Amniotic Fluid Embolism

/

Read along: SMFM Clinical Guideline 9: AFE: diagnosis and management 

AFE: Background/Presentation

  • AFE is a clinical diagnosis characterized by a triad of sudden onset symptoms:

    • Sudden hypoxia 

    • Hypotension, often resulting in cardiac arrest / cardiovascular collapse

    • Followed by coagulopathy in 83% of cases

      • Coagulopathy may be in conjunction with cardiopulmonary symptoms, or follow them.

      • Often profound with bleeding from venipuncture or surgical sites, hematuria, GI hemorrhage, vaginal bleeding, epistaxis. 

  • Importantly, the diagnosis is clinical. Based on this triad and exclusion of other potential causes.

    • Cases are often dramatic - preceded not infrequently by impending sense of doom from patient, change in mental status, agitation.

      • Fetal status may also change with sudden profound decelerations, loss of variability, and terminal bradycardia.

    • No lab test can confirm or refute the diagnosis.

  • A national registry reports with respect to case timing:

    • 70% occur during labor

    • 11% after vaginal delivery

    • 19% during cesarean delivery

  • Incidence is hard to know given its rarity - likewise, predicting AFE is also impossible - there are no defined and true risk factors.

    • There is some potential relation related to moments where, “exchange of fluids between fetal and maternal compartments is more likely,” such as operative or cesarean delivery, placenta previa, placenta accreta, abruption

What causes AFE? What's the pathophysiology? 

  • It’s unclear what exactly causes AFE, but again, it’s often reported at the time of some disruption of maternal-fetal interface. 

    • Whether amniotic fluid passing into maternal circulation is the underlying cause or not, there are a fair number of subsequent clinical manifestations that can be observed.

  • First, there is massive pulmonary vasoconstriction and possible mechanical obstruction of pulmonary vasculature due to amniotic fluid components.

    • This vasoconstriction results in acute cor pulmonale - or sudden right ventricular failure.

    • Accompanying this is acute respiratory failure and severe hypoxemia.

      • The best way to think about these coming together (and potentially a valid way to think pathophysiologically too) is a massive, anaphylactoid reaction. 

    • With the massive afterload on the RV, on echocardiogram you can see a dilated RV with ballooning of the ventricular septum towards the left.

      • TTE and/or TEE during an event may help to visualize this concern in AFE.

  • Cor pulmonale in this acute fashion leads then to left-ventricular failure - there’s no blood going forward to the LV! - which results in profound systemic hypotension. 

  • Finally, it is thought that the amniotic fluid or inflammatory insult activates factor VII in the coagulation cascade → thus activating platelets and consuming them in a process that ultimately results in DIC.

    • The hemorrhage that results further exacerbates the hemodynamic instability at the level of the heart, and multiorgan failure can result.

SMFM Clinical series: afe


How should AFE be managed?

  • First, suspicion: AFE should be considered in the differential for any sudden cardiopulmonary collapse in pregnant or recently postpartum patients.

  • Next, high quality CPR: BLS/ACLS. 

    • Management does not differ initially with cardiac arrest due to any other cause, so the most important thing you can do is to be BLS and ACLS-certified. 

    • Chest compressions should be initiated immediately - take a listen back to our maternal cardiac arrest episode for a refresher on CPR. Recall the major points, though:

      • Same rate of compressions as for non-pregnant individuals (100/min), aiming for compression depth of 2 inches.

      • Switch compressors every 2 minutes to prevent fatigue.

      • If undelivered, tilt to left lateral decubitus or displace the uterus leftward to prevent aortocaval compression.

      • Resuscitative hysterotomy (aka perimortem cesarean) at 4 minutes without ROSC if not imminently delivering vaginally. 

    • And important to a high-quality ACLS resuscitation is having a diverse team - anesthesia, RT, critical care, OB/MFM, nursing, blood bank, and pediatrics should all be part of the care and emergency response!

  • There are no well-studied medication protocols to treat AFE, and none are discussed in the SMFM Clinical Guidelines.

    • The most discussed one in many circles is the “A-OK” protocol, which consists of:

      • Atropine 1mg - reversing parasympathetic activity that may contribute to pulmonary vasospasm

      • Ondansetron 8mg - blocks serotonin receptors that may be found in vagal terminals of heart and lungs, and would in turn contribute to pulmonary vasoconstriction 

      • Ketorolac 30mg - blocks thromboxane, which is a major platelet activator

        • The idea behind this therapy is to potentially interrupt these vasoconstricting/inflammatory pathways felt to contribute to AFE; however, this is obviously very difficult to study in a systematic or rigorous way.

  • Post-arrest care is also extremely important.

    • MAP goal of 65 mmHg.

    • Appropriate oxygenation with attempt to wean oxygen to minimal possible to avoid ischemia-reperfusion injury. 

    • Laboratories: essentially, draw the rainbow to be broad. 

      • But checking in on CBC, CMP, troponins, BNP, and coag profile (fibrinogen, PT/aPTT) are good places to start.

    • If not already initiated, preparation for massive transfusion with ongoing/impending coagulopathy.

      • TXA can be considered.

      • Treating atony remains important - the uterus may become atonic in the context of profound hypotension/arrest.

        • One major challenge as a surgeon is to see the bleeding and atony, and be tempted into performing a hysterectomy. Don’t be tempted! 

          • It may very well serve you in the setting of an AFE not to perform a hysterectomy, as further incisions may give further sites of bleeding that are difficult to control. Wait for the products to get on board and resuscitation to catch up.

      • Transfusion using best practice of 1:1:1 ratio (RBC:plasma:platelet).

    • Managing airway concerns and right ventricular failure, if present on echo

      • There are a variety of agents that can be used RV failure, including sildenafil, pressors such as dobumtamine or norepi, and inhaled nitric oxide or prostacyclins.

      • ECMO can also be considered

        • Admittedly, these will be in the purview of our anesthesia/critical care colleagues so we won’t focus much more on them! 

  • In your hospital, verify if you have a protocol or checklist to help with AFE management.