BRIEF COMMUNICATION Intravenous injection of autologous amniotic fluid induces transient thrombocytopenia in a gravid rabbit model of amniotic fluid embolism B. Rannou 1 , G.-E. Rivard 2 , M. J. Gains 1 , C. Be ´ dard 1 1 Department of Pathology and Microbiology, Faculty of Veterinary Medicine, Universite ´ de Montre ´ al, Montre ´ al, Que ´ bec, Canada; and 2 Centre Hospitalier Universitaire Sainte-Justine, Montre ´ al, Que ´ bec, Canada Key Words Animal model, coagulation, hypercoagulability, pregnancy, TEG Correspondence B. Rannou, VetAgro Sup, Unite ´ de Biochimie et d’Endocrinologie, 1 Avenue Bourgelat, 69280 Marcy l’E ´ toile, France E-mail: b.rannou@vetagro-sup.fr DOI:10.1111/j.1939-165X.2011.00369.x Background: Amniotic fluid embolism (AFE) is a rare but catastrophic complication of pregnancy characterized by severe hypotension, cardiovas- cular collapse, and massive consumptive coagulopathy. Several animal models of this syndrome have been proposed, but most have yielded incon- clusive results. Objectives: The objective of this study was to develop a suitable animal model of AFE. Methods: Twelve rabbits in late gestation (25 days) were used. Amniotic fluid was collected from the fetal amniotic sacs after laparotomy, and autol- ogous fluid was injected into 6 rabbits via the left auricular vein. Six other rabbits received saline (control group). Blood pressure, platelet counts, and coagulation variables were measured at baseline and at various intervals for 60 minutes after injection. The in vitro effect of amniotic fluid on coag- ulation was assessed by thrombelastographic (TEG) analysis. Results: Injection of amniotic fluid did not reproduce clinical signs of AFE and had no effect on activated partial thromboplastin time (aPTT), pro- thrombin time (PT), or Factor VIII activity. However, significant thrombo- cytopenia was observed 5 minutes after administration of amniotic fluid and resolved by 60 minutes. In vitro addition of amniotic fluid to blood resulted in accelerated clotting on TEG tracings. Conclusions: The syndrome of AFE was not reproduced in this rabbit model. However, injection of autologous amniotic fluid induced a transient and severe thrombocytopenia. Moreover, TEG analysis indicated that amniotic fluid could initiate the coagulation cascade. Other factors such as the presence of meconium in amniotic fluid may be needed to provoke more severe clinical signs. Amniotic fluid embolism (AFE) is a rare but cata- strophic complication of pregnancy in woman that typically occurs during labor and delivery or in the immediate postpartum period. 1 It is initiated by the entry of amniotic fluid into maternal circulation and is generally characterized by the sudden onset of severe dyspnea, tachypnea, and cyanosis. 2,3 These clinical signs are provoked by severe hypotension and cardio- vascular collapse that may lead to cardiac arrest and death. 4,5 If the patient survives this initial event, bleed- ing frequently occurs secondary to massive consump- tive coagulopathy. 2,6 Specific prodromes or risk factors have not been clearly identified. 2,3,7,8 Given the unpredictable nature and the rarity of AFE, its pathophysiology is poorly understood. Although cardiovascular signs were thought histori- cally to be secondary to embolization of amniotic cells and amorphous elements of amniotic fluid or meco- nium, many studies have suggested that those signs resulted from biochemical mediators released after embolization occurs. 9–11 To better understand the pathophysiology of AFE, several animal models have been developed; however, many models have failed to reproduce the syndrome, possibly due to use of male animals and nonpregnant females, as well as to injec- tion of heterologous (usually human) amniotic fluid or Vet Clin Pathol 40/4 (2011) 524–529 ©2011 American Society for Veterinary Clinical Pathology 524 Veterinary Clinical Pathology ISSN 0275-6382