Amniotic Fluid Embolism
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
Last updated: April 16, 2010
Citation
"Amniotic Fluid Embolism." Pocket ICU Management, PocketMedicine.com, Inc, 2010. Anesthesia Central, anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534006/all/Amniotic_Fluid_Embolism.
Amniotic Fluid Embolism. Pocket ICU Management. PocketMedicine.com, Inc; 2010. https://anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534006/all/Amniotic_Fluid_Embolism. Accessed November 25, 2024.
Amniotic Fluid Embolism. (2010). In Pocket ICU Management. PocketMedicine.com, Inc. https://anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534006/all/Amniotic_Fluid_Embolism
Amniotic Fluid Embolism [Internet]. In: Pocket ICU Management. PocketMedicine.com, Inc; 2010. [cited 2024 November 25]. Available from: https://anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534006/all/Amniotic_Fluid_Embolism.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC
T1 - Amniotic Fluid Embolism
ID - 534006
Y1 - 2010/04/16/
BT - Pocket ICU Management
UR - https://anesth.unboundmedicine.com/anesthesia/view/Pocket-ICU-Management/534006/all/Amniotic_Fluid_Embolism
PB - PocketMedicine.com, Inc
DB - Anesthesia Central
DP - Unbound Medicine
ER -