Amniotic fluid embolism
|Amniotic fluid embolism|
|Classification and external resources|
Amniotic fluid embolism (AFE) is a rare and incompletely understood obstetric emergency in which amniotic fluid, fetal cells, hair, or other debris enters the mother's blood stream via the placental bed of the uterus and trigger an allergic reaction. This reaction then results in cardiorespiratory (heart and lung) collapse and coagulopathy. It was first formally characterized in 1941. While it is estimated to be the fifth most common cause of maternal mortality in the world, there has been discrepancy with respect to the incidence and mortality of amniotic fluid embolism. One likely explanation for this inconsistency is the lack of sensitive and specific diagnostic studies to definitively identify cases of amniotic fluid embolism, leading to both over- and underreporting.
The condition is so rare (between 1 in 8000 and 1 in 80,000 deliveries, although more recent studies show 1 in 20,464 deliveries for a more precise number) that most doctors will never encounter it in their professional careers, and as a result the exact process is poorly understood.
It is believed however that once the fluid and fetal cells enter the maternal pulmonary circulation in general terms there will be profound respiratory failure with deep cyanosis and cardiovascular shock followed by convulsions and profound coma; however this does occur in two phases detailed below:
The patient experiences acute shortness of breath and hypotension. This rapidly progresses to cardiac failure leading to a reduction of perfusion to the heart and lungs. This may be accompanied by other "premonitory symptoms" such as shivering, coughing, vomiting, and an unpleasant taste in the mouth. Not long after this stage the patient will lose consciousness due to circulatory collapse. While previously believed to have a maternal mortality rate of 60-80%, more recently it has been reported at 26.4%.
Although many women do not survive beyond the first stage, about 40 percent of the initial survivors will pass onto the second phase. This is known as the hemorrhagic phase due to excessive bleeding as the blood loses its ability to clot. Collapse of the cardiovascular system leads to fetal distress and death unless the child is delivered swiftly.
It is thought that this condition results from amniotic fluid entering the maternal circulation via the uterine veins, which then has either a direct effect on the lungs, or triggers an immune response in the mother. 
In order for amniotic fluid to enter the maternal circulation, there are three prerequisites:
- Ruptured membranes (a term used to define the rupture of the amniotic sac)
- Ruptured uterine or cervical veins
- A pressure gradient from uterus to vein
Although exposure to fetal tissue is common and thus finding fetal tissue within the maternal circulation is not significant, in a small percentage of women this exposure leads to a complex chain of events resulting in collapse and death.
There is some evidence that AFE may be associated with abdominal trauma  or amniocentesis. A 2006 study showed that the use of drugs to induce labor, such as misoprostol, nearly doubled the risk of AFE. A maternal age of 35 years or older, caesarean or instrumental vaginal delivery, polyhydramnios, cervical laceration or uterine rupture, placenta previa or abruption, eclampsia, and fetal distress were also associated with an increased risk.
There is no specific treatment for amniotic fluid embolism, and initial emergency management is the same as for any other cause of sudden maternal collapse - with cardiovascular and respiratory resuscitation and correction of the coagulopathy.  One emergency intervention which has been applied is an immediate caesarean section.
- Alfredo Gei, Gary D. V. Hankins: Amniotic fluid embolus: An update. Contemp Ob/Gyn 45 (2000), pp. 53–66, online.
- Stafford I, Sheffield J (2007). "Amniotic fluid embolism". Obstet. Gynecol. Clin. North Am. 34 (3): 545–53, xii. doi:10.1016/j.ogc.2007.08.002. PMID 17921014.
- Moore J, Baldisseri MR (2005). "Amniotic fluid embolism". Crit. Care Med. 33 (10 Suppl): S279–85. doi:10.1097/01.CCM.0000183158.71311.28. PMID 16215348.
- Ellingsen CL, Eggebø TM, Lexow K (2007). "Amniotic fluid embolism after blunt abdominal trauma". Resuscitation 75 (1): 180–3. doi:10.1016/j.resuscitation.2007.02.010. PMID 17467876.
- Gilbert WM, Danielsen B (June 1999). "Amniotic fluid embolism: decreased mortality in a population-based study". Obstet Gynecol 93 (6): 973–7. doi:10.1016/s0029-7844(99)00004-6. PMID 10362165.
- N J McDonnell, V Percival, M J Paech (Aug 2013). "Amniotic fluid embolism: a leading cause of maternal death yet still a medical conundrum". International journal of obstetric anesthesia. doi:10.1016/j.ijoa.2013.08.004.
- Dodgson J, Martin J, Boswell J, Goodall HB, Smith R (May 1987). "Probable amniotic fluid embolism precipitated by amniocentesis and treated by exchange transfusion". Br Med J (Clin Res Ed) 294 (6583): 1322–3. doi:10.1136/bmj.294.6583.1322. PMC 1246486. PMID 3109636.
- Kramer, M.S.; Rouleau, Jocelyn; Baskett, Thomas F; Joseph, KS (2006). "Amniotic-fluid embolism and medical induction of labour: a retrospective, population-based cohort study". The Lancet 368 (9545): 1444–1448. doi:10.1016/S0140-6736(06)69607-4. PMID 17055946.
- N.F. Collins, M. Bloor, N.J. McDonnell (2013). "Hyperfibrinolysis diagnosed by rotational thromboelastometry in a case of suspected amniotic fluid embolism". International Journal of Obstetric Anesthesia 22 (1): 71–76. doi:10.1016/j.ijoa.2012.09.008.
- Stehr SN, Liebich I, Kamin G, Koch T, Litz RJ (2007). "Closing the gap between decision and delivery--amniotic fluid embolism with severe cardiopulmonary and haemostatic complications with a good outcome". Resuscitation 74 (2): 377–81. doi:10.1016/j.resuscitation.2007.01.007. PMID 17379383.