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Amniotic Fluid Embolism [AFE] Approach to Management
Amniotic fluid embolism (AFE) is a rare but life-threatening condition during pregnancy with complex causes and serious consequences for both mother and infant, accompanied by high mortality rates. Diagnosis is challenging and often requires exclusion of other conditions, with symptoms including sudden respiratory distress and abnormal bleeding. Effective management involves aggressive treatment and monitoring, as maternal mortality can arise from cardiac arrest, hemorrhage, or respiratory failure.
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Amniotic Fluid Embolism [AFE] Approach to Management
- 5. Nevertheless, these andother frequently cited risk factors are not consistently observed and at the present time Experts agree that this condition is not preventable.
- 12.
- 20. Management of AFE Coagulopathy •DIC results in the depletion of fibrinogen, platelets, and coagulation factors, especially factors V, VIII, and XIII. The fibrinolytic system is activated as well. • Most patients will have hypofibrinogenemia, abnormal PT and aPTT and low Platelet counts • Treat coagulopathy with FFP for a prolonged aPTT, cryoprecipitate for a fibrinogen level less than 100 mg/dL, and transfuse platelets for platelet counts less than 20,000/mm3
- 22. Sympathomimetic Vasopressor agent •Dopamine increases myocardial contractility and systolic BP with little increase in diastolic BP. Also dilates the renal vasculature, increasing renal blood flow and GFR. • DOSE: 2-5 mcg/kg/min IV; titrate to BP and cardiac output. • Contraindications: ventricular fibrillation, hypovolemia, pheochromocytoma. • Precautions: Monitor urine flow, cardiac output, pulmonary wedge pressure, and BP during infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful
- 23. Maternal Mortality inAFE • Maternal death usually occurs in one of three ways: (1) sudden cardiac arrest, (2) hemorrhage due to coagulopathy, or (3) initial survival with death due to acute respiratory distress syndrome (ARDS) and multiple organ failure • For women diagnosed as having AFE, mortality rates ranging from 26% to as high as 86% have been reported. • The variance in these numbers is explained by dissimilar case definitions and possibly improvements in intensive care management of affected patients.
- 25. SUMMARY • AFE isa sudden and unexpected rare but life threatining complication of pregnancy. • It has a complex pathogenesis and serious implications for both mother and infant • Associated with high rates of mortality and morbidity. • Diagnosis of exclusion. • Suspect AFE when confronted with any pregnant patient who has sudden onset of respiratory distress, cardiac collapse, seizures, unexplained fetal distress, and abnormal bleeding • Obstetricians should be alert to the symptoms of AFE and strive for prompt and aggressive treatment.
Editor's Notes
- #3 Amniotic fluid embolism (AFE) is a rare obstetric emergency in which it is postulated that amniotic fluid, fetal cells, hair, or other debris enter the maternal circulation, causing cardiorespiratory collapse. In 1941, Steiner and Luschbaugh described AFE for the first time after they found fetal debris in the pulmonary circulation of women who died during labor. Current data from the National Amniotic Fluid Embolus Registry suggest that the process is more similar to anaphylaxis than to embolism, and the term anaphylactoid syndrome of pregnancy has been suggested because fetal tissue or amniotic fluid components are not universally found in women who present with signs and symptoms attributable to AFE.[1]
- #4 The diagnosis of AFE has traditionally been made at autopsy when fetal squamous cells are found in the maternal pulmonary circulation; however, fetal squamous cells are commonly found in the circulation of laboring patients who do not develop the syndrome. In a patient who is critically ill, a sample obtained by aspiration of the distal port of a pulmonary artery catheter that contains fetal squamous cells is considered suggestive of but not diagnostic of AFE syndrome.[2] The diagnosis is essentially one of exclusion based on clinical presentation. Other causes of hemodynamic instability should not be neglected.
- #7 The pathophysiology of AFE is poorly understood. Based on the original description, it was theorized that amniotic fluid and fetal cells enter the maternal circulation, possibly triggering an anaphylactic reaction to fetal antigens. However, fetal material is not always found in the maternal circulation in patients with AFE, and material of fetal origin is often found in women who do not develop AFE. Benson et al[3] tested 2 hypotheses concerning the pathophysiology of AFE: (1) Clinical symptoms result from mast cell degranulation with the release of histamine and tryptase, or (2) Clinical symptoms result from activation of the complement pathway. Nine women with AFE were compared with 22 women with normal labors. Serum from patients with AFE was collected within 14 hours of symptom onset and frozen. Urine was collected within 12-24 hours after symptom onset. Control patients had complement levels measured on admission, during labor, and the day after delivery.
- #8 Six of the 9 women with AFE died, and all 9 required blood transfusions for disseminated intravascular coagulation (DIC). Seven women had no evidence of mast cell degranulation (ie, either urinary histamine or serum tryptase). Compared with postpartum control patients, complement levels in the AFE group were severely depressed. C3 in the AFE group was 44 compared with 117.2 in the postpartum group. C4 was 10.7 in the AFE group versus 29.4 in the postpartum group. These differences were statistically significant. This suggests that complement activation may play an important role in the pathophysiology of AFE. Farrar and Gherman[4] reported the case of a 40-year-old multipara in active labor with acute onset of facial erythema, seizures, hypoxia, cardiac arrest, DIC, and ultimately death. Fetal squames and fibrin thrombi were found in the pulmonary tree at autopsy. Blood drawn 2 hours after symptom onset had a serum tryptase level of 4.7 ng/mL (normal < 1 ng/mL). A case reported by Marcus et al[5] , in which AFE developed after a spontaneous rupture of membranes, demonstrated no increase in mast cells or degranulation in lung tissue as shown by Giemsa staining. Serum tryptase levels were 11.4 ng/mL (normal < 11.4 ng/mL). The initiating event is poorly understood. However, usually during labor or other procedure, amniotic fluid and debris, or some as yet unidentified substance, enters the maternal circulation; this may trigger a massive anaphylactic reaction, activation of the complement cascade, or both. Progression usually occurs in 2 phases. In phase I, pulmonary artery vasospasm with pulmonary hypertension and elevated right ventricular pressure cause hypoxia. Hypoxia causes myocardial capillary damage and pulmonary capillary damage, left heart failure, and acute respiratory distress syndrome. Women who survive these events may enter phase II. This is a hemorrhagic phase characterized by massive hemorrhage with uterine atony and DIC; however, fatal consumptive coagulopathy may be the initial presentation.
- #9 AFE is considered an unpredictable and unpreventable event with an unknown cause. In the national registry, 41% of patients had a history of allergies. Reported risk factors for development of AFE include multiparity, advanced maternal age, male fetus, and trauma. In a retrospective review of a 12-year period encompassing 180 cases of AFE, of which 24 were fatal, medical induction of labor increased the risk of AFE.[10] In the same study, AFE was positively associated with multiparity, cesarean section or operative vaginal delivery, abruption, placenta previa, and cervical laceration or uterine rupture
- #11 Amniotic fluid embolism (AFE) usually occurs during labor but has occurred during abortion, after abdominal trauma, and during amnioinfusion. A woman in the late stages of labor becomes acutely dyspneic with hypotension; she may experience seizures quickly followed by cardiac arrest. Massive DIC-associated hemorrhage follows and then death. Most patients die within an hour of onset. Currently no definitive diagnostic test exists. The United States and United Kingdom AFE registries recommend the following 4 criteria, all of which must be present to make the diagnosis of AFE.[7, 1, 9] Acute hypotension or cardiac arrest Acute hypoxia Coagulopathy or severe hemorrhage in the absence of other explanations All of these occurring during labor, cesarean delivery, dilation and evacuation, or within 30 minutes postpartum with no other explanation of findings
- #12 In case reports, patients are described as developing acute shortness of breath, sometimes with a cough, followed by severe hypotension. The following signs and symptoms are indicative of possible AFE: Hypotension: Blood pressure may drop significantly with loss of diastolic measurement. Dyspnea: Labored breathing and tachypnea may occur. Seizure: Tonic clonic seizures are seen in 50% of patients. Cough: This is usually a manifestation of dyspnea. Cyanosis: As hypoxia/hypoxemia progresses, circumoral and peripheral cyanosis and changes in mucous membranes may manifest. Fetal bradycardia: In response to the hypoxic insult, fetal heart rate may drop to less than 110 beats per minute (bpm). If this drop lasts for 10 minutes or more, it is a bradycardia. A rate of 60 bpm or less over 3-5 minutes may indicate a terminal bradycardia. Pulmonary edema: This is usually identified on chest radiograph. Cardiac arrest Uterine atony: Uterine atony usually results in excessive bleeding after delivery. Failure of the uterus to become firm with bimanual massage is diagnostic. Coagulopathy or severe hemorrhage in absence of other explanation (DIC occurs in 83% of patients.)[9] Altered mental status/confusion/agitation
- #15 Differential Diagnoses Anaphylaxis Aortic Dissection Cholesterol Embolism Myocardial Infarction Pulmonary Embolism Septic Shock