Amniotic Fluid Embolism

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What the Anesthesiologist Should Know before the Operative Procedure

Amniotic fluid embolism (AFE) is a rare and devastating complication of pregnancy. The incidence of AFE in North America is approximately 1:15,200 (95% CI, 1:13,900 to 1:16,700). Amniotic fluid embolism accounted for 7.5% of pregnancy-related deaths in the United States between 1998 and 2005. In contrast to maternal mortality rates of 20-60%, neonatal survival is high (80%), however, many of the neonates do not survive neurologically intact. Intact neurologic survival for infants is related to the cardiac arrest-to-delivery interval.

Amniotic fluid embolism typically presents during labor, however, it has also been described elsewhere in peripartum or early postpartum period, as well as intraoperatively during cesarean deliveries without prior labor. In postpartum patients, it can develop during the first 30 minutes after birth or during dilation and evacuation procedures. Rare occurrences have been reported 6 to 12 hours after delivery. And it may occur in the presence of sudden fetal demise during labor, placental abruption, or postpartum uterine atony.

The classic signs of AFE are dyspnea, hypoxemia, cardiovascular collapse, coma, and bleeding.

This clinical syndrome may also manifest with premonitory symptoms (restlessness, numbness, tingling, agitation), non-reassuring fetal status (fetal hypoxia, category II and III tracings), hypotension, disseminated intravascular coagulation (DIC), seizures or altered mental status, and/or cardiac arrest.

The differential diagnosis should include anesthetic complications (high neuraxial block, local anesthetic toxicity), medication error/anaphylaxis, pulmonary embolism (air, thromboembolism), cardiac complications (myocardial infarction, postpartum cardiomyopathy, valvular disease such as severe mitral stenosis), eclampsia, placental abruption, hemorrhage of any etiology (uterine rupture, atony, placental abruption, birth canal laceration, etc.), and sepsis/septic shock.

The etiology is unknown but most likely the syndrome occurs with (1) the presence of amniotic fluid with or without meconium in the circulation or (2) complement activation from the presence of immunologic components and vasoactive and procoagulant substances in the amniotic fluid (Figure 1).

Figure 1

AFE etiology.

1. What is the urgency of the surgery?

What is the risk of delay in order to obtain additional information?

AFE presents nearly always as a medical emergency. Maternal death and fetal demise are extremely common. Long-term neurologic sequelae and renal damage in the surviving patients are very frequent occurrences. Airway management, resuscitation, and cardiovascular support should begin as soon as the diagnosis is considered.

Emergent: AFE most often presents as sudden cardiovascular collapse, altered mental status, bleeding, and DIC. The delay in either considering the diagnosis or initiating aggressive treatment increases an already high maternal and fetal mortality rate. If possible, laboratory tests should be sent while resuscitating the patient.

2. Preoperative evaluation

Patients are usually in labor or have delivered recently or are undergoing a cesarean delivery or a D&E. They should have had a medical history completed by the delivery team (obstetrician, midwife, or anesthesiologist).

Risk factors from population-based cohort studies are maternal age greater than 35 years, grand multiparity, multiple pregnancy, minority ethnic groups, cesarean delivery, forceps or vacuum-assisted delivery, placenta previa or abruption, polyhydramnios, eclampsia, macrosomia, induction of labor with oxytocin, artificial rupture of membranes, cervical laceration, and uterine rupture.

As soon as possible, obtain complete blood count (CBC), coagulation profile with DIC panel including fibrinogen, arterial blood gas for oxygenation and base deficit, serum tryptase.

Also, draw a heparinized central line sample for specific or special stains and antibodies to confirm the presence of amniotic fluid or its components in the central circulation.

3. What are the implications of co-existing disease on perioperative care?

What are the implications of AFE?

AFE can be catastrophic to both mother and child. In a parturient with sudden cardiovascular collapse who has not delivered, prompt delivery of the fetus should be attempted in an effort to improve neonatal outcome as well as maternal resuscitation.

Steps to improve overall outcome are based on prompt and aggressive resuscitation, expediting delivery, cardiorespiratory stabilization, and critical care support.

b. Cardiovascular system

Patients manifest with acute cardiovascular collapse. Other presenting signs can include hypotension, cardiopulmonary arrest, and chest pain. Differential diagnosis of most common causes of cardiovascular collapse during labor and treatment options are shown in Figure 2.

Figure 2

Differential diagnosis.

If maternal cardiovascular instability is present, attempts should be made to stabilize the mother while preparations to deliver the fetus are under way. If a terminal cardiac rhythm is present, delivery of the fetus should be attempted as soon as possible.

In acute/unstable conditions, AFE manifests as a biphasic response. The initial phase consists of pulmonary vasoconstriction with increased pulmonary vascular resistance causing right ventricular failure, initiating cardiovascular collapse. If the patient survives this phase, left ventricular failure ensues.

c. Pulmonary

Dyspnea, hypoxia, pulmonary edema, or acute respiratory distress syndrome (ARDS) can be present. Cyanosis, bronchospasm, and cough can also present as the initial manifestation of AFE.

d. Coagulation

Bleeding either may be a presenting symptom and the initial manifestation of AFE or may manifest during the first hour after the embolic phenomenon/insult and the anaphylactoid reaction. It is associated with a consumptive coagulopathy and DIC.

e. Renal-GI:


f. Neurologic:

Hypotension can cause altered mental and neurologic status secondary to cerebral hypoperfusion. Seizures can be present and the differential diagnosis of eclampsia should be considered.

g. Endocrine:


h. Additional systems/conditions which may be of concern in a patient undergoing this procedure and are relevant for the anesthetic plan (e.g., musculoskeletal in orthopedic procedures, hematologic in a cancer patient)


4. What are the patient's medications and how should they be managed in the perioperative period?

Any medication suspected to cause anaphylaxis to the patient should be stopped immediately. Latex should be eliminated from the patient's contact if a latex allergy is confirmed or suspected.

h. Are there medications commonly seen in patients undergoing this procedure and for which should there be greater concern?


i. What should be recommended with regard to continuation of medications taken chronically?


j. How to modify care for patients with known allergies


k. Latex allergy- If the patient has a sensitivity to latex (e.g., rash from gloves, underwear, etc.) versus anaphylactic reaction, prepare the operating room with latex-free products.

l. Does the patient have any antibiotic allergies? (common antibiotic allergies and alternative antibiotics)


m. Does the patient have a history of allergy to anesthesia?


5. What laboratory tests should be obtained and has everything been reviewed?


CBC, platelets, coagulation profile (PT, PTT, INR, D-dimer, and fibrinogen) to guide specific treatment with blood and blood products to maintain adequate hemoglobin levels and coagulant factors in the presence of bleeding. Do not delay necessary treatments or transfusion of the patient during hemorrhage while waiting for results from laboratory.


May be normal or altered. When treating these patients, activate the massive transfusion protocol and correct electrolytes such as calcium and potassium as needed.


Patients will nearly always be too unstable to be transported for imaging. Chest radiography will reveal cardiomegaly and pulmonary edema. Bedside transesophageal echocardiography (TEE) or transthoracic echocardiography (TTE) is extremely useful for diagnosis and to guide fluid and vasopressor therapy.

Other tests

Serial blood gas analyses are needed to aid in diagnosis and treatment of respiratory and metabolic acidosis and to follow the effectiveness of resuscitation. An anaphylactic panel that includes histamine and serum tryptase level (as a marker for mast cell degranulation) is helpful in excluding anaphylaxis but also supports the diagnosis of AFE as an anaphylactoid reaction to fetal antigens.

Intraoperative Management: What are the options for anesthetic management and how to determine the best technique?

Resuscitation should focus on three priority areas: (1) maintenance of oxygenation; (2) hemodynamic support; and (3) correction of coagulopathy. If maternal cardiac arrest occurs or if maternal stabilization is obtained, prompt delivery should be accomplished. When maternal cardiac arrest ensues, time to delivery should ideally be less than 5 minutes to provide more effective CPR and optimize newborn outcome.

a. Regional anesthesia

Regional anesthesia is generally contraindicated as patients presenting with AFE often present with cardiovascular instability, hypoxia, altered mental status, and coagulopathy.

b. General anesthesia

Benefits: With an unstable patient, general anesthesia is the best choice to ensure adequate ventilation and airway protection. It frees the anesthesiologist to focus on cardiovascular support and transfusion of necessary blood products and coagulation factors.

Drawbacks: Difficult airway should be anticipated, especially in the presence of fragile capillaries, bleeding, and mucosal edema.

Airway concerns: The patient will be unstable, and difficult airway should be anticipated in these patients. Fluid shifts will be significant and the airway should be secured early in the course of AFE.

c. Monitored anesthesia

Monitored anesthesia is contraindicated.

6. What is the author's preferred method of anesthesia technique and why?

When the patient becomes unstable and has cardiovascular collapse, intubation, ventilation, and intensive hemodynamic support form our technique of choice.


Most patients will require intubation and ventilation with 100% oxygen. In severely hypoxic patients, especially those with pulmonary edema, consider positive end-expiratory pressure (PEEP) while closely following blood pressure and cardiac output.


Large-bore IV lines are required for fluid resuscitation. Central line placement, even in the presence of coagulopathy, may be essential to guide fluid and vasopressor therapy, which is required in most cases. Even though arterial line placement may be difficult in a patient with cardiovascular collapse, it is necessary. The arterial line tracing and repeated blood gas analysis help guide vasopressor therapy and resuscitation. Pulmonary artery catheter with cardiac output measurement may help distinguish between the two different phases of AFE. TEE can be used to help optimize vasopressor and inotrope choices as well as fluid resuscitation.

As a coagulopathy will often ensue, it is critical to activate institutional massive hemorrhage protocols so as to mobilize blood products. Correct the coagulopathy with fresh frozen plasma (FFP), platelets, and cryoprecipitate. Cryoprecipitate replaces both fibrinogen and fibronectin, which helps the reticuloendothelial system clear circulating microaggregates. Cardiopulmonary bypass, nitric oxide, and prostacyclin have been used for right ventricular outflow obstruction or refractory hypoxemia.


Vasopressors, such as vasopressin, dobutamine, and milrinone may be necessary during resuscitation. Dobutamine infusion is a useful inotropic agent to consider in patients with pulmonary hypertension or ventricular failure.

Steroids have been used successfully in some patients who survived AFE, perhaps because of the similarity to anaphylaxis. Consider activating a massive hemorrhage protocol in patients with excessive bleeding. Consider factor VII and antifibrinolytic therapy in some cases for continued bleeding. Interventional Radiology techniques have also been used.

What prophylactic antibiotics should be administered?

None should be administered. If anaphylaxis is suspected, possible drugs such as antibiotics should be eliminated.

What can I do intraoperatively to assist the surgeon and optimize patient care?

If maternal cardiac arrest ensues before the delivery of the baby, efforts to deliver the fetus should be made within 5 minutes of maternal arrest.

What are the goals of management and support?

Oxygenation, maintenance of cardiac output and blood pressure, and resolution of the severe coagulopathy should be the goals for treatment. Crystalloid and blood product administration and vasopressors should be used to improve cardiac preload. Component therapy to treat bleeding and DIC should be accomplished with packed red blood cells (PRBCs), FFP, cryoprecipitate, and platelets, guided by lab values and the clinical picture.

What other supportive treatments can be considered in these cases?

Recently, case reports have mentioned the use of the following treatments to be effective with successful maternal outcomes: (1) prompt initiation of cardiovascular bypass, (2) intra-aortic balloon pump with extracorporeal membrane oxygenation, (3) ventricular assist devices, (4) inhaled nitric oxide, and (5) recombinant factor VIIa.

a. Neurologic:


b. If the patient is intubated, are there any special criteria for extubation?

Most patients remain intubated and ventilated due to the need for fluid and blood product replacement. It is prudent to follow ICU criteria for extubation.

c. Postoperative management

What analgesic modalities can I implement? This is not applicable until the patient is conscious and hemodynamically stable.

What level bed acuity is appropriate? If the patient survives the initial event, ICU care is necessary.

What are common postoperative complications, and ways to prevent and treat them?

Bleeding, coagulation abnormalities, and respiratory abnormalities are frequent. Renal damage is a concern and renal function should be assessed frequently. Renal function may return to normal after adequate resuscitation but in some cases may require hemodialysis during the first days.

Among the survivors of AFE and cardiac arrest, less than 10% are neurologically intact: a similar percentage of all in-hospital cardiac arrest survivors.

What's the Evidence?

Benson, MD, Kobayashi, H, Silver, RK. "Immunologic studies in presumed amniotic fluid embolism". Obstet Gynecol. vol. 97. 2001. pp. 510-4.

Berg, CJ, Callaghan, WM, Syverson, C, Henderson, Z.. "Pregnancy-related mortality in the United States, 1998 to 2005". Obstet Gynecol. vol. 116. 2010. pp. 1302-9.

Clark, SL, Hankins, GD, Dudley, DA. "Amniotic fluid embolism: analysis of the national registry". Am J Obstet Gynecol. vol. 172. 1995. pp. 1158-67.

Clark, SL. "Amniotic fluid embolism". Clin Obstet Gynecol. vol. 53. 2010. pp. 322-8.

Conde-Agudelo, A, Romero, R. "Amniotic fluid embolism: an evidence-based review". Am J Obstet Gynecol. vol. 201. 2009. pp. e441-3.

Davies, S. "Amniotic fluid embolus: a review of the literature". Can J Anesth. vol. 48. 2001. pp. 88-98.

Gei, AF, Vadhera, RB, Hankins, GD. "Embolism during pregnancy: thrombus, air, and amniotic fluid". Anesthesiol Clin North Am. vol. 21. 2003. pp. 165-82.

Gist, RS, Stafford, IP, Leibowitz, AB, Beilin, Y. "Amniotic fluid embolism". Anesth Analg. vol. 108. 2009. pp. 1599-602.

Knight, M, Tuffnell, D, Brocklehurst, P, Spark, P, Kurinczuk, JJ. "Incidence and risk factors for amniotic fluid embolism". Obstet Gynecol. vol. 115. 2010. pp. 910-7.

Knight, M, Berg, C, Brocklehurst, P. "Amniotic fluid embolism incidence, risk factors and outcomes: a review and recommendations". BMC Pregnancy Childbirth. vol. 12. 2012. pp. 7.

Leighton, BL, Wall, MH, Lockhart, EM. "Use of recombinant factor VIIa in patients with amniotic fluid embolism: a systematic review of case reports". Anesthesiology. vol. 115. 2011. pp. 1201-8.

O'Shea, A, Eappen, S. "Amniotic fluid embolism". Int Anesthesiol Clin. vol. 45. 2007. pp. 17-28.

Roberts, CL, Algert, CS, Knight, M, Morris, JM. "Amniotic fluid embolism in an Australian population-based cohort". BJOG. vol. 117. 2010. pp. 1417-21.

"Amniotic fluid embolism: diagnosis and management". Am J Obstet Gynecol. vol. 215. 2016. pp. B16-24.

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