Is the current system of staging lung cancer the best it can be?
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Biomedical subjects
Publications and source records attributed to R B Wagner.
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Conservative resection of a second primary lung cancer is desirable but not always feasible. We recently carried out three left pneumonectomies for the removal of metachronous primary lung cancers in patients who had previously undergone right upper lobe resection for the treatment of bronchogenic carcinoma. In each patient, the results of pulmonary function tests plus the findings from quantitative perfusion lung scans predicted a postpneumonectomy forced expiratory volume in 1 second of at least 1.00 L. All 3 patients had uncomplicated postoperative courses, and were doing satisfactorily at follow-up 2 to 6 months later. One patient died 5 months after pneumonectomy due to unrelated causes, another died 8 months after pneumonectomy from infection after resection of a brain metastasis, and the third is doing well 15 months after pneumonectomy. The rarity of previously reported cases suggests that performing a pneumonectomy after contralateral lobectomy may be considered too radical. Our experience indicates the procedure may be considered if the patient's pulmonary function meets the standard criteria for pneumonectomy.
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Thoracic surgery is undergoing major changes. In addition to the well publicized political and economic upheavals, our patients and the diseases targeted are rapidly evolving. Much of the change is driven by an explosion of new biology that many in the field have little or no familiarity with. As molecular biology, immunology, and information about cytokines pervade our literature and practices, it is imperative that thoracic surgeons develop a basic understanding of these and other unique concepts. The best link between our clinical practice and the new biology is thoracic surgical scientists who are exposed to current information.
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Our purpose was to examine changes in pulmonary hemodynamics for patients with pulmonary contusion. Pulmonary vascular resistance index (PVRI) and shunt fraction were calculated from standard measurements in 25 traumatized patients. The percent of lung volume injured, measured as air-space filling disease (ASF), was quantitated from computed tomograms using a previously described technique. The amount of reactive pulmonary vasoconstriction per unit of injury (PVRI/ASF) identified 3 groups of patients: 5 were reactors (PVRI/ASF greater than 15), 10 were weak-reactors (PVRI/ASF = 5 to 15), and 10 were nonreactors (PVRI/ASF less than 5). In the reactor group PVRI increased as the size of contusion (ASF) increased (r = 0.99). In weak-reactors PVRI also increased with the size of contusion (r = 0.93), but the slope was less pronounced. In both groups shunt fraction did not rise above 0.31. In the nonreactors, PVRI remained normal while shunt fraction increased with the extent of injury (r = 0.95). These results indicate that pulmonary vasoconstriction often occurs after pulmonary contusion. The vasoconstriction most probably represents a compensatory mechanism to limit perfusion of traumatized parenchyma, thereby minimizing increases in shunt fraction. Some patients (nonreactors) not demonstrating this response have unchecked increases in shunt fraction. This insight into the hemodynamic sequelae of pulmonary contusions may enhance our ability to provide optimal care for patients suffering from this injury.
Two patients with traumatic rupture of the mid-descending aorta successfully repaired are presented. Most clinical series of aortic tears do not include this entity. A review of the world literature reveals only 9 previous cases. In 6 of the 11 patients the diagnosis was either missed or delayed. In 4 patients the diagnosis was delayed or missed because of the absence of a superior mediastinal hematoma, and in 2 patients the diagnosis was delayed because of inadequate (single-plane) aortography. Suspicion may be lacking because of absence of the upper mediastinal hematoma considered to be the sine qua non for the diagnosis of aortic rupture. Although deceleration is considered to be the mechanism of injury in tears at the isthmus, severe hyperextension (often associated with fracture dislocation of the underlying thoracic vertebra) is considered to be the causative factor in descending aortic tears. Experience with the 2 patients presented here demonstrates that a high index of suspicion and complete two-plane aortography is required to avoid the potential for catastrophic outcome subsequent to overlooking a tear of the mid-descending aorta.
Long-term successes in treating carcinoid tumors suggest that in poor-risk patients endobronchial resection, when possible, be considered the treatment of choice.
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The basic principles of the pathology, physiology, diagnosis, and management of nonpenetrating chest trauma evolved to a significant degree before World War II. The advances in the past 40 years include more frequent use of endotracheal intubation, improved ventilatory assistance, better control of blood volume, antibiotics, the clinical application of blood-gas studies, diagnostic imaging, and specialized nursing and monitoring in intensive care units. Thus, the improvement in survival is not primarily attributable to operative measures but rather to enhanced supportive measures.
In thoracic trauma, as in all of medicine, diagnosis precedes therapy. Over the past 5 years, we have liberally used chest CT examinations to improve diagnosis in the severely injured patient. This approach has significantly increased our diagnostic yield and permitted early diagnosis and treatment of unsuspected injuries. Confidence in our method of quantitation has helped us to assess the severity of pulmonary parenchymal injuries. Correlation of the CT findings with histologic study has changed our concept of pulmonary contusion from that of interstitial disease to that of pulmonary laceration with blood pneumonia.
Sixty-nine patients with nonpenetrating pulmonary trauma were studied by chest computed tomography (CT) within 24 hours of admission. The percentage of air-space filling was quantitated and compared with the requirement for ventilatory support. Pulmonary intraalveolar hemorrhage always is gravity dependent originating at the site of injury. Utilizing CT, the patients' pulmonary status was classified into three separate clinicoradiologic groups: Grade I injury (less than 18% air-space filling, no ventilator support required), Grade II injury (18-28% air-space filling, ventilator support sometimes required), and Grade III injury (greater than 28 air-space filling, ventilator support always required). The CT quantitation correlated with clinical functional studies and was useful in the therapeutic management of nonpenetrating lung injury.
Pulmonary contusion, implying interstitial and alveolar injury without significant laceration, has been accepted as the primary lung injury in nonpenetrating chest trauma. Computed tomographic (CT) findings were compared with those of chest radiography in 85 consecutive patients with chest trauma in which there was a pulmonary radiodensity consistent with pulmonary contusion or patients with a history of severe chest trauma with normal parenchyma despite rib fractures, hemothorax, pneumothorax, or widened mediastinum. CT was found to be more sensitive than radiography in that 151 abnormalities (excluding rib fractures) were demonstrated on radiographs versus 423 abnormalities on CT scans, and 99 lacerations were seen on CT scans versus five on radiographs. Pulmonary lacerations were classified into four types on the basis of CT findings and mechanism of injury: compression rupture, compression shear, rib penetration, and adhesion tears. In these cases, pulmonary laceration was shown to be an integral component of the mechanism of injury in pulmonary contusion, pulmonary hematoma, pulmonary cyst or pneumatocele, or cavitation in pulmonary contusion.
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