Fluid Embolism

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© Springer Nature Singapore Pte Ltd. 2020
A. Sharma (ed.)Labour Room Emergencieshttps://doi.org/10.1007/978-981-10-4953-8_42



42. Amniotic Fluid Embolism



Kiran Pandey1   and Amrita Singh1  


(1)
Department of OBGYN, GSVM Medical College, Kanpur, Uttar Pradesh, India

 



 

Kiran Pandey (Corresponding author)


 

Amrita Singh


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).

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Fig. 42.1

Classical triad of AFE


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 ).

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Fig. 42.2

Mortality rate according to antecedent cause on time scale


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.


42.2.2 Recurrence


According to a review by Agustin Conde et al published in American Journal of Obstetrics & Gynaecology, 2009, a total of 9 cases of successfull pregnancy following AFE have been reported.


On the basis of available limited experience and evidences, AFE is found to be nonrecurrent[ 3].


42.3 Predisposing Causes


In order for amniotic fluid to enter circulation, there are three prerequisites:


  1. 1.

    Ruptured membranes


     

  2. 2.

    Ruptured uterine or cervical vein


     

  3. 3.

    Pressure gradient from the uterus to vein


     

Various risk factors include[ 4]:



  • Maternal age >35 years



  • Placenta previa and abruption



  • Cesarean sections or assisted delivery procedures (forceps, vacuum)



  • Eclampsia



  • Fetal distress



  • Induction/augmentation of labor



  • Meconium-stained amniotic fluid



  • Tears in uterine or other large pelvic veins


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:



  • Endocervical veins



  • Placental insertion site



  • Site of uterine trauma (Figs. 42.3 and 42.4)


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Fig. 42.3

Pathophysiology of amniotic fluid embolism


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Fig. 42.4

Proposed hypothesis and mechanisms


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






  • Respiratory distress



  • Chest pain



  • Light-headedness



  • Restlessness



  • Panic



  • Tingling in fingers



  • 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).

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Fig. 42.5

First and second phase of AFE


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).


     

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Fig. 42.6

HRCT of the chest showing ground glass infiltrate in AFE

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Mar 28, 2021 | Posted by in OBSTETRICS | Comments Off on Fluid Embolism

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