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Amniotic Fluid Embolism: Recognizing the Signs

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Contact Hours: 4

This educational activity is credited for 4 contact hours at completion of the activity.

Course Purpose

The purpose of this course is to provide healthcare professionals with a brief overview of the incidence of amniotic fluid embolism in the United States, differential diagnoses, treatment options, nursing considerations, and the importance of immediate management to improve patient survival.

Overview

An amniotic fluid embolism (AFE) is a rare but life-threatening pregnancy complication. It occurs when amniotic fluid or fetal elements enter the mother’s bloodstream (maternal pulmonary circulation) and set off a series of reactions to induce severe cardiovascular and respiratory collapse. Amniotic fluid embolism is the second leading cause of maternal death and peripartum cardiac arrest in the United States, yet only occurs in less than 1% of pregnancies. This course discusses the clinical presentation of an amniotic fluid embolism, its incidence in the United States, differential diagnoses, and treatment options. This course will also discuss nursing considerations and the importance of immediate management to improve the survival of patients with AFE.

Course Objectives

Upon completion of the independent study, the learner will be able to:

  • Describe amniotic fluid embolism and common signs and symptoms
  • Review the causative factors of  amniotic fluid embolism, and how those causes can be mitigated to reduce the risk of amniotic fluid embolism
  • Differentiate amniotic fluid embolism from other medical conditions that may pose similar signs and symptoms
  • Review treatment options to improve the chance of survival of a patient with an amniotic fluid embolism
  • Discuss nursing considerations as they relate to amniotic fluid embolism

Policy Statement

This activity has been planned and implemented in accordance with the policies of FastCEForLess.com.

Disclosures

Fast CE For Less, Inc and its authors have no disclosures. There is no commercial support.

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Definitions
Acute Fetal DistressOccurs when the fetus does not receive adequate amounts of oxygen during pregnancy or labor.
Acute Pulmonary Arterial Obstruction (Pulmonary Embolism)An obstruction of the pulmonary arteries.
Acute Tubular Necrosis (ATN)A serious condition that damages the tiny tubes in the kidneys that filter blood.
Amniotic FluidThe fluid surrounding a fetus within the amnion.
Amniotic Fluid Embolism (AFE)A rare but serious condition that occurs when amniotic fluid – the fluid that surrounds a baby in the uterus during pregnancy, or fetal material, such as fetal cells, enters the mother’s bloodstream.
Anaphylactoid Syndrome of PregnancyA widespread, proinflammatory, anaphylactic-like reaction that can occur when amniotic fluid enters the maternal blood circulation.
AnaphylaxisA serious life-threatening allergic reaction which usually occurs within a few seconds or minutes of exposure to allergic substances. 
AntepartumAlso referred to as prenatal care, consists of the all-encompassing management of a woman throughout pregnancy. 
BronchiThe two large tubes that carry air from the windpipe (trachea) into the lungs and back out again. 
BronchiolesAir passages in the lungs that deliver air to the alveoli
BronchoconstrictionWhen the airways in the lungs become narrow and make it hard to breathe.
Cardiac OutputThe amount of blood the heart pumps in one minute.
Cardiopulmonary BypassA life-saving technique that replaces the function of the heart and lungs during surgery or critical illness.
CephaladToward the head or anterior end of the body.
Clotting FactorsAny of several plasma components (as fibrinogen, prothrombin, and thromboplastin) that are involved in the clotting of blood.
CoagulopathyA disorder that affects blood clotting, which normally stops bleeding from injuries.
CyanosisBluish skin color due to decreased amounts of oxygen.
Congestive Heart FailureA progressive heart disease that affects pumping action of the heart muscles.
Disseminated Intravascular Coagulation (DIC)A rare but serious condition that causes abnormal blood clotting throughout the body’s blood vessels.
EchocardiographyA test that uses sound waves to create images of the heart and its blood vessels
EclampsiaA life-threatening condition during pregnancy or shortly after giving birth characterized by the development of seizures.
EmbolismBlockage in the arterial (oxygen rich blood which flows from the heart to rest of the body) or venous (which carry deoxygenated blood from the organs to the heart) blood flow due to a blood clot.
Extracorporeal Membrane Oxygenation (ECMO)When blood is pumped outside of the body to a heart-lung machine that removes carbon dioxide and sends oxygen-filled blood back to tissues in the body. 
Fibrinolytic PathwaysA process that helps dissolve blood clots from the body.
HypoxemiaOccurs when levels of oxygen in the blood are lower than normal.
Hypoxic-Ischemic EncephalopathyA dangerous condition that happens when the brain does not receive enough blood and oxygen. 
Intra-Aortic Balloon Pump (IABP)A mechanical device that helps the heart pump blood.
Peripartum Cardiomyopathy (PPCM)Also known as postpartum cardiomyopathy, is an uncommon form of heart failure that happens during the last month of pregnancy or up to five months after giving birth. 
PlacentaEnables the exchange of oxygen and nutrients between the bloodstreams of mother and baby without mixing them. 
Pulmonary ArteryThe two major arteries coming from right ventricle of the heart.
Pulmonary EdemaA buildup of fluid in the lungs.
Right Ventricular Assist Device (RVAD)A device that helps the heart pump blood when the pumping muscle has become weak.
SepsisAn infection of the blood stream resulting in a cluster of symptoms such as drop in a blood pressure, increase in heart rate and fever.
Septic ShockA medical emergency that occurs because of severe infection in the body.
TachypneaTo breathe faster and shallower than normal.
Tricuspid RegurgitationMalfunctioning of the valve between two right heart chambers resulting in backflow of the blood. 
Uterine Artery EmbolizationA way to shrink fibroids, benign tumors in the uterus, without surgery.
Uterine AtonySoft and weak uterus after childbirth.
Venous Air Embolism (VAE)Occurs when air or gas is introduced to the venous system. 
Introduction

An amniotic fluid embolism (AFE) is a rare but life-threatening pregnancy complication. It occurs when amniotic fluid or fetal elements enter the mother’s bloodstream (maternal pulmonary circulation) and set off a series of reactions to induce severe cardiovascular and respiratory collapse.1

This rapid onset is like an extreme immune response such as anaphylaxis as opposed to a typical embolism, which is a physical blockage in a blood vessel. For this reason, AFE is also known as an anaphylactoid syndrome of pregnancy. 1

Amniotic fluid embolism is the second leading cause of maternal death and peripartum cardiac arrest in the United States, yet only occurs in less than 1% of pregnancies.This rarity makes AFE considerably difficult to study, which is why its exact physiopathology, associated risk factors, and long-term maternal outcomes are unknown.2 Amniotic fluid embolism has also been reported in healthy pregnancies with no underlying conditions or other pregnancy complications. Additionally, it can happen at any time during pregnancy, labor, or birth. As a result, AFEs are very difficult to predict and diagnose early, making them one of the most challenging obstetric emergencies to effectively treat before complications become fatal.3

This course discusses the clinical presentation of an amniotic fluid embolism, its incidence in the United States, differential diagnoses, and treatment options. This course will also discuss nursing considerations and the importance of immediate management to improve the survival of patients with AFE.

Physiology of Amniotic Fluid Embolism (AFE)

To fully understand the characteristics of an amniotic fluid embolism, it is first critical to understand the features and functionality of the placenta, a transient or temporary organ formed during pregnancy and expelled after birth. This specialized organ develops within the first few weeks of pregnancy. It is essentially the fetus’s lungs, liver, gut, kidneys, and endocrine system, carrying out vital biological processes while fetal organs and systems are still developing. While its principal function is to supply the fetus with nutrients and oxygen and remove waste, it is also a selective barrier that keeps maternal and fetal blood circulation separate.5 The role of the placenta as a barrier is a critical function. Not only does the placenta protect the fetus from external environmental pollutants, foreign bodies, and maternal hormones, it also protects the mother from harmful waste produced by the fetus.5

What is interesting to note is despite this life-saving function, the placenta barrier is basically a thin membrane between the two circulatory systems. It is highly susceptible to damage and disruption, which creates a pathway for amniotic fluid and fetal matter to pass through unhindered.This disruption can be caused by several factors, such as the abnormal development of the placenta itself, which can occur because of a chromosomal abnormality or external factors such as a drug. In addition, surgical incisions to the uterine wall, abdominal trauma, or micro-tears in the placenta, uterus, or cervical veins can all create space for fetal matter to pass through to reach maternal circulation. The matter can include amniotic fluid and fetal elements such as hair, meconium, mucin, and squamous cells.1,5 Once the material enters the maternal pulmonary arterial network, intense vasoconstriction occurs, where the blood vessels inside the lungs significantly narrow, which causes an immediate domino effect of reactions in such rapid succession that it seems simultaneous.

First, the mother will experience bronchoconstriction, where the smooth muscle around the bronchi and bronchioles in the lungs tighten, making breathing difficult. The pregnant mother will experience shortness of breath and begin wheezing.6 This reaction will cause the pulmonary artery to constrict, making it harder for blood to reach the lungs from the heart. This condition is known as acute pulmonary arterial obstruction. It makes it difficult for the body to absorb oxygen and release carbon dioxide, which, in turn, reduces blood oxygen levels.7 This change is accompanied by the dilatation of the right ventricle and the right atrium, which makes it more difficult for the heart to pump blood. While the exact reason for this response is unknown, some research suggests it could be a response to the constriction of the pulmonary artery and the need to bring more blood to the heart. However, a side effect of this response is significant tricuspid regurgitation, which causes blood to flow back in the opposite direction, thus stopping the heart valve flaps from closing properly. The disruption affects the overall flow of blood within the heart chambers, creating a negative feedback loop that further constricts the pulmonary artery, increases ventricle dilation, and decreases cardiac output to its lowest limit.9As a result, the pregnant mother experiences hypoxemia and hypotension.1,2

Hypoxemia is an abnormal deficiency of oxygen in the blood, and hypotension is abnormally low blood pressure. These two conditions combined result in cardiovascular and pulmonary collapse as the body is no longer able to circulate blood and absorb oxygen effectively.1,2 However, this is just one part of the underlying reactions seen in AFE. As lung and heart function collapse, another domino effect of reactions occurs in the bloodstream. Pregnancy increases procoagulant activity, so there are higher levels of clotting factors such as X, IX, and VIII in the blood, which are also affected by the presence of amniotic fluid or fetal elements.10

When amniotic fluid or fetal elements enter the maternal circulation, these clotting factors are triggered into action, activating the coagulation cascade, which creates blood clots and fibrinolytic pathways, which breaks blood clots down.10

Within a relatively short period of time, a combination of inflammatory and clotting responses occurs rapidly, using up and breaking down specialized proteins needed to control bleeding. Moreover, the speed of this response is much faster than protein production, so normal levels cannot be restored. This imbalance causes the natural blood clotting mechanisms of the body to fail, and this condition is known as coagulopathy.11

Coagulopathy results in an abnormal blood clotting condition known as disseminated intravascular coagulation (DIC), where internal bleeding cannot be controlled from the uterus, puncture sites, and surgical incisions. Also known as DIC-related hemorrhaging, this condition is seen in approximately 80% of AFE cases and leads to severe, unrelenting, and fatal internal bleeding if left untreated.12

Additionally, if the amniotic fluid and fetal elements infiltrate the uterus right before, during, or after labor, it can cause severe uterine atony, which occurs when the uterus fails to contract. This issue further exacerbates the hemorrhage, making it even more difficult to stop internal bleeding.13

It is important to note that lung and heart failure, coagulopathy, DIC, and uterine atony are a few of the more prevalent complications of AFE. Autopsy studies of women who have succumbed to an AFE have also shown other complications such as fluid in the lungs (pulmonary edema), amniotic component emboli in the lungs, alveolar hemorrhage, heart attack (myocardial infarction), acute kidney failure from acute tubular necrosis, and ischemic stroke (cerebral infarctions).1, 2, 14

With all the sudden reactions, AFE can also affect the fetus, raising concerns about its well-being. Amniotic fluid embolism can result in acute fetal distress because the blood supply of nutrients and oxygen essentially stops. Depending on the stage of pregnancy, fetal development may be compromised, as processes will be disrupted. In severe cases, AFE can lead to miscarriage, stillbirth, or neonatal death.1, 2

If AFE leads to preterm labor and premature birth, this can greatly diminish the baby’s survival rate, especially if immediate care is not available. Infants that survive birth have a higher risk of developing hypoxic-ischemic encephalopathy, cerebral palsy, or other cognitive disabilities.1, 2

Amniotic Fluid Embolism Incidences

Amniotic fluid embolisms have the second highest maternal mortality rate in the US but are among the most challenging pregnancy-related complications to study because of their low incidence. General estimates suggest 1 in every 8,000 – 30,000 pregnant women may suffer from an AFE, resulting in 0.8 – 7.7 cases per 100,000 live births.14

Recent evidence suggests that at least one in five AFE cases are most likely incorrectly diagnosed, thus making it harder to accurately estimate the true numbers of AFE cases.14

A recent retrospective cohort study conducted at the University of Southern California, Los Angeles, examined 14.6 million deliveries in the National Inpatient Sample and found 880 women with AFE after examining clinical, pregnancy, and delivery findings with maternal outcomes. The study found AFE to be closer to 6 per 100,000 live births in the US.14 The study also confirmed the dismal outcomes for pregnancies complicated by AFE. The overall fail-to-rescue (FTR) rate (mortality after failed or delayed intervention) after an AFE was 17%, which is significantly high, especially when compared to the overall maternal mortality rate of 1.7%. 14

The rate exceeded 30% if it occurred with other severe symptoms. Consider the failure-to-rescue rates of the most severe complications seen with AFE in the table below: 14

ComplicationsFTR Rate
AFE with cardiac arrest and coagulopathy45.8%
AFE with cardiac rhythm conversions and shock,43.2%
AFE with cardiac arrest, coagulopathy, and shock38.6%
AFE with placenta accreta (or any other condition on the PA spectrum)42.9%
AFE with placental abruption31.3%

It is important to note that mortality rates are with some form of treatment, albeit delayed. Without any intervention, mortality after an AFE may increase to 60%, depending on the speed of onset and severity. Reports have shown that up to 50% of patients die within the first hour, and two-thirds succumb within five hours of cardiovascular collapse.1,2

Of the women who survive an AFE, approximately 66% are left with serious cardiovascular, pulmonary, and neurologic damage that may progress to long-term chronic conditions such as renal failure, pulmonary failure, cardiac failure with left ventricular impairment, pulmonary edema, arrhythmias, myocardial ischemia, or infarctions.2

Amniotic fluid embolism reoccurrence rates are unknown, and experiencing an AFE once does not indicate a reoccurrence in subsequent pregnancies. In fact, reports have shown AFE survivors going on to have normal pregnancies in the future.1,2 

Babies born to mothers who suffer an AFE have been shown to have a mortality rate of approximately 30%, but this is subject to the when in the pregnancy the AFE occurs, its severity, and co-occurring complications. 1,2 

Amniotic fluid embolism causes considerable fetal distress, increasing the risk of stillbirth and life-threatening complications immediately after birth. Also, the time that has elapsed between maternal cardiac arrest and delivery determines the neurological status of the baby. Delivering the fetus as soon as possible has shown to be the most effective treatment to increase the likelihood of survival.1,2

Causes

Historically, it was believed that an AFE resulted from the accumulation of amniotic fluid and fetal elements that caused a mechanical obstruction in the pulmonary arteries, hence the condition being categorized as an embolism.15 However, research has revealed otherwise, showing amniotic fluid is soluble and fetal elements are too small to cause a clot and create a significant obstruction. Additionally, it is now understood that an AFE is a systemic reaction like an allergic response such as an anaphylactic shock.15

Therefore, it is now believed that an AFE is caused by some type of immune-mediated disorder that causes an overwhelming inflammatory response in the mother’s body, damaging healthy tissue and structures.1, 2, 15

From the case information available, potential risk factors that may increase the chances of an AFE include the presence of micro-tears in the cervix or uterus, intense contractions during labor or inducing labor, and requiring a cesarean delivery. Pregnant women older than 35, those with five or more pregnancies, and those who have multiple babies at once also seem to have a higher risk of developing AFE.1, 2

Certain pregnancy-related complications have also been shown to increase the onset of AFE, including early separation of the placenta from the uterine wall, placenta previa, eclampsia, and fetal distress or death.

However, there is no conclusive evidence to verify these risk factors, which makes it exceedingly challenging to predict or prevent the onset of an amniotic fluid embolism.1, 15

Signs and Symptoms

Typically, a woman in the early phases of an AFE may experience several nonspecific symptoms including, but not limited to, headaches, cough, chest pain, nausea, sweating, chills, vomiting, and palpitations.1, 3, 15 However, these signs are very similar to normal pregnancy symptoms and are often dismissed without further investigation.

As AFE progresses, these symptoms are often followed by more characteristic signs such as difficulty breathing, shortness of breath, and increasing feelings of agitation, confusion, and anxiety. Very quickly, these issues can intensify to signal marked hypoxemia and significant hypotension.1, 3, 15

Other symptoms include rapid shallow breathing (tachypnea), abnormally rapid heart rate (tachycardia), purple-bluish coloring to the skin (cyanosis), and DIC-associated bleeding from the vagina, surgical incisions or IV sites, which ranges from minimal to massive.

If AFE occurs before delivery, it can trigger early labor, but if the uterus is unable to contract properly, this can indicate uterine atony. In the most severe cases, AFE can cause seizures and cardiac arrest, such that the patient is gasping for breath, is not breathing, or becomes completely unresponsive and comatose. Throughout AFE progression, the body temperature will remain normal.1,3,15

Diagnostics tests and imaging may also reveal other complications, such as fluid in the lungs, a prominent pulmonary artery, and an enlarged heart. Minute bubbles may be visible in the retinal arteries via a fundoscopy, and a holosystolic high-pitched murmur loudest at the lower left sternal border and radiating to the right sternal edge may be auscultated, signaling tricuspid regurgitation.1,3,15

Blood sample tests will also show abnormal levels, such as low levels of hemoglobin, platelets, and fibrinogen levels, along with increased prothrombin time, activated partial thromboplastin time, and possibly fetal squamous cells.1,3,15

Differential Diagnoses

As no definitive diagnostic tests or pathological markers can diagnose AFE, differential diagnoses are made to rule out other potential conditions that can cause similar symptoms.15

The differential diagnosis of a woman who sustains a complete cardiovascular collapse during or close to the time of delivery followed by major hemorrhaging should include pulmonary embolism (PE), peripartum cardiomyopathy, septic shock, myocardial infarction, venous air embolism, eclampsia, anaphylaxis and cephalad spread of spinal anesthetic.1

Pulmonary Embolism

A pulmonary embolism (PE) is the obstruction of a pulmonary artery, often caused by a moving clot known as an embolus. The most common symptoms include sharp and sudden chest pain, shortness of breath, heart palpitations, dizziness, coughing with bloody mucus, and leg pain or swelling.16 While a pulmonary embolism (PE) mimics many symptoms seen in AFE, it does not present with ongoing coagulopathy; therefore, if a patient has this condition, PE can be ruled out.

Peripartum Cardiomyopathy

Peripartum cardiomyopathy (PPCM) is defined as heart failure between the last month of pregnancy and five months post-delivery.16 However, PPCM is generally seen in the late antepartum period or during the first-month post-delivery. Amniotic fluid embolism, on the other hand, can occur at any time during late pregnancy, labor, or after birth.

Additionally, PPCM symptoms show predominantly left-sided congestive heart failure, which will show significant ST-T wave changes on electrocardiography. 17 A bedside echocardiography can easily make this differential as the results of a PPCM will be different from the classic right ventricular dilatation, overload pattern, and septal bowing into the left ventricle seen in AFE.1

Septic Shock

Septic shock reveals a systemic inflammatory response like AFE, with hypotension and organ failure as the body lacks sufficient oxygen18. However, septic shock also presents with elevated or lowered body temperature, which is generally not seen in sudden cardiopulmonary collapse.

Myocardial Infarction

Myocardial infarction, more commonly known as a heart attack, is caused by decreased blood flow to the heart muscles. Myocardial infarction has the potential to progress to a cardiac arrest and shows typical ST-T wave changes and elevated serial cardiac enzymes.19 A bedside echocardiography would show characteristic ventricular wall motion abnormalities of myocardial infarction, which are different from an AFE.1, 19

Venous Air Embolism

Venous air embolism (VAE) is a gas bubble in the venous circulation that can obstruct blood flow, most often caused by improper vessel cannulation or syringe injection.20 Patients may present with wheezing, gasping, and chest pain before cardiovascular collapse, but they do not have ongoing coagulopathy or DIC-related hemorrhaging.1, 20

Eclampsia

Eclampsia is a serious pregnancy complication that poses a life-threatening risk to both the mother and fetus.21 While it does present with a few similar symptoms, such as seizures before the cardiovascular collapse, eclampsia is a hypertensive disorder.21 Therefore, it is associated with abnormally high blood pressure, unlike AFE, which is associated with hypotension.

Anaphylaxis

Anaphylaxis is like AFE as it includes a sudden onset of hypotension from a serious immune response. However, anaphylaxis is caused by a known agent with evidence of allergy, such as oropharyngeal and lip swelling, inspiratory stridor, and hives.22

Cephalad Spread of Spinal Anesthetic

Cephalad distribution of spinal anesthetic can cause severe hypotension in pregnant women, weakness of the upper extremities, an elevated sensory level, bradycardia, dysphagia, and difficulty in speaking, which are not associated with AFE.1, 23

Treatment Options

An AFE is a medical emergency. Treatment must be aggressive with a focus on prompt cardiopulmonary resuscitation of the mother and rapid delivery of the fetus.

For the mother, breathing and heart function is stabilized by resuscitation and securing the airway. Mechanical ventilation will help reverse the effects of hypoxemia.1,2,3,4 If the patient also suffers from DIC-related bleeding, blood transfusions are started immediately until the internal bleeding can be controlled. Additionally, vasoactive medications may be administered to raise the blood pressure. Other medications are also given to stop the DIC and reduce fluid accumulation around the heart and lungs. 1,2,3,4

The fetus is delivered as soon as possible if its gestation is over 23 weeks, even if the mother is still being resuscitated. The baby should be placed in intensive care for continued monitoring and treatment.1,2,3,4

Once the fetus is delivered, surgical intervention may be necessary to alleviate the mother’s uterine hemorrhaging. If it is determined to be excessive, an emergency hysterectomy may be the best treatment option. 1,2,3,4

Nursing Considerations

While it is difficult to predict who is most at risk of an AFE, steps can be taken to reduce the risk. First, trauma to the uterus must be avoided during any medical procedure, such as the insertion of a pressure catheter. Also, incisions to the placenta must be avoided during cesarean delivery to prevent an AFE during or after birth.24

If a healthy pregnant woman experiences naturally intense labor contractions, these should be controlled by administering intravenous β-adrenergic drugs or magnesium sulfate, as intense labor is a risk factor for an AFE. 24

For the best health outcomes, early detection is key. Healthcare professionals must recognize the early-stage symptoms, including being aware of increased agitation and panic in the mother, low oxygen saturation with hyperventilation and shortness of breath, coarse or wet-sounding coughing, and a bluish tinge to lips or fingertips.3,4 By catching the signs early, preventative treatment can reduce the severity of AFE and increase the chance of survival for both the mother and fetus.1,2,3,4

Once early symptoms present, supportive and resuscitative measures should be implemented, in addition to monitoring the fetus for fetal distress.24 Vasopressors are generally needed depending on the severity of AFE and the clinical situation. The most common agents used include epinephrine and phenylephrine.24 Fluid resuscitation is also used to counter hypotension. This therapy may include restoring blood volume with rapid volume infusion of isotonic crystalloid and colloid solutions. Packed red blood cell transfusions may be necessary to restore the circulation’s oxygen-carrying capacity.24

In addition to vasopressors and fluid management, mechanical ventilation should also be considered to correct the initial hypoxia and hypotension, thus preventing the negative feedback from reaching organ failure.24

The patient should also frequently be examined for signs of bleeding around IV sites, the uterus, and any surgical incisions.1,2,3,4 In the case of coagulopathy, administrating blood and blood products may be recommended to correct it. This includes Fresh frozen plasma (FFP), cryoprecipitate, and platelets.24

If the fetus is still in-utero, left uterine displacement is critical. Tilting the pelvis and abdomen by at least 15 degrees can relieve pressure off the aorta and vena cava, thus reducing hypotension and lowering the risk of fetal distress.24

An emergency cesarean delivery is recommended if the fetus is older than 23 weeks, even if the mother has not been fully resuscitated. 1,2,3,4  Reports suggest that fetal evacuation within five minutes of maternal cardiovascular arrest can significantly improve neonatal neurological recovery and maternal outcomes.

In the case of persistent uterine bleeding, an emergency hysterectomy after delivery may be necessary to control excessive blood loss. However, this should be done cautiously, as some reviews suggest that this procedure can worsen maternal health outcomes.24

Other successful novel approaches to treating AFE include exchange transfusion, cardiopulmonary bypass, a right ventricular assist device, extracorporeal membrane oxygenation (ECMO), uterine artery embolization, and intra-aortic balloon pump.25,26,27,28

If the mother or infant survives this ordeal, educating the family on the risk of medical impairments the mother or infant may face is also important. Ongoing care and rehabilitation may be necessary to recover from this serious complication. 1,2,3,4

Conclusion

An amniotic fluid embolism is a rare but catastrophic pregnancy complication with few preventative measures or predicting diagnostics. The condition is exceptionally complex by nature and can progress rapidly to severe internal bleeding and sudden cardiopulmonary collapse.

Trauma to the uterus must be avoided at all costs, as any micro-tear can create an opening for fetal elements and amniotic fluid to pass through to maternal circulation. Even in a cesarean delivery where a surgical incision must be made, caution must be practiced to avoid the placenta to reduce the likelihood of trauma. While these precautions may reduce the chances of an AFE, there is no guarantee. Therefore, vigilance remains of the utmost importance. If an AFE is suspected, immediate and aggressive treatment by a multidisciplinary team is the best course of action. Recommended therapies should consider the complications presented with AFEs, and, if possible, the fetus should be evacuated as soon as possible.1,2

With early recognition and effective coordination between the multidisciplinary team, a rapid response is possible, and symptoms can be managed, improving health outcomes, and reducing long-term complications for both the mother and the baby.

References
  1. Amniotic fluid embolism. (2016). Pulmonary Embolism, 182-183. https://doi.org/10.1002/9781119039112.ch35
  2. Mazza, G. R., Youssefzadeh, A. C., Klar, M., Kunze, M., Matsuzaki, S., Mandelbaum, R. S., Ouzounian, J. G., & Matsuo, K. (2022). Association of Pregnancy Characteristics and Maternal Mortality With Amniotic Fluid Embolism. JAMA Network Open, 5(11), e2242842. https://doi.org/10.1001/jamanetworkopen.2022.42842
  3. Fitzpatrick, K. E., van den Akker, T., Bloemenkamp, K. W. M., Deneux-Tharaux, C., Kristufkova, A., Li, Z., Schaap, T. P., Sullivan, E. A., Tuffnell, D., & Knight, M. (2019). Risk factors, management, and outcomes of amniotic fluid embolism: A multicountry, population-based cohort and nested case-control study. PLoS Medicine, 16(11). https://doi.org/10.1371/journal.pmed.1002962
  4. Kaur, K., Bhardwaj, M., Kumar, P., Singhal, S., Singh, T., & Hooda, S. (2016). Amniotic fluid embolism. Journal of Anaesthesiology, Clinical Pharmacology, 32(2), 153–159. https://doi.org/10.4103/0970-9185.173356
  5. Burton, G. J., & Fowden, A. L. (2015). The placenta: a multifaceted, Transient Organ. Philosophical Transactions of the Royal Society B: Biological Sciences, 370(1663), 20140066. https://doi.org/10.1098/rstb.2014.0066
  6. Bacsi, A., Pan, L., Ba, X., & Boldogh, I. (2016). Pathophysiology of Bronchoconstriction: Role of Oxidatively Damaged DNA Repair. Current Opinion in Allergy and Clinical Immunology, 16(1), 59–67. https://doi.org/10.1097/ACI.0000000000000232
  7. Pulmonary Artery Occlusion – an overview | ScienceDirect Topics. (n.d.). Www.sciencedirect.com. Retrieved June 13, 2023, from https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/pulmonary-artery-occlusion#:~:text=Acute%20pulmonary%20artery%20obstruction%20increases
  8. Beitzke, D., Wolf, F., Edelhauser, G., Lammer, J., & Loewe, C. (2011). Right heart dilatation in adult congenital heart disease: imaging appearance on cardiac magnetic resonance. The British Journal of Radiology, 84(998), 188–193. https://doi.org/10.1259/bjr/13711325
  9. Chan, K. M. (2016). Anatomy of the tricuspid valve and pathophysiology of functional tricuspid regurgitation. Functional Mitral and Tricuspid Regurgitation, 157-162. Yoon, H.-J. (2019). Coagulation abnormalities and bleeding in pregnancy: an anesthesiologist’s perspective. Anesthesia and Pain Medicine, 14(4), 371–379. https://doi.org/10.17085/apm.2019.14.4.371
  10. Liao, C.-Y. (2016). Amniotic Fluid Embolism with Isolated Coagulopathy: A Report of Two Cases. JOURNAL of CLINICAL and DIAGNOSTIC RESEARCH. https://doi.org/10.7860/jcdr/2016/21720.8615
  11. Gara, M., Draouil, A., Ben Saad, A., Njima, M., Ladib, A., Cherif, O., Jlali, A., & Grati, L. (2021). Disseminated intravascular coagulation type of amniotic fluid embolism: a challenging case report with favorable outcome. Pan African Medical Journal, 38. https://doi.org/10.11604/pamj.2021.38.325.23434
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