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Pulmonary hemorrhage (PHEM) complicates the hospital course of 3-5% of preterm infants with respiratory distress syndrome (RDS), and bears a high mortality rate. Impaired thrombin generation and poor clot formation in premature neonates affect PHEM severity.We evaluated the impact of surfactant upon in-vitro clot formation in order to assess the role of surfactant in the pathogenesis of PHEM.Blood samples were obtained from healthy volunteers for measuring complete blood count, PT, PTT, and platelet function. Surfactant at increasing concentrations was added to blood samples, and whole blood clotting assays were performed using rotation thromboelastogram (ROTEM®, Pentapharm Munich, Germany) and whole blood platelet adhesion and aggregation (Impact-R®, Diamed, Switzerland).The mean PT level increased from 10.05 ± 033 to 11.64 ± 0.85 sec (p=0.06) in the presence of surfactant. Platelet aggregation with the agonists adenosine diphosphate and epinephrine significantly decreased with escalating surfactant concentration (p0.001). Adhesion, manifested by surface coverage (SC), significantly decreased with increasing surfactant concentration: mean SC 9.25 ± 2.96 compared to 6.1 ± 0.96 and 0.05 ± 0.058 with 0/0.1/5mg/ml surfactant, respectively, p0.001 Whole blood ROTEM studies showed a trend towards lengthening of clotting time with increased surfactant concentration and lower clot strength.The presence of surfactant impairs coagulation in-vitro. The risk of PHEM may therefore be greater in extremely premature infants. Future studies are required to assess the clinical significance and relevance of our preliminary findings.

Summary. Objectives: The hypothesis that the administration of fibrinogen concentrate enables restoration of impaired clot formation and increased bleeding in severe thrombocytopenia was tested. Methods: Thirty pigs were anesthetized, instrumented for blood sampling (routine coagulation tests, modified thrombelastography ROTEM®), hemodynamic monitoring and platelet apheresis to a target below 30 × 109 L−1 after splenectomy. Thereafter 10 each of the animals randomly received two apheresis platelet concentrates, 250 mg kg−1 fibrinogen concentrate or normal saline solution. A standardized liver injury was subsequently inflicted to induce uncontrolled hemorrhage. Results: Median (Q1, Q3) clot firmness increased significantly more in thrombocytopenic pigs after fibrinogen administration (42 mm (41, 43) to 60 mm (57, 63)) than following platelet transfusion (40 mm (37, 45) to 52 mm (48, 55), P = 0.0004) or placebo (45 mm (41, 48) to 45 mm (43, 46), P = 0.0002). Median blood loss velocity after liver injury was significantly less with fibrinogen (33 mL min−1, P = 0.005) than with platelets (62 mL min−1, P = 0.037) or saline (84 mL min−1, P = 0.005), and median survival time after liver injury was 55 min in the fibrinogen, 26 min in the platelet (P = 0.035) and 19 min in the saline group (P =

Objective. The purpose of this study was to evaluate postoperative bleeding in patients treated with oral anticoagulant drugs who underwent dental extractions without interruption of the treatment and to compare the effect of 3 different hemostatic modalities. Study design. A total of 150 patients who underwent dental extractions were divided into 3 groups. Local hemostasis was carried out as follows: group 1 (119 extractions), with gelatin sponge and sutures; group 2 (117 extractions), with gelatin sponge, sutures, and mouthwash with tranexamic acid; group 3 (123 extractions), with fibrin glue, gelatin sponge, and sutures. Results. Of 150 patients, 13 (8.6%) presented with postoperative bleeding: 3 patients from group 1, 6 patients from group 2, and 4 patients from group 3. Conclusions. Dental extractions can be performed without interruption in patients treated with oral anticoagulant. Local hemostasis with gelatin sponge and sutures is sufficient. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:137-40)