Brain-dead donors are the major source of lungs for transplantation. Brain death is characterized by two hemodynamic phases. Initially, massive sympathetic discharge results in a hypertensive crisis. This is followed by neurogenic hypotension. Up-regulation of pro-inflammatory mediators occurs in all organs and lung injury develops; this can adversely affect graft function post-transplantation. The mechanisms of the systemic and lung inflammation are unknown. We hypothesized that the hemodynamic changes are responsible for these inflammatory phenomena. Brain death was induced by intra-cranial balloon inflation in rats. This resulted in hypertensive crisis, followed by hypotension. There was a significant increase in blood neutrophil CD11b/CD18 expression and pro-inflammatory cytokine levels in serum and bronchoalveolar lavage, compared with control animals. Rupture of the capillary-alveolar membrane was demonstrated by electron microscopy. Elimination of the hypertensive response by a -adrenergic antagonist pre-treatment prevented inflammatory lung injury, reduced the systemic inflammatory markers and preserved capillary-alveolar membrane integrity. Correction of the neurogenic hypotension with noradrenaline ameliorated the systemic inflammatory response and improved oxygenation. We conclude that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension. Management of the brain-dead donor with early anti-inflammatory treatment and vasoconstrictors is warranted.

The paucity of suitable lung donors and the high early mortality as the result of primary graft failure remain major challenges in pulmonary transplantation. There is evidence that the lung is injured in the donor by the process of brain death and often is made unusable or fails posttransplantation after amplification of the injury by the process of ischemia-reperfusion. An understanding of the mechanism of donor lung injury could lead to the development of new treatment strategies for the donor to reduce lung injury, increase the number of donors with acceptable lungs, and improve the results of transplantation. The pathophysiology of brain death is complex and involves sympathetic, hemodynamic, and inflammatory mechanisms that can injure the lung. The literature is reviewed, and these mechanisms are discussed together with their possible interrelations.

(2015). Indications for red blood cell transfusion in cardiac surgery: A systematic review and meta-analysis. Lancet Haematology, 2(12), e543-e553. DOI: 10.1016/S2352-3026 (15) University of Bristol -Explore Bristol Research General rightsThis document is made available in accordance with publisher policies. Please cite only the published version using the reference above. Full terms of use are available:

Sympathetic discharge and hypertensive crisis often accompany brain death, causing neurogenic pulmonary edema. Progressive systemic inflammatory response develops, which can injure the lung further. We investigated whether (a) early hemodynamic injury during donor brain death increases reperfusion injury after lung transplantation and (b) delaying lung recovery would augment reperfusion injury further, because of the progressive systemic inflammatory response in the donor. Brain death was induced by intracranial balloon inflation in rats, with or without a-adrenergic blockade pretreatment to prevent the hypertensive crisis. Another group of rats had a sham procedure. Lungs were retrieved 15 min after brain death or sham procedure and reperfused using recipient rats. In a fourth group, brain death was induced and the lungs were retrieved 5 h after brain death and reperfused. Postreperfusion, lungs retrieved early from untreated brain-dead donors developed more severe reperfusion injury, as assessed by functional parameters and inflammatory markers, than those from sham or alpha-blockadetreated donors. Lungs retrieved late from brain-dead donors had similar inflammatory markers after reperfusion to those retrieved early, but significantly lower pulmonary vascular resistance. Early hemodynamic damage during donor brain death increases reperfusion injury after lung transplantation. Delaying retrieval may allow the lung to recover from the hemodynamic injury.

Primary lymphoma of the liver is extremely rare, and is more common among immunocompromised patients. It typically occurs during the fifth decade of life and has a male predominance. Abdominal pain, weight loss, and fever are the normal symptoms. Liver function tests are usually upset. Ultrasonography, computed tomography, and magnetic resonance imaging can help in the diagnosis, which can be confirmed only by histological examination of a liver biopsy specimen. Treatments include surgery, chemotherapy, and radiotherapy all of which give good results. Surgical resection when feasible is beneficial.