Amniotic Fluid Embolus

The EMS unit you are staffing is dispatched for a patient complaining of respiratory distress. Your response time is 12 minutes to the scene. Upon your arrival at the patient you note an obviously pregnant female who is being held unresponsive in her husband’s arms. The patient’s husband relates to you that she is due to deliver at any time, and she began to have weak contractions this morning. The couple presented to the hospital for the delivery, but was told it was too soon to be admitted. They were to return to the hospital when the patient’s contractions were stronger and closer together. Tonight the patient was at rest in bed where she began to complain of shortness of breath that began very suddenly. The patient’s husband called 9-1-1 immediately.

The patient is pale, cool, diaphoretic, and not responding to any stimuli. Your partner immediately secures an airway utilizing endotracheal intubation and begins to ventilate the patient with 100% oxygen. The patient’s heart rate is a regular sinus rhythm at 130 beats per minute. Despite your best efforts and aggressive ventilation the patient’s heart rate rapidly declines until she has an idioventricular heart rate of 12 beats per minute. The patient and fetus are both pronounced dead on arrival at the hospital. Several days later you find out from the emergency room attending physician that the patient most likely had suffered an amniotic fluid embolism.

Unpreventable and catastrophic to the patient and fetus, amniotic fluid embolism (AFE) is the leading cause of death during labor and during the first few postpartum hours.1 Impacting one of every 8,000–80,000 live births, AFE has a maternal death rate of anywhere from 50%–85%. The fetal death rate is not as great as the maternal rate, though it is still in the area of 21%. However, 50% of the surviving neonates experience permanent neurologic injury secondary to hypoxia.2 Much is still unknown about this devastating illness, with the diagnosis of amniotic fluid embolus still being made largely by clinical suspicion or after a postmortem exam.

Description and Etiology

Normally, amniotic fluid does not enter the maternal circulation because the fluid remains contained within the amniotic sac, safely tucked into the uterus. In amniotic fluid embolus, the barrier that exists between maternal circulation and the amniotic sac becomes breached, which allows amniotic fluid and fetal debris to enter maternal central circulation. The most common routes for this to happen are uterine/placental trauma, the endocervical veins or through the placenta itself.

The amount of amniotic fluid that enters the bloodstream does not appear to influence whether the patient will have a reaction. With some women, the fetal debris and amniotic fluid that enter the blood- stream do not cause any signs or symptoms of distress. With other women, the entry of only minute amounts of amniotic fluid or fetal debris can cause devastating results.

Because of the inconsistent symptoms in patients who are exposed to amniotic fluid and fetal debris, there are several different philosophies regarding amniotic fluid embolus. A recent study has likened the reaction more to an allergic reaction than to an embolic reaction, and has proposed the term “anaphylactoid syndrome of pregnancy” instead of amniotic fluid embolus, because of the close resemblance to anaphylaxis.3 Additional studies have indicated that the embolus may actually be caused by a physical obstruction of the vessels by amniotic fluid and fetal debris, more consistent with the classic presentation of an embolus.

Clinical Presentation

The most common time for the presentation of an AFE is during the third trimester of pregnancy or immediately postpartum. However, the patient can experience an AFE at any time during pregnancy. It remains virtually unknown what factors, if any, predicate AFE. A study examining 46 cases of AFE found that 70% of patients experienced their first symptoms during labor, 11% after vaginal delivery, and 19% during cesarean section (during or without labor).4

While assessing the patient for AFE, any chance of successful outcome is predicated on early recognition of symptoms and aggressive resuscitation. Commonly, the first presenting signs or symptoms of AFE are shortness of breath or cyanosis, followed by hypotension, pulmonary edema, shock and neurological manifestations such as confusion, loss of consciousness and seizures.

As maternal hypoxia and hypotension set in, the fetus begins to show signs of distress, as evidenced by a lower heart rate. Decreases in maternal oxygen will rapidly produce unreassuringly slow heart rates. Occasionally, the fetal distress indicated by the change in heart rates will be among the first signs of maternal distress.

Within several minutes of the presentation of symptoms, approximately half of the patients suffering from AFE decompensate into cardiac arrest. Of patients in witnessed cardiac arrest (in hospital), approximately 40% are successfully resuscitated with aggressive Advanced Cardiac Life Support (ACLS) treatment. After resuscitation, the surviving patients are likely to experience noncardiac pulmonary edema and severe coagulopathy.

Treatment

Treatment for AFE is generally based on the patient’s presentation. If the patient does not succumb into cardiac arrest, the care is generally aimed at restoring fetal perfusion. As with any maternal patient, she should be placed on her left side to prevent the weight of the gravid uterus from compressing the inferior vena cava and compromising cardiac filling. The remainder of patient treatment should be aimed at supporting oxygenation, circulation and fetal perfusion.

Airway

Carefully monitor the patient’s airway for adequacy of respirations.

Deliver oxygen in concentrations close to 100% by the best available means. If the patient ceases to have an adequate respiratory effort, or shows signs of hypoxia, secure the airway utilizing more definite means, including intubation. After the airway is secured and confirmed using appropriate ACLS airway guidelines, ventilate the patient with a high concentration of inspired oxygen. The objective of oxygen therapy in the AFE patient is to keep arterial oxygen saturation above 90%.

Perfusion

Keeping blood pressure up and cardiac output adequate requires that several measures be accomplished simultaneously. The simple measure of placing the patient with her legs in the shock position helps improve venous blood return. If available, placing the patient in a true Trendelenburg position not only helps venous blood return, but also facilitates improved perfusion to the nervous system. The patient should have continuous ECG monitoring to allow early detection and correction of dysrhythmias.

To maintain blood pressure at 90 mmHg systolic, the first appropriate choice in treating hypotension is to provide rapid volume expansion utilizing a crystalloid solution. The end point of fluid boluses is a matter of local policy. Be cautious about overusing fluids, as the patient may become overhydrated. Inotropic agents to pharmacologically assist with cardiac function and blood pressure may be indicated after fluids have proved ineffective. Some of the commonly used inotropes include dopamine, dobutamine, and Levophed to maintain blood pressure and improve end-organ profusion.

Control of Hemorrhage and Coagulopathy

If you are transporting a woman who is immediately postpartum and is experiencing uterine hemorrhage, several modalities could be employed.

Contracting the uterus to achieve hemorrhage control could be achieved by uterine massage or the use of intravenous Pitocin.

Resuscitation Pitfalls

Aggressive cardiopulmonary resuscitation on a pregnant female is more difficult because of the anatomic and physiologic changes that take place during gestation.

The pregnant female has decreased gastric motility, increased gastric emptying times, and a relaxation of the lower esophageal sphincter. These factors make it more likely that the patient will aspirate during the aggressive compressions and ventilations used during common CPR. This aspiration risk necessitates that the patient’s airway be controlled definitively early in the resuscitation, utilizing endotracheal intubation.

The gravid uterus causes changes in lung volume significantly in the second half of pregnancy, decreasing functional residual lung capacity by 9.5% to 25%. It also increases serum progesterone levels, stimulating the respiratory centers in the brain and resulting in hyperventilation and a maternal sense of dyspnea.

Blood volume rises during pregnancy, with the plasma content raised as much as 50% over nonpregnant values. The mass of maternal red cells rises as well, but not as much as the plasma levels. This inequality of plasma to red blood cells creates the relative anemia found in pregnancy. This anemia impacts the oxygenation of vital organs during resuscitation, lessening their ability to respond to therapy.

Maternal oxygen consumption rises remarkably as a result of the oxygen consumption of placenta, uterus and fetus. Uterine blood flow accounts for roughly 10% of the patient’s cardiac output. During proficient CPR, a maximum of 30% of the patient’s cardiac output is achieved. With only 30% of the patient’s normal cardiac output being achieved, it is unlikely that either the mother or the fetus will receive enough oxygen to successfully facilitate resuscitation.

Fetal Considerations

The best outcomes with AFE occur after delivery of the fetus. The infant is not impacted by the event because he no longer resides within the maternal host. The mother is therefore not taxed by the physiologic hurdles of the placenta and fetus, and the gravid uterus can no longer place weight on the inferior vena cava to decrease maternal blood flow.

When the AFE occurs before or during delivery, the fetus is impacted quickly by any hypoxia. If the fetus is deemed viable outside the maternal host, consider quick transport to a facility prepared for a crash cesarean section.

Family Considerations

As long as it doesn’t interfere with ongoing treatment or transport, families should be given unrestricted access to their loved ones. It is not uncommon for expectant or new fathers and other family members to want to watch medical care delivered to their families. This request should be honored, but an informed member of the crew should be assigned to the family to provide accurate information about the resuscitation and its progress. The patient’s family must always be well-informed about the ongoing care and condition of their loved ones.

If the resuscitation is terminated and the patient won’t be transported, allow accompanied visitation of the deceased by her loved ones. After initial contact has been made and all questions have been answered, allow family members to be left alone with the deceased, with medical personnel standing close by.

If the infant dies after delivery, allow family members to hold it. Some in-hospital policies dictate that pictures of the newborn should be taken and offered to the family as keepsakes. All of the infant clothing, blankets or identification bracelets that are used during treatment should be kept and given to the family. Some labor and delivery units give “memory boxes” to the family to contain all of the infant’s belongings.

Summary

Amniotic fluid embolus remains among the most fatal obstetrical emergencies, with an extremely high maternal and fetal death rate. There is no way to predict who is at risk for this often catastrophic malady. Increased awareness by the medical community of the signs and symptoms of AFE may allow us to provide earlier aggressive treatment to these patients. Early recognition and treatment remain the best way to start early aggressive intervention aimed at successful outcomes for both mother and child.

References

1. Davies S. Amniotic fluid embolus: A review of the literature. Can J Anesth 48:88–98, 2001.
2. Ladewig PW, et al. Essentials of Maternal-Newborn Nursing. New York: Addison-Wesley Nursing, 1990.
3. Masson RG. Amniotic fluid embolism. Clin Chest Med 13:657–665, 1992.
4. Ray B, et al. Amniotic fluid embolism with second trimester pregnancy termination: A case report. Can J Anesth 51:139–144, 2004.
5. Turner R, et al. Massive amniotic fluid embolism. Ann Emerg Med 13:359–361, 1984.