AMNIOTIC FLUID EMBOLISM
Dr SREENIVASULUYADAV SURINENI
Assistant Professor
SV Medical College, Tirupathi
AMNIOTIC FLUID EMBOLISM
Often referred to as the anaphylactoid syndrome of pregnancy
Is the second leading cause of peripartummaternal death
It occurs when amniotic fluid enters the maternal bloodstream.
Obstetric emergency marked by sudden cardiorespiratory collapse
and disseminated intravascular coagulation (DIC).
INCIDENCE
•The incidence ranges from 1.9 to 6.1 per 100,000 births,
•In the United States, affects 2.2 to 7.7 per 100,000 deliveries,
contributing to 7.5% of maternal deaths.
•In developing countries, the mortality rate ranges from 1.8 to
5.9 per 100,000 deliveries
PATHOPHYSIOLOGY
Abnormal placentation, surgical trauma Theory
Breach of barrier between maternal blood and amniotic fluid
Amniotic fluid enters systemic circulation
Physical obstruction of pulmonary circulation
Amniotic fluid in systemic circulation –second theory :
Activates inflammatory mediators
❑Platelet activating factor
❑Cytokines
❑Bradykinin
❑Leukotrienes
❑Thromboxane
CLINICAL PRESENTATION
May occur during labor, after instrumental vaginal deliver/ C
section, even upto 48hours post delivery.
Acute onset respiratory distress
Hypotension
coagulopathy
seizures
Bronchosapsm
Uterine atony
Fetaldistress
DIAGNOSIS
DIAGNOSIS IS BY EXCLUSION
The American Society for Maternal-Fetal Medicine (SMFM)
established objective criteria for Amniotic Fluid Embolism.
➢Sudden cardiopulmonary collapse or hypotension (systolic
blood pressure <90 mmHg) with hypoxia (SpO2 <90%).
➢Severe hemorrhage or DIC according
➢Symptomatology occurs either during labor or placental
delivery (or up to 30 minutes later).
➢Absence of fever or other explanations for the observed
findings.
The classic triad of AFE consists of hypoxia,
hypotension, and coagulopathy, with a normal body
temperature.
Fundus examination may detect minute bubbles in
retinal arteries.
high-pitched murmur of tricuspid regurgitation.
Full-blown DIC is observed in approximately 83% of
patients.
Non specific tests
Complete blood count : low Hemoglobin and platelets
Coagulation profile : increased PT,APTT ; low fibrinogen
ABG: Hypoxemia, raised pCO2
Chest x ray : normal or pulmonary edema or cardiomegaly
Ecg : Right ventricular strain pattern
V/Q Scans: V/Q mismatch
Echocardiogram: Right Ventricular dysfunction,
Low ejection fraction
SPECIFIC TESTS
Broncho alveolar sample : presence of squamous cells coated
with neutrophils, Fetal debris
Elevated serum tryptase levels
Elevated plasma concentration of Zinc coproporphyrin
Elevated Sialyl Tn antigen
MANAGEMENT
Goals of management:
Early recognition
Oxygenation
Resuscitation and hemodynamic stability
Maintain uterine tone
Correction of DIC
Delivery of Fetus
Taking care of ABCs
Secure the airway and administer 100% 02 with positive pressure
ventilation as early as possible
Optimise pre load and reduce pulmonary vascular resistance
Fluid resuscitation with crystalloids and colloids for hemodynamic
instability
Arterial line, Trans thoracic echocardiography to guide fluid
management
Vasoressors to maintain mean arterial pressure > 65 mm Hg
Plan for Packed cell transfusion in ongoing hemorrhage due to
uterine atony
Pharmacological treatment:
❑Vasopressors and Inotropic support
❑Epinephrine is first line agent as AFE is anaphylactoid
❑Noradrenaline and dopamine are other choices
❑In Right heart failure : Milrinone is considered
❑Steroids, to reduce inflammation induced by amniotic fluid
❑Uterotonic agents like Oxytocin
Methergine & Carboprost.
Treating DIC
❑Blood and blood products- Platelets, FFP and cryoprecipitate to
be administered early in resuscitation
❑Monitor platelet count and coagulation profile to guide further
transfusion
❑If fibrinogen <100mg/dl administer cryoprecipitate
❑Each unit of cryoprecipitate raises fibrinogen by 10 mg/dl
❑Visco elastic hemostatic assay(VHA) to guide transfusion of
blood and blood products
Uterine artery embolisation and
Hysterectomy may be required in those with
persistent uterine hemorrhage to control
blood loss
Rx pulmonary hypertension
Pulmonary hypertension and right heart failure are
mainstay in AFE
Administer after load reducing agents
Milrinone causes pulmonary vascular dilation,
decreases right ventricular after load
Epoprostenol inhaled or intravenous reduces
pulmonary hypertension
Inhaled nitric oxide causes pulmonary vasodilation
ECMO
ECMO has proven successful for refractory hypoxemia and severe
right ventricular failure not responding to medical management
Provides respiratory and hemodynamic support, improves RV
function
Any patient presenting in cardiopulmonary collapse femoral
arterial and venous 4 Fr sheaths placed in anticipation of ECMO
Anticoagulation free ECMO to be considered if ongoing
hemorrhage
Early decision making and transferring to facilities capable of
ECMO improves survival.
PROGNOSIS
Case fatality ranges between 11% to 26%
Death has been noted 1 to 12 hours after AFE
UK AFE registry reported 37% mortality rate
Early recognition and effective management of cardiac arrest
significantly improves survival rate.