The Annals of thoracic surgery
-
Postpneumonectomy syndrome, a late complication of pneumonectomy, is secondary to shift of the mediastinum and remaining lung toward the pneumonectomy side, leading to tracheobronchial compression between the vertebral body and the aorta or pulmonary artery. Obstructive airway symptoms are usually due to tracheobronchial tree compression, however, secondary airway malacia may develop. We report herein a case of postpneumonectomy syndrome with secondary bronchomalacia after left pneumonectomy in a patient with normal mediastinal vascular anatomy.
-
The responsibility for those of us involved in residency training programs is to foster the development of future leaders in thoracic surgery. Although the actual training of female surgeons is no different than training male surgeons, academic advancement after training can be more difficult for women due to a variety of reasons. The education and training of female surgeons has its origin in admission to medical school followed by recruitment into a residency program. ⋯ Specific recommendations are made for retainment of faculty. In addition to academic promotion and financial reward, creating the proper environment is an important consideration to allow women the chance to succeed in medicine. This report addresses the training aspects involved in the thoracic residency program and the state of professional academic advancement at the Johns Hopkins University School of Medicine.
-
Randomized Controlled Trial Clinical Trial
Cardiac ischemic preconditioning improves lung preservation in valve replacement operations.
Previous work has shown that cardiac ischemic preconditioning reduces cardiac reperfusion injury. We investigated whether cardiac ischemic preconditioning can improve lung preservation in patients who undergo valve replacement. ⋯ Cardiac ischemic preconditioning improves lung preservation in patients having valve replacement. The mechanism may be that cardiac ischemic preconditioning reduces the accumulation of polymorphonuclear leukocytes in lung tissue and decreases the formation of oxygen free radicals.
-
Neurocognitive decline, often produced by atherosclerotic plaque embolization, remains a frequent complication of cardiopulmonary bypass. Plaque fragments may initiate local thrombosis, which, in turn, aggravates the embolic insult. Prothrombotic genetic factors may exacerbate this process. We investigated whether the PlA2 polymorphism of platelet GPIIIa, a prothrombotic risk factor in other cardiovascular settings, is associated with early neurocognitive decline after cardiopulmonary bypass. ⋯ This study demonstrates a link between the PlA2 allele of platelet GPIIIa and more severe neurocognitive decline after cardiopulmonary bypass. Although the mechanism is unknown, it could represent exacerbation of platelet-dependent thrombotic processes associated with plaque embolism.
-
Cardiopulmonary bypass is associated with a systemic inflammatory response, a spectrum of pathophysiologic changes ranging from mild organ dysfunction to multisystem organ failure. Complications include coagulation disorders (bleeding diathesis, hyperfibrinolysis) from platelet defects and plasmin activation, as well as pulmonary dysfunction from neutrophil sequestration and degranulation. Diverse injuries are a consequence of multiple inflammatory mediators (complement, kinins, kallikrein, cytokines). ⋯ Specifically, inhibition of factor XII, bradykinin, C5a, neutrophil integrin expression, elastase activity, and airway nitric oxide production are observed. Clinical correlates include reduced capillary leak, preserved systemic vascular resistance and blood pressure, and improved myocardial recovery following ischemia. Overall, evidence indicates that aprotinin attenuates the systemic inflammatory response associated with cardiopulmonary bypass.