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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 veinso Placental insertion siteo Site of uterine trauma

Why Anaphylactoid Syndrome of Pregnancy?

1. A lag period2. Amniotic debris in non-AFES mother3. Variability of clinical s/s and its severity

Proposed Mechanisms~

1. Host immune responses2. Abnormal amniotic fluid, atypical substance

Clinical Presentation

Onset most commonly during labor & deliveryClinical Presentation of a Review

272 cases ~o Nonspecific symptoms: chills, nausea, vomiting, agitationo Cardiorespiratory collapse occurred at presentation in the majorityo Some had tonic-clonic seizure

Major clinical findings ~o Hypoxia & respiratory failureo Cardiogenic shocko Disseminated intravascular coagulation

Each of the above can be the dominant presentation

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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 50% 1st 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 fluid2. 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. Hemorrhage2. Air or pulmonary embolism3. Anesthetic complications4. Anaphylaxis5. Sepsis6. Aspiration of gastric contents7. Myocardial infarction

Some authors require the amniotic fluid debris (eg. squamous and trophoblastic cells, mucin, lanugo) from the distalport 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 ofAFES

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Management

Aggressive monitor About maternal & fetal hypoxia Pharmacologic therapy Fluid support Correct coagulopathy as neededManagement ---- 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)

PEEPManagement ---- Fetal Hypoxia

65% fatal AFES present before delivery

Prevention of Fetal Hypoxiao Maternal PO2 keep > 47 mmHg; best above 65 mmHgo Fetal umbilical vein PO2 >32 mmHg

Fetal compensation by elevated Hb level & cardiac outputo Immediate delivery decreases fetal morbidity

Pharmacologic Therapy

Inotropic & vasoactive agentso Norepinephrineo Dopamineo Dobutamine (often use norepinephrine in combination)

Fluid management

Pulmonary artery catheter insertion first, if possibleo Avoid exacerbating pulmonary edemao Initial management with vasopressor is preferred

Correct coagulopathy with blood product as needed