in particular in cerebral contusions with longer survival the estimate of the age of the injury is only approximate.
Myocardial contusion remains an elusive clinical entity, which consumes a disproportionate amount of scarce and expensive critical care resources for the purpose of cardiac monitoring. This study attempts to define a group of patients at high risk who can be identified from the available data present at the time of admission. All patients admitted with the suspicion of a myocardial contusion over a 3-year period were retrospectively studied. The records were examined for history, physical findings, electrocardiographic (ECG) results, creatine kinase levels, Injury Severity Score (ISS), and echocardiographic findings. A diagnosis of a myocardial contusion was made if patients had an ECG consistent with acute injury, increased creatine kinase-MB, or an abnormal echocardiogram consistent with acute injury. Patients were stratified into two groups: Group 1 patients satisfied the criteria for a myocardial contusion and Group 2 patients lacked sufficient evidence to substantiate this diagnosis. The records were then examined for the presence of factors available in the emergency room that might be predictive of a myocardial contusion or its complications. A total of 88 patients were evaluated; 27 of these were found to have a myocardial contusion (Group 1) with 61 patients placed in Group 2 (no myocardial contusion). Group 1 patients had an abnormal admission ECG (p less than 0.05), and an ISS greater than or equal to 10 (p less than 0.05). Multivariate analysis identified two factors predictive of a myocardial contusion: an abnormal ECG and an ISS greater than 10. When these two predictors were absent, the probability of a myocardial contusion was 1%. No predictors of a complication of a myocardial contusion were identified. These data suggest that a combination of easily obtained variables in the emergency department can be used to select a patient population at high risk for myocardial contusion. Prospective evaluation of these variables is necessary.
BACKGROUND: Bone contusions are often identified at magnetic resonance imaging (MRI) in the acutely injured knee. Contusions of both surfaces of the joint are known as kissing contusions. OBJECTIVE: To determine the frequency, type, and distribution of kissing contusions occurring in association with injuries of the knee joint. METHODS: 255 MRI examinations in athletes with acutely injured knees (197 men; 58 women; mean age 24.2 years) were reviewed by two independent examiners; 219 MRIs were done within the first month after the injury and 36 within two to four months. None of the knees had been injured before. No fractures were present on x ray. RESULTS: Bone contusions were diagnosed in 71 cases (27.8%); 55 (22.5%) were identified as single contusions and 16 (6.3%) as kissing contusions. Eight of the kissing contusions were associated with anterior cruciate ligament tears, three with menisceal tears, four were isolated lesions, and one was delayed, following a menisceal tear. The 32 bone contusions (16 kissing contusions) were located as follows: lateral femoral condyle (n = 14; 8 type I, 6 type II); lateral tibial condyle (n = 9; 3 type I, 1 type II, 5 type III); medial tibial condyle (n = 7; 2 type I, 5 type III); medial femoral condyle (n = 2; both type I). The associated injuries were confirmed by arthroscopy in 12/16 patients. CONCLUSIONS: Kissing contusion is a significant injury often associated with ligamentous or menisceal injuries. Type I lesions are most common on the lateral femoral condyle and type III on the lateral tibial condyle.
OBJECTIVES: To assess the usefulness of transesophageal echocardiography in diagnosing cardiac contusions in patients with blunt trauma. BACKGROUND: For more than a decade, noninvasive tests, including ECGs, cardiac enzymes, nuclear studies, and transthoracic echocardiography have been utilized in an attempt to identify trauma patients with cardiac injuries. These tests have been imperfect in identifying the patients at high risk for mortality. METHODS: We retrospectively reviewed the charts in 22 patients with transesophageal echocardiographically diagnosed cardiac contusions noting age, race, sex, transthoracic echocardiographic examinations, study quality, and outcome. We also noted the Injury Severity Score, which is a measure of the severity of illness in trauma patients. Higher scores correlate more severe injury and higher mortality. We defined cardiac contusions as presence of wall motion abnormality, including either or both ventricles, in the absence of transmural myocardial infarction on ECG following nonpenetrating chest trauma. RESULTS: Over a 30-month period, 81 transesophageal echocardiographic examinations were performed on trauma patients. Among this group, 22 patients were diagnosed as having cardiac contusions. There were 15 patients with right ventricular contusions, 7 patients with left ventricular contusions, and 2 patients with both ventricles involved. We compared this group with all ICU trauma patients admitted to the hospital during this time period. Overall, the contusion patients had an average Injury Severity Score of 27 and a mortality of 27% compared with the overall trauma group with an Injury Severity Score of 33 and a corresponding mortality of 9% (p < 0.001). Corresponding ECGs were nondiagnostic in 73% of patients with cardiac contusion. There were no complications related to the transesophageal examinations. CONCLUSIONS: Transesophageal echocardiographically diagnosed cardiac contusion in trauma patients carries a high mortality rate. Transesophageal examinations are safe and provide excellent quality images where transthoracic examinations were inadequate. Right ventricular contusions are approximately twice as common as left ventricular contusions.
Bacterial infections frequently,complicate pulmonary contusion and are the leading cause of death in such patients. This study evaluated the effects of pulmonary contusion alone and contusion associated with other factors on the ability to clear aerosolized bacteria from the lung. Lung bacterial clearance of Staphylococcus aureus and Klebsiella pneumoniae was studied in animals with isolated pulmonary contusion, or contusion associated with blood loss, rapid crystalloid infusion, or steroid administration. An isolated pulmonary contusion produced no impairment of the ability of the contused lung to clear either gram-negative or gram-positive organisms. The addition of acute blood loss and crystalloid infusion resulted in decreased clearance from the contused lung; steroid administration caused a marked depression in lung bacterial clearance from the noninjured lung as well. The canine model described allowed for study of regional differences in bacterial clearance. The data presented support several conclusions; (1) the contused lung is not more susceptible to bacterial infection than the normal lung: (2) acute blood loss renders the contused lung less able to clear bacteria; (3) crystalloid infusion markedly depresses lung bacterial clearance; and (4) steroids have a deleterious antibacterial effect on both contused and noncontused lungs.
Pulmonary contusion is the most commonly identified thoracic soft tissue injury in an automobile crash and after blunt chest trauma and affects 10-17% of all trauma admissions. The mortality associated with pulmonary contusions is significant and is estimated to be 10-25%. Thus, there is a need to develop a finite element model based injury metric for pulmonary contusion for the purpose of predicting outcome. This will enable current and future finite element models of the lung to incorporate an understanding of how stress and strain may be related to contusion injuries. This study utilizes 14 impacts onto male Sprague-Dawley rats. In 5 of these tests, a calibrated weight (46 g) is dropped from a height of 44 cm directly onto the lungs of intubated, anesthetized rats in situ. Contused volume is estimated from MicroPET scans of the lung and normalized on the basis of liver uptake of 18F-FDG. The lungs are scanned at 24 hours, 7 days, and 28 days (15 scans), and the contused volume is measured. In addition, 9 controlled mechanical tests on in situ rat lung are used for model development and validation. Identical impacts are performed on a finite element model of the rat lung. The finite element model is developed from CT scans of normal rat and scaled to represent average rat lung volume. First principal strain is chosen as a candidate injury metric for pulmonary contusion. The volume of contused tissue at the three time points measured using PET is compared to the strain level achieved by a corresponding volume in the finite element model. For PET scans (n=5 scans per time point), the average contusion volume was 4.2 cm3 at 24 hours, 2.8 cm3 at 7 days, and 0.39 cm3 at 28 days. These volumes were used to identify threshold peak first principal strain levels measured by the finite element model. Maximum first principal strain from the finite element model for the three volume levels (4.2, 2.8, and 0.39 cm3) was 3.5%, 8.8%, and 35% strain, respectively. Furthermore, the lung model exhibited exponential decay in principal strain threshold as more of the lung volume was considered, correlating to the precise and well defined volume of the contusion as it healed. The results of this study may be used to establish an injury metric to predict pulmonary contusion due to an impact to the lungs. The results may be used to improve finite element models of the human body, which may then be used to tune stiffnesses of interior components of automobiles and tune safety systems for maximum mitigation of this serious injury.
BACKGROUND: The aims of the Langendorff-perfused rabbit heart study were to evaluate the arrhythmogenic consequences of myocardial contusion and to determine the mechanism of arrhythmia. METHODS: Six hearts were in the control group, and 24 hearts (intact heart protocol) were submitted to one of four different contusion kinetic energies (75, 100, 150, or 200 millijoules [mJ]; n = 6). Occurrence of arrhythmia, of an electrically silent area (i.e., area with no electrical activity), and of line of fixed conduction block were reported before and for 1 h after contusion. In 16 hearts (frozen hearts) submitted to cryoprocedure and contusion impact of 100 or 200 mJ, ventricular conduction velocities, anisotropic ratio, wavelengths, ventricular effective refractory period, and its dispersion were measured before and for 1 h after contusion. Using high-resolution mapping, arrhythmias were recorded and analyzed. RESULTS: The intact heart study showed that the number and seriousness of contusion-induced arrhythmias increased with increasing contusion kinetic energy, as did the number of electrically silent areas (five of six ventricular fibrillations and five of six electrically silent areas at 200 mJ). In the frozen heart study, immediately after contusion ventricular effective refractory periods were shortened and dispersed, and wavelengths were also shortened. The arrhythmia analysis showed that all ventricular tachycardias but one were based on reentry developed around an electrically silent area or a line of fixed conduction block. CONCLUSIONS: Myocardial contusion has direct arrhythmogenic effects, and the seriousness of arrhythmia increases with the level of contusion kinetic energy. The mechanism of arrhythmia was mainly based on reentrant circuit around a fixed obstacle.
OBJECTIVES: To quantify pulmonary contusions on chest x-ray film and to evaluate factors correlating with the size of the pulmonary contusions, changes in the first 24 hours, the need for ventilatory assistance, and death. METHODS: The medical records and chest x-ray films of 103 patients with blunt chest trauma diagnosed as having a pulmonary contusion were reviewed. RESULTS: A pulmonary contusion score was developed (3 = one third of a lung; 9 = an entire lung). In the emergency department, pulmonary contusions were not present in 11, were mild (one ninth to two ninths of a lung) in 15 patients, moderate-severe (three ninths to nine ninths of a lung) in 53 patients, and very severe in 24 patients. Within 24 hours, the pulmonary contusion score increased in 26 patients by 7.9 +/- 5.5 (SD). The 26 patients with an increasing contusion had a higher mortality rate (38% vs. 17%) (p = 0.044) and tended to need ventilatory assistance more frequently (73% vs. 49%) (p = 0.061). The 35 patients with very severe pulmonary contusions (pulmonary contusion score = 10-18) had the lowest PaO2:FIO2 ratio at 24 hours (175 +/- 103 mm Hg), longest hospital length of stay (28 +/- 35 days), and the highest Injury Severity Score (26 +/- 9). The factors correlating highest with a need for ventilatory support (57/103) were the 24 hour or initial PaO2/FIO2 ratio < 300, an Injury Severity Score > or = 24, Revised Trauma Score < 6.4, Glasgow Coma Scale score < or = 12, and shock or need for blood in the first 24 hours (p < 0.001). Death correlated highly with a need for ventilatory assistance, Injury Severity Score > or = 26, Revised Trauma Score < or = 6.3, and Glasgow Coma Scale score < or = 11 (p < 0.001). CONCLUSION: Quantifying and noting changes in the extent of the pulmonary contusions and PaO2/FIO2 ratio during the first 24 hours may be of value in determining the need for ventilatory assistance and predicting outcome.
STUDY OBJECTIVE: Myocardial contusion may induce life-threatening complications, but its diagnosis is difficult. Circulating cardiac troponin T is considered a highly sensitive and specific marker of myocardial cell injury. We investigate the value of cardiac troponin T measurement in the diagnosis of myocardial contusion. DESIGN: Prospective study. SETTING: Level 1 trauma center. METHODS: We prospectively measured circulating cardiac troponin T and performed echocardiography and continuous Holter monitoring in patients who had suffered blunt trauma. Myocardial contusion was diagnosed in patients who fulfilled one of the following criteria: (1) an abnormal echocardiography compatible with myocardial contusion; (2) severe cardiac rhythm abnormalities; (3) severe cardiac conduction abnormalities; and (4) hemopericardium. MEASUREMENTS AND RESULTS: One hundred twenty-eight patients were included and myocardial contusion was diagnosed in 29 patients. Patients with myocardial contusion had more severe trauma, experienced more frequently associated thoracic lesions, and had a lower left ventricular ejection fraction area (48 +/- 15 vs 61 +/- 10%; p < 0.001). Elevated circulating cardiac troponin T concentrations were significantly more frequent in patients with a myocardial contusion (31 vs 9%; p < 0.007). An elevated circulating cardiac troponin T concentration (> or = 0.5 microgram/L) was more accurate than MB fraction of creatine kinase (CK) (CK-MB) and CK-MB/CK ratio in the diagnosis of myocardial contusion, as shown by an area under the receiver operating characteristic (ROC) curve (AROC), which was significantly different from 0.50 (AROC = 0.69; 95% confidence interval, 0.56 to 0.80). However, this improvement was not clinically acceptable (sensitivity, 0.31; specificity, 0.91). CONCLUSIONS: Circulating cardiac troponin T measurement had a slightly greater diagnostic value than usual biological parameters (CK-MB, CK-MB/CK) in myocardial contusion. Nevertheless, it was concluded that an elevated circulating cardiac troponin T concentration has no important clinical value in the diagnosis of myocardial contusion.