~ Amniotic Fluid Embolism ~
§ Background:
Recently, the term anaphylactoid syndrome of pregnancy
has been proposed
instead of AFE (amniotic fluid embolism), to better
characterize this condition as
a multisystemic reaction to toxins rather than an embolic
phenomenon.
§ Incidence:
z True incidence of AFE: may
not be known, 1/8000 to 1/83000 deliveries
z Growing
awareness of the syndrome, rather than a true increase in incidence or
idiosyncrasies
in obstetric practice, is responsible for these difference.s
§ Mortality:
z AFE constitute
the leading cause of mortality during labor and the first few postpartum hours.
Maternal death usually occurs because of sudden cardiac
arrest, hemorrhage due to
coagulopathy, or acute respiratory distress syndrome, and
multiple organ failure
z 5% to 18% of all maternal
deaths are due to AFE.
z 7.8 to 12 deaths per million
births
z For women diagnosed as having
AFE, mortality rates ranging from 26% to
86% have been reported.
§ Pathophysiology:
z Anaphylaxis plays a role in
the syndrome.
z Clinically, the reaction to
AFE comprises three distinct phases. Besides, the
syndrome seems to have a logarithimic presentation with
decreasing
intensity, frequency, and mortality as time elapses from the
onset of
symptoms. If a patient survives with or without intervention,
the morbidity
and mortality are dramatically lower.
Amniotic fluid enters the venous systemic circulation,
for reasons not completely known.
z The first phase:
Cardiogenic and noncardiogenic pulmonary edema
Intrapulmonary shunting
Bronchoconstriction
Desaturation
1). Blue phase: respiratory, including respiratory
distress and cyanosis
Decreased coronary blood flow
Decreased inotropism
Decreased cardiac output
Pulmonary congestion
2). White phase: hemodynamic, with pulmonary edema and
shock
3). Neurologic, including seizures, confusion or coma
ø These
presentations can occur separately or in combination, and indifferent degrees
Amniotic fluid enters the arterial systemic circulation
z The second phase:
Thromoplasins
1). Intravascular coagulopathy
2). Red phase: hemorrhage
ø Of patients who
survive the initial acute cardiorespiratory insult, 40% to 50% enter
the second phase. In some women, this may be the
first and only clinical
manifestation.
z The third phase: Gray
phase
The acute symptoms are
over and tissue injury (brain, lung, or renal) is for
the most part already established.
During this
convalescent period, which may last weeks, affected patients
can die as a result of severe lung or brain injury,
multisystemic organ
failure, or infections.
Fetal hypoxia, fetal
bradycardia, or fetal death may follow as a result of
systemic hypotension.
§ Diagnosis:
z Establishment of diagnosis of
AFE: ~ by a pathologist
Finding in maternal tissue of epithelial squamous cells,
lanugo hair, fat
derived from vernix caseosa, mucin derived from infant’s
intestinal mucus,
or bile derived from meconium.
z Presumption of diagnosis of
AFE:
? Symptoms/signs and their
temporal relationship:
Eg. sudden onset of respiratory distress, cardiac collapse,
seizures,
unexplained fetal distress, and abnormal bleeding
‚ Clinical
conditions associated with AFE:
- Onset of labor
- Rupture of membranes
- Fetal death
- Trauma
- Uterine overdistension by multiple gestation,
polyhydramnios, or fetal macrosomia
ƒ Aids for diagnosis
of AFE: (see table 2)
z Differential diagnosis of AFE:
Coagulopathy/bleeding:
Uterine atony
Placental abruption
Retained products of conception
Urogenital tract laceration
Sepsis |
Fever:
Sepsis
Pulmonary thromboembolism
Thyroid storm |
§ Management:
z Prompt and aggressive
treatment of an acutely ill pregnant patient,
regardless of the cause:
· Write down the time. Call
for help. Get code cart to the room. Ask relatives to step
outside the room or better yet, ask somebody to escort
them.
· Airway patency.
Check and maintain patency. Start O2 via the quickest way avaliable
· Breathing. Check
for spontaneous respiration. Evaluate breathing effort. Prepare for
intubation. Proceed when possible.
· Check pulse and blood
pressure. If none registered, begin CPR and order somebody to
say the time out loud. Place defibrillator pads ASAP.
Obtain EKG tracing. Prepare for
defibrillation. Call local Code Team.
· Displacement of
the patient hips or the uterus to the left will improve venous return and
uterine blood flow.
· Endovascular access:
- Place 2 large-bore (ideally 14 or 16) peripheral IV lines
- Obtain at least 40 mL of blood for laboratory samples.
(More if patient is febrile to touch, for cultures)
- Do a bedside glucose if arrest not witnessed. Tell
glucose results out loud
· Fluid, fetus, and
Foley:
- Begin crystalloids in both sides, full open.
- Monitor the fetus.
- Place Foley catheter. Keep a urine sample. Quantify
amount. Notify others if blood
present.
· Good or go:
- Prepare the team caring for the patient for the
performance of a bedside C/S.
- Ask for the time since arrest called and proceed if
deemed necessary.
- If the situation is “good” (or improving) defer; if
“not good” go ahead and proceed
to deliver the infant.
z Medications:
? To maintain systolic blood
pressure ³ 90 mmHg, with acceptable
peripheral organ perfusion (manifested by urine output ³
25 mL/hour)
and to maintain patient’s sensorium:
Crystalloids
Inotropics (rapid
digitalization + b -adrenergics)
Pressors
(ephedrine, dopamine, dobutamine, norepinephrine infusions)
ø After
hypotension has been corrected, fluid therapy should be restricted to
maintenance levels, to minimize pulmonary edema due to
developing ARDS.
Corticosteroids
(hydrocortisone 500 mg iv q6h)
‚ To maintain arterial
PO2 > 60 mmHg or hemoglobin
saturation ³ 90%:
As in any other
conditions when oxygenation and airway patency
may be compromised due to seizures, shock, or severe
respiratory
distress, securing an airway through endotracheal
intubation is
advisable.
1) Mechanical ventilation and high levels of fractional
inspired oxygen (FIO2)
When still poor oxygenation despite of FIO2 >
0.6
2) Mechanical ventilation and positive end-expiratory
pressure (PEEP)
ƒ To correct coagulation
abnormalities:
Packed red blood
cells
Fresh frozen
plasma
Cryoprecipitates:
- Rich in both fibrinogen and fibronectin, the latter
facilitating the uptake of
cellular and particulate debris (such as amniotic
fluid contents) from the blood
via the reticuloendothelial system
Platelets
Oxytocin and
other uterotonics for uterine atony
ø The shock seen
in these patients is out of proportion to the amount of bleeding,
so vasopressors are an indicated adjunct to blood
replacement.
ø If the patient
has an epidural catheter, it is prudent to remove it as soon as possible.
However, if bleeding occurs around the device, it may
be better to leave it in place
to tamponade the site until further diagnostic testing.
After removal of the catheter,
the patient should be monitored closely for any signs
of subarachnoid or epidural
hemorrhage.
§ Prognosis:
z Data gathered from the
National AFE Registry:
- Maternal mortality rate: 61%
- Rate of survival without neurologic sequelae: 15%
- Rate of survival in the presence of maternal cardiac
arrest: 7.5%
Only 8% of those survivors were without neurologic
impairment.
Neonatal survival rate: 68%, with only 32% having normal
neurologic outcome
- Neonatal survival rate: 79%
Only 50% of the surviving infants were neurologically normal.
The infant’s prognosis was adversely affected by maternal
cardiac arrest.
z Data from a recently
published population-based study from California:
- Maternal survival rate: 73.6%
Intact maternal survival rate: 87%
- Neonatal survival rate: 95%
Intact neonatal survival rate: 72%
§ References:
1. Amniotic fluid embolism: an update. Alfredo Gei, MD, and
Gary DV Hankins, MD.
Contemporary OB/GYN Jan. 2000: 53-62
Filename: Amniotic Fluid Embolism
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