First Things First (assess and treat for the following)

• Amniotic fluid embolism (AFE) occurs when there is a breach in the barrier between maternal circulation and amniotic fluid. Fetal material has been documented in the pulmonary circulation of asymptomatic women.

• The postulated mechanisms include:
  • Obstruction of pulmonary vasculature from fetal debris
  • Inflammatory mediators leading to vasoconstriction and bronchospasm rather than mechanical factors

• It is likely due to a combination of these factors that leads to:
  • Development of acute pulmonary hypertension and cor pulmonale
  • Sudden decrease in blood flow to the left ventricle, leading to vascular collapse
  • Ventilation/perfusion mismatches, leading to hypoxemia and its attendant complications
  • Activation of the extrinsic coagulation pathway, leading to disseminated intravascular coagulation (DIC)

History & Physical (assess for the following)

• Signs & symptoms
  • Hypoxemia
  • Hypotension
  • Coagulopathy
  • Altered mental status
  • Seizures
  • Fetal distress
  • Fever
  • Chills
  • Headache
  • Nausea
• The diagnosis of AFE is suspected when women present with above-mentioned signs and symptoms during:
  • Labor
  • Delivery
  • Immediate postpartum period
  • Rarely in the late postpartum period
• AFE has also been reported following:
  • Amniocentesis
  • Therapeutic abortion
  • Abdominal trauma in pregnant individual
  • Intrapartum amnioinfusion
• Differential diagnosis
  • Venous thromboembolism
  • Air embolism
  • Myocardial infarction
  • Septic shock
  • Preeclampsia/eclampsia
  • Postpartum hemorrhage
  • Anaphylaxis
  • Anesthetic complication
  • Transfusion reactions

Diagnostic Tests

• The diagnosis of AFE is essentially a diagnosis of exclusion.

• There is no laboratory or bedside investigation that can confirm the diagnosis.

• It is suspected when a woman who is pregnant or in the immediate postpartum period acutely presents with shock along with severe respiratory distress.

• Although most patients present in this manner, there is a subset of patients in whom the initial presentation may be severe hemorrhage secondary to DIC.

• Occasionally the presentation may be subtle, with restlessness, altered mental status and/or hypoxemia.

• It is important to exclude other fulminant conditions like sepsis, myocardial infarction, anaphylaxis, and transfusion reactions.

• Labs: More than a diagnostic aid, these tests are useful in guiding resuscitation.
  • Arterial blood gas to evaluate ventilation and hypoxemia
  • DIC profile: These patients may develop DIC, as evidenced by elevated PT, PTT, low fibrinogen level and elevated fibrin split products (FSP).
  • Complete blood count: In the presence of DIC, hemoglobin and hematocrit tend to drop. Patients often develop thrombocytopenia and they usually have reactive leukocytosis.
  • Serum chemistries
• Experimental studies have suggested that certain lab tests may be helpful:
  • Serum tryptase and histamine markers of mast cell activation (high)
  • Sialyl Tn - Fetal antigen (high)
  • Complement C3 & C4 (low)
  • Zinc coproporphyrin (high)
  • Although touted to be specific for AFE, they have no established role in confirming the diagnosis of AFE and remain experimental tools.

• Radiographic findings are not diagnostic. Most of these patients show diffuse infiltrates suggestive of pulmonary edema.

• An electrocardiogram should be obtained to look for signs of ischemia.
• Echocardiogram to evaluate pulmonary artery pressure, right ventricular and left ventricular function
• Historically, it was believed that the amniotic fluid debris found by aspirating blood from the distal port of a pulmonary artery catheter was pathognomonic of AFE; however, recent studies have shown that fetal elements can be found in some asymptomatic pregnant women.

General Management Principles

• Given the rapidity with which AFE presents, it is essential to be vigilant and respond quickly.

• The cornerstone of therapy is supportive care.

• Hypoxemia
  • Supplemental oxygen while monitoring oxygen saturation
  • If hypoxemia with hemodynamic instability is present, intubation and mechanical ventilation is indicated.
  • AFE patients with ARDS should be placed on low tidal volume and high PEEP while monitoring the plateau pressure as recommended by the ARDS network.

• Hemodynamic instability
  • These patients need to be resuscitated with fluids and vasopressors.
  • Transthoracic or transesophageal echocardiogram may be useful in guiding fluid therapy.
  • If patients are noted to have left-sided failure with pulmonary edema, therapy should include a combination of dobutamine along with either phenylephrine or norepinephrine.
  • The goal is to maintain a mean arterial pressure >65 mmHg.

• Cardiac arrest
  
  • Advanced Cardiac Life Support including medications should be instituted immediately.
  • During cardiopulmonary resuscitation before delivery the uterus should be displaced to the left to avoid compression of aorta & inferior vena cava.
  • The goal is to restore maternal hemodynamics and deliver the fetus as soon as possible.

• DIC
  
  • Frequent monitoring of the coagulation profile, including complete blood count and fibrinogen levels
  • Blood transfusion for hemorrhage
  • Patients need to be transfused with fresh frozen plasma & cryoprecipitate to correct coagulation abnormalities.
  • Platelet transfusions for patients with thrombocytopenia who are actively bleeding
  • Given the increased risk of bleeding with a coexisting coagulopathy, uterine atony must be treated aggressively with standard medical and surgical methods, including uterotonic medications, uterine artery embolization or ligation and hysterectomy.

• Fetus
  • ~2/3 of patients are in labor when they are diagnosed. In these instances immediate delivery of the fetus is mandated to prevent further hypoxic damage.

Specific Management

• N/A

Ongoing Assessment

• AFE patients should be continuously monitored in an intensive care unit.
• Continuous fetal monitoring until delivery is mandatory.
• All patients need central venous IV access as well as arterial lines.

Complications

• Maternal outcome

• • Mortality 13-86%
  • 7-85% of the survivors have neurologic deficits.

• Fetal outcome
  • Mortality 21-22%
  • 29-50% of the survivors have neurologic deficits.

Authors

• Jijo John, MD, and Gary T. Kinasewitz, MD