Amniotic fluid embolism occurs when some amniotic fluid gains access to the maternal circulation, often in massive volumes and with catastrophic consequences. It was discovered for the first time by Ricardo Juvenal Meyer in 1926, who was extremely surprised to find whole chunks of foetal tissue (skin cell, lanugo hairs, intestinal mucin) in the pulmonary vessels of dead mothers. Clearly that was an abnormal finding, but nobody really put two and tow together until a whole case series of sudden maternal deaths was linked to pulmonary embolism of amniotic fluid by Steiner and Lushbaugh (1941). Death occurs typically due to circulatory collapse, or (if that doesn't get you) respiratory failure and severe hypoxia.
Though Question 28 from the first paper of 2017 was the first time the college had asked for some detail about this condition, it comes up now and again as a differential in the lists of possible reasons for DIC (for example), or sudden peri-Caesarian cardiovascular catastrophe, or possibly as a part of a particularly vicious viva station. The question specifically asked for clinical features and risk factors. Potentially, vicious viva scenarios may in the future ask the candidates to make an echo diagnosis, or to manage the situation (which may or may not progress to cardiac arrest).
As far as published literature goes, one cannot go past Moore's article from Critical Care Medicine (2005). That would probably be enought to satisfy the requirements of the time-poor exam candidate who does not wish to pay UpToDate subscription fees.
Question 28 from the first paper of 2017 asked the candidates to outline the important clinical features of amniotic fluid embolism. The college answer listed the following features, making them canonically "important":
This list likely represents the maximum expected of a candidate. The British AFE Register (Tuffnell et al, 2005) used something very similar to identify cases for record-keeping purposes. The hypoxia hypotension and DIC are what you migth call "cardinal signs". Other associated features are listed by Moore et al (2005):
Differentials are also offered by the same article, which is helpful:
Amniotic fluid gains access to the circultaion by a number of possible routes:
Let's say that there is some sort of direct venous blood/amniotic fluid interface, at the breach of some venous blood vessel somewhere in the uterus. Amniotic fluid will get into the venous circulation though this opening by a variety of mechanisms:
Now, amniotic fluid is not some sort of crystal-clear mountain stream straight from some sanitised fairytale description of pregnancy. A sopering realism is introduced by Doke Uyeno (1919) who described its properties in horriic detail.
The amniotic fluid is slimy, yellowish white or pale yellow, and cloudy like soap water (rarely clear); it almost always contains much mucous flocks and has a peculiar odor.
This magical material has interesting physicochemical properties and a complex composition, largely consiting of:
So, a volume of this material entering the circulation can only the most disastrous of consequences, being equivalent to the intravenous injection of sewer water.
These are due to several components, elegantly illustrated in these diagrams from Moore et al (200%):
The hypoxia is due to the crude effects of V/Q mismatching which occurs when amniotic fluid emboli clog the lungs. Several pathophysiologies contribute to the hypoxia:
The shock is initially obstructive (giving rise to characteristic intraopetaive TOE findings) and subsequently distributive with a sepsis-like capillary leak.
This is though to be due to a systemic inflammatory response with activation of complement and the activation of the coagulation cascade throughout the circulation. It can start rapidly, within 10-30 minutes.
Moore et al (2005) attributes the neurological findings in AFE to severe hypoxia.
Question 28 from the first paper of 2017 asked fro six risk factors. The college answer gives us eight, which (judging by the wording) all came from UpToDate.
Knight et al (2010 and 2012) adds a few more risk factors:
A specific risk factor labor which UpToDate and the college describe as "tumultuous", implying bizarrely that all other labour is a calm and peaceful process.
This is usualy a diagnosis of exclusion, and based on a strong clinical suspicion.
Gold standard of diagnosis is the totally unrealistic manoeuvre of sucking some amniotic fluid debris out of a distal port of the PA catheter.
Foetal debris in maternal sputum is a more civilised alternative, but again unlikely to be game-changing if you already strongly suspect AFE.
Foetal antigen serology looking for TKH-2 antibodies ( or insulin-like growth factor binding protein-1) are apparently not well validated
Specific management:
Supportive management:
Unique aspects:
-
Moore, Jason, and Marie R. Baldisseri. "Amniotic fluid embolism." Critical care medicine 33.10 (2005): S279-S285.
Meyer, JR "Embolia pulmonar amnio caseosa". Brasil Medico. 1926; 2:301.
Attwood, H. D. "The histological diagnosis of amniotic‐fluid embolism." The Journal of Pathology 76.1 (1958): 211-215.
Steiner, Paul E., and Clarence Chancelum Lushbaugh. "Maternal pulmonary embolism by amniotic fluid: as a cause of obstetric shock and unexpected deaths in obstetrics." Journal of the American Medical Association 117.15 (1941): 1245-1254.
Tuffnell, D. J. "United Kingdom amniotic fluid embolism register." BJOG: An International Journal of Obstetrics & Gynaecology 112.12 (2005): 1625-1629.
Conde-Agudelo, Agustín, and Roberto Romero. "Amniotic fluid embolism: an evidence-based review." American journal of obstetrics and gynecology 201.5 (2009): 445-e1.
Tamura, Naoaki, et al. "Amniotic fluid embolism: Pathophysiology from the perspective of pathology." Journal of Obstetrics and Gynaecology Research43.4 (2017): 627-632.
Sideris, Ioannis G., and Kypros H. Nicolaides. "Amniotic fluid pressure during pregnancy." Fetal diagnosis and therapy 5.2 (1990): 104-108.
Uyeno, Doko. "The physical properties and chemical composition of human amniotic fluid." Journal of Biological Chemistry 37.1 (1919): 77-103.
Lim, Y., et al. "Recombinant factor VIIa after amniotic fluid embolism and disseminated intravascular coagulopathy." International Journal of Gynecology & Obstetrics 87.2 (2004): 178-179.
Davies, Sharon. "Amniotic fluid embolism and isolated disseminated intravascular coagulation." Canadian Journal of Anesthesia 46.5 (1999): 456-459.
Kaneko, Yuhko, et al. "Continuous Hemodiafiltration for Disseminated Intrav ascular Coagulation and Shock due to Amniotic Fluid Embolism: Report of a Dramatic Response." Internal medicine 40.9 (2001): 945-947.
Awad, I. T., and G. D. Shorten. "Amniotic fluid embolism and isolated coagulopathy: atypical presentation of amniotic fluid embolism." European journal of anaesthesiology 18.6 (2001): 410-413.
Waters, Jonathan H., et al. "Amniotic fluid removal during cell salvage in the cesarean section patient." The Journal of the American Society of Anesthesiologists 92.6 (2000): 1531-1536.
Knight, Marian, et al. "Incidence and risk factors for amniotic-fluid embolism."Obstetrics & Gynecology 115.5 (2010): 910-917.
Knight, Marian, et al. "Amniotic fluid embolism incidence, risk factors and outcomes: a review and recommendations." BMC pregnancy and childbirth12.1 (2012): 7.