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Cardiac contusion in the patient with multiple injuries.

We have treated 20 patients with multiple injuries and concomitant myocardial contusion. The diagnosis of myocardial contusion was based mainly on serial ECG tracings which showed arrhythmias, dynamic ischaemic patterns or conduction disturbances. The clinical and laboratory findings of cardiac contusion are sometimes indistinguishable from those found in multiple injuries. Furthermore, they are overshadowed by the overt manifestation of cerebral, thoraco-abdominal and skeletal injuries. Awareness and prompt diagnostic measures are essential in the diagnosis of cardiac injury. Strict cardiac monitoring following multiple trauma will prevent serious or even fatal outcome of cardiac injury.

Accidents, Traffic↗

Cardiac contusion in patients wearing seat belts.

The incidence of myocardial contusion in patients wearing seat belts and requiring admission to hospital after road traffic accidents was examined. The criteria used for diagnosing contusion were serial electrocardiograms (ECGs) and estimation of CK-MB isoenzymes using the Isomune-CK (Roche) kit. Nine of the 14 patients (64 per cent) showed evidence of myocardial contusion. We suggest long-term studies to establish the true incidence among patients wearing seat belts.

Accidents, Traffic↗

Maximal contraction lessens impact response in a muscle contusion model.

The effect of muscle contraction on a contusion injury model was studied in the gastrocnemius muscle of anesthetized rats. Both limbs of 18 rats received a contusion injury with a blunt non-penetrating impact. One hind limb was relaxed during impact and the other was electrically stimulated to tetanic contraction. The impact was produced using a drop-mass technique (mass = 171 g, height = 101 cm, spherical radius of impactor tip = 6.4 mm). The impact response was determined by sampling (10 kHz) the transmitted impact force and the displacement of the impactor. In a subgroup of nine rats, the severity of the contusion injury was measured by recording contractile tension in twitch and tetanus within two hours of injury. We found that the peak impact force was significantly less (p < 0.01), while the peak impact displacement was significantly greater (p < 0.01) in the contracted limb. Correspondingly, the impact stiffness of the contracted limb was significantly less (p < 0.01) than the impact stiffness in the relaxed limb. Both impacts produced significant injuries relative to an uninjured control group. The tetanic tension (31 +/- 4 N) generated by the muscles that were contracted during impact was significantly (p < 0.03) greater than that generated by the muscles that were relaxed during impact (27 +/- 4 N). The findings from this specific model indicate that the impact response of the limbs with relaxed muscle was dominated by the underlying bone, while maximally contracted muscle decreased the influence of the bone and lessened the impact response. Maximally contracted muscle was not more susceptible to injury and may act as protective mechanism against some impacts.

Animals↗

The relevance of the detection of troponins to the forensic diagnosis of cardiac contusion.

The forensic diagnosis of cardiac contusion has hitherto been based mainly on anamnesis, concomitant thoracic injuries and the detection of macroscopic changes to the heart. Parallel histological and serological investigations of the heart-specific troponins have been conducted with varying results. This paper aims to show whether heart-specific troponins are suitable as a means of securing the diagnosis in proven cases of cardiac contusion and of determining which of the three heart-specific troponins cTnT, cTnI and cTnC are most significant in serology and histology for postmortem diagnosis. In the study, 25 cases of known cardiac contusion and 11 controls without vital myocardial trauma taken from autopsy material were prospectively investigated. Investigation of the venous serum revealed significant differences in the concentrations of the case and control groups for troponin T (mean value 5.5056 versus 0.4982; p=0.014), for troponin C (mean value 263.9280 versus 68.5640; p=0.001) and for troponin I (mean value 1404.0560 versus 36.1650; p=0.003). In histology there are also significantly different depletions between the groups investigated (cTnT: p=0.002; cTnC: p=0.003; cTnI: p<0.001) taking into account the autolysis time.

Case-Control Studies↗

Indocyanine green angiographic features of choroidal rupture and choroidal vascular injury after contusion ocular injury.

PURPOSE: To report features of choroidal rupture and choroidal vascular injury after contusion ocular injury on indocyanine green angiography. METHODS: In a prospective study, nine patients (nine eyes) with choroidal rupture after ocular contusion underwent initial fluorescein angiography and indocyanine green angiography within 19 days after trauma. Eyes that had a distinct abnormality of the retinal pigment epithelium were excluded from this study. Subtraction indocyanine green angiography was also performed. Follow-up fluorescein angiographic and indocyanine green angiographic findings were also studied. RESULTS: Initial ophthalmoscopic examination revealed subretinal hemorrhage in all nine eyes. In five of the nine eyes, choroidal rupture was not seen on initial ophthalmoscopic or fluorescein angiographic examination because it was hidden beneath the subretinal hemorrhage, but it was detected on subsequent examinations. In the remaining four eyes, choroidal rupture was observed by ophthalmoscopy at the time of initial examination, and these eyes exhibited hyperfluorescent streaks on fluorescein angiography in the region of the subretinal hemorrhage. On initial indocyanine green angiography of all nine eyes, observed hypofluorescent streaks became more obvious with time. For each eye, there were more hypofluorescent streaks on indocyanine green angiography than hyperfluorescent streaks on fluorescein angiography. In one eye, the location of indocyanine green leakage nearly coincided with the location of a hyperfluorescent streak on fluorescein angiography. In this case, crescentic streaks of hypofluorescence were seen on the temporal side of the subretinal hemorrhage on indocyanine green angiography, although choroidal rupture was not observed in that region by ophthalmoscopy or fluorescein angiography. In two of the nine eyes, indocyanine green angiography and the subtraction technique demonstrated disturbance of flow into choroidal vessels, especially at the choroidal rupture site. CONCLUSION: After ocular contusion injury, various features of choroidal rupture and choroidal vascular injury were observed on indocyanine green angiography. This technique may contribute to the diagnosis of choroidal rupture and to the understanding of the clinical course after injury.

Accidents, Traffic↗

Predictors of mortality in pulmonary contusion.

BACKGROUND: Associated injuries and central nervous system (CNS) trauma are historically associated with poor outcome in patients with pulmonary contusions, but the value of specific factors reflecting shock, fluid resuscitation requirement and pulmonary parenchymal injury in predicting mortality in this population is not well established. METHODS: The medical records of 100 consecutive patients with pulmonary contusion, admitted over a 5-year period, were retrospectively reviewed. Survivors and nonsurvivors were compared in terms of age, Injury Severity Score (ISS), Glasgow Coma Score (GCS), PaO2/FiO2 (oxygenation ratio), the severity and adequacy of shock resuscitation reflected in plasma lactate, resuscitation volume and transfusion requirements, using one-way ANOVA. To determine the contribution of individual, interdependent variables to mortality, the data were then analyzed using multivariable analysis. RESULTS: ISS and transfusion requirement were significantly higher, and GCS and PaO2/FiO2 at 24 and 48 hours after admission were significantly lower in nonsurvivors than in survivors. After multiple regression analysis, the factors most strongly associated with mortality included patient age, oxygenation ratio at 24 hours after admission, and resuscitation volume. CONCLUSIONS: Outcome in patients with pulmonary contusion is dependent upon a number of variables including the severity of pulmonary parenchymal injury as reflected in PaO2/FiO2 ratio.

Adult↗

The asymptomatic patient with suspected myocardial contusion.

Diagnostic criteria and guidelines for hospital admission for suspected myocardial contusion (MCC) remain unclear. This study defines and examines the clinical sequelae of patients admitted with a suspicion of MCC. Criteria for observation following isolated, minor blunt chest trauma are suggested. Hospital and trauma registry records of patients admitted over a 33-month period with suspected MCC were reviewed. Conventional evaluation criteria, cardiac-related complications, and associated injuries were analyzed for 524 patients. Twenty-eight cardiac-related complications occurred in 27 of 524 patients (5%). These complications included 23 dysrhythmias, 3 infarctions, and 2 pericardial effusions. There were 23 patients with abnormal admission electrocardiograms and 4 with normal ones. Of the latter, one patient developed dysrhythmia 4 hours after admission, and three had other major multi-system injuries requiring admission to the intensive care unit. The overall incidence of cardiac-related complications in minimally injured patients was 0.1%. There were no complications in patients with isolated chest wall contusions, a normal admission electrocardiogram, and a normal rhythm at 4 hours. There was no significant association between creatine phosphokinase isoenzymes or echocardiogram and cardiac-related complications. The complete absence of significant cardiac sequelae in patients with isolated chest wall contusion, normal admission and 4-hour electrocardiograms, and no other associated major injuries suggests that these patients need not be admitted.

Adult↗

Ventilatory management of pulmonary contusion patients.

BACKGROUND: The goal of this study was to evaluate two modes of mechanical ventilation in patients with pulmonary contusion: pressure-controlled ventilation (PCV) and volume-controlled ventilation (VCV). METHODS: One hundred and thirty-five patients with pulmonary contusion, defined as an infiltrate on admission chest x-ray and hypoxemia, were treated over 45 months; 59 patients who required more than 48 hours of mechanical ventilation were initially managed with VCV. RESULTS: Twenty patients were converted from VCV to PCV when pulmonary function deteriorated. With PCV, peak inspiratory pressure decreased from 49 +/- 1 to 31 +/- 1 cm H2O, the alveolar-arterial oxygen difference decreased from 491 +/- 36 mm Hg to 300 +/- 36 mm Hg. These findings were significantly different (P < 0.05, by Student's paired t-test). Twenty patients managed with PCV had equivalent duration of mechanical ventilation and days in intensive care units to 39 patients with less pulmonary dysfunction managed with VCV. None of the 10 patients who died expired from pulmonary failure. CONCLUSIONS: PCV is an alternative mode to VCV in patients with poorly compliant lungs after pulmonary contusion.

Adolescent↗

Induction of heme oxygenase-1 (HO-1) in the contused spinal cord of the rat.

The induction of heme oxygenase-1 (HO-1) was studied in intact spinal cords and injured spinal cords after a moderate, thoracic contusion injury. HO-1 was immunolocalized in the normal cord and along the axis of the cord at 1, 2, 3 and 4 days after contusion. Induction of this enzyme in astrocytes and microglia/macrophages was evaluated using immunofluorescent double labeling with monoclonal antibodies to HO-1 and either glial fibrillary acidic protein or the complement C3bi receptor. HO-1 was expressed in neurons in the normal spinal cord. After contusion, HO-1 was induced in both gray and white matter at the impact site. In segments of cord that were 1 cm proximal or distal to the injury, HO-1 was primarily induced in the dorsal columns and occasionally in the lateral white matter. This pattern of induction was noted at all time points. The HO-1 was induced primarily in microglia/macrophages. The distribution of the HO-1 positive cells closely correlated with the pattern of intraparenchymal hemorrhage. These findings demonstrate acute induction of HO-1 in non-neuronal cells in the injured spinal cord. Induction of HO-1 in glia may be a consequence of multiple factors including exposure to heme proteins, hypoxia and oxidative stress.

Animals↗

Diagnosis of myocardial contusion in blunt chest trauma.

Of 20 patients with blunt chest trauma who underwent cardiac scanning, serial electrocardiography and cardiac monitoring to rule out myocardial contusion, four had positive cardiac scans. All four had electrocardiographic abnormalities: three had nonspecific ST-T wave changes, and the fourth had electrocardiographic evidence of an acute subendocardial infarction. Of the 16 patients with negative scans, five had normal electrocardiograms. In the remaining 11 patients, factors other than myocardial contusion were suspected causes of electrocardiographic abnormalities. On the basis of this data, electrocardiogram changes in the traumatized patient have various causes. Cardiac scanning appears to be a useful adjunct to electrocardiography in confirming the presence of myocardial contusion.

Adult↗

Changes in contused lung volume and oxygenation in patients with pulmonary parenchymal injury after blunt chest trauma.

Although it is well known that pulmonary parenchymal injury impairs oxygenation, the relationship between hypoxemia and volume of the contused lung after blunt chest trauma remains unknown. We studied 23 blunt chest trauma patients who underwent thoracic computed tomography (CT) within 24 hours after admission and also underwent follow-up CT at 1-week intervals until abnormal lung findings disappeared. Contused lung volume was determined quantitatively by CT. CT findings of parenchymal injury were either a diffuse lesion that disappeared within 1 week (n = 9 patients, group 1), or a solitary lesion that remained a few weeks after resolution of the diffuse lesion (n = 14 patients, group 2). PaO2/FiO2 was positively correlated with the volume of contused lung during the first 24 hours in both groups, however, there was no significant correlation after 1 week after injury. Degree of impaired oxygenation is related to the volume of the diffuse lesion that is recognized soon after injury.

Adolescent↗

[Pulmonary contusion after blunt chest trauma--an experimental model (author's transl)].

A model in the rat for pulmonary contusion after blunt chest trauma is described. It is possible to avoid trauma of the mediastinal organs, liver and spleen; therefore it is possible to produce pulmonary contusion with a good reproducebility. The parameter for the extent of contusion was the lungweight which rose statistically with a specific force of trauma. Simultaneous injection of high doses of prednisolone with the blunt chest trauma inhibits the increase of the lung weight.

Animals↗

Bcl-xL expression after contusion to the rat spinal cord.

After contusion-derived spinal cord injury, (SCI) there is localized tissue disruption and energy failure that results in early necrosis and delayed apoptosis, events that contribute to chronic central pain in a majority of patients. We assessed the extent of contusion-induced apoptosis of neurons in a known central pain-signaling pathway, the spinothalamic tract (STT), which may be a contributor to SCI-induced pain. We observed the loss of STT cells and localized increase of DNA fragmentation and cytoplasmic histone-DNA complexes, which suggested potential apoptotic changes among STT neurons after SCI. We also showed SCI-associated changes in the expression of the antiapoptotic protein Bcl-xL, especially among STT cells, consistent with the hypothesis that Bcl-xL regulates the extent of apoptosis after SCI. Apoptosis in the injured spinal cord correlated well with prompt decreases in Bcl-xL protein levels and Bcl-xL/Bax protein ratios at the contusion site. We interpret these results as evidence that regulation of Bcl-xL may play a role in neural sparing after spinal injury and pain-signaling function.

Animals↗

Abnormal cerebral blood volume in regions of contused and normal appearing brain following traumatic brain injury using perfusion magnetic resonance imaging.

Following traumatic brain injury, there may be secondary alterations in cerebrovascular parameters leading to ischemia and further cellular damage. To assess possible subacute hemodynamic disturbances following traumatic brain injury, we used conventional and perfusion magnetic resonance imaging (MRI) in 18 patients, on average 10 days following injury. Six of the 18 patients had focal contusions or edema visible on conventional MRI. These six patients had a significantly reduced normalized regional cerebral blood volume (rCBV) in the regions of focal pathology compared to equivalent areas in control subjects (patients 0.47 +/- 0.20 [means +/- SD], controls 1.02 +/- 0.11, p < 0.001). In addition, four of these six patients had an increased rCBV (outside control range) in the region of normal appearing brain immediately surrounding the contusion. These six patients were more significantly injured and had a worse clinical outcome compared to the remaining patients (p = 0.004,p = 0.03, respectively). There were five patients who had a region of reduced rCBV (outside control range) in a quadrant of normal appearing white matter, away from any visible abnormality, who were not more significantly injured than the remaining patients but went on to have a significantly poorer clinical outcome (p = 0.27, p = 0.01, respectively). Traumatic brain injury is a heterogeneous insult causing a variety of pathology, not all of which is visible using conventional imaging methods. The current study has shown that regions of both normal appearing and contused brain may have an abnormal rCBV and that alterations in rCBV may play a role in determining the clinical outcome of patients.

Adult↗

Spinal cord edema, 5-hydroxytryptamine, lipid peroxidation, and lysosomal enzyme release after acute contusion and compression injury in primates.

Physical and biochemical changes in the spinal cord of monkeys at 1/2, 2, and 4 hours following 200 g cm contusion injury and 50 g of compression injury and 2 hours of decompression following 4 hours of compression were studied. The pathophysiologic changes were milder in compression compared to contusion injury. Following contusion injury, at 1/2 and 2 hours there was significant increase in % water content, lipid peroxidation, and alpha-L-fucosidase. alpha-D-Mannosidase was significantly increased at all time periods, and beta-D-hexosaminidase was increased at 1/2 and 4 hours. At 4 hours following injury, serotonin (5 HT) and 5-hydroxyindole-3-acetic acid (5-HIAA) showed a significant increase. From 10 minutes to 2 hours there was increased platelet aggregation. In compression injury, a significant increase in water content and 5 HT was observed only at 1/2 hour. Lipid peroxidation had increased at all time periods, whereas B-D-hexosaminidase, beta-D-galactosidase, and 5-HIAA were increased at 2 hours. alpha-D-Mannosidase had increased at 1/2 and 2 hours, and alpha-L-fucosidase had increased at 4 hours. After 2 hours decompression following 4 hours compression, water content, beta-D-galactosidase, and alpha-D-Mannosidase were significantly increased. An attempt was made to correlate the findings and to understand the sequential pathophysiologic changes in the first 4 hours following spinal cord trauma, providing a baseline for evaluation of the efficacy of any therapeutic maneuvers.

Acute Disease↗

A mouse model of graded contusive spinal cord injury.

A mouse model of spinal cord injury (SCI) could further increase our basic understanding of the mechanisms involved in injury and recovery by taking advantage of naturally-occurring and genetically engineered mutations available in mice. We have, therefore, investigated whether methods used to produce and evaluate graded experimental contusive SCI in the rat could be modified to produce a mouse model of traumatic SCI. C57BL6 mice were anesthetized with 2,2,2-tribromoethanol and a restricted laminectomy performed at the T8 vertebral level. The spinal column was stabilized and a weight drop technique used to produce contusive injury. Experimental groups were distinguished by the amount of weight or the height from which the weight was dropped onto an impounder resting on the dura (1 g x 2.5 cm, 2 g x 2.5 cm, 3 g x 2.5 cm, and 3 g x 5.0 cm). Functional deficits over time were examined up to 28 days after SCI by testing hindlimb reflex responses and coordinated motor function. Chronic lesion histopathology was evaluated by light microscopy and analyzed with morphometric techniques. All groups demonstrated profound functional deficits after injury followed by gradual recovery. Recovery correlated with the weight dropped and percent of white matter spared that was 41.3+/-6.0% (mean +/- SEM) in the 2 g x 2.5 cm group and 24.3+/-5.0% in the 3 g x 2.5 cm group. A replicate experiment confirmed reproducibility of the injury. This new mouse model of contusive SCI could pave the way for in vivo studies of the effect of genetic modifications produced by specific mutations on injury and recovery processes after spinal cord trauma.

Animals↗

Selective management of flail chest and pulmonary contusion.

Four hundred and twenty-seven patients with severe blunt chest trauma were treated resulting in (1) flail chest, (2) pulmonary contusions, (3) pneumothorax, (4) hemothorax, or (5) multiple rib fracture. The need for endotracheal intubation and mechanical ventilation was determined selectively by standard clinical criteria. Avoidance of fluid overload and vigorous pulmonary toilet was attempted in all patients. Three hundred and twenty-eight patients were treated by nonintubation; 318 patients (96.6%) had a successful outcome, while ten required intubation. Only one patient died. The 99 patients who required intubation and mechanical ventilation had a high mortality because of associated shock and head injury; however, the total mortality for the entire group of patients was 6.5%, with only 1.4% mortality caused by pulmonary injury. The incidence of pneumonia was high (51%), but there was only a 4% incidence of tracheostomy complications. Flail chest and pulmonary contusion without flail chest occurred in 95 and 135 patients, respectively. Half of the flail chest patients were intubated, but 69.5% were intubated less than three days. Twenty per cent of the patients with pulmonary contusion required mechanical ventilation, usually for less than three days. This study demonstrates that patients with severe blunt chest trauma can be managed safely by selective intubation and mechanical, ventilation and that the incidence of complications associated with controlled mechanical ventilation can be greatly reduced.

Adolescent↗

Myocardial contusion: a case study of a myocardial infarction.

Injuries from blunt trauma can occur from a variety of causes. Myocardial contusion is the most common injury resulting from blunt, nonpenetrating trauma to the chest. The potential hemodynamic changes seen with a blunt chest trauma victim are often insidious and confusion. Diagnosing a myocardial contusion concomitant with other traumatic injuries can often be delayed, especially in light of the fact that immediate cardiac dysfunction may be slow in manifesting symptoms. Through use of a case study approach, this article demonstrates that a myocardial contusion has many similarities in terms of pathophysiologic changes with that of a myocardial infarction, often confusing symptoms and therefore diagnosis and treatment.

Contusions↗