42.1 Introduction

Amniotic fluid embolism is an obstetric emergency in which amniotic fluid, fetal cells, hair, or other debris enters mother’s bloodstream through placental bed and thereby initiates allergic reaction resulting in cardiopulmonary collapse, respiratory compromise, and coagulopathy leading to massive hemorrhage.

Amniotic fluid embolism (AFE) was first described in 1926 by J.R. Meyer, but its real significance as a killer disease was probably recognized in 1941 when Steiner and Lushbaugh, who published an autopsy series of eight pregnant women who died due to sudden shock during labor, believed that AFE was the commonest cause of death in the first 10 h after delivery.

The term AFE is a misnomer now also known as “sudden obstetric collapse syndrome” and “anaphylactoid syndrome of pregnancy”.

AFE is classically characterized by a triad of hypoxia, hypotension, and consumptive coagulopathy; however many a times nonclassical presentation may also dominate (Fig. 42.1).

42.2 Incidence

AFE is more likely underreported in many medical communities as it is a diagnosis of exclusion with no specific diagnostic tests.

AFI is a rare condition ranging from 1 in 8000 to 1 in 80,000 deliveries as per the study done by Gilbert and Danielsen [1]. Reported incidence varies from 1.9/100,000 to 6/100,000 according to some studies.

42.2.1 Maternal Mortality

The case fatality of all the cases ranges from 11% to 43% (Fig. 42.2 ).

AFE is the fifth most common cause of mortality[ 2]. Traditionally AFE was associated with an 80% mortality rate. More recent reports would suggest the mortality is between 20% and 40%, with some as low as 13%.

Neonatal outcome is poor, if AFE develop antenatally and survivors however have long-term neurological impairments.

42.3 Predisposing Causes

Association of uterine hypertonus appears to be an effect rather than cause of AFI. It is likely because uterine blood flow ceases when intrauterine pressure exceeds 35–40 mmHg [5].

42.4 Pathogenesis

The pathogenesis of AFE is complicated and not clear; its development envisages mechanical obstruction of the pulmonary vessels by amniotic fluid components leading to release of humoral and immunological factors.

42.4.1 Pathophysiology [6]

Entrance of amniotic fluid to maternal circulation:

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  Endocervical veins

  
  
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  Placental insertion site

  
  
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  Site of uterine trauma (Figs. 42.3 and 42.4)

42.4.2 Clinical Presentation [7] (Table 42.1)

Table 42.1

Symptoms of AFE in diagnosed cases

Hypotension	60%	Cyanosis	90%
Fetal distress	90%	Coagulopathy	50%
Pulmonary edema or ARDS	45%	Dyspnea	75%
Cardiopulmonary arrest	65%	Seizures	15%

Warning Signs

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  Respiratory distress

  
  
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  Chest pain

  
  
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  Light-headedness

  
  
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  Restlessness

  
  
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  Panic

  
  
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  Tingling in fingers

  
  
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  Nausea, vomiting

First phase:

In the first phase, the patient experiences acute shortness of breath due to pulmonary hypertension. This rapidly progresses to cardiac failure because of pressure overload leading to a reduction of perfusion to the heart, lungs, and finally brain. Not long after this stage, the patient will lose consciousness due to circulatory collapse leading to death of mother unless managed on war footing.

Second phase:

About 40% of the initial survivors will pass onto the hemorrhagic phase after left heart failure. The blood loses its ability to clot and there is excessive bleeding. Collapse of the cardiovascular system leads to fetal distress and death unless the child is delivered swiftly (Fig. 42.5).

Various systemic changes are as follows[ 4]:

1. 1.
   
   
   

   Cardiovascular system: severe pulmonary hypertension leading to right heart failure and subsequently left heart failure too.

   
   
    
   
   
2. 2.
   
   
   

   Hematological changes:

   
   

   Within 4 h there is rise in APTT and PT with fall in fibrinogen level.

   
   
    
   
   
3. 3.
   
   
   

   Respiratory changes:

   
   

   Hypoxia secondary to:
   

   
   

   
   
   1. (a)
      
      
      

      Pulmonary vasoconstriction and cardiogenic pulmonary edema because of left heart failure

      
      
       
      
      
   2. (b)
      
      
      

      Inflammation of pulmonary vasculature leading to capillary leak and noncardiogenic pulmonary edema.

      
      
       
   
   
    
   
   
4. 4.
   
   
   

   Neurological changes

   
   

   Encephalopathy and seizures due to hypoxia (Fig. 42.6).