Hiroshi Kobayashi1. 1. Professor, Department of Obstetrics and Gynecology, Nara Medical University, Nara, Japan.
Abstract
PROBLEM: Amniotic fluid embolism (AFE) is a rare but severe emergency in obstetrics. The aim of the present study was to investigate the pathophysiology of AFE. METHODS: A search was conducted between 1966 and 2014 through the English-language literature (online MEDLINE PubMed database) using the keyword amniotic fluid embolism combined with anaphylaxis, anaphylactoid, complement activation, mast cells, fetal antigens, and idiosyncratic. RESULTS: Amniotic fluid embolism is a rare clinical entity but a severe obstetric emergency that can be lethal even in previously healthy women in labor or in the early postpartum period. There appears to be at least 2 mechanisms. First, adverse reactions in AFE are usually unexpected and fetal antigen dose dependent. Given the disastrous entry of amniotic fluid into the maternal circulation, they experience a sudden cardiopulmonary collapse (mechanical obstruction subtype). Second, anaphylactic and anaphylactoid reactions of the remaining AFE are also relatively unexpected and fetal antigen dose independent and can occur at the first exposure to amniotic fluid components. They are associated with complement activation and subsequent postpartum hemorrhage. Cardiac mast cells constitute a central pathogenesis of anaphylactic (immunoglobulin E-dependent) and anaphylactoid (immunoglobulin E-independent) reactions. CONCLUSIONS: Recent immunologic studies provide a new approach to the study of the pathophysiology of AFE.
PROBLEM: Amniotic fluid embolism (AFE) is a rare but severe emergency in obstetrics. The aim of the present study was to investigate the pathophysiology of AFE. METHODS: A search was conducted between 1966 and 2014 through the English-language literature (online MEDLINE PubMed database) using the keyword amniotic fluid embolism combined with anaphylaxis, anaphylactoid, complement activation, mast cells, fetal antigens, and idiosyncratic. RESULTS:Amniotic fluid embolism is a rare clinical entity but a severe obstetric emergency that can be lethal even in previously healthy women in labor or in the early postpartum period. There appears to be at least 2 mechanisms. First, adverse reactions in AFE are usually unexpected and fetal antigen dose dependent. Given the disastrous entry of amniotic fluid into the maternal circulation, they experience a sudden cardiopulmonary collapse (mechanical obstruction subtype). Second, anaphylactic and anaphylactoid reactions of the remaining AFE are also relatively unexpected and fetal antigen dose independent and can occur at the first exposure to amniotic fluid components. They are associated with complement activation and subsequent postpartum hemorrhage. Cardiac mast cells constitute a central pathogenesis of anaphylactic (immunoglobulin E-dependent) and anaphylactoid (immunoglobulin E-independent) reactions. CONCLUSIONS: Recent immunologic studies provide a new approach to the study of the pathophysiology of AFE.