amniotic fluid embolism

武功密笈

小黃藏書

OBS
GYN
Gyn Oncology
Infertility
Urogynecology

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~ 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