Haemocompatibility of paediatric membrane oxygenators with heparin-coated surfaces

Extracorporeal circulation (ECC) in paediatric patients with heparin-coated oxygenation systems is rarely investigated. The objective of this study was to evaluate, preclinically, the haemocompatibility of paediatric membrane oxygenators with heparin-coated surfaces. We compared 16 paediatric membrane oxygenators (Minimax, Medtronic) in an in vitro heart-lung machine model with fresh human blood. Eight of these oxygenation systems had a covalent heparin coating (Carmeda bioactive surface). After 90 min simulated ECC, the heparin-coated systems showed significantly higher platelet count, lower platelet-factor 4 release, reduced contact activation (factor XIIa and kallikrein), and lower neutrophil elastase levels ( p &lt; 0.05), compared to the noncoated oxygenator group. More biocompatible materials for paediatric operations may ameliorate the various postperfusion syndromes arising from ECC procedures, particularly unspecific inflammation, hyperfibrinolysis and blood loss. </jats:p

Aprotinin in fibrin tissue adhesives induces specific antibody response and increases antibody response of high-dose intravenous application

AbstractBackground: In cardiac operations, aprotinin therapy is used either locally as a component of commercially available fibrin tissue adhesives, intravenously, or combined. Our aim was to examine the formation of aprotinin-specific antibodies with regard to the application mode. Methods: Sera of 150 patients who had undergone cardiac operations and were receiving aprotinin therapy for the first time were sampled before the operation and at medians of 3.5 and 13.3 months after the operation. Aprotinin-specific IgG including all subgroups and aprotinin-specific IgE were analyzed. Aprotinin was given locally (as contained in fibrin sealant; n = 45; median dose, 6000 KIU), intravenously (n = 46; 2.000 × 106 KIU), and combined (n = 59; 2.012 × 106 KIU). Results: At 3.5 months, the prevalence of aprotinin-specific IgG antibodies was 33% (15/45 patients) after local, 28% (13/46 patients) after intravenous, and 69% (41/59 patients) after combined exposure (P = .0001). At 13.3 months, the prevalence of aprotinin-specific IgG antibodies was 10% (4/41 patients) after local, 31% (13/42 patients) after intravenous, and 49% (28/57 patients) after combined exposure. Total aprotinin dose was similar in patients who were antibody positive and negative. Before the operation, no aprotinin-specific antibodies were detected. Aprotinin-specific IgE were not found after the operation. Conclusion: Local aprotinin contact induces a specific immune response and reinforces that of intravenous exposure. The antibody spectrum is identical to the immune response induced by intravenous exposure. Any exposure should be documented. For use in cardiac operations as a hemostyptic, the necessity itself and alternatives for aprotinin as a stabilizing agent merit consideration. (J Thorac Cardiovasc Surg 1999;118:348-53

Fibrin sealant, aprotinin, and immune response in children undergoing operations for congenital heart disease

AbstractObjective: Most commercially available fibrin sealants contain aprotinin in doses of 1500 kallikrein inactivator units per milliliter. They are used in many operative disciplines. An elevated risk of hypersensitivity reactions exists at reexposure to aprotinin. Our aim was to examine the immunogenic potency of aprotinin as a fibrin sealant content. Methods: We investigated 49 children with operatively treated congenital heart disease. All patients received aprotinin only topically as contained in fibrin sealant. Serum samples were drawn preoperatively, 1 week, 2 weeks, 6 weeks, and approximately 1 year after operation. They were analyzed for aprotinin-specific immunoglobulin G antibodies with a standard enzyme-linked immunosorbent assay and a fluorescence enzyme immunoassay for aprotinin-specific immunoglobulin E antibodies. Results: At 1 week, 2 weeks, 6 weeks, and 1 year, we found prevalences of 8% (2 of 26), 8% (2 of 24), 6% (3 of 49), and 0% for aprotinin-specific Immunoglobulin E, and for aprotinin-specific immunoglobulin G 8% (2 of 26), 17% (4 of 24), 39% (19 of 49), and 12% (5 of 41). The doses of aprotinin given did not differ significantly in antibody-negative and antibody-positive patients; no significant factors could predict the immune response. Conclusions: Our findings show the existence of a subgroup of patients who had aprotinin-specific antibodies develop after topical aprotinin application. Any use of aprotinin must be carefully documented. If aprotinin use is planned in patients who previously underwent a surgical procedure, preexposure to aprotinin in any form must be sought to avoid unexpected anaphylactic reactions. The necessity itself and alternatives for aprotinin as a stabilizing agent in fibrin sealants merit consideration. (J Thorac Cardiovasc Surg 1998;115:883-9