Amniotic Fluid Embolism

Amniotic fluid embolism

I. What every physician needs to know.

Amniotic fluid embolism is a cause of respiratory distress, hypotension, cardiac arrest, altered mental status, seizure, or coagulopathy in pregnant women. Although it has been reported to occur with other gynecologic procedures, symptoms usually occur during labor or immediately after labor.

The pathophysiology is not fully elucidated but it is not solely related to amniotic fluid material entering the maternal circulation and causing pulmonary vascular obstruction. Diagnosis is clinically based and also one of exclusion. Treatment is supportive. Mortality and morbidity is high for the mother and fetus.

II. Diagnostic Confirmation: Are you sure your patient has amniotic fluid embolism?

Diagnostic criteria for amniotic fluid embolism by national registries require patients to have (1) acute hypotension or cardiac arrest, (2) acute hypoxia diagnosed by dyspnea, cyanosis or respiratory arrest, and (3) coagulopathy or severe hemorrhage.

All clinical components need to have occurred within an appropriate timeframe which can occur during labor or cesarean delivery, 30 minutes after delivery, or during dilation and evacuation. Additionally, patients can have no other explanation for symptoms.

A. History Part I: Pattern Recognition:

Respiratory distress
Hypotension or cardiac arrest
Altered mental status or seizure
Coagulopathy
Occurring during or immediately after delivery

B. History Part 2: Prevalence:

The prevalence is 14.8 per 100,000 multiparous deliveries and 6 per 100,000 primigravid deliveries. Data correlating increased risk with specific conditions varies by demographic population. Although rare, amniotic fluid embolism is one of the leading cause of maternal morbidity and mortality and is accountable for approximately 10% of maternal deaths in developed countries. The perinatal death rate is roughly 25% with approximately 50% of surviving neonates being neurologically intact. However, data consistently suggest that aminiotic fluid embolism is more common with maternal age of 35 years or older, cesarean delivery, forceps or vacuum assisted vaginal delivery, placenta previa, abruption placenta, eclampsia, and fetal distress.

C. History Part 3: Competing diagnoses that can mimic amniotic fluid embolism.

Pulmonary embolism
Eclampsia
Peripartum cardiomyopathy
Septic shock
Hemorrhage
Myocardial infarction

D. Physical Examination Findings.

There are no specific physical exam findings for amniotic fluid embolism except for evidence of cardiopulmonary compromise with hypotension, tachypnea, tachycardia, and hypoxia. There are three phases of this syndrome. The initial phase usually occurs within the first 30 minutes of delivery and is characterized by transient pulmonary and systemic hypertension that results in hypoxemia due to ventilation perfusion mismatch and possible concurrent myocardial injury. Mortality is the highest during this acute phase. The second phase is characterized by a profound depression of left ventricular function, myocardial depression and hypoxia secondary to amniotic fluid embolism associated pulmonary injury. Pulmonary manifestations occur due to profound intrapulmonary shunting with subsequent lung injury patterns consistent with acute respiratory distress. The third phase is marked by heart failure, acute respiratory distress, and coagulopathy. The fetus may also have signs of distress.

E. What diagnostic tests should be performed?

Amniotic fluid embolism is a clinical diagnosis where other possible diagnoses have also been excluded. No laboratory or radiographic studies are specific and the focus of diagnostic tests is to rule out other treatable causes.

Tests to consider are complete blood count, chemistries, arterial blood gas, disseminated intravascular coagulation (DIC) panel, cardiac enzymes, blood and urine cultures, electrocardiogram, chest x-ray, computed tomography (CT) angiogram of lungs, transthoracic echocardiogram, and transesophageal echocardiogram in conjunction with the obstetric evaluation.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

After other diagnoses are ruled out, results of laboratory studies in patients with amniotic fluid embolism may reveal mild leukocytosis, anemia and rarely thrombocytopenia. Also, patients may have DIC with elevated prothrombin and partial thromboplastin time. Patients may also have low complement component 3 and 4 (C3 and C4) levels, elevated serum tryptase levels and elevated sialyl TN antigen levels (a fetal antigen present in both meconium and amniotic fluid). Insulin-like growth factor is a protein synthesized by the placenta decidua and can be measured in both maternal serum and amniotic fluid. Comparing the ratio of this growth factor between amniotic fluid and maternal serum might make this marker potentially useful for diagnosis. Several novel and potentially viable biomarkers using protein, lipid, and transcriptomic profiles of extracellular vesicles have diagnostic potential. These vesicles are ejected into the maternal circulation early in the course of the disease process and can be detected even before clinical manifestations are present, making them potentially useful in early diagnosis. Sensitivity and specificity of these biomarkers remain poor, which limits their current use.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Again imaging is mainly done to rule out other potential diagnoses. Chest radiograph may reveal diffuse, bilateral homogenous opacities. Echocardiograms can have evidence of increased pulmonary pressures with right side strain and leftward deviation of the interatrial and interventricular septum.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

N/A

III. Default Management.

N/A

A. Immediate management.

Immediate management is maintenance of oxygenation and potentially intubation, if needed. Attention to blood pressure and cardiac output should be managed with fluids and vasopressors or inotropes if needed, to maintain systolic blood pressure above 90 mm/Hg. Since DIC coagulation can be associated with severe hemorrhage, correction of coagulopathy with transfusion of fresh frozen plasma, platelets, and/or cryoprecipitate may be necessary.

Inhaled nitric oxide or inhaled epoprostenol can be used in refractory hypoxemia to produce pulmonary vasodilation. In the event of a cardiac arrest, prompt delivery improves the likelihood of good outcome and should occur in less than 5 minutes of maternal cardiac arrest. Pregnant patients requiring cardiopulmonary resuscitation should be placed in left lateral decubitus position to relieve uterine weight off inferior vena cava and improve blood return. In patients unresponsive to advanced life support measures, sodium bicarbonate has been proposed for pulmonary vasodilation. If the aforementioned fail, extracorporeal membrane oxygenation may be considered. Decisions regarding advanced therapies should be made in consultation with a specialist and may include intra-aortic balloon counterpulsation, cardiopulmonary bypass, intraoperative cell salvage, uterine artery embolization, and placement of a Bakri balloon to create a postpartum intrauterine tamponade for temporary control and reduction of postpartum hemorrhage. In the setting of hypoxic brain injury, there is anecdotal evidence that therapeutic hypothermia for 12-24 hours may have benefit. Due to the rare occurrence of amniotic fluid embolism, clinical data on these newer treatments are extremely limited.

B. Physical Examination Tips to Guide Management.

Physical exam should identify the degree of hypotension, tachycardia, tachypnea, and hypoxia. Emergent cardiopulmonary stabilization of the mother and fetus is needed and should be addressed first.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

None

D. Long-term management.

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E. Common Pitfalls and Side-Effects of Management

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