Amniotic Fluid Embolism

Amniotic Fluid Embolism 

7 Interesting Facts of Amniotic Fluid Embolism

  1. Amniotic fluid embolism is a rare and potentially fatal complication of childbirth that occurs in the peripartum period
  2. It is thought to be a severe allergic reaction that is triggered in some women by amniotic fluid and fetal debris entering the bloodstream 
  3. Cardinal findings include cardiocirculatory and pulmonary collapse, severe hypoxemia and hypotension, and disseminated intravascular coagulopathy and/or hemorrhage 
  4. Physical signs and symptoms occur suddenly and include shortness of breath, cough, hypotension, chest pain, lightheadedness, chills, tingling in hands and feet, cyanosis, nausea, vomiting, confusion, anxiety, and panic
  5. There is no specific diagnostic test; diagnosis is made on the basis of clinical findings and by exclusion of other conditions 
    • Ultimately, if a laboring or recently delivered woman becomes agitated and restless and complains of dyspnea, amniotic fluid embolism must be considered
  6. Treatment is multidisciplinary and primarily supportive
    • Involves managing the hemodynamic status of the patient, providing ventilatory and cardiocirculatory support, delivering the fetus or performing uterine evacuation, and resolving coagulopathy and hemorrhage
  7. Mortality rate has declined to 22% in the last 35 years
    • Morbidity rate among patients is still elevated (61% of women and 50% of infants develop long-lasting neurologic complications) 


  • Late recognition of signs and symptoms may prevent a prompt, effective medical response
  • Many signs and symptoms are similar to other conditions, which can lead to misdiagnosis
  • Amniotic fluid embolism is a life-threatening anaphylactic reaction caused by amniotic fluid and fetal debris entering the maternal bloodstream 
    • Causes collapse/failure of respiratory and cardiocirculatory systems, which can result in cardiopulmonary arrest and death 
  • Defined by the following findings, which occur during delivery or within 30 minutes post partum and for which there is no alternative explanation: 
    • Acute hypoxia
    • Acute hypotension or cardiac arrest
    • Disseminated intravascular coagulation (22%-83% of patients) or severe hemorrhage

Clinical Presentation


  • Occurs during labor (70% of cases), during delivery, or in the postpartum period (within 15-45 minutes or as late as 48 hours after delivery) 
  • Several symptoms are premonitory of the pulmonary and cardiovascular collapse characteristic of amniotic fluid embolism and can manifest alone or in combination 
    • Symptoms of respiratory distress
      • Dyspnea (48%-72% of cases) 
      • Chest pain 
      • Persistent dry cough 
    • Symptoms of poor tissue oxygenation
      • Altered mental status (eg, anxiety, confusion, agitation, panic; 80%-100% of cases) 
      • Chills and shivering 
      • Lightheadedness 
      • Tingling in extremities 
      • Nausea and vomiting 
  • Once symptoms manifest, death can occur within 1 to 7 hours 

Physical examination

  • Most common signs (up to 100% of patients)
    • Sudden and severe hypotension (blood pressure less than 90/60 mm Hg) 
    • Respiratory distress 
    • Cyanosis 
  • If amniotic fluid embolism occurs before delivery, fetal heart rate monitoring may indicate decelerations, loss of beat-to-beat variability, and terminal bradycardia as oxygenated blood is directed away from uterus and uterine perfusion decreases 
    • Fetal distress is present in 50% to 100% of cases 
  • Other clinical signs include:
    • Pulmonary edema (51%-100%) 
    • Acute hypoxemia (50%-100%) 
    • Cardiopulmonary arrest (30%-87%) 
    • Seizure or coma (10%-48%) 
    • Severe hemorrhage (eg, from uterus, gastrointestinal tract, urinary tract, vaginal lacerations, venipuncture sites, or recent incision sites) 
    • Uterine atony 


  • Abnormal release of trophoblasts or other fetal material into maternal circulation causing an immune-mediated reaction that triggers cardiorespiratory collapse 
    • Pathogenesis is not fully understood 
    • Likely has no direct relationship to either amniotic fluid or an embolism despite the name 
  • Pregnancy complications, procedural complications, or accidental events that cause breach in maternal-fetal barrier include:
    • Placenta previa 
    • Placental abruption 
    • Eclampsia/ preeclampsia 
    • Operative vaginal delivery
      • Forceps-assisted 
      • Vacuum-assisted 
    • Cesarean delivery 
    • Cervical laceration or uterine rupture 
    • Polyhydramnios 
    • Induction of labor 
    • Amniocentesis 
    • Therapeutic abortion 
    • Amnioinfusion 
    • Abdominal trauma 

Risk factors and/or associations

  • Higher incidence in women older than 35 years 
  • 2-fold higher incidence observed in non-Hispanic Black population compared with other races 
Other risk factors/associations
  • Risk factors may also include:
    • Multiparity 
    • Intrauterine fetal demise 
    • Chorioamnionitis 
    • Older maternal age 

Diagnostic Procedures

Primary diagnostic tools

  • Diagnosis depends on history and physical examination findings, exclusion of other likely causes, and a high index of suspicion 
    • Cardinal findings during labor or delivery or within 48 hours post partum and for which there is no alternative explanation include:
      • Acute hypoxia 
      • Acute hypotension or cardiac arrest 
      • Disseminated intravascular coagulation or severe hemorrhage 
      • Altered mental status 
    • Clinical diagnosis is made during labor (65%-70% of cases) or post partum (11% of cases); 19% of cases occur during cesarean delivery 
  • No particular tests can reliably confirm the diagnosis of amniotic fluid embolism 
  • Nonspecific tests are performed when the diagnosis is suspected, with the goal of managing the clinical findings at initial presentation 
    • Pulse oximetry and end-tidal carbon dioxide measurement are used in all patients
    • Measure arterial blood gas levels as soon as possible in all patients (to determine degree of hypoxemia and adequacy of ventilation)
    • Obtain the following tests in all patients with suspected amniotic fluid embolism after any initial efforts to stabilize the patient (eg, basic or advanced cardiac life support); do not delay resuscitative efforts to obtain any of these tests
      • Serum electrolyte levels
        • Especially calcium and magnesium levels
      • Coagulation profile (ie, prothrombin time/INR, advanced partial thromboplastin time, fibrinogen, and fibrin degradation products)
      • CBC with platelet count
    • Point-of-care visco-elastometric testing (rotational thromboelastometry) may identify coagulopathy and exclude pulmonary embolism in the acute setting 
    • Obtain 12-lead ECG in all patients for evidence of ischemia or infarction once initially stabilized
      • Obtain cardiac troponin level in all patients who show evidence of cardiac ischemia or new infarction
    • If available, transthoracic or transesophageal echocardiography may be performed at bedside once patient is initially stabilized
      • Echocardiography is useful in diagnosing amniotic fluid embolism–induced pulmonary hypertension, in identifying other similarly presenting conditions, and in fluid management
  • If amniotic fluid embolism occurs before delivery, fetal heart rate monitoring may indicate nonreassuring fetal status before symptoms are observed in the woman 
    • Decelerations, loss of beat-to-beat variability, and terminal bradycardia are observed as oxygenated blood is directed away from uterus and uterine perfusion decreases
    • Nonreassuring fetal status is present in 50% to 100% of cases of amniotic fluid embolism 


  • Arterial blood gas analysis
    • Obtain in all patients
    • Results indicative of poor ventilation and hypoxemia are:
      • Decreased PaO₂ levels (PaO₂ less than 80 mm Hg; reference range, 80-100 mm Hg) 
      • Increased PaCO₂ levels (PaCO₂ greater than 45 mm Hg; reference range, 35-45 mm Hg) 
      • Decreased pH levels (pH less than 7.35; reference range, 7.35-7.45) 
  • Coagulation profile
    • Obtain in all patients after initial stabilization
    • Results indicative of disseminated intravascular coagulopathy are:
      • Failure of blood to clot 
      • Elevated prothrombin time and partial thromboplastin time 
      • Reduced platelet count (rare finding; less than 20,000 cells/μL)
      • Reduced fibrinogen level (less than 100 mg/dL)
      • Presence of products of fibrin degradation 
  • CBC
    • Obtain in all patients after initial stabilization 
    • Results characteristic of severe hemorrhage with an acute-phase response are: 
      • Low hemoglobin level (less than 10 g/dL) and low hematocrit (less than 20%) 
      • Elevated WBC count (more than 9000-25,000 cells/μL) (acute-phase response)
      • Reduced platelet count (rare; less than 20,000 cells/μL)
  • Serum troponin level
    • Obtain in all patients who show evidence of cardiac ischemia or new infarction on ECG results
    • Results indicative of cardiac injury are:
      • Elevated troponin level (more than 0.035 mcg/L; reference range, less than 0.01 mcg/L) 


  • Transthoracic or transesophageal echocardiography
    • Indications for bedside echocardiography
      • Evaluation of response to preload in mechanically ventilated patients
      • Evaluation of suspected pulmonary hypertension
      • Evaluation of suspected or possible pulmonary embolism
        • Perform lower extremity ultrasonographic evaluation for thrombi
        • Used in evaluation of amniotic fluid embolism; helps to differentiate from pulmonary embolism that presents similarly
      • Evaluation of shock and hemodynamic instability
    • Results indicating acute right-sided heart failure due to pulmonary hypertension (early phase of amniotic fluid embolism) are:
      • Diminished right ventricular contractility and systolic function 
      • Enlargement of right ventricle 
      • Pulmonary valve regurgitation (significant) and tricuspid regurgitation (moderate), paired with systolic pulmonary artery pressure of 60 mm Hg or higher 
    • Results indicating acute left-sided heart failure are:
      • Diminished left ventricular contractility and decreased ejection fraction 
      • Dilated left ventricle 

Functional testing

  • Pulse oximetry
    • Obtain in all patients
    • Sudden drop in arterial oxygen saturation is indicative of hypoxemia 
  • End-tidal carbon dioxide measurement
    • Result indicative of insufficient ventilation is:
      • Widened difference (or gradient) between end-tidal CO₂ concentration and PaCO₂ (from 2-5 mm Hg [normal gradient] to 20 mm Hg or higher) in patients whose status is consistent with ventilation-perfusion mismatch (high ventilation-perfusion ratio) 
  • ECG
    • Results indicating ischemia or infarction and cardiovascular collapse are: 
      • Tachycardia with right ventricular strain pattern in early stage of condition
      • Abnormal ST segment and T waves
      • Cardiac arrhythmias or asystole (seen with severe cardiovascular collapse)
        • Ventricular fibrillation, pulseless electrical activity, and asystole are the 3 classic dysrhythmias in patients with amniotic fluid embolism who are in cardiac arrest 

Other diagnostic tools

  • Diagnostic criteria have been developed; primarily for research purposes but may be clinically useful
    • Amniotic fluid embolism can be diagnosed when all of the following conditions are present 
      • Sudden onset of cardiorespiratory arrest, or both hypotension (systolic blood pressure lower than 90 mm Hg) and respiratory compromise (dyspnea, cyanosis, or peripheral capillary oxygen saturation lower than 90%)
      • Overt disseminated intravascular coagulation following appearance of these initial signs or symptoms, documented using the scoring system of the Scientific and Standardization Committee on Disseminated Intravascular Coagulation of the International Society on Thrombosis and Haemostasis, modified for pregnancy
        • Coagulopathy must be detected before loss of sufficient blood to itself account for dilutional or shock-related consumptive coagulopathy
      • Clinical onset during labor or within 30 minutes of delivery of placenta
      • No fever (temperature 38 °C or higher) during labor
    • This may not identify patients with atypical amniotic fluid embolism. A French study reported that less than two-thirds of patients who died from amniotic fluid embolism exhibited all 4 of these criteria, with documented disseminated intravascular coagulation the most common missing criterion 

Differential Diagnosis

Most common

  • Conditions presenting with chest pain, dyspnea, or abrupt cardiopulmonary compromise
    • Pulmonary thromboembolism
      • Also presents with chest pain and pulmonary edema 
      • Peak risk of pulmonary thromboembolism is immediately postpartum, continuing for 4 to 6 weeks afterward
      • Less likely to be present in a profusely bleeding patient 
      • Differentiated by presence of venous thrombosis in lower limbs detected by imaging (eg, CT) 
        • Doppler ultrasonography may identify lower extremity thrombosis, particularly in patients unable to undergo CT angiography
    • Drug-induced anaphylactic reaction
      • Severe systemic immediate hypersensitivity reaction caused by IgE release in response to a pharmaceutic agent (eg, local anesthetic)
      • Cardiovascular/respiratory collapse and seizures are manifestations similar to those of amniotic fluid embolism
      • Characterized by cutaneous presentation, including urticaria and angioedema 
      • Differentiated clinically by examination findings and history
        • Symptoms typically manifest within minutes after drug administration
    • Peripartum cardiomyopathy/arrhythmia
      • Disease of pregnancy occurring in high-risk patients (eg, those with preeclampsia, cesarean delivery, or multiple gestation) 
        • Idiopathic heart failure in the absence of identifiable heart disease
        • Associated with family history of cardiac disease
      • Arrhythmias may develop, placing the patient at risk for sudden cardiac death
      • Heart failure may develop during the last month of pregnancy and up to 5 months post partum
      • Disseminated intravascular coagulation does not develop in peripartum cardiomyopathy, nor is seizure activity present
      • Diagnosed by marked elevation of natriuretic peptide levels and echocardiographic and ECG findings indicative of dilated cardiomyopathy and heart failure 
        • Echocardiographic criteria include:
          • Reduced left ventricular ejection fraction less than 0.45 and/or M-mode fractional shortening less than 30%
          • End-diastolic dimension greater than 2.7 cm/m²
    • Myocardial infarction
      • Peripartum myocardial infarction occurs mainly in women older than 30 years and is predominantly an anterior ST-segment elevation myocardial infarction 
      • Chest pain and dyspnea, leading up to cardiac arrest, may occur
      • Difficult to differentiate clinically except that myocardial infarction is not usually associated with disseminated intravascular coagulation or seizures
      • Diagnosed by characteristic ECG changes and elevation of serum troponin levels
    • Acute aortic dissection
      • Presents with chest pain, dyspnea, nausea, vomiting, agitation, collapse, and cardiac arrest 
      • Differentiated by association with history of connective tissue disorders, cardiac valve variants, or chest trauma 
      • Ultrasonography may be used for initial detection of aortic aneurysm; CT or MRI confirm and define the dissection and leakage 
    • Sepsis
      • Systemic inflammatory state associated with infection
      • Depending on type of infection, symptoms similar to those of amniotic fluid embolism include chills, fever, altered mental status, difficulty breathing, cough, nausea, and vomiting
        • Cardiovascular collapse and disseminated intravascular coagulation may occur 
      • Differentiated by evidence of infection (eg, signs of bacterial infection, fever, hypothermia); furthermore, the presentation of sepsis and its sequelae is usually not as dramatic and sudden as that of amniotic fluid embolism 
    • Blood transfusion reaction
      • Acute complication of blood transfusion, including hemolytic, allergic, or anaphylactic reactions 
      • Presents with:
        • Dyspnea, chest pain, hypotension, diffuse bleeding, nausea, and vomiting (with severe form of hemolysis) 
        • Coagulopathy, especially in massive transfusion (replacement of a patient’s total blood volume in less than 24 hours) 
      • Distinguishing features include:
        • Mild urticarial reactions (pruritus) or anaphylactic shock
        • Fever, rigors, renal dysfunction (eg, hemoglobinuria, oliguria, anuria), and pain at the infusion site, in the back, and/or in the abdomen (with acute hemolytic transfusion reaction)
      • Differentiated by history of recent blood transfusion
  • Conditions presenting with seizures
    • Eclampsia 
      • Seizures occurring during pregnancy, associated with pregnancy-induced hypertension
      • Seizure and coma are features similar to those of amniotic fluid embolism
      • Differentiated by presence of hypertension, proteinuria, and edema 
        • Typically accompanied by elevation of liver function test results and thrombocytopenia
        • Eclampsia is suspected especially in women with a diagnosis of preeclampsia or pregnancy-induced hypertension
      • Diagnostic tests include blood pressure measurement showing repeated values of 140/90 mm Hg or higher and detection of proteinuria of 300 mg or more in a 24-hour urine collection specimen 
  • Conditions presenting with hemorrhage
    • Postpartum hemorrhage
      • Hemorrhage occurring after delivery
        • Associated with uterine atony, ruptured uterus, inverted uterus, placental abruption, and placenta previa 
        • Also occurs owing to significant lacerations within the birth canal
      • Differentiated by low central venous pressure and the absence of cyanosis in postpartum hemorrhage 
      • Diagnosis is based on identification of bleeding site (eg, uterus, vaginal canal, cervix) in the absence of marked coagulopathy 

Treatment Goals

  • Resuscitate the woman
  • Achieve survival of the fetus (if viable)
  • Maintain oxygenation
  • Reverse cardiovascular and pulmonary failure
  • Correct coagulopathy

Admission criteria

Criteria for ICU admission
  • Directly admit to the ICU any patients who demonstrate at least 1 of the premonitory symptoms of cardiovascular collapse (eg, hypoxia, hypotension, cardiac arrest), respiratory distress, coagulopathy, or severe hemorrhage

Recommendations for specialist referral

  • Multidisciplinary approach allows the best management
    • Refer to obstetrician if needed for assistance with rapid delivery or cesarean delivery
    • Refer to neonatologist for resuscitation and management of delivered fetus, if viable
    • Refer to critical care specialist to assist with ICU care
    • Refer patients surviving cardiac arrest to cardiologist to manage hypothermic therapy and assess cardiovascular status
  • Psychological counseling
    • Amniotic fluid embolism is a traumatic and life-altering event, especially if it results in fetal loss

Treatment Options

If a patient with suspected amniotic fluid embolism has cardiopulmonary arrest: 

  • Begin immediate high-quality cardiopulmonary resuscitation following the standard American Heart Association Advanced Cardiovascular Life Support (ACLS) guidelines for adult cardiopulmonary resuscitation with minor adaptions 
    • Manually displace uterus (preferred) or tilt laterally during resuscitation 
    • Avoid hyperventilation, which can lead to decreased uterine blood flow 
    • Intubation with a smaller endotracheal tube (6-7 mm diameter) is recommended 
  • Perform perimortem cesarean section delivery or ‘resuscitative hysterotomy’ within 4 minutes of commencing resuscitation to increase the probability of a successful outcome 
    • Prompt cesarean delivery may be lifesaving for a viable fetus (at or beyond 23 weeks of gestation) and may improve maternal survival even if fetus is nonviable or cannot be resuscitated 
    • Recommended for maternal benefit in women with a uterine size at or above the umbilicus (20 weeks of gestation or more) 
    • Releases the weight of the gravid uterus on the inferior vena cava, which improves venous return and helps increase cardiac output 
    • Performed at the patient’s current location to save time; do not move to operating room unless it can be accomplished within 1 to 2 minutes 
  • Once the infant is delivered, the next steps consist of preventing and managing uterine atony, hemorrhage, and coagulopathy 

If a patient is suspected to have amniotic fluid embolism but has not yet progressed to cardiopulmonary arrest: 

  • Place patient in a full left lateral decubitus position to relieve aortocaval compression 
  • Prepare for urgent cesarean delivery (or operative vaginal delivery) if fetal gestation is at or beyond 23 weeks
    • If fetus is nonviable, timing of uterine evacuation is individualized and may allow for the mother to be stabilized
  • Simultaneously provide respiratory and hemodynamic support 
  • Treat uterine atony and hemorrhage
    • Administer uterotonic agents
      • Oxytocin is the first line drug 
      • Methylergometrine is the most effective uterotonic agent but may cause hypertension, nausea, and vomiting 
      • Prostaglandins or their analogues are recommended in low resource settings where other drugs are not available, with attention to possible adverse effects such as hypersensitivity (carboprost) or fever and shivering (misoprostol) 
    • Perform bimanual uterine massage 
    • Examine for other sources of bleeding (eg, pelvic lacerations) and repair as needed 
    • Uterovaginal packing followed by uterine artery embolization or surgical ligation if needed when bimanual uterine massage and uterotonic agents alone are insufficient 
      • Necessary with severe hemorrhage (blood loss greater than 1000 mL) 
        • Uterovaginal packing requires administration of broad-spectrum antibiotics 
    • Hysterectomy
      • Used as last resort to treat severe bleeding
    • Give tranexamic acid if disseminated intravascular coagulation or hemorrhage develops 
  • Therapeutic hypothermia is recommended after resuscitation to reduce neurologic complications in patients who have survived cardiac arrest and do not manifest significant disseminated intravascular coagulation or bleeding 
    • In pregnant patients, there is concern that therapeutic hypothermia may increase the risk of hemorrhage
    • Targeting a temperature of 36 °C (as opposed to lower temperatures with a concomitant increased risk of hemorrhage) is an option 
    • Optimal timing for initiation of hypothermia and optimal duration of hypothermia are not established 
      • Begin hypothermia initiation as soon as possible after resuscitation

Ongoing management of amniotic fluid embolism (eg, after initial resuscitation)

  • Manage pulmonary hypertension and right ventricular failure
    • Consider monitoring with pulmonary artery catheter or echocardiography to guide treatment 
    • Initial phase of amniotic fluid embolism is mainly right ventricular failure
      • Inotropes such as dobutamine and milrinone are recommended to improve right ventricular output
      • Sildenafil, inhaled or IV epoprostenol, or inhaled nitric oxide may decrease pulmonary vascular resistance and improve oxygenation
      • Norepinephrine (or vasopressin) is recommended to treat hypotension
        • Maintain systolic blood pressure of 90 mm Hg or higher 
        • Maintain urinary output of 0.5 mL/kg/hour or higher 
    • Minutes to hours later, right ventricular function improves, and left ventricular failure with pulmonary edema manifests
      • Optimize preload
      • Treat hypotension with vasopressors (eg, norepinephrine) to help sustain coronary perfusion pressure; use inotropes to improve left ventricular contractility
      • Avoid fluid overload
    • Maintain oxygen saturation at 94% to 98%
    • Consider extracorporeal membrane oxygenation in cases with prolonged cardiopulmonary resuscitation or refractory heart failure 

Drug therapy

  • Vasopressors/inotropes
    • Indicated for initial hemodynamic inotropic support of predominately right heart failure and as further inotropic support as failure becomes more left sided
      • Dobutamine
        • Dobutamine Hydrochloride Solution for injection; Adults: 0.5 to 1 mcg/kg/minute continuous IV infusion; titrate to clinical response. Usual dosage range: 2 to 20 mcg/kg/minute. Max: 40 mcg/kg/minute.
      • Milrinone
        • Milrinone Lactate Solution for injection; Adults: 50 mcg/kg IV load, then 0.125 to 0.75 mcg/kg/minute continuous IV infusion.
    • For treatment of hypotension and to help sustain coronary perfusion pressure as heart failure becomes more left sided
      • Norepinephrine
        • Norepinephrine Bitartrate Solution for injection; Adults: 0.1 mcg/kg/minute (weight-based) or 8 to 12 mcg/minute (flat-dose) continuous IV infusion, initially. Titrate by 0.02 mcg/kg/minute (or more in emergency cases) to clinical response. Usual dosage range: 0.05 to 0.4 mcg/kg/minute (weight-based) or 2 to 4 mcg/minute (flat-dose). Infusion rates up to 3.3 mcg/kg/minute have been used.
      • Epinephrine
        • Epinephrine Hydrochloride Solution for injection; Adults: 0.01 to 2 mcg/kg/minute continuous IV infusion. Titrate by 0.05 to 0.2 mcg/kg/minute every 10 to 15 minutes to clinical response.
      • Dopamine
        • Dopamine Hydrochloride Solution for injection; Adults: 2 to 5 mcg/kg/minute continuous IV infusion, initially. Titrate by 5 to 10 mcg/kg/minute until desired hemodynamic and/or renal response is attained. Usual dosage: 2 to 20 mcg/kg/minute. Max: 50 mcg/kg/minute
  • Pulmonary vasodilators
    • To decrease pulmonary vascular resistance and improve oxygenation
      • Sildenafil
        • Sildenafil Citrate Oral tablet [Pulmonary Hypertension]; Adults: 50 mg PO twice daily and 25 mg PO every 8 hours decreased pulmonary artery pressure and improved exercise capacity and symptoms in clinical studies. The effect of sildenafil treatment on mortality in patients with PH has not been studied.
        • Sildenafil Citrate Solution for injection [Pulmonary Hypertension]; Adults: 2.5 mg or 10 mg IV bolus 3 times per day; use for continued treatment in patients temporarily unable to take oral drugs.
      • IV epoprostenol, the synthetic analogue of endogenous prostacyclin (prostaglandin I₂) 
        • Epoprostenol Sodium Solution for injection; Adults: Begin with initial infusion rate of 1 to 2 ng/kg/minute IV through a central line. Titrate to desired effect.
      • Inhaled nitric oxide
        • Inhaled Nitric Oxide; Adults: 5 to 40 ppm. Follow methemoglobin levels every 6 hours for elevation, and avoid abrupt discontinuation.
  • Uterotonic agents
    • To control postpartum uterine bleeding
    • Oxytocin
      • Oxytocin Solution for injection; Adult females: 10 to 40 units may be added to existing IV drip infusion (max concentration: 40 units added per 1,000 mL), after delivery of the placenta. The infusion rate must be adjusted to sustain uterine contraction and control uterine atony.
      • Oxytocin Solution for injection; Adult females: 10 units IM after delivery of the placenta.
    • Methylergonovine (methylergometrine)
      • Methylergonovine Maleate Solution for injection; Adult females: 0.2 mg IM or IV, after delivery of the anterior shoulder, after delivery of the placenta, or during the puerperium; may repeat as required, at intervals of 2 to 4 hours.
    • Prostaglandins and their analogues
      • Carboprost (an analogue of prostaglandin F₂α)
        • Carboprost Tromethamine Solution for injection; Adults: 250 mcg (1 mL) IM is advised; if hemostasis is inadequate, additional doses may be administered every 15—90 minutes as determined by the attending physician. Do not exceed the Maximum Dosage Limit of 2 mg (8 mL).
        • Carboprost Tromethamine Solution for injection; Adults: 250 mcg (1 mL) by intramyometrial injection; if hemostasis is inadequate, repeat dose once at 5 minutes. Treatment failure after 2 doses necessitated surgical intervention in 2 of 5 women with postpartum hemorrhage following cesarean section.
      • Misoprostol (an analogue of prostaglandin E₁) 
        • Misoprostol Oral tablet; Adult females: 600 to 1,000 mcg PO, SL, or PR as a single dose has been used in this setting.

Nondrug and supportive care

Oxygen administration

  • Maintain oxygen saturation above 90% 
  • Maintenance of PaO₂ of 60 mm Hg or higher is recommended 

Fluid administration

  • Optimize preload with rapid infusion of isotonic crystalloid solutions 
  • Use of pulmonary artery catheter or bedside transthoracic or transesophageal echocardiography (evaluates left ventricular filling) to manage fluid therapy is recommended
  • Fluid management parameters include:
    • Maintenance of urinary output to at least 0.5 mL/kg/hour or a volume greater than 25 mL/hour
    • Maintenance of systolic blood pressure at 90 mm Hg or higher
  • With ongoing blood loss, before receipt of packed RBCs, infuse solution in a volume approximately 3 times that of the lost blood 


  • Packed RBCs: priority given to this treatment to sustain tissue oxygen delivery; maintain hemoglobin level of at least 7 g/dL Fresh frozen plasma: given when prothrombin time is prolonged 
    • When prothrombin time/INR is greater than 1.6
  • Cryoprecipitate: given to treat coagulation abnormalities (ie, hypofibrinogenemia) in lieu of fresh frozen plasma when fibrinogen levels are less than 1 g/L 
    • American Association of Blood Banks Technical Manual recommends dosing of cryoprecipitate as follows: 
      • Blood volume = weight (kg) × 70 mL/kg
      • Plasma volume = blood volume × (1 − hematocrit)
      • Volume (mg) of fibrinogen required = (desired fibrinogen level − current fibrinogen level in mg/dL) × plasma volume/100 mL/dL
      • Bags of cryoprecipitate required = mg of fibrinogen/250 mg
  • Platelets: when platelet count is less than 50,000/μL in bleeding patients 
Urgent operative vaginal delivery

General explanation

  • Vacuum-assisted suction cup or metal forceps is applied to fetal head to extract fetus from birth canal 


  • Fetal gestational age of 23 weeks or more 
  • Rapid and progressive deterioration of maternal clinical status
  • In cases where delivery of fetus may facilitate maternal cardiopulmonary resuscitation 


  • Unengaged fetal head
  • Unknown fetal position
  • Malpresentation
  • Suspected cephalopelvic disproportion


  • Maternal
    • Perineal lacerations
    • Anal sphincter injury
  • Fetal
    • Intracranial hemorrhage
    • Cephalohematoma
    • Laceration
    • Facial nerve palsy
    • Corneal abrasions
    • Brachial plexus injury
Cesarean delivery 

General explanation

  • Surgical delivery of fetus through incisions in abdomen and uterine wall
  • Performed if gestational age of fetus is 23 weeks or more 
  • Referred to as perimortem cesarean delivery or resuscitative hysterotomy if performed to aid maternal resuscitation


  • Performed to assist with cardiopulmonary resuscitation of mother 


  • Intraoperative
    • Uterine lacerations
    • Bladder lacerations
    • Ureter injury
    • Bowel injury
    • Uterine atony
  • Postoperative
    • Infection
      • Endomyometritis
      • Chorioamnionitis
      • Urinary tract infection
      • Septic pelvic thromboembolism
    • Thromboembolic disease
    • Fascial dehiscence
Bimanual uterine massage 

General explanation

  • Compression of uterus by pressing on fundus both internally through vagina and externally through abdominal wall 
  • Principle is based on the fact that uterine hemostasis depends on the contractions of the myometrial smooth muscles 


  • Performed in combination with uterotonic agents to stop hemorrhage caused by uterine atony 
Uterine packing 

General explanation

  • Uterine tamponade to stop bleeding using a balloon (eg, Bakri balloon) or gauze


  • Performed when uterotonic agents and bimanual massage are unsuccessful
  • Useful to stabilize patient until a surgical procedure is arranged
  • May prevent surgery in some cases


  • Overt pelvic or vaginal infection (provide broad-spectrum antibiotics for patients with packing inserted)
  • Settings where tamponade is unlikely to be effective (eg, uterine rupture)
  • Uterine anomalies (eg, large leiomyoma, uterine didelphys)
  • Allergy to the material (silicone)


  • Uterine infection
Uterine embolization 

General explanation

  • Gelatin sponge particles or spring coils to obstruct blood flow to uterus are injected through small catheter inserted in femoral artery 


  • Uncontrolled uterine bleeding 


  • Hemorrhage
  • Infection
  • Reduced fertility

General explanation

  • Surgical removal of uterus


  • Refractory postpartum hemorrhage 


  • Infection
  • Hemorrhage
  • Urinary tract injury
  • Thrombosis
  • Bowel injury
  • Fascial dehiscence
Therapeutic hypothermia 

General explanation

  • Patient who regains spontaneous circulation after resuscitation of cardiac arrest is cooled actively to between 32 and 36 °C for cerebral protection 
    • As lower temperatures are associated with increased risk of hemorrhage in postpartum patients, targeting a temperature of 36 °C is an option in patients with amniotic fluid embolism 
    • Patient is kept hypothermic for at least 24 hours, although the optimal time has yet to be determined 
    • Shivering is prevented pharmacologically (eg, propofol or midazolam as sedatives plus fentanyl or hydromorphone as analgesics)
  • Cooling techniques include:
    • Surface cooling devices and feedback-controlled endovascular catheters
    • Cooling blankets and frequent ice bag application
    • Initiation of cooling with iced isotonic saline combined with other cooling methods to maintain cooling
  • Rewarming
    • Begin rewarming 12 to 24 hours after cooling is initiated
    • The optimal rate of rewarming has not been determined 
    • Avoid hyperthermia (using cooling blankets if needed)


  • For cerebral protection to increase chances of survival after resuscitation


  • Significant disseminated intravascular coagulation with bleeding


  • Shivering
  • Bradycardia with hypotension
  • Hyperglycemia
  • Hypokalemia
  • Decreased immunity


  • Postresuscitation, all patients have cardiac monitoring with continuous telemetry, and respiratory monitoring with pulse oximetry and end-tidal carbon dioxide monitor 
    • If fetus has not been delivered, fetal monitoring (tocometry) should be continuous
    • Hemodynamic management may be guided by central venous or pulmonary artery catheter placement
  • During induced hypothermia, monitor the following:
    • Arterial oxygen saturation
      • Maintain at 94% to 98%, reducing FIO₂ to avoid prolonged exposure to 100% oxygen
    • Blood glucose
      • Measure at least hourly to detect hyperglycemia; treat when glucose levels exceed 200 mg/mL
    • Serum potassium
      • Measure at least every 4 to 6 hours to detect hypokalemia, correcting to maintain potassium above 3.5 mEq/L


  • Complications or sequelae affecting patients who survive amniotic fluid embolism may lead to multiple organ dysfunction or permanent damage and include:
    • Hypoxic-ischemic injury (especially in patients who suffered cardiac arrest)
      • Neurologic deficits are common as the result of brain hypoxia/ischemia (up to 85% of survivors), including: 
        • Altered mental status 
        • Seizures 
        • Hemiplegia
        • Memory loss
      • Fetal complications resulting in death or permanent damage 
        • Hypoxic ischemic encephalopathy (18% to 29% of surviving fetuses) 
        • Cerebral palsy (6% of surviving fetuses) 
    • Renal sequelae after ischemia and reperfusion injury
      • Acute oliguric or nonoliguric renal failure 
    • Cardiac complications or long-term injuries
      • Heart failure with left ventricular impairment 
      • Myocardial ischemia and infarction
      • Arrhythmias 
    • Pulmonary/respiratory sequelae or long-term injuries
      • Refractory bronchospasm 
      • Cardiogenic or noncardiogenic pulmonary edema 
    • Circulatory complications associated with disseminated intravascular coagulation
      • Long-term coagulopathy 
      • Thrombosis 


  • Mortality may be as high as 50% during the first hour of presentation because of cardiopulmonary manifestations 
    • Maternal mortality has decreased to 22% as a result of improved reporting and improvements in treatment 
  • According to a national study, amniotic fluid embolism accounted for just over 9% of maternal mortality cases in France 
  • Morbidity among survivors is still significantly elevated. According to the national registry, 61% of women and 50% of infants are permanently affected by neurologic damage 
  • Women with poor outcome were less likely to have received treatments such as fresh-frozen plasma, platelets, or tranexamic acid; received lower doses of tranexamic acid; and were less likely to have had an obstetrician and/or anesthesiologist present at the time the amniotic fluid embolism occurred 
  • Fetal outcome is especially poor if amniotic fluid embolism develops before delivery 
    • 79% of fetuses survive but 50% suffer neurologic impairment 

Screening and Prevention


  • Amniotic fluid embolism is unpredictable and there are no preventive measures against its occurrence 
  • Accurate monitoring of patient condition is fundamental to recognize the early onset of symptoms and guarantee a prompt and correct therapeutic response 


Conde-Agudelo A et al: Amniotic fluid embolism: an evidence-based review. Am J Obstet Gynecol. 201(5):445.e1-13, 2009


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