AMNIOTIC FLUID EMBOLISM

Introduction
1926, Ricardo Meyer 1941, Steiner & Luschbaugh autopsy series of 8 woman died of sudden shock during labor Other studies revealed amniotic fluid debris in maternal kidney, liver, spleen, pancreas, brain Amniotic fluid embolism (AFES), or anaphylactoid syndrome of pregnancy Incidence: 1/8000 ~ 1/80000 Maternal mortality: 60 ~ 90 % AFES & Pulmonary thromboembolism 20% perinatal maternal mortality

Pathophysiology
Entrance of amniotic fluid to maternal circulation: o Endocervical veins o Placental insertion site o Site of uterine trauma Why Anaphylactoid Syndrome of Pregnancy? 1. A lag period 2. Amniotic debris in non-AFES mother 3. Variability of clinical s/s and its severity Proposed Mechanisms~ 1. Host immune responses 2. Abnormal amniotic fluid, atypical substance

Clinical Presentation
Onset most commonly during labor & delivery Clinical Presentation of a Review 272 cases ~ o Nonspecific symptoms: chills, nausea, vomiting, agitation o Cardiorespiratory collapse occurred at presentation in the majority o Some had tonic-clonic seizure Major clinical findings ~ o Hypoxia & respiratory failure o Cardiogenic shock o Disseminated intravascular coagulation Each of the above can be the dominant presentation

 Symptoms/Signs similar to anaphylactoid or septic shock Risk factors unknown? Etiology unkown? Major clinical findings ~ Hypoxia & respiratory failure Cardiogenic shock Disseminated intravascular coagulation Hypoxemia Due to Ventilation/Perfusion mismatching Some (15%) cases had bronchospasm st 50% 1 hour death were due to hypoxia and cardiogenic shock May result in neurologic impairment 70% who initially survived developed pulmonary edema May be cardiogenic or noncardiogenic Evidence for endothelial-alveolar membrane damage capillary leak 1. High protein concentration in lung edema fluid 2. Amniotic fluid debris in sputum & alveoli Major clinical findings ~ Hypoxia & respiratory failure Cardiogenic shock Disseminated intravascular coagulation Cardiovascular Collapse Pulmonary artery & pulmonary capillary wedge pressures Cardiac output LV stroke index PA catheter data usually show CO with relatively small increase in pulmonary vascular resistance Arrhythmia, PEA, asystole may occur Major clinical findings ~ Hypoxia & respiratory failure Cardiogenic shock Disseminated intravascular coagulation DIC 80% AFES develop DIC The temporal correlation is not constant among DIC, cardiogenic shock, hypoxia When AFES occurs postpartum and DIC is the major early finding, diagnosis may be delayed due to s/s mimics hemorrhage!

Diagnosis
Via symptoms & signs suspicion of AFES Other causes of sudden cardiorespiratory failure ~ 1. Hemorrhage 2. Air or pulmonary embolism 3. Anesthetic complications 4. Anaphylaxis 5. Sepsis 6. Aspiration of gastric contents 7. Myocardial infarction Some authors require the amniotic fluid debris (eg. squamous and trophoblastic cells, mucin, lanugo) from the distal port of a pulmonary artery catheter to make the diagnosis o But, amniotic fluid components commonly are present in the maternal circulation in women with no s/s of AFES

Management
Aggressive monitor About maternal & fetal hypoxia Pharmacologic therapy Fluid support Correct coagulopathy as needed Management ---- Monitoring SpO2 EKG Arterial line Fetal monitor if onset prior to delivery Echocardiography CVP alone is not sufficient Pulmonary artery catheterization Management ---- Maternal Hypoxia Secure airway Intubation & Ventilation o Small tidal volume (6 ~ 8 ml/kg) o Normocapnia (~32 mmHg) PEEP Management ---- Fetal Hypoxia 65% fatal AFES present before delivery Prevention of Fetal Hypoxia o Maternal PO2 keep > 47 mmHg; best above 65 mmHg o Fetal umbilical vein PO2 >32 mmHg Fetal compensation by elevated Hb level & cardiac output o Immediate delivery decreases fetal morbidity Pharmacologic Therapy Inotropic & vasoactive agents o Norepinephrine o Dopamine o Dobutamine (often use norepinephrine in combination) Fluid management Pulmonary artery catheter insertion first, if possible o Avoid exacerbating pulmonary edema o Initial management with vasopressor is preferred Correct coagulopathy with blood product as needed