Amniotic fluid embolism: Pathophysiology and new strategies for management

Abstract

The registry program of amniotic fluid embolism (AFE) in Japan started in 2003. More than 400 hundred clinical diagnosed amniotic fluid embolism has been accumulated. Those data showed that there were two etiologies of AFE: the fetal materials create physical obstructions in the maternal microvessels in various organs, such as the lung; and (ii) the liquids cause an anaphylactoid reaction that leads to pulmonary vasospasm and activation of platelets, white blood cells and/or complements. The clinical findings showed that AFE was characterized mainly by cardiopulmonary collapse, the other involves the presence of disseminated intravascular coagulation (DIC) and atonic bleeding. Zinc coproporphyrin-1, sialyl Tn antigen (STN), complement C3, C4 and interleukin-8 have been used as serum markers of AFE. The levels of zinc coproporphyrin-1 and STN were increased in cardiopulmonary collapse type AFE, and a marked reduction of C3 and C4 was observed in DIC type AFE. At the primary medical institution, initial treatments for shock airway management, vascular management, fluid replacement, administration of anti-DIC therapy such as antithrombin, and administration of fresh frozen plasma should be provided. C1 esterase inhibitor activity in AFE cases was significantly lower than those of normal pregnant women. C1 esterase inhibitor may be a promising candidate of treatment of AFE.

Amniotic fluid embolism

“…Recently, recombinant factor VIIa has been tried in such scenarios, but was associated with worse outcomes and thus is no longer recommended [41,42]. C1INH concentrates have been shown to revert hereditary angioedema in C1INH deficient patients; thus the administration of C1INH may turn out to be a promising treatment in some cases of AFE [1].…”

“…AFE appears to involve an abnormal activation of humoral and immunologic mechanisms leading to a massive inflammatory reaction following the entry into the maternal circulation of fetal antigens. Although classically associated with delivery process, it has been described in the settings of abortion, maternal trauma, amniocentesis, cervical lacerations, and manual removal of the placenta [1][2][3][4][5][6][7]. Despite its infrequent occurrence, AFE continues to be one of the leading causes of maternal mortality in the United States, and is estimated to be causative in roughly 10% of maternal deaths in developed countries [8].…”

Amniotic Fluid Embolism: An Update of the Evidence

“…Additionally, instrumental vaginal and caesarean deliveries are associated with the occurrence of AFE post-natally [5]. In fact, the rupture of the membranes followed by the inflow of amniotic fluid into maternal circulation occurs easily in cases of cesarean delivery, forceps/vacuum delivery, placenta previa, abruption placenta and eclampsia, because these conditions are ascribed to injury of the birth canal or injury of trophoblasts [14]. In keeping with this assumption, 91% women had ruptured membranes at or before AFE presentation in the recent UKOSS survey [5].…”

“…Rarer clinical manifestations are: seizures, acute confusion and, in extreme cases, unconsciousness/coma (15% to 50%) or life-threatening hemorrhage resulting from coagulopathy (≤ 12%) [3,16]. Kanayama and Tamura proposed that two-thirds of AFE cases present with atonic bleeding, and only one-third with cardiopulmonary collapse [14].…”

“…Maternal post-partum care is based on several procedures, including: I) prevention of atony through immediate administration of uterotonics and hysterectomy in case of treatment refractarity [7]; II) differentiated use of catecholamines optimized using TEE [16] and possible additional inotropy support; III) cardiac pump function monitoring [16]; IV) prompt optimization of coagulation status through initial administration of tranexamic acid to treat hyperfibrinolysis and subsequent use of fibrinogen concentrate (for fibrinogen levels below 2 g/L) possibly using rotational thromboelastometry [18]; V) Replacement of red blood cell concentrates and fresh-frozen plasma (FFP) according to blood loss/severity of bleeding and in line with the risk profile of the patient, paying attention to volume overload that can possibly lead to pulmonary oedema (Optimal RBC to FFP ratio 1:1-1.5 [14]; VI) administration of recombinant factor VIIa if the above treatments are ineffective for improving DIC [14].…”