Clinical Update on Amniotic Fluid Embolism

AFE is a rare but serious obstetric emergency. We all wish we don’t have to experience this during our career. For those of you who provide obstetric care to patients, it is crucial that we need to know what to do and how to optimize the patient when it happens. The new mortality rate is actually a lot lower than what we learned in textbook which is roughly 20-30%. It mostly occurs during labor but could happen before labor or after delivery. Severe symptoms include hypotension, cardiac arrest, dyspnea, cyanosis, respiratory arrest and coagulopathy. We all know there is really no cure for AFE but supportive management of ABC. But there are some new insights on the MOA of AFE . If s**t hit the fan, might as well try something that may get you out of trouble. It is known as AOK treatment, atropine, ondansetran and ketorolac.

Pathophysiology of AFE in animal model:

  • Just barely lethal amount of material embolized into pulmonary arteries (blood clot, marrow, fat, microsphere)
  • Platelets degranulate
  • Thromboxane, serotonin cause intense pulmonary vascoconstriction, stimulate vagal reflex
  • Peripheral vasodilation, bradycardia are the final lethal events.

Animal Pulmonary Embolism Events:

  • Embolsim
  • Platele activation and degranulation
  • Pulmonary hypertension due to serontonin and thromboxane.
  • Systemic hypotension and bradycardia due to reflex vagal stimulation and PTH
  • Death

Serotonin

  • About half of the vagal afferent terminals in the lung and the heart are serotonergic, not cholinergic.
  • Leanos OL et al. injected rabbit with marrow; compared platelet depletion, vagotomy, 5-HT3 blocker, vagal stimulation
  • Vagotomy prevented SBP decrease, few death, no effect on PAP
  • 5-5H3 antagonist=vagotomy
  • Vagal stimulation caused severe SBP decrease and death.

AOK treatment:

  • Atropine: vagolysis
  • Ondansetron to block serotonin receptors and for vagolysis
  • Ketorolac 30mg to block throboxane production

AFE patient #1

  • 28 yo G2P1 39 wks, elective c/s, uterine incision, tachypnea, restlessness, gasp, decerebrate posturing, apnea, PEA
  • Intubated, chest compression, epinephrine 1mg, vasopressin 40 units with brief weak pulse, no BP
  • Atropine 0.9mg, Ondansetron 4mg, Ketorolac 30mg at minute 5
  • Strong pulse and BP 105/80 within 1 min.
  • No further cardiac meds needed.
  • Echo: RV dilation. DIC 1hr later.
  • Survived neurologically intact.

picture2

AFE patient #2

  • 41 yo G8P3 39wks, labor induction, 10cm
  • Dyspnea, SpO2 80%, cardiac arrest
  • Forceps delivery, 31 min ACLS
  • Atropine 1mg, ondansetron 8mg, ketorolac 30mg
  • Pulse and stable vital signs with pressor support within 2 min.
  • Echo: RV dilation. DIC 1hr later
  • Survived with minor neuro deficits.picture3

2 Comments Add yours

  1. OBJim says:

    Interesting that both patients wound up in DIC. I wonder whether that was from the natural history of survived AFE or somehow promoted by blockade of thrombocyte serotonin and thromboxane….

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  2. Behind The Drape says:

    Thank you OB for your comment. When the patient has cardiac arrest due to significant AFE, it is reasonable to postulate that there is significant amount of foreign substance in this case amniotic fluid in the mother’s circulation. Hence, the body elicits massive inflammatory and immune responses. The manifestation in this type of cases would be DIC. There is no research that has shown the relationship between the blockade of serotonin and thromboxane degranulation and DIC.

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