ABSTRACT
Lung transplantation is an established therapeutic option for selected patients with various end stage pulmonary diseases which prolongs survival and improves quality of life. A multitude of pulmonary and non-pulmonary complications can lead to significant morbidity thus impairing short and long-term survival. Early recognition and fast treatment of these complications are fundamental measures to prevent secondary destructive incidents. This article reviews the most frequent complications arising after lung transplantation.
ABSTRACT
Despite immediate surgical repair of the entry site in acute thoracic aortic dissection with visceral malperfusion, the results are poor. Primary restitution of visceral flow by intervention might be one way to cope with this problem, but probably causes ischemia/reperfusion associated problems after prolonged complete visceral ischemia. In this report, we demonstrate a successful attempt of controlled delay of thoracic aortic surgical repair after visceral flow restitution with stable hemodynamics.
Subject(s)
Aortic Aneurysm, Thoracic/surgery , Aortic Dissection/surgery , Blood Vessel Prosthesis Implantation , Critical Care , Ischemia/surgery , Radiography, Interventional , Reperfusion Injury/prevention & control , Viscera/blood supply , Aged, 80 and over , Aortic Dissection/complications , Aortic Dissection/diagnostic imaging , Aortic Dissection/physiopathology , Aortic Aneurysm, Thoracic/complications , Aortic Aneurysm, Thoracic/diagnostic imaging , Aortic Aneurysm, Thoracic/physiopathology , Cardiopulmonary Bypass , Fatal Outcome , Female , Humans , Ischemia/diagnostic imaging , Ischemia/etiology , Ischemia/physiopathology , Male , Middle Aged , Regional Blood Flow , Reperfusion Injury/diagnostic imaging , Reperfusion Injury/etiology , Reperfusion Injury/physiopathologyABSTRACT
OBJECTIVE: Clinical complications arising from extracorporeal circulation (ECC) have been linked to disturbances in the microcirculation. Hyperoxia, a mainstay of supportive treatment, is clinically used for a variety of pathological states. In previous in vivo animal experiments we found increased leukocyte/endothelial (L/E) cell interaction following ECC due to oxygen derived free radicals. This study was carried out to investigate the link between arterial pO2 during ECC and the potential damage to the microcirculation, supposedly caused by oxygen derived radicals. METHODS: Intravital fluorescence microscopy was used on the dorsal skinfold chamber preparation in syrian golden hamsters. ECC was introduced via a micro-rollerpump (0.7 ml/min) and a 60 cm silicon tube (1 mm inner diameter) shunted between the carotid artery and the jugular vein after application of 300 IE Heparin/kg/bw. Experiments were performed in chronically instrumented, awake animals (age: 10-14 weeks, weight: 65-75 g). Control inspired room air, experimental group 1 inspired 100% oxygen, group 2 received 100% oxygen and 2000 IE of Heparin i.v. (n=7/group), that releases endothelial bound superoxide dismutase, a natural scavenger of oxygen derived free radicals in the hamster. RESULTS: Normobaric inhalation of 100% oxygen increased arterial pO2 from 64+/-8.1 mmHg to 512+/-124 mmHg (P<0.05 vs. baseline). ECC under 100% oxygen reduced functional capillary density (FCD) to 70% of baseline values 8 h after ECC (P<0.05). Adherent leukocytes in postcapillary venules and arterioles increased significantly (P<0.05). 2000 IE Heparin prevented the reduction in FCD and decreased the number of adherent leukocytes. CONCLUSIONS: Reduction in FCD, increased leukocyte adherence to the microvascular endothelium of postcapillary venules and arterioles under hyperoxia compared to ECC under room air conditions, demonstrates harmful effects of oxygen during ECC in vivo. A high dose of Heparin enhances functional capillary density, thus attenuating the microvascular dysfunction/damage in the period after ECC.
