RESUMEN
BACKGROUND: Amniotic fluid embolism is an unpredictable and sometimes lethal complication of childbirth. Fibrinogen γ-chain peptide-coated, ADP-encapsulated Liposomes (H12-(ADP)-liposomes), which were developed as a platelet substitute, may be useful to control postpartum hemorrhage with consumptive coagulopathy. OBJECTIVE: This study aimed to establish a hemodynamically stable amniotic fluid embolism animal model and evaluate the efficacy of H12-ADP-liposome infusion in the initial management of postpartum hemorrhage complicated with amniotic fluid embolism-involved coagulopathy. STUDY DESIGN: Pregnant New Zealand white rabbits (28th day of pregnancy or normal gestation period of 29-35 days) underwent cesarean delivery, followed by intravenous administration of amniotic fluid (a total of 3.0 mL administered in 4 doses over 9 minutes). Thereafter, uncontrolled postpartum hemorrhage was induced by transecting the right midartery and concomitant vein in the myometrium. After initial bleeding for 5 minutes, rabbits received isovolemic fluid resuscitation through the femoral vein with an equivalent volume of blood loss every 5 minutes for 60 minutes. The transfusion regimens included platelet-rich plasma, platelet-poor plasma, and a bolus administration of H12-ADP-liposomes followed by platelet-poor plasma transfusion (8 rabbits per group). Moreover, 60 minutes after initiation of bleeding, rabbits received surgical hemostasis by ligation of bleeding vessels, except in cases with spontaneous hemostasis. RESULTS: The administration of amniotic fluid caused thrombocytopenia (56±3â¯×â¯103/µL) and prolonged both clotting time (before administration: 130.0±3.0 to 171.0±5.0 seconds) and prothrombin time (4.5±0.1 to 4.7±0.1 seconds). After the initial 5-minute bleeding in the rabbits, the mean arterial pressure fell to 43±2 mm Hg. Platelet-poor plasma transfusion alone further prolonged clotting time and prothrombin time at 60 minutes (192.0±10.0 and 5.2±0.1 seconds, respectively) with decreasing mean arterial pressure to <40 mm Hg. By contrast, the administration of H12-ADP-liposomes followed by platelet-poor plasma transfusion reduced the prolonged clotting time (153.0±5.0 seconds) and prothrombin time (4.9±0.1 seconds) similar to platelet-rich plasma transfusion (154.0±11.0 and 4.9±0.1 seconds, respectively) at 60 minutes. These rabbits maintained a mean arterial pressure of >45 mm Hg throughout the experiment. H12-ADP-liposome infusion and platelet-poor plasma transfusion and platelet-rich plasma transfusion yielded spontaneous hemostasis in 4 of 8 rabbits, whereas platelet-poor plasma transfusion did not stop bleeding in any of the rabbits. The total blood loss was 59±17 mL in the H12-ADP-liposomes and platelet-poor plasma group, which was half of that in the platelet-poor plasma group (124±10 mL). CONCLUSION: H12-ADP-liposome infusion may be effective in the initial management of postpartum hemorrhage complicated with amniotic fluid embolism, resulting in mitigation of consumptive coagulopathy.
RESUMEN
A 54-year-old woman was admitted for mitral valvular repair. After folding plasty to A3, a 30 mm Cosgrove-Edwards ring was placed. There was no mitral regurgitation jet observed by transesophageal echocardiography (TEE) during the operation. However, high blood pressure was monitored and treated in the intensive care unit, hemolytic anemia developed, and the serum lactate dehydrogenase level was elevated. Two weeks after the operation, serum lactate dehydrogenase was again elevated. TEE showed mild mitral regurgitation and the regurgitation jet colliding with the annuloplasty ring. Multiple transfusions of red blood cells were required. Repeat surgery was therefore undertaken. Lam and associates previously studying patients on hemolysis after mitral valvular repair noted high grade mitral regurgitation jets fragmented or accelerated. In the present case, mitral regurgitation was mild, but the high velocity and manner of regurgitation (collision with the annuloplasty ring) could cause hemolytic anemia. In the present case, high blood pressure might have caused chordae rupture. Furthermore, a flexible ring, such as the Cosgrove-Edwards ring, is likely to cause hemolytic anemia. As contributing factors to hemolysis after mitral valvular repair, perioperative blood pressure management and type of ring are significant.