Amniotic fluid embolism: Pathophysiology from the perspective of pathology.

Amniotic fluid embolism (AFE) is recognized as a type of syndrome characterized by the abrupt onset of hypoxia, hypotension, seizures, or disseminated intravascular coagulopathy (DIC), occurring during labor, delivery, or immediately postpartum, caused by the inflow of amniotic components into the maternal circulation. AFE is a rare condition but one of the most serious obstetrical complications, resulting in a high mortality rate among pregnant women. Despite earlier recognition and intensive critical management, we often encounter patients who unfortunately do not recover from the exacerbation of AFE-related conditions. A major concern is that there are no effective evidence-based therapies for AFE, because its pathophysiology is still not well understood. This article reviewed AFE, focusing on the pathology and currently proposed pathophysiology.

Histological characteristics of the myometrium in the postpartum hemorrhage of unknown etiology: a possible involvement of local immune reactions.

The aim of this study was to evaluate the histological characteristics of the myometrium obtained in postpartum hemorrhage (PPH) of unknown etiology secondary to uterine atony. These characteristics were selected from among registered cases of clinically suspected amniotic fluid embolism (AFE) and classified as PPH of unknown etiology because of no obvious cause of PPH at Hamamatsu University School of Medicine, a registration center for clinical AFE in Japan. Immunohistochemical studies were performed on myometrium using anti-mast cell tryptase, anti-neutrophil elastase, anti-CD68, anti-CD88, anti-CD3, and anti-ZnCP-1 antibodies. Massive infiltrations of inflammatory cells with mast cell degranulation within the myometrium secondary to complement activation were observed in PPH of unknown etiology (n=34), but not in control pregnant women (n=15) or after delivery in women without PPH (n=18). The concomitant immunohistochemical detection of meconium in myometrium suggests that amniotic fluids or fetal materials are one of the candidates for inducing maternal local immune activation in the PPH of unknown etiology. Postpartum acute myometritis in the absence of an infective etiology may be a histological characteristic of PPH of unknown etiology.

C1 esterase inhibitor activity in amniotic fluid embolism.

OBJECTIVES: Amniotic fluid embolism exhibits activation of the complement system and the kallikrein-kinin and coagulofibrinolytic systems. C1 esterase inhibitor is a major inhibitor of C1 esterase and can inhibit plasma kallikrein and also factors XIIa and XIa. Its activity has been shown to be significantly lower in pregnancy and labor than in the nonpregnant state. The purpose of this study was to determine C1 esterase inhibitor activity levels in amniotic fluid embolism. DESIGN: Retrospective study. SETTING: A single university-based center. PATIENTS: One hundred six cases with amniotic fluid embolism in a total of 194 singleton pregnant women between January 2010 and December 2011. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: One hundred six cases of amniotic fluid embolism had applied to the Japan amniotic fluid embolism registration center in Hamamatsu University School of Medicine between January 2010 and December 2011. In amniotic fluid embolism cases, 85 cases were nonfatal and 21 cases were fatal. Eighty-eight women who delivered without amniotic fluid embolism were regarded as a control. C1 esterase inhibitor activity levels were significantly lower in amniotic fluid embolism patients (30.0% ± 1.8%) than in control women (62.0% ± 2.0%) (p < 0.0001). C1 esterase inhibitor activity levels in fatal amniotic fluid embolism cases (22.5% ± 3.4%) were significantly lower than those in nonfatal amniotic fluid embolism cases (32.0% ± 2.1%) (p < 0.05). CONCLUSIONS: These results demonstrated that low C1 esterase inhibitor activity levels were closely associated with the pathogenesis of amniotic fluid embolism suggesting that C1 esterase inhibitor activity levels have potential as a prognosis factor of amniotic fluid embolism.