Blunt Chest Injury Research Articles

Late respiratory sequelae of blunt chest injury: a preliminary report.

Eighty-six survivors of blunt chest injury were assessed for pre- and post-injury respiratory symptoms using a standardised questionnaire. A comparison was made between observed and expected symptom prevalence and lung function. Respiratory symptom prevalence after injury was greater than expected, 23 survivors (27%) claiming a persistent productive cough, 18 (21%) persistent wheezing, and 22 (26%) grade 2 dyspnoea. After injury persistent productive cough (p less than 0.05) and occasional wheezing (p less than 0.01) were more common among smokers and ex-smokers when compared with non-smokers. Mean forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) were not statistically different from expected values. We concluded that respiratory sequelae of blunt chest injury are common and that smokers and ex-smokers are at particular risk.

Anatomic and cardiopulmonary responses to trauma with associated blunt chest injury.

Myocardial dysfunction may result from severe trauma. Therefore, left (LV) and right ventricular (RV) function were prospectively assessed by ECG-gated blood pool radionuclide (RN) angiography in 25 consecutive patients who had sustained severe trauma including blunt chest injuries. Focal abnormalities of RV and LV wall motion were defined in 17 patients; 12, RV; two, LV; and three, biventricular. In two patients traumatic tricuspid insufficiency was also demonstrated, and subsequently verified by contrast angiography. Other means to detect myocardial contusion (enzymatic, electrocardiographic, and Tc-99m pyrophosphate scintigraphy) proved to be insensitive when compared to RN angiography. Two of the five deaths in the group were attributed to refractory arrhythmias. Surgical or post-mortem evidence of traumatic myocardial injury was obtained in five instances when RN angiography indicated contusion. Of the 13 patients available for followup examinations, 11 showed complete or partial resolution of the abnormality and two were unchanged. Comprehensive cardiopulmonary monitoring revealed an inverse relationship between right ventricular ejection fraction (RVEF) and pulmonary vascular resistance (PVR) (R2 = 0.42; p < 0.01) and between the PVR and left ventricular ejection fraction (LVEF) (R2 = 0.48; p < 0.01) and left ventricular end-diastolic volume (LVEDV) (R2 = 0.69; p < 0.01). Further, as right ventricular end-diastolic volume (RVEDV) was increased in trauma, left ventricular function and compliance were reduced. In blunt chest trauma RV contusion occurs more frequently than previously recognized and positive RN angiography constitutes prima facie evidence of direct myocardial injury. Further, LV function remains preload dependent, but may be depressed by elevated PVR impeding the blood flow from RV to LV and/or decreases in LV compliance.

The use of inotropic drugs in myocardial contusion 2 case reports

Myocardial contusion is a common complication of blunt chest injury. Severe heart failure and shock may result. The haemodynamic consequences of myocardial contusion in two patients are described; both received inotropic agents. In the first patient dobutamine was successful in improving myocardial function; dopamine had similar effects on the heart. In the second patient dopamine, preferred for its renal effects, produced a short-term improvement in myocardial function. The rational use of pharmacological agents in this condition demands precise understanding of the underlying haemodynamic disturbances.

Extensive pulmonary laceration caused by blunt trauma

During the past five years, 210 patients were treated for lung injury resulting from blunt trauma. Thirteen failed to respond to traditional conservative measures and underwent emergency thoracotomy. In each, an extensive pulmonary laceration was found. The indications for thoracotomy were massive hemothorax in 10 patients, profuse air leak not responding to chest tube suction in two patients, and severe intratracheal bleeding in one patient. Rib fractures were present in every patient, but in only 10 patients was the pulmonary laceration directly produced by the sharp end of a fractured rib. In three the laceration was far removed from the rib fractures and evidently was caused by a shearing force. The lacerations were treated by pulmonary resection in eight patients and by suture repair in four. One patient died during thoracotomy but prior to definitive repair. Four patients survived, two of whom had undergone lobectomy and two, suture repair. Death was caused primarily by extra-thoracic injuries in six of the nine who died. Extensive pulmonary laceration is a significant cause of morbidity and death among patients with blunt chest injury. The initial clinical and roentgenographic findings are similar to those found in the larger group of patients with lesser injury. However, continued and uncontrollable hemorrhage and massive air leakage characterized this entity. Awareness of the condition, a high degree of suspicion in patients who do not respond to conservative measures, and prompt thoracotomy may be life-saving.

Electrocardiographic changes in traumatized patients

Traumatized patients who sustain a severe physical or psychological insult may develop myocardial ischemic changes, espicially those patients over the age of 40 years. The electrocardiogram (EKG) findings in 34 chest injury patients out of 200 multiple injury cases over a period of two years were studied. Two types of myocardial changes were found: injury pattern (of a permanent character) and ischemic pattern (of a transient nature). The first type was more frequent in the penetrating noncardiac chest injury cases, and the second more common in the blunt chest injury cases. It is necessary to make early and serial EKG tracings on traumatized patients in order to detect myocardial changes.

Coronary Artery Occlusion Resulting From Blunt Trauma

SEVERE, frontal, nonpenetrating chest trauma is a common event that frequently results in a variety of intrathoracic injuries. The occurrence of a blunt injury to a major coronary artery resulting in coronary occlusion has been rarely reported. A cause and effect relationship between blunt chest injury and coronary occlusion may, at times, be difficult to prove because of the presence of preexisting atheromatous stenosis in the coronary vessels. 1-5 We report the occurrence of complete obstruction of the left anterior descending coronary artery following severe, frontal, nonpenetrating chest injury sustained in an automobile accident. Report of a Case A 16-year-old white teen-ager was admitted to Baptist Memorial Hospital on Aug 25, 1972, following an automobile accident. He was riding in the seat next to the driver and recalled striking his chest and chin on the steering wheel and dashboard. He sustained multiple facial fractures with obstruction of the upper airway

Pre-Operative Clinical Diagnosis in Pericardial Rupture

Although pericardial ruptures are not uncommon in major blunt chest trauma, these lesions are very seldom diagnosed clinically prior to operation. A characteristic “splashing” murmur, first described by Morel-Lavallee, is diagnostic. In a 54-year-old male sustaining blunt chest injury, this characteristic murmur was observed and the clinical diagnosis of pericardial rupture was verified at thoracotomy. A brief review of the literature is presented.

Cardiac tamponade resulting from non-penetrating chest injury, with reports of two cases.

Two cases are described in which cardiac tamponade resulted from blunt chest injury. The significance of various clinical features and the value of special investigations are discussed. It is emphasized that early diagnosis is facilitated by an awareness that this complication may be caused by such injury. Management is detailed, and the relevance of early and late follow up is indicated.

Traumatic Rupture of the Thoracic Aorta Following Blunt Chest Injury

Traumatic Rupture of the Thoracic Aorta Following Blunt Chest Injury