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2014 Version
Risk factors
Hypertonic uterine action
effect of amniotic fluid embolism rather than the cause
uterine blood flow ceases completely when IUP exceeds 35 to 40mmH
least likely time for fetomaternal exchange to take place.
Caesarean section
Polyhydramnios
Precipitate labour.
Oxytocin stimulated labour
Rupture of membrane
Multiparity
Placental abruption
Most cases do not have risk factors as mentioned above
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nd
Clinical Presentation
linked to precipitous labor, uterine hyperstimulation, and the use of
oxytocin
analysis of national registry data has questioned the strength of these
associations.
12% of the cases occurred in women with intact membrane, 70% during
labour, 11% after vaginal delivery and 19% during C/S with or without
labour
onset usually during labor and delivery or in the immediate postpartum
period
classically a women in the late stages of labour or immediately postpartum
begins gasping for air &then rapidly suffers seizures or cardiorespiratory
arrest complicated by DIC.
Rarely, has been reported up to 48 hours postpartum, or following
cesarean delivery, first and second trimester abortions, or amniocentesis.
abrupt and fulminant onset of:
Hypoxia and respiratory failure
Cardiogenic shock
Disseminated intravascular coagulation
Rapid cardiorespiratory collapse.
Nonspecific symptoms
chills, nausea, vomiting, agitation, may precede the onset of
dyspnea and hypotension
tonic-clonic seizure activity may be present. Clinical
presentation similar to septic or anaphylactic shock but a clear
etiologic agent or antibody-mediated reaction has not been
identified.
Hypoxaemia
Results from severe ventilation/perfusion mismatching.
Bronchospasm in 15% of patients.
Hypoxia accounts for approximately 50% of the deaths observed in the first
hour after presentation, and may also result in severe neurologic
impairment or brain death in the mother.
Up to 70% of patients who survive the first several hours develop
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Cardiovascular collapse
Primarily the result of left ventricular dysfunction.
Cardiac dysrhythmias, including pulseless electrical activity, bradycardia,
ventricular fibrillation, and asystole, may further complicate management.
Pulmonary artery catheter data usually show a diminished cardiac output
with relatively small increases in pulmonary vascular resistance.
Approximately 86% of patients diagnosed with AFES die from cardiogenic
shock or its complications.
Disseminated intravascular coagulation - as many as 80% of patients
develop DIC Causes haemorrhage.
Diagnosis
No single clinical or laboratory finding is available.
Primarily a clinical diagnosis.
Profound shock and severe respiratory compromise during labor or
immediately postpartum.
At postmortem,demonstrate fetal squames or debris in the pulmonary
artery vasculature.
Surviving patients identification of amniotic fluid debris in the bronchial
washings or blood from right atrium or ventricle washings or fetal squames
in sputum.
ECG (R ventricular strain pattern,tachycardia),blood gas-(reduced
PaO2,PaCO2 &metabolic acidosis),coagulation screen(evidence of
DIC),CXR-(perihilar infiltrates) may be helpful.
Other causes of sudden cardiorespiratory failure, such as air or pulmonary
embolism, hemorrhage, anesthetic complications, anaphylaxis, sepsis,
aspiration of gastric contents, and myocardial infarction, must be excluded
Some authors require amniotic fluid debris (squamous and trophoblastic
cells, mucin, and lanugo) in samples from the distal port of a pulmonary
artery catheter in order to make the diagnosis. However, amniotic fluid
components commonly are present in the maternal circulation in women
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Differential Diagnosis
PTE, septic shock, MI, aspiration pneumonia, allergy to anaesthetic
agents.
Pathophysiology
Because AFES is an uncommon clinical event, understanding the cause of
this syndrome has been based to a large degree upon animal models.
Introduction of amniotic fluid into the venous circulation of laboratory
animals results in the rapid development of pulmonary hypertension, acute
cor pulmonale, and systemic hypotension.
These responses appear secondary to occlusion and vasospasm of the
maternal pulmonary vasculature due to the local presence of amniotic
fluid.
Passage of amniotic fluid debris into the maternal circulation during or just
after childbirth,together with surrounding platelet-fibrin thrombi,obstructs
pulmonary circulation.This results in,
brief initial phase of pulmonary & systemic hypertension,there is
decreased systemic vascular resistance & left ventricular stroke work
index.
Transient but profound oxygen desaturation seen in initial phase result in
neurological injury in most survivors.
Who live beyond the initial CV collapse, a secondary phase of lung injury
occurs in 70% which may in turn lead to ARDS & coagulopathy in 40%
which may manifest by persistent bleeding from IV sites or surgical
incisions, often ensues.
Haemodynamic changes
In humans, amniotic fluid most commonly enters the maternal circulation
through the endocervical veins, the placental insertion site, or at a site of
uterine trauma.
In humans, the principal hemodynamic alteration in AFES is left ventricular
failure rather than pulmonary hypertension with right ventricular failure:
pulmonary artery and pulmonary capillary wedge pressures are elevated,
cardiac output is decreased, and the left ventricular stroke work index is
severely reduced, indicating left ventricular dysfunction.
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Inflammation
Immunologic or inflammatory events may be required for the clinical
syndrome to develop.
Asymptomatic embolization of amniotic material is not uncommon,
supporting the theory that specific maternal responses are necessary to
produce AFES.
Several mechanisms have been proposed to explain the time lag between
amniotic fluid embolism and disease as well as the inconsistent
occurrence of the clinical syndrome:
Abnormal amniotic fluid may be required.
Exposure to atypical substances within the amniotic fluid, such as
leukotrienes or other arachidonic acid metabolites, may produce the
principal hemodynamic responses, including left heart failure,
pulmonary capillary injury, and coagulopathy.
Host immune responses may be necessary to affect organ function.
Variability in severity and intensity of clinical features may reflect
varied immunologic stimulation by fetal-associated antigens.
Management
The three main goals of the treatment are:
oxygenation
maintaining cardiac output and BP
correcting coagulopathy- give uterotonics, and uterine massage,
blood transfusion and blood components (FFP, cryoprecipitate,
platelets)
As per management of cardiorespiratory arrest, resuscitation consists of
the A, B and Cs
securing airway through endotracheal intubation
mechanical ventilation with high inspired fraction oxygen, and the
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Monitoring
Monitoring should include continuous pulse oximetry, electrocardiography,
arterial blood pressure monitoring, and electronic fetal monitoring, if illness
occurs prior to delivery.
Invasive hemodynamic monitoring with pulmonary artery catheterization is
essential to the management of both the cardiovascular and respiratory
components of AFES.
Serial measurements of the pulmonary capillary wedge pressure and
cardiac output are useful in the fluid management of this syndrome, and
can guide therapy in cases of cardiogenic and noncardiogenic pulmonary
edema.
Central venous pressure assessment alone is generally not sufficient for
the management of these complex, hemodynamically compromised
patients.
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Pharmacologic therapy
Cardiogenic shock requires the use of inotropic and vasoactive agents.
Norepinephrine and dopamine are the drugs of choice for the initial
maintenance of cardiac output and blood pressure.
In the patient with severe left ventricular dysfunction and pulmonary
edema, dobutamine may offer the potential advantage of increasing the
low cardiac output and decreasing the high filling pressures.
Dobutamine infusion may result in hypotension caused by a drop in
systemic vascular resistance, and use of a vasopressor (generally
norepinephrine) in combination with this inotrope may be required.
Patients with AFES who are managed with appropriate inotropic support
and use of vasoactive agents as guided by central haemodynamic
monitoring may have an overall improved survival rate.
Fluid management
Vigorous fluid resuscitation should be withheld, if possible, until a
pulmonary artery catheter can guide management.
Intravenous fluids may result in, or exacerbate, pulmonary edema, and
initial management with vasopressors is preferred.
Blood product transfusion may be required for the correction of clinically
significant coagulopathy.
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References
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