Incidence: hyper acute lung transplant rejection has become a rare type of rejection (due to more sensitive and specific pre-transplant screening for HLA antibodies
Physiology
Reaction of Preformed Recipient Donor-Specific Antibodies, Usually Directed Against Foreign Donor Human Leukocyte Antigens (HLA)
Less commonly, antibodies may be directed against donor ABO blood group or endothelial antigens
Bronchoalveolar Lavage (BAL): useful to examine the bronchial anastomosis, assess for alveolar hemorrhage, and obtain microbiologic samples
Transbronchial Biopsy (TBB) (see Bronchoscopy, [[Bronchoscopy]]): risk of TBB may be prohibitive
Open Lung Biopsy
Marked neutrophilic interstital infiltrate, alveolar edema, small arteriolar platelet and fibrin thrombi -> alveolar capillaries are the primary target of injury in hyperacute rejection
Cross-Match Between Recipient Serum and Donor Cells Demontrating Incompatibility
Diagnostic
Presence of Pre-Transplant Donor-Specific Antibodies in Recipient’s Serum
Diagnostic
Clinical Manifestations
General Comments
Onset: min-hours (usually within 24 hrs post-transplant)
Bortezomib (Velcade) (see Bortezomib, [[Bortezomib]]): proteasome inhibitor, which has pro-apoptotic effects on plasma cells -> decreases antibody synthesis
Corticosteroids (see Corticosteroids, [[Corticosteroids]]): while patients are typically receiving corticosteroids as part of their induction regimen, they are not believed to be useful in the management of hyperacute rejection
Cyclophosphamide (Cytoxan) (see Cyclophosphamide, [[Cyclophosphamide]])
Eculizumab (Soliris) (see Eculizumab, [[Eculizumab]]): anti-complement C5 antibody
Intravenous Immunoglobulin (IVIG) (see Intravenous Immunoglobulin, [[Intravenous Immunoglobulin]]): causes B-lymphocyte apoptosis, blocks binding of donor-reactive antibodies, and inhibits complement activation
Plasmapheresis (see Plasmapheresis, [[Plasmapheresis]]): rapidly removes anti-donor antibodies from peripheral blood to prevent further allograft damage