Pulmonary amniotic fluid embolism in a rhesus macaque (Macaca mulatta).

A pregnant female rhesus macaque died spontaneously during stage two labor. Gross and histopathologic findings included severe pulmonary edema, with low numbers of blood vessels containing pale basophilic mucinous material (Alcian Blue positive and PTAH negative), consistent with intravascular amniotic fluid-derived mucin resulting in pulmonary amniotic fluid embolism.

Intravenous injection of autologous amniotic fluid induces transient thrombocytopenia in a gravid rabbit model of amniotic fluid embolism.

BACKGROUND: Amniotic fluid embolism (AFE) is a rare but catastrophic complication of pregnancy characterized by severe hypotension, cardiovascular collapse, and massive consumptive coagulopathy. Several animal models of this syndrome have been proposed, but most have yielded inconclusive 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 autologous 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 coagulation 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), prothrombin time (PT), or Factor VIII activity. However, significant thrombocytopenia 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.

Oximetry for amniotic fluid embolism detection in mini-pigs: tail or snout?

The continuous, non-invasive real-time monitoring of arterial oxygenation (pulse oximetry) has become a standard of care in both human and veterinary medicine. It allows reliable, simple and inexpensive assessment of the arterial oxygenation status. In pigs, commonly used sites for oximetry-probe placement are the ear, snout or tongue, while more recently the 'pig-tail oximetry' has been suggested. In a study regarding the coagulation system during amniotic fluid embolism (AFE) in mini-pigs, we compared tail and snout for oximetry-probe placement and compared them with the 'gold standard': blood-gas analysis (BGA). In both the AFE group and the control group, the tail measurements were slightly lower and the snout measurements were slightly higher than the BGA results. In the experimental model used, both tail and snout measurements were able to detect a temporary desaturation immediately after amniotic fluid embolism (AFE). Blood-gas analysis (BGA) performed on blood drawn from a large artery missed the event. Clinically, there is no significant difference between snout and tail as oximetry-probe placement sites: both are reliable oximetry sites in mini-pigs.