NONPENETRATING TRAUMA
Blunt chest trauma is especially common after steering wheel impact from an automobile accident. It may produce myocardial contusion, resulting in myocardial hemorrhage and at times some degree of necrosis. Often there is little or no residual myocardial scar once healing is complete. Large contusions may lead to myocardial scars, cardiac or septal rupture, congestive heart failure, or formation of true or false aneurysms. Necrosis or hemorrhage involving the cardiac conduction system can produce intraventricular or atrioventricular block. Coronary artery laceration, valvular damage, or pericardial tears may occasionally occur after blunt trauma. The chest pain of myocardial contusion is similar to that of myocardial infarction and is often confused with musculoskeletal pain from the chest trauma. The electrocardiogram at the time of injury may show a diffuse injury pattern similar to that of pericarditis. Later, the electrocardiogram may reveal serial development of Q waves similar to that of acute myocardial infarction if significant necrosis has occurred. Bradyarrhythmias and tachyarrhythmias are common. Contractile abnormalities are usually not severe unless concomitant injury to a valve or the septum has occurred. The MB fraction of creatine kinase is elevated. Myocardial contusion is usually treated similarly to myocardial infarction with initial monitoring and subsequent progressive ambulation. Anticoagulants should not be administered to patients with myocardial contusion. If the patient survives the acute-episode,, his long-term prognosis is usually good, although late complications such as ventricular arrhythmias occasionally occur.
Rupture of the aorta is a common consequence of blunt trauma. It most commonly occurs just distal to the take-off of the left subclavian artery. The patient may complain of pain in the back or chest similar to that of aortic dissection. The chest x-ray usually reveals widening of the mediastinum. Many patients demonstrate increased arterial pressure in the upper extremities and decreased arterial presure and pulse pressure in the lower extremities. Signs of decreased renal or spinal cord perfusion may become evident. The diagnosis is usually confirmed by aortography, and the treatment is surgical.
- CARDIAC PACEMAKERS
- Lidocaine
- DISORDERS ASSOCIATED WITH MALABSORPTION
- CLASSIFICATION AND PATHOPHYSIOLOGY
- Mesangioproliferative Glomerulonephritis
- The Fanconi Syndrome
- TUMORS OF THE PLEURAL SPACE
- MYOCARDIAL METABOLISM
- Clinical Manifestations
- PNEUMOTHORAX
- Pathology
- Other Cystic Diseases
- APPROACH TO THE PATIENT WITH RENAL DISEASE
- CLINICAL CLASSIFICATION OF JAUNDICE
- SPECIFIC MANIFESTATIONS OF RENAL DISEASE
- Diagnosis
- DIAGNOSIS AND EVALUATION
- NAUSEA AND VOMITING
- MEDIASTINAL DISEASE
- PHYSIOLOGICAL EFFECTS OF PULMONARY HYPERTENSION ON CARDIAC FUNCTION
- Sigmoidoscopy and Colonoscopy
- Outcome and Prognosis
- Pulmonary Infiltrates with Eosinophilia PIE
- GAS TRANSFER
- CLINICAL FEATURES OF PULMONARY HYPERTENSION
- Miscellaneous
- Blood Chemistries
- ANTIBIOTICS
- RAYNAUD’S PHENOMENON
- Esophagogastroduodenoscopy
- Important NEPHROTOXIRIS
- CLINICAL MANIFESTATIONS OF MALABSORPTION
- CHRONIC RENAL FAILURE
- SPECIFIC CLINICAL DISORDERS
- GLOMERULAR DISEASE