The document describes amniotic fluid embolism (AFE), a rare but life-threatening complication during pregnancy and childbirth. AFE occurs when amniotic fluid enters the mother's bloodstream, which can cause respiratory failure, shock, disseminated intravascular coagulation, and other symptoms. It has a high mortality rate of 70-80%. The document discusses two case studies of AFE and provides details on risk factors, pathogenesis, clinical presentation, diagnosis, differential diagnosis, and management of AFE. Treatment aims to restore cardiovascular and pulmonary function, correct coagulation abnormalities, and provide supportive care.
The document describes amniotic fluid embolism (AFE), a rare but life-threatening complication during pregnancy and childbirth. AFE occurs when amniotic fluid enters the mother's bloodstream, which can cause respiratory failure, shock, disseminated intravascular coagulation, and other symptoms. It has a high mortality rate of 70-80%. The document discusses two case studies of AFE and provides details on risk factors, pathogenesis, clinical presentation, diagnosis, differential diagnosis, and management of AFE. Treatment aims to restore cardiovascular and pulmonary function, correct coagulation abnormalities, and provide supportive care.
The document describes amniotic fluid embolism (AFE), a rare but life-threatening complication during pregnancy and childbirth. AFE occurs when amniotic fluid enters the mother's bloodstream, which can cause respiratory failure, shock, disseminated intravascular coagulation, and other symptoms. It has a high mortality rate of 70-80%. The document discusses two case studies of AFE and provides details on risk factors, pathogenesis, clinical presentation, diagnosis, differential diagnosis, and management of AFE. Treatment aims to restore cardiovascular and pulmonary function, correct coagulation abnormalities, and provide supportive care.
The document describes amniotic fluid embolism (AFE), a rare but life-threatening complication during pregnancy and childbirth. AFE occurs when amniotic fluid enters the mother's bloodstream, which can cause respiratory failure, shock, disseminated intravascular coagulation, and other symptoms. It has a high mortality rate of 70-80%. The document discusses two case studies of AFE and provides details on risk factors, pathogenesis, clinical presentation, diagnosis, differential diagnosis, and management of AFE. Treatment aims to restore cardiovascular and pulmonary function, correct coagulation abnormalities, and provide supportive care.
Download as PPT, PDF, TXT or read online from Scribd
Download as ppt, pdf, or txt
You are on page 1/ 46
Amniotic Fluid Embolism
Dr. Lizhan Department of gynecology and obstetrics of Chaoyang hospital Capital Medical University Case 1 A healthy 34-year-old multipara; 41 weeks; induction for labor; Meconium staining, fetal distress; Caesarean section with anaesthesia; …… Case 1 A few minutes after delivery of the baby… Arterial desaturation, hypotension; Abnormal bleeding; DIC; Perform a hysterectomy; ICU; Multiple organ faliure… Case 2 A healthy 23-year-old primigravida; 38 weeks; spontaneous in labor; Strong uterine contraction; Membranes ruptured; precipitate delivery; …… Case 2 A few minutes after delivery of the baby… Chest distress; Seizure ; Shock ; Postpartum heamorrage; ICU; Multiple organ faliure… Final diagnosis:
Amniotic fluid embolism
What is Amniotic fluid embolism ? Amniotic fluid Embolism Definition
Amniotic Fluid Embolism is a complex disorder
during labor characterized by amniotic fluid entering into the maternal circulation which causes acute pulmonary embolism, shock, DIC, acute renal failure or abrupt death. Backgroud Ricardo Meyer (1926); reported the presence of fetal cellular debris in the maternal circulation. Steiner and Luschbaugh (1941) described the autopsy findings of eight cases of AFE. Until 1950, only 17 cases had been reported. AFE was not listed as a distinct heading in causes of maternal mortality until 1957 when it was labeled as obstetric shock. The first well-documented case with ultimate survival was published in 1976 (Resnik R, et al. Obstet Gynecol 1976;47:295-8). Overview
An devastating complication during labor
Mortality: up to 70%~80% May occur in the first and second trimester abortions Recently, it is also termed “anaphylactoid syndrome of pregnancy” Risk factors of AFE Advanced maternal age Placenta accreta Multiparity Polyhydramnios Meconium Uterine rupture Cervical laceration Maternal history of allergy or Intrauterine fetal death atopy Very strong frequent or uterine Chorioamnionitis tetanic contractions Macrosomia Sudden fetal expulsion (short Male fetal sex labor) Oxytocin (controversial) Why amniotic fluid can enter into the maternal circulation? Three factors
Disruption of fetal membrane
Greater intensity of uterine contractions Breaching blood vessel Pathogenisis There is a breach in vein or blood sinus at the trauma site of cervix and the body of uterine Higher pressure of amniotic cavity After disruption of fetal membrane, amniotic fluid enters into the maternal circulation through the breached vein and blood sinus Main reason: greater contraction and high pressure of amniotic cavity Common clinic causative factor
Greater contraction → rupture of fetal membrane
Fetal membrane separate from cervical wall Pathologic blood sinus breach: cervical laceration, rupture of uterus, placenta previa, placental abruption or caesarean section Amniocentesis and curettage or scraping What happen after the amniotic fluid enter into the maternal circulation? pathophysiology
Respiratory Tissue damage acidosis Left ventricular regurgitation volume↓ Left ventricular output↓ bleeding Acute pulmonary edema
Circulation Acute renal failure
failure Acute right ventricular failure
shock Clinical presentation
Acute amniotic fluid embolism: occur acutely
Shock Typical: three phages Hemorrhage due to DIC Acute renal failure
Bulk colporrhagia (occur mainly after delivery)
Atypical: shock Diagnosis According to the typical clinic manifestation, we can make the preliminary diagnosis and salve the patients immediately While salving the patients do the necessary auxiliary examination, including:
a. collecting blood from arteria pulmonalis and inferior
vena, and finding components of amniotic fluid b. X-ray c. ECG d. the basis of laboratory examination for DIC Basis of laboratory examination for Hypoxia
Arterial blood gas (ABG) levels: Expect changes
consistent with hypoxia/hypoxemia. Decreased pH levels (reference range = 7.40-7.45) Decreased PO2 levels (reference range = 104-108 mm Hg) Increased PCO2 levels (reference range = 27-32 mm Hg) Base excess increased Basis of laboratory examination for DIC
PLT＜ 100 ╳109/L or it was gradually decrease
fibrinogen <1.5g/L PT >15 s plasm protamine paracoagulation test (+) CT >30 minites Obtrite RBC in blood smear Imaging Studies Histologic Findings Differential diagnosis Respiratory distress Pulmonary embolism (thrombus, fluid, air, fat) Pulmonary edema Anesthesia complications Aspiration Hypotension and shock-related symptoms Septic shock Hemorrhagic shock Anaphylactic reaction Myocardial infarction Cardiac arrhythmias Differential diagnosis Hemorrhage and bleeding disorders Disseminated intravascular coagulation Placental abruption Uterine rupture Uterine atony Neurological and seizure-related conditions Eclampsia Epilepsy Cerebrovascular accident Hypoglycemia Management of AFE GOALS OF MANAGEMENT: Restoration of cardiovascular and pulmonary equilibrium - Maintain systolic blood pressure >90 mm Hg. - Urine output > 25 ml/hr - Arterial pO2 > 60 mm Hg. Re-establishing uterine tone Correct coagulation abnormalities Management of AFE As intubation and CPR may be required it is necessary to have easy access to the patient, experienced help, and a resuscitation tray with intubation equipment, DC shock, and emergency medications. IMMEDIATE MEASURES : - Set up IV Infusion, O2 administration. - Airway control endotracheal intubation maximal ventilation and oxygenation. LABS : CBC,ABG,PT,PTT,fibrinogen,FDP. Management of AFE Treat hypotension, increase the circulating volume and cardiac output with crystalloids. After correction of hypotension, restrict fluid therapy to maintenance levels since ARDS follows in up to 40% to 70% of cases. Steroids may be indicated (recommended but no evidence as to their value) Dopamine infusion if patient remains hypotensive (myocardial support). Other investigators have used vasopressor therapy such as ephedrine or levarterenol with success (reduced systemic vascular resistance) Management of AFE To assess the effectiveness of treatment and resuscitation, it is prudent to continuously monitor ECG, pO2, CO2, and urine output. There is support in literature for early placement of arterial, central venous, and pulmonary artery catheters to provide critical information and guide specific therapy. Management of AFE
Central venous pressure monitoring is important to diagnose
right ventricular overload and guide fluid infusion and vasopressor therapy. Blood can also be sampled from the right heart for diagnostic purposes. Pulmonary artery and capillary wedge pressures and echocardiography are useful to guide therapy and evaluate left ventricular function and compliance. An arterial line is useful for repeated blood sampling and blood gases to evaluate the efficacy of resuscitation. Sympathomimetic Vasopressor agent Dopamine • 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. Management of AFE Anti-anaphylacic
Hydrocortisone Glucocorticosteroid Hexadecadrol 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 Restoration of uterine tone
Uterine atony is best treated with massage, uterine
packing, and oxytocin or prostaglandin analogues. Improvement in cardiac output and uterine perfusion helps restore uterine tone. Extreme care should be exercised when using prostaglandin analogues in hypoxic patients, as bronchospasm may worsen the situation. Obstetric management antepartum intrapartum post partum
amnionic fluid embolism
drug treatment
Cervical is not open Cervical is
or not fully open fully dilatting Without postpartum cesarean section delivery hemorrhage Forcep delivery
Without hemorrage postpartum hemorrhage
Go on the expectant treatment uterectomy Go on the expectant treatment
Main goals of treatment :
(1) oxygenation, (2) maintaining cardiac output and blood pressure, (3) correcting coagulopathy. Further issues in the Management
Prevent or cure ARF and infection
Prevent ARF: Prevent infection aware of urinary using antibiotic drug volume with low toxicity Furosemide Further issues in the Management Transfer: Transfer to a level 3 hospital may be required once the patient is stable. Prevention Artificial rupture of membrane without stripping of membrane Don’t conduct artificial rupture of membrane when uterine is constricting Master the indication of oxytocin application Protect the vessel during the caesarean section Avoid precipitate labor, birth trauma, rupture of uterus, cervical laceration Aware of the predisposing factor Summary AFE is a sudden and unexpected rare but life threatening complication of pregnancy; AFE has a complex pathogenesis and serious implications for both mother and infant; Associatied 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,seizure,unexplained fetal distress, and abnormal bleeding; Obstericians should be alert to the symptoms of AFE and strive for prompt and aggressive treatment. Thank you!
