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Pulmonary contusion and embolism are frequent complications of trauma. The radionuclide imaging finding of pulmonary embolism, a segmental ventilation/perfusion mismatch, has been documented in the literature to occur in pulmonary contusion, without, however, excluding concurrent pulmonary embolus by arteriography. The authors report a case of ventilation/perfusion mismatch due to pulmonary contusion with normal pulmonary arteriography.
During a consecutive 17 month period, 15 trauma patients were diagnosed as having a myocardial contusion on the basis of abnormal ECG in 14 patients, elevated creatinine phosphokinase (CPK) in 13 patients, and elevated CPK-Muscle Brain (CPK-MB) isoenzyme determination in 11 patients. Using these screening modalities, the incidence of myocardial contusion in patients with blunt chest trauma increased from 7% when viewed retrospectively to 15% when viewed prospectively. Five patients had determinations of cardiac index of which 4 were less than 2.9 L/min . M2. An additional 9 patients underwent a standard fluid challenge of 500 ml of 5% plasma protein faction infused over 30 min allowing construction of a Starling myocardial performance curve. Of these patients, 6 had biventricular dysfunction, 1 had isolated abnormal left ventricular function, and 2 had isolated abnormal right ventricular function in the absence of chronic obstructive pulmonary disease or preexisting heart disease. Multiple gated acquisition scans (MUGA) were abnormal in 6 patients and normal in 4 patients. Of the latter group, 3 had biventricular dysfunction and 1 had depressed cardiac index. Morbidity and mortality for myocardial contusion occurred in 40% (6 of 15) of patients in this series. Direct hemodynamic measurement with construction of a Starling curve was useful in monitoring the degree of impairment and subsequent recovery of myocardial function. This information was important in delaying semiurgent operations or in determining the best alternative of otherwise equally acceptable methods of patient management.
We wanted to evaluate whether current screening techniques effectively determine a patient's need for hospital admission and intensive care monitoring after blunt chest trauma. Consequently, we reviewed 104 consecutive admissions for "blunt chest trauma; rule out cardiac contusion." Neither clinical findings, cardiac enzyme levels, chest x-rays, nor ECGs predicted the high-risk patients who would subsequently develop complications related to myocardial contusion. Since only 23% of the study patients developed such complications, the plurality of study patients did not require admission and monitoring. There is, therefore, a definite need to develop new, accurate screening tests for patients at risk for myocardial contusion complications.
Myocardial contusion secondary to nonpenetrating chest trauma can occur in the absence of any identifiable large vessel coronary artery occlusion or injury. It has also been reported in association with coronary artery atheromata, thrombosis, rupture, and fistula formation. After reviewing the clinical and experimental research literature, we conclude that myocardial contusion necrosis results from changes in perfusion of small vessels and the coronary microvasculature. Coronary arteriography and emergency coronary artery bypass surgery do not appear promising as therapeutic modalities to reduce myocardial necrosis in this condition. More appropriate therapeutic emphasis may result from research efforts to develop pharmacologic interventions to preserve contused myocardium similar to those currently being evaluated in the management of patients with ischemic myocardium secondary to coronary artery disease.
Pulmonary contusion is a common lesion occurring in patients sustaining severe blunt chest trauma. Alveolar hemorrhage and parenchymal destruction are maximal during the first 24 hours after injury and then usually resolve within 7 days. The diagnosis of traumatic lung injury is usually made clinically with confirmation by chest x-ray films. The chest computed tomography scan is highly sensitive in identifying pulmonary contusion and may help predict the need for mechanical ventilation. Respiratory distress is common after lung trauma, with hypoxemia and hypercarbia greatest at about 72 hours. Although management of patients with pulmonary contusion is supportive, pneumonia and adult respiratory distress syndrome with long-term disability occur frequently.
OBJECTIVE: To determine visual outcomes, incidence of posterior segment abnormalities, and prognostic factors in eyes undergoing lens removal for cataract or lens subluxation-dislocation secondary to ocular contusion injuries. DESIGN: Retrospective, noncomparative, interventional case series. PARTICIPANTS: Forty eyes in forty consecutive patients undergoing lens extraction for ocular contusion-related cataract or lens subluxation, all with a minimum of 6 months' follow-up. INTERVENTION: Lens extraction in the traumatized eye. MAIN OUTCOME MEASURE: Final best-corrected visual acuity. RESULTS: Final best-corrected visual acuity was 20/40 or better in 55% of eyes, and ambulatory vision (>5/200) was achieved in 88%. Preoperative factors associated with poorer visual outcome (<20/40) were the presence of an afferent pupillary defect or an iridodialysis (P < 0.05). Seventy percent of eyes were determined to have significant posterior segment injuries. The cause of final visual acuity less than 20/40 included macular scarring (23%), retinal detachment (15%), and optic atrophy (5%). CONCLUSION: Cataract or lens subluxation secondary to ocular contusion injuries is often associated with severe posterior segment sequelae and poor visual outcomes.
From July 1988 to July 1990, 159 consecutive cases of major blunt chest injury were evaluated prospectively for myocardial contusion with serial electrocardiographic monitoring, cardiac isoenzyme studies, and two-dimensional echocardiography. One hundred and forty-seven cases in the series were assessable; 97 of the patients were male, and 50 were female. They ranged in age from 2 to 97 years (average, 38.5 years). There were five deaths, none of cardiac origin. Total lactate dehydrogenase (LDH) values were elevated in 115 patients (78%); total creatine phosphokinase (CPK) values were elevated in 100 (68%). Cardiac isoenzyme patterns were consistent with myocardial contusion in 18 patients (12%). Seventy-five patients had abnormal electrocardiograms, and 10 of these had ectopic rhythms. Two-dimensional echocardiograms were completed in 58 cases; 12 of these (21%) were abnormal. Nineteen patients (25%) with abnormal rhythms had elevated LDH values, and 26 (35%) had elevated CPK values. One patient (10%) with ectopy had an abnormal echocardiogram. Two patients (11%) with abnormal isoenzyme patterns experienced dysrhythmias. Costs for hospitalization and studies amounted to $1,886 per patient. Given the poor predictive value of laboratory testing in patients with significant (ie, symptomatic) cardiac contusion, observation alone with electrocardiographic monitoring and treatment of symptomatic dysrhythmias is an adequate and cost-conscious treatment.
PURPOSE: This cohort study was designed to evaluate risk factors for the development of posttraumatic glaucoma after ocular contusion. METHODS: Data from the United States Eye Injury Registry (USEIR) were obtained from a total of 6021 patients who experienced blunt ocular contusion. Logistic regression was used to evaluate the association between these baseline structural and functional ocular characteristics and posttraumatic glaucoma. Odds ratios with 95% confidence intervals were obtained. RESULTS: The 6-month incidence of developing posttraumatic glaucoma was 3.39%. The development of glaucoma was independently associated with: advancing age (OR = 1.02; 95% CI = 1.02, 1.03), visual acuity worse than 20/200 (OR = 1.92; 95% CI = 1.19, 3.10), iris injury (OR = 1.60; 95% CI = 1.05, 2.44), lens injury (OR = 1.86; 95% CI = 1.11, 3.11), hyphema (OR = 2.23; 95% CI = 1.40, 3.54), or angle recession (OR = 1.71; 95% CI = 1.00, 2.90). CONCLUSION: This study provides an estimate for the risk of developing glaucoma after ocular contusion in a large cohort of patients and has determined several independently predictive factors that were significantly associated with the development of posttraumatic glaucoma including poor initial visual acuity, advancing age, lens injury, angle recession, and hyphema.
BACKGROUND: Chemokines direct leukocytes to areas of inflammation or injury. In general, CC chemokines (MCP-1, MIP-1alpha, RANTES) are chemoattractants for mononuclear cells and CXC (CINC-1, MIP-2alpha) for polymorphonuclear cells (PMNs). Herein we describe an open chest model of pulmonary contusion (PC) in a rodent (rat) and have identified a possible role for CC and CXC chemokines in the pathogenesis of PC. METHODS: Sprague-Dawley rats (350 g) underwent thoracotomy. The exposed lung was struck with a piston at 5.2 m/s (150 J/M2). Blood, bronchoalveolar lavage (BAL), and lung tissue were collected at 3 hours and 24 hours after injury. PaO2/FiO2 (P/F) ratio was calculated at 15-minute intervals for 3 hours after contusion. Serum was evaluated for cytokine and chemokine expression using ELISA. Cell count/differential was performed on BAL, and lung tissue was obtained for histologic analysis, protein expression and wet to dry weights. Data are reported as pg/mL +/- SE. Data were analyzed using Student's t test to identify significant differences (p < or = 0.05 significant) between sham and injured animals. RESULTS: Piston impact caused PC based upon morphologic and histologic criteria. BAL cell count and lung wet to dry weights were increased and P/F ratio was decreased after PC. Systemic levels of IL-ra, MCP-1, and the CXC chemokines MIP-2alpha and CINC-1 were significantly elevated at 3 hours when sham and injured animals were compared. All chemokines were found to be significantly elevated at 24 hours, consistent with the early PMN and subsequent mononuclear infiltration observed in the contused lung. Pulmonary expression of TNF-alpha, IL-1beta, CINC-1, MIP-2alpha, ICAM-1, and elastase were increased and activated systemic neutrophils showed increased CD-11b. CONCLUSION: A model of PC is described in which innate inflammation is activated locally and systemically. Systemic levels of CC and CXC chemokines are increased after PC. This correlates with elevated PMN CD-11b expression, enhanced pulmonary ICAM-1 expression, and mononuclear and PMN infiltration into the lung and alveolar space. Elevated levels of CC and CXC chemokines are seen after PC and may be involved in the lung's inflammatory response to injury.
Cardiac contusion is an infrequent but occasionally serious complication of deceleration injury. According to ATLS teaching, the true diagnosis of contusion can only be established by direct inspection of the myocardium. The clinically important sequelae of myocardial contusion are hypotension and arrhythmia. Despite recent advances in investigative techniques, myocardial trauma remains an important diagnostic and management challenge. This paper presents an evidence-based review of the topic.
Bone marrow contusions are frequently identified at magnetic resonance imaging after an injury to the musculoskeletal system. These osseous injuries may result from a direct blow to the bone, from compressive forces of adjacent bones impacting one another, or from traction forces that occur during an avulsion injury. The distribution of bone marrow edema is like a footprint left behind at injury, providing valuable clues to the associated soft-tissue injuries. Five contusion patterns with associated soft-tissue injuries occur in the knee: pivot shift injury, dashboard injury, hyperextension injury, clip injury, and lateral patellar dislocation. The classic bone marrow edema pattern seen following the pivot shift injury involves the posterolateral tibial plateau and the midportion of the lateral femoral condyle. Edema occurs in the anterior aspect of the proximal tibia following the dashboard injury. Hyperextension results in the "kissing" contusion pattern involving the anterior aspect of the proximal tibia and distal femur. The clip injury results in a prominent area of edema involving the lateral femoral condyle and a smaller area of edema involving the medial femoral condyle. Finally, lateral patellar dislocation results in edema involving the inferomedial patella and anterior aspect of the lateral femoral condyle. In many instances, the mechanism of injury can be determined by studying the distribution of bone marrow edema, which then enables one to predict with accuracy the specific soft-tissue abnormalities that are likely to be present.
A 3 year study of 117 quadriceps contusions in West Point cadets was undertaken to document the effectiveness of a three-phased therapy program to return these young athletes to full activity with a normal knee range of motion and without recurrence of injury. The treatment protocol of this study was modeled after the 1973 West Point study of Jackson and Feagin with two major changes: 1) resting the injured leg in flexion (versus extension) and 2) emphasizing early flexion exercises (versus extension). Classification of contusions was based on knee range of motion at 12 to 24 hours after the injury (mild, greater than 90 degrees; moderate, 45 degrees to 90 degrees; severe, less than 45 degrees). The average disability time was 13 days for mild, 19 days for moderate, and 21 days for severe contusions. Myositis ossificans developed in 9% of cadets and was associated with five risk factors (knee motion less than 120 degrees, injury occurring during football, previous quadriceps injury, delay in treatment greater than 3 days, and ipsilateral knee effusion.
Muscle injuries are a challenging problem in traumatology, and the most frequent occurrence in sports medicine. Muscle contusions are among the most common muscle injuries. Although this injury is capable of healing, an incomplete functional recovery often occurs, depending on the severity of the blunt trauma. We have developed an animal model of muscle contusion in mice (high energy blunt trauma) and characterized the muscle's ability to heal following this injury using histology and immunohistochemistry to determine the level of muscle regeneration and the development of scar tissue. We have observed a massive muscle regeneration occurring in the first 2 wk postinjury that is subsequently followed by the development of muscle fibrosis. Based on these observations, we propose that the enhancement of muscle growth and regeneration, as well as the prevention of fibrotic development, could be used as approach(es) to improve the healing of muscle injuries. In fact, we have identified three growth factors (bFGF, IGF-1, and NGF) capable of enhancing myoblast proliferation and differentiation in vitro and improving the healing of the injured muscle in vivo. Furthermore, the ability of adenovirus to mediate direct and ex vivo gene transfer of beta-galactosidase into the injured site opens possibilities of delivering an efficient and persistent expression of these growth factors in the injured muscle. These studies should help in the development of strategies to promote efficient muscle healing with complete functional recovery following muscle contusion.
Cardiac contusion is an infrequent complication of blunt chest trauma. The definite diagnosis of myocardial contusion is complex and needs a number of examinations such as electrocardiography, echocardiography, cardiac enzyme and radionuclide perfusion scan. We present a patient who had a blunt chest trauma from a car accident resulting in an acute myocardial infarction without injury to coronary arteries. The non-viable myocardium was diagnosed with (18)F-fluorodeoxyglucose positron emission tomography (FDG PET) combined with (201)Tl perfusion single photon emission tomography (SPECT). This is the first report of FDG PET for the diagnosis of myocardial contusion in blunt myocardial trauma.
In the present study we evaluated the morphological aspect and changes in the area and incidence of muscle fiber types of long-term regenerated rat tibialis anterior (TA) muscle previously submitted to periodic contusions. Animals received eight consecutive traumas: one trauma per week, for eight weeks, and were evaluated one (N = 8) and four (N = 9) months after the last contusion. Serial cross-sections were evaluated by toluidine blue staining, acid phosphatase and myosin ATPase reactions. The weight of injured muscles was decreased compared to the contralateral intact one (one month: 0.77 +/- 0.15 vs 0.91 +/- 0.09 g, P = 0.03; four months: 0.79 +/- 0.14 vs 1.02 +/- 0.07 g, P = 0.0007, respectively) and showed abundant presence of split fibers and fibers with centralized nuclei, mainly in the deep portion. Damaged muscles presented a higher incidence of undifferentiated fibers when compared to the intact one (one month: 3.4 +/- 2.1 vs 0.5 +/- 0.3%, P = 0.006; four months: 2.3 +/- 1.6 vs 0.3 +/- 0.3%, P = 0.007, respectively). Injured TA evaluated one month later showed a decreased area of muscle fibers when compared to the intact one (P = 0.003). Thus, we conclude that: a) muscle fibers were damaged mainly in the deep portion, probably because they were compressed against the tibia; b) periodic contusions in the TA muscle did not change the percentage of type I and II muscle fibers; c) periodically injured TA muscles took four months to reach a muscle fiber area similar to that of the intact muscle.
OBJECTIVE: To document pulmonary function, ventilator management, and outcome of dogs with thoracic trauma that required mechanical ventilation because of severe pulmonary contusions. DESIGN: Retrospective study. ANIMALS: 10 dogs that required mechanical ventilation because of severe pulmonary contusions caused by blunt thoracic trauma. PROCEDURE: Signalment, historical data, arterial blood gas values, oxygen tension-based indices, ventilator settings, peak inspiratory pressure, positive end-expiratory pressure, tidal volume, and minute ventilation values were retrieved from medical records. RESULTS: All 10 dogs required positive-pressure ventilation because of dyspnea following trauma and had severely abnormal pulmonary function. Survival rate to discharge was 30%. Dogs were categorized into 2 groups; group A included 5 dogs in which pulmonary function improved during ventilation, whereas group B included 5 dogs that were euthanatized because of progressive lung dysfunction (n = 4) or cardiac arrest (1). Mean +/- SD body weight of group-A dogs (30.9 +/- 15.9 kg [68 +/- 35 lb]) was significantly greater than that of group-B dogs (7.6 +/- 1.8 kg [16.7 +/- 4 lb]). Dogs with improved lung function had peak inspiratory pressure that decreased progressively, whereas lung compliance deteriorated in dogs in group B. CONCLUSIONS AND CLINICAL RELEVANCE: Dyspneic dogs with severe pulmonary contusions may require and benefit from positive-pressure ventilation Prognosis is better for dogs that weigh > 25 kg (55 lb).
We present five patients with acute traumatic hemarthrosis of the knee who also had hemorrhage within the bone marrow around the knee detected by magnetic resonance imaging. No additional bony, ligamentous, meniscal or osteochondral injuries were evident from clinical examination, initial and repeated plain radiographs, or magnetic resonance imaging. The main symptoms were sharply localized pain and tenderness of the contused area. When hemarthrosis was demonstrated at the first office visit, three cases had fat droplets in the blood. Two patients with hemarthrosis of the knee undergoing arthroscopy showed no obvious lesions of intra-articular structures. Instead they showed congestion of the joint capsule located in accordance with the traumatic episode. Magnetic resonance imaging demonstrated marrow abnormalities as diffusely low and high signal intensity areas in T1-weighted and T2-weighted images, respectively, in locations consistent with the traumatic episode and the symptoms. These disappeared within an average of 13 weeks (range in 4 cases, 12 to 16 weeks). These findings were considered diagnostic of bone contusion. Symptom duration was about 2 weeks in all cases. In conclusion the clinician should consider the possibility of coexisting bone contusion in cases of acute traumatic hemarthrosis of the knee with no evidence of bone or intra-articular lesions on clinical examination and conventional radiographs.
OBJECT: The authors tested the hypothesis that breach of the blood-spinal cord barrier (BSCB) will produce evidence of oxidative stress and that a similar staining pattern will be seen between 4-hydroxynonenal (HNE)/protein complexes and extravasated immunoglobulin G (IgG). METHODS: Adult female Fischer 344 rats, each weighing 200 to 225 g, were subjected to a spinal cord contusion at T-10 by means of a weight-drop device. Spinal cord tissue was assessed for oxidative stress by localizing extravasated plasma contents with a monoclonal antibody for rat IgG and protein conjugation with HNE, which is an aldehyde byproduct of lipid peroxidation. The animals were killed at 1 and 6 hours, and 1, 2, and 7 days after surgery. Maximum HNE/protein staining was observed at 2 days postinjury, and HNE/protein and IgG manifested similar staining patterns. Analysis revealed a graduated but asymmetrical rostral-caudal response relative to the T-10 injury site. Both HNE/protein complex and IgG staining revealed that the caudal levels T-11 and T-12 stained significantly more intensely than the rostral levels T-9 and T-8, respectively. A higher percentage of neurons positive for HNE/protein immunostaining was observed in spinal cord levels caudal to the injury site compared with equidistant rostral regions. Protein dot-blot assays also revealed a similar asymmetrical rostral-caudal HNE/protein content. To analyze the timing of the BSCB breach, another group of animals received identical contusions, and horseradish peroxidase (HRP) was injected 10 minutes before or at various times after injury (1, 3, and 6 hours, and 1, 2, and 7 days). Maximum HRP permeability was seen immediately after injury, with a significant decrease occurring by 1 hour and a return to control levels by 2 days posttrauma. CONCLUSIONS: Data from this study indicate possible compromise of neuronal, axonal, glial, and synaptic function after trauma, which may be a factor in motor deficits seen in animals after spinal cord contusion. The colocalization of the IgG stain with the HNE/protein stain is consistent with the hypothesis of a mutual cause-effect relationship between BSCB and oxidative stress in central nervous system trauma.