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{{SI}}
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{{CMG}} {{AIDA}}
{{CMG}} {{AE}} {{AIDA}} ; {{MIR}}


{{SK}} AFE
{{SK}} AFE; Amnioembolism; Pulmonary amnioembolism.


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==Overview==
''Amniotic fluid embolism'' (AFE) is a rare and incompletely understood [[obstetric]] emergency in which [[amniotic fluid]], [[fetal]] cells, hair or other debris enters the mother's blood stream via the [[placenta]]l bed of the [[uterus]] and triggers an [[allergic reaction]]. This reaction then results in [[cardiopulmonary|cardiorespiratory]] ([[heart]] and lung) collapse and [[coagulopathy]]. The condition is so rare (less than 1 in 20,000 deliveries) that most doctors will never encounter it in their professional careers, and as a result the exact process is poorly understood. However, it is believed that once the fluid and [[fetal]] cells enter the maternal [[pulmonary]] circulation a two-phase process occurs. First phase: The patient experiences [[acute]] [[dyspnea|shortness of breath]] and [[hypertension]]. This rapidly progresses to [[cardiac arrest]] as the chambers of the heart fail to dilate and there is a reduction of oxygen to the heart and lungs. Not long after this stage the patient will lapse into a [[coma]]. 50% die within the first hour of [[symptom]]s. Second phase: Although many women do not survive beyond the first stage, about 40 per cent of the initial survivors will pass onto the second phase. This is known as the [[hemorrhagic]] phase and may be accompanied by severe [[shivering]], [[cough]]ing, [[vomit]]ing and the sensation of a bad taste in the mouth. This is also accompanied by excessive bleeding as the blood loses its ability to [[clot]]. Collapse of the [[cardiovascular system]] leads to [[fetal distress]] and death unless the child is delivered swiftly.


==Overview==
==Historical Perspective==
''Amniotic fluid embolism'' (AFE) is a rare and incompletely understood [[obstetric]] emergency in which [[amniotic fluid]], [[fetal]] cells, hair or other debris enters the mother's blood stream via the [[placenta]]l bed of the [[uterus]] and triggers an [[allergic reaction]]. This reaction then results in [[cardiopulmonary|cardiorespiratory]] (heart and lung) collapse and [[coagulopathy]].
* In 1926, Meyer was first who described the underlying pathophysiology of amniotic fluid embolism (AFE).<ref name="pmid26715344">{{cite journal |vauthors=West M |title=Amniotic fluid embolism: a historical perspective in diagnosis and management |journal=BJOG |volume=123 |issue=1 |pages=110 |date=January 2016 |pmid=26715344 |doi=10.1111/1471-0528.13528 |url=}}</ref>
* In 1949, Shotton and Taylor described the contemporary symptoms of sudden and profound shock, [[dyspnea]], [[cyanosis]], and [[pulmonary edema]] as the associated symptoms.<ref name="pmid12698839">{{cite journal |vauthors=Gei AF, Vadhera RB, Hankins GD |title=Embolism during pregnancy: thrombus, air, and amniotic fluid |journal=Anesthesiol Clin North America |volume=21 |issue=1 |pages=165–82 |date=March 2003 |pmid=12698839 |doi= |url=}}</ref>
 
==Pathophysiology==
 
=== Pathogenesis: ===
* The exact pathophisiology of AFE is unknown.<ref name="pmid28188959">{{cite journal |vauthors=Tamura N, Farhana M, Oda T, Itoh H, Kanayama N |title=Amniotic fluid embolism: Pathophysiology from the perspective of pathology |journal=J. Obstet. Gynaecol. Res. |volume=43 |issue=4 |pages=627–632 |date=April 2017 |pmid=28188959 |doi=10.1111/jog.13284 |url=}}</ref> Abnormal maternal response to fetal tissue exposure during [[vaginal delivery]], [[cesarean]], second trimester of pregnancy or even post delivery could be the initial step resulting AFE.<ref name="pmid27816160">{{cite journal |vauthors=Shamshirsaz AA, Clark SL |title=Amniotic Fluid Embolism |journal=Obstet. Gynecol. Clin. North Am. |volume=43 |issue=4 |pages=779–790 |date=December 2016 |pmid=27816160 |doi=10.1016/j.ogc.2016.07.001 |url=}}</ref>
* It has been suggested the main reason of AFE is [[Immune system|immune response]] not embolic process.<ref name="pmid8832353">{{cite journal |vauthors=Syed SA, Dearden CH |title=Amniotic fluid embolism: emergency management |journal=J Accid Emerg Med |volume=13 |issue=4 |pages=285–6 |date=July 1996 |pmid=8832353 |pmc=1342736 |doi= |url=}}</ref>
* [[Amniotic fluid]] caused intravascular [[coagulation]] by having procoagulant products such as platelet-activating factor, [[cytokines]], [[bradykinin]], and [[thromboxane]]. Also, [[Complement]] system activation might play a role in causing AFE.<ref name="pmid12634603">{{cite journal |vauthors=Tuffnell DJ |title=Amniotic fluid embolism |journal=Curr. Opin. Obstet. Gynecol. |volume=15 |issue=2 |pages=119–22 |date=April 2003 |pmid=12634603 |doi=10.1097/01.gco.0000063546.93768.ba |url=}}</ref>
 
=== Hemodynamic Consequences ===
*The most common complication and presentation of amniotic fluid embolism is in the pulmonary vessels.
*Hemodynamic complications and the nature of the clinical manifestations of a pulmonary amniotic fluid embolism depends on a number of factors:<ref name="Hellas">Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.</ref>
** The size of the [[embolus]] and the degree to which it occludes the vascular tree and its subsequent branches 
** The presence of any preexisting cardiopulmonary conditions
** The role of chemical [[vasoconstriction]] as it is insinuated by [[platelets]] releasing [[serotonin]] and [[thromboxane]] in addition to other vasoconstrictors


The condition is so rare (less than 1 in 20,000 deliveries) that most doctors will never encounter it in their professional careers, and as a result the exact process is poorly understood. However, it is believed that once the fluid and [[fetal]] cells enter the maternal [[pulmonary]] circulation a two-phase process occurs:
* Pulmonary amniotic fluid embolism results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the [[capillary]] by the [[embolism]], but also due to pulmonary vasoconstriction.  Pulmonary vasoconstriction can be either biochemically mediated, hypoxia induced, or reflex-induced.<ref name="pmid1555481">{{cite journal| author=Elliott CG| title=Pulmonary physiology during pulmonary embolism. | journal=Chest | year= 1992 | volume= 101 | issue= 4 Suppl | pages= 163S-171S | pmid=1555481 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1555481  }} </ref><ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>


First phase: The patient experiences [[acute]] [[dyspnea|shortness of breath]] and [[hypertension]]. This rapidly progresses to [[cardiac arrest]] as the chambers of the heart fail to dilate and there is a reduction of oxygen to the heart and lungs. Not long after this stage the patient will lapse into a [[coma]]. 50% die within the first hour of [[symptom]]s.
* Several mediators are involved the pulmonary [[vasoconstriction]] that occurs in the setting of acute pulmonary amniotic fluid embolism, such as:
** [[Thromboxane A2]] (end product of [[arachidonic acid]] metabolism)<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
** [[Serotonin]] (vasoconstrictor in the pulmonary circulation and vasodilator in the systemic circulation)<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
** [[Endothelin 1]]<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
** [[Prostaglandin F2α]]<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
** [[Thrombin]]<ref name="pmid14656907">{{cite journal| author=Goldhaber SZ, Elliott CG| title=Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. | journal=Circulation | year= 2003 | volume= 108 | issue= 22 | pages= 2726-9 | pmid=14656907 | doi=10.1161/01.CIR.0000097829.89204.0C | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14656907  }} </ref>
** [[Histamine]]<ref name="pmid14656907">{{cite journal| author=Goldhaber SZ, Elliott CG| title=Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. | journal=Circulation | year= 2003 | volume= 108 | issue= 22 | pages= 2726-9 | pmid=14656907 | doi=10.1161/01.CIR.0000097829.89204.0C | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14656907  }} </ref>


Second phase: Although many women do not survive beyond the first stage, about 40 per cent of the initial survivors will pass onto the second phase. This is known as the [[hemorrhagic]] phase and may be accompanied by severe [[shivering]], [[cough]]ing, [[vomit]]ing and the sensation of a bad taste in the mouth. This is also accompanied by excessive bleeding as the blood loses its ability to [[clot]]. Collapse of the [[cardiovascular system]] leads to [[fetal distress]] and death unless the child is delivered swiftly.
* The embolus may start local inflammatory response which will lead to:
** Release of cytokines [[serotonin]] and [[thromboxane A2]] that are mainly produced by activated [[platelets]]
** The vascular wall and pulmonary neuroendocrine cells might also be the source of some [[vasoconstrictor]]s<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>


==Historical Perspective==
* [[Prostacyclin]] is a vasodilator produced by the [[endothelial cells]] in response to the hemodynamic changes induced by the acute pulmonary amniotic fluid embolism.<ref name="pmid11033105">{{cite journal| author=Smulders YM| title=Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction. | journal=Cardiovasc Res | year= 2000 | volume= 48 | issue= 1 | pages= 23-33 | pmid=11033105 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11033105  }} </ref>
AFE is first described in 1926. <ref name="pmid26715344">{{cite journal |vauthors=West M |title=Amniotic fluid embolism: a historical perspective in diagnosis and management |journal=BJOG |volume=123 |issue=1 |pages=110 |date=January 2016 |pmid=26715344 |doi=10.1111/1471-0528.13528 |url=}}</ref><ref name="pmid12698839">{{cite journal |vauthors=Gei AF, Vadhera RB, Hankins GD |title=Embolism during pregnancy: thrombus, air, and amniotic fluid |journal=Anesthesiol Clin North America |volume=21 |issue=1 |pages=165–82 |date=March 2003 |pmid=12698839 |doi= |url=}}</ref>


==Classification==
* When pulmonary vascular resistance occurs following an acute pulmonary amniotic fluid embolism, the rapid increase in the right ventricular [[afterload]] might lead to the dilatation of the right ventricular wall and subsequent [[right heart failure]]. In addition, the elevated pulmonary vascular resistance causes a decrease in the [[LV|left ventricular]] [[preload]] and consequently leads to systemic [[hypotension]].<ref name="pmid3916797">{{cite journal| author=Wiedemann HP, Matthay RA| title=Acute right heart failure. | journal=Crit Care Clin | year= 1985 | volume= 1 | issue= 3 | pages= 631-61 | pmid=3916797 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3916797  }} </ref><ref name="pmid7484782">{{cite journal| author=Lualdi JC, Goldhaber SZ| title=Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. | journal=Am Heart J | year= 1995 | volume= 130 | issue= 6 | pages= 1276-82 | pmid=7484782 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7484782  }} </ref> In patients with underlying cardiopulmonary disease, the [[cardiac output]] suffers substantial deterioration in overall output as compared to otherwise healthy individuals.
There is no classification for AFE.


==Pathophysiology==
* [[Right heart failure]], as well as systemic [[hypotension]], can attenuate coronary perfusion and contribute to subsequent [[coronary ischemia]].<ref name="pmid3916797">{{cite journal| author=Wiedemann HP, Matthay RA| title=Acute right heart failure. | journal=Crit Care Clin | year= 1985 | volume= 1 | issue= 3 | pages= 631-61 | pmid=3916797 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3916797  }} </ref><ref name="pmid7484782">{{cite journal| author=Lualdi JC, Goldhaber SZ| title=Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. | journal=Am Heart J | year= 1995 | volume= 130 | issue= 6 | pages= 1276-82 | pmid=7484782 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7484782  }} </ref>
The exact pathophisiology of AFE is unknown. <ref name="pmid28188959">{{cite journal |vauthors=Tamura N, Farhana M, Oda T, Itoh H, Kanayama N |title=Amniotic fluid embolism: Pathophysiology from the perspective of pathology |journal=J. Obstet. Gynaecol. Res. |volume=43 |issue=4 |pages=627–632 |date=April 2017 |pmid=28188959 |doi=10.1111/jog.13284 |url=}}</ref> Abnormal maternal response to fetal tissue exposure during [[vaginal delivery]], [[cesarean]], second trimester of pregnancy or even post delivery could be the initial step resulting AFE<ref name="pmid27816160">{{cite journal |vauthors=Shamshirsaz AA, Clark SL |title=Amniotic Fluid Embolism |journal=Obstet. Gynecol. Clin. North Am. |volume=43 |issue=4 |pages=779–790 |date=December 2016 |pmid=27816160 |doi=10.1016/j.ogc.2016.07.001 |url=}}</ref>. It has been suggested the main reason of AFE is [[Immune system|immune response]] not embolic process. <ref name="pmid8832353">{{cite journal |vauthors=Syed SA, Dearden CH |title=Amniotic fluid embolism: emergency management |journal=J Accid Emerg Med |volume=13 |issue=4 |pages=285–6 |date=July 1996 |pmid=8832353 |pmc=1342736 |doi= |url=}}</ref> [[Amniotic fluid]] caused  intravascular [[coagulation]] by having procoagulant products such as platelet-activating factor, [[cytokines]], [[bradykinin]], and [[thromboxane]]. <ref name="pmid12634603">{{cite journal |vauthors=Tuffnell DJ |title=Amniotic fluid embolism |journal=Curr. Opin. Obstet. Gynecol. |volume=15 |issue=2 |pages=119–22 |date=April 2003 |pmid=12634603 |doi=10.1097/01.gco.0000063546.93768.ba |url=}}</ref> [[Complement]] system activation might play a role in causing AFE.


== Causes ==
== Causes ==
Line 33: Line 54:
Although exposure to [[fetal]] tissue is common and thus finding [[fetal]] tissue within the maternal [[circulation]] is not significant, in a small percentage of women this exposure leads to a complex chain of events resulting in collapse and death.  
Although exposure to [[fetal]] tissue is common and thus finding [[fetal]] tissue within the maternal [[circulation]] is not significant, in a small percentage of women this exposure leads to a complex chain of events resulting in collapse and death.  
* Drugs causing amniotic fluid embolism
* Drugs causing amniotic fluid embolism
:* Dinoprostone.
:* Dinoprostone


==Differentiating Amniotic fluid embolism from other Diseases==
==Differentiating Amniotic fluid embolism from other Diseases==
Line 53: Line 74:


===Race===
===Race===
*There is no racial predilection for [disease name].
*There is no racial predilection for AFE.
*[Disease name] usually affects individuals of the [race 1] race.
*[Race 2] individuals are less likely to develop [disease name].
   
   
==Risk Factors==
==Risk Factors==
Line 67: Line 85:


== Natural History, Complications and Prognosis==
== Natural History, Complications and Prognosis==
*The majority of patients with [disease name] remain asymptomatic for [duration/years].  
The overal prognosis of AFE is very poor. Early diagnosis and resuscitative measures can save the patient's life. Neurological impairment, [[renal failure]], respiratory and [[cardiac failure]] are the complications of AFE.
*Early clinical features include [manifestation 1], [manifestation 2], and [manifestation 3].
 
*If left untreated, [#%] of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].
*Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].
*Prognosis is generally [excellent/good/poor], and the [1/5/10­year mortality/survival rate] of patients with [disease name] is approximately [#%].
== Diagnosis ==
== Diagnosis ==
===Diagnostic Criteria===
===Diagnostic Criteria===
Line 104: Line 118:


== Treatment ==
== Treatment ==
=== Medical Therapy ===
The important key in treating AFE is diagnosing it as soon as possible.
*There is no treatment for [disease name]; the mainstay of therapy is supportive care.
 
=== Medical Therapy <ref name="pmid23724386">{{cite journal |vauthors=Thongrong C, Kasemsiri P, Hofmann JP, Bergese SD, Papadimos TJ, Gracias VH, Adolph MD, Stawicki SP |title=Amniotic fluid embolism |journal=Int J Crit Illn Inj Sci |volume=3 |issue=1 |pages=51–7 |date=January 2013 |pmid=23724386 |pmc=3665120 |doi=10.4103/2229-5151.109422 |url=}}</ref> ===
*The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
*Keep patient's vital sign stable by fluid [[resuscitation]], giving oxygen and transfusion of packed [[red blood cells]] if needed.
*[Medical therapy 1] acts by [mechanism of action 1].
*Platelet transfusion if platelets are <20,000/μL without any bleeding, or platelets are 20,000-50,000/μL with bleeding, transfuse [[platelets]] at 1-3 U/10 kg/day.
*Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
*If any [[coagulopathy]] is present, it can be treated with activated recombinant factor VIIa. Acticated recombinant factor VIIa can be used with a dosage of 20-120 mcg/kg in order to prevent serious bleedings associated with amniotic fluid embolism.<ref name="pmid15491576">{{cite journal |vauthors=Lim Y, Loo CC, Chia V, Fun W |title=Recombinant factor VIIa after amniotic fluid embolism and disseminated intravascular coagulopathy |journal=Int J Gynaecol Obstet |volume=87 |issue=2 |pages=178–9 |date=November 2004 |pmid=15491576 |doi=10.1016/j.ijgo.2004.08.007 |url=}}</ref>
*If [[coagulopathy]] is present,the first line treatment is to start with [[FFP]] for a prolonged [[aPTT]], [[cryoprecipitate]] for lower than 100 mg/dL [[fibrinogen]] level, and [[Platelet transfusions|platelet transfusion]] if [[thrombocytopenia]] is present.
 
=== Surgery ===
=== Surgery ===
*Surgery is the mainstay of therapy for [disease name].
In case of severe persistent uterine hemorrhage, hysterectomy should be done.
*[Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
 
*[Surgical procedure] can only be performed for patients with [disease stage] [disease name].
=== Prevention ===
=== Prevention ===
*There are no primary preventive measures available for amniotic fluid embolism.
*Avoid any trauma to the [[uterus]] during labor.
==References==
==References==
{{reflist|2}}
{{reflist|2}}

Latest revision as of 19:41, 23 October 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aida Javanbakht, M.D. ; Mahshid Mir, M.D. [2]

Synonyms and keywords: AFE; Amnioembolism; Pulmonary amnioembolism.

Overview

Amniotic fluid embolism (AFE) is a rare and incompletely understood obstetric emergency in which amniotic fluid, fetal cells, hair or other debris enters the mother's blood stream via the placental bed of the uterus and triggers an allergic reaction. This reaction then results in cardiorespiratory (heart and lung) collapse and coagulopathy. The condition is so rare (less than 1 in 20,000 deliveries) that most doctors will never encounter it in their professional careers, and as a result the exact process is poorly understood. However, it is believed that once the fluid and fetal cells enter the maternal pulmonary circulation a two-phase process occurs. First phase: The patient experiences acute shortness of breath and hypertension. This rapidly progresses to cardiac arrest as the chambers of the heart fail to dilate and there is a reduction of oxygen to the heart and lungs. Not long after this stage the patient will lapse into a coma. 50% die within the first hour of symptoms. Second phase: Although many women do not survive beyond the first stage, about 40 per cent of the initial survivors will pass onto the second phase. This is known as the hemorrhagic phase and may be accompanied by severe shivering, coughing, vomiting and the sensation of a bad taste in the mouth. This is also accompanied by excessive bleeding as the blood loses its ability to clot. Collapse of the cardiovascular system leads to fetal distress and death unless the child is delivered swiftly.

Historical Perspective

  • In 1926, Meyer was first who described the underlying pathophysiology of amniotic fluid embolism (AFE).[1]
  • In 1949, Shotton and Taylor described the contemporary symptoms of sudden and profound shock, dyspnea, cyanosis, and pulmonary edema as the associated symptoms.[2]

Pathophysiology

Pathogenesis:

Hemodynamic Consequences

  • The most common complication and presentation of amniotic fluid embolism is in the pulmonary vessels.
  • Hemodynamic complications and the nature of the clinical manifestations of a pulmonary amniotic fluid embolism depends on a number of factors:[7]
    • The size of the embolus and the degree to which it occludes the vascular tree and its subsequent branches
    • The presence of any preexisting cardiopulmonary conditions
    • The role of chemical vasoconstriction as it is insinuated by platelets releasing serotonin and thromboxane in addition to other vasoconstrictors
  • Pulmonary amniotic fluid embolism results in the elevation of the pulmonary vessel resistance as a consequence of not only mechanical obstruction of the capillary by the embolism, but also due to pulmonary vasoconstriction. Pulmonary vasoconstriction can be either biochemically mediated, hypoxia induced, or reflex-induced.[8][9]
  • The embolus may start local inflammatory response which will lead to:
  • Prostacyclin is a vasodilator produced by the endothelial cells in response to the hemodynamic changes induced by the acute pulmonary amniotic fluid embolism.[9]
  • When pulmonary vascular resistance occurs following an acute pulmonary amniotic fluid embolism, the rapid increase in the right ventricular afterload might lead to the dilatation of the right ventricular wall and subsequent right heart failure. In addition, the elevated pulmonary vascular resistance causes a decrease in the left ventricular preload and consequently leads to systemic hypotension.[11][12] In patients with underlying cardiopulmonary disease, the cardiac output suffers substantial deterioration in overall output as compared to otherwise healthy individuals.

Causes

It is mostly agreed that this condition results from amniotic fluid entering the uterine veins and in order for this to occur there are three prerequisites:

Although exposure to fetal tissue is common and thus finding fetal tissue within the maternal circulation is not significant, in a small percentage of women this exposure leads to a complex chain of events resulting in collapse and death.

  • Drugs causing amniotic fluid embolism
  • Dinoprostone

Differentiating Amniotic fluid embolism from other Diseases

Epidemiology and Demographics

The exact incidence of AFE is unknown but it has been reported between 1 in 8000 and 1 in 80,000 deliveries.[13]

The mortality rate is between 13-26%. If it happens during pregnancy the mortality death in neonate is around 10%.[14]

Age

  • Although older maternal age is considering a risk factor, but AFE can happen in all pregnant ladies in all ages.

Gender

AFE happens in female.

Race

  • There is no racial predilection for AFE.

Risk Factors

Maternal risk factors: [15]

Fetal risk factors:

  • Male baby

Natural History, Complications and Prognosis

The overal prognosis of AFE is very poor. Early diagnosis and resuscitative measures can save the patient's life. Neurological impairment, renal failure, respiratory and cardiac failure are the complications of AFE.

Diagnosis

Diagnostic Criteria

AFE is a diagnosis of exclusion. Classic triad of sudden hypoxia, hypotension, and subsequent coagulopathy in mother especially after labor could be AFE. [16]

Symptoms

Physical Examination

Laboratory Findings

Imaging Findings

  • There are no specific findings associated with AFE.

Other Diagnostic Studies

Transesophageal echocardiography: right ventricular dilation due to pulmonary vasoconstriction [20]

Treatment

The important key in treating AFE is diagnosing it as soon as possible.

Medical Therapy [21]

  • Keep patient's vital sign stable by fluid resuscitation, giving oxygen and transfusion of packed red blood cells if needed.
  • Platelet transfusion if platelets are <20,000/μL without any bleeding, or platelets are 20,000-50,000/μL with bleeding, transfuse platelets at 1-3 U/10 kg/day.
  • If any coagulopathy is present, it can be treated with activated recombinant factor VIIa. Acticated recombinant factor VIIa can be used with a dosage of 20-120 mcg/kg in order to prevent serious bleedings associated with amniotic fluid embolism.[22]
  • If coagulopathy is present,the first line treatment is to start with FFP for a prolonged aPTT, cryoprecipitate for lower than 100 mg/dL fibrinogen level, and platelet transfusion if thrombocytopenia is present.

Surgery

In case of severe persistent uterine hemorrhage, hysterectomy should be done.

Prevention

  • Avoid any trauma to the uterus during labor.

References

  1. ↑ West M (January 2016). "Amniotic fluid embolism: a historical perspective in diagnosis and management". BJOG. 123 (1): 110. doi:10.1111/1471-0528.13528. PMID 26715344.
  2. ↑ Gei AF, Vadhera RB, Hankins GD (March 2003). "Embolism during pregnancy: thrombus, air, and amniotic fluid". Anesthesiol Clin North America. 21 (1): 165–82. PMID 12698839.
  3. ↑ Tamura N, Farhana M, Oda T, Itoh H, Kanayama N (April 2017). "Amniotic fluid embolism: Pathophysiology from the perspective of pathology". J. Obstet. Gynaecol. Res. 43 (4): 627–632. doi:10.1111/jog.13284. PMID 28188959.
  4. ↑ Shamshirsaz AA, Clark SL (December 2016). "Amniotic Fluid Embolism". Obstet. Gynecol. Clin. North Am. 43 (4): 779–790. doi:10.1016/j.ogc.2016.07.001. PMID 27816160.
  5. ↑ Syed SA, Dearden CH (July 1996). "Amniotic fluid embolism: emergency management". J Accid Emerg Med. 13 (4): 285–6. PMC 1342736. PMID 8832353.
  6. ↑ Tuffnell DJ (April 2003). "Amniotic fluid embolism". Curr. Opin. Obstet. Gynecol. 15 (2): 119–22. doi:10.1097/01.gco.0000063546.93768.ba. PMID 12634603.
  7. ↑ Kostadima, E., & Zakynthinos, E. (2007). Pulmonary Embolism: Pathophysiology, Diagnosis, Treatment. Hellenic Journal of Cardiology, 94-107.
  8. ↑ Elliott CG (1992). "Pulmonary physiology during pulmonary embolism". Chest. 101 (4 Suppl): 163S–171S. PMID 1555481.
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 Smulders YM (2000). "Pathophysiology and treatment of haemodynamic instability in acute pulmonary embolism: the pivotal role of pulmonary vasoconstriction". Cardiovasc Res. 48 (1): 23–33. PMID 11033105.
  10. ↑ 10.0 10.1 Goldhaber SZ, Elliott CG (2003). "Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis". Circulation. 108 (22): 2726–9. doi:10.1161/01.CIR.0000097829.89204.0C. PMID 14656907.
  11. ↑ 11.0 11.1 Wiedemann HP, Matthay RA (1985). "Acute right heart failure". Crit Care Clin. 1 (3): 631–61. PMID 3916797.
  12. ↑ 12.0 12.1 Lualdi JC, Goldhaber SZ (1995). "Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications". Am Heart J. 130 (6): 1276–82. PMID 7484782.
  13. ↑ Gist RS, Stafford IP, Leibowitz AB, Beilin Y (May 2009). "Amniotic fluid embolism". Anesth. Analg. 108 (5): 1599–602. doi:10.1213/ane.0b013e31819e43a4. PMID 19372342.
  14. ↑ Moore J, Baldisseri MR (October 2005). "Amniotic fluid embolism". Crit. Care Med. 33 (10 Suppl): S279–85. PMID 16215348.
  15. ↑ Benson MD (2012). "Current concepts of immunology and diagnosis in amniotic fluid embolism". Clin. Dev. Immunol. 2012: 946576. doi:10.1155/2012/946576. PMC 3182579. PMID 21969840.
  16. ↑ Sundin CS, Mazac LB (2017). "Amniotic Fluid Embolism". MCN Am J Matern Child Nurs. 42 (1): 29–35. doi:10.1097/NMC.0000000000000292. PMID 27755062.
  17. ↑ Hankins GD, Snyder RR, Clark SL, Schwartz L, Patterson WR, Butzin CA (April 1993). "Acute hemodynamic and respiratory effects of amniotic fluid embolism in the pregnant goat model". Am. J. Obstet. Gynecol. 168 (4): 1113–29, discussion 1129–30. PMID 8475957.
  18. ↑ Rudra A, Chatterjee S, Sengupta S, Nandi B, Mitra J (2009). "Amniotic fluid embolism". Indian J Crit Care Med. 13 (3): 129–35. doi:10.4103/0972-5229.58537. PMC 2823093. PMID 20040809.
  19. ↑ Leighton BL, Wall MH, Lockhart EM, Phillips LE, Zatta AJ (December 2011). "Use of recombinant factor VIIa in patients with amniotic fluid embolism: a systematic review of case reports". Anesthesiology. 115 (6): 1201–8. doi:10.1097/ALN.0b013e31821bdcfd. PMID 21720243.
  20. ↑ Stanten RD, Iverson LI, Daugharty TM, Lovett SM, Terry C, Blumenstock E (September 2003). "Amniotic fluid embolism causing catastrophic pulmonary vasoconstriction: diagnosis by transesophageal echocardiogram and treatment by cardiopulmonary bypass". Obstet Gynecol. 102 (3): 496–8. PMID 12962931.
  21. ↑ Thongrong C, Kasemsiri P, Hofmann JP, Bergese SD, Papadimos TJ, Gracias VH, Adolph MD, Stawicki SP (January 2013). "Amniotic fluid embolism". Int J Crit Illn Inj Sci. 3 (1): 51–7. doi:10.4103/2229-5151.109422. PMC 3665120. PMID 23724386.
  22. ↑ Lim Y, Loo CC, Chia V, Fun W (November 2004). "Recombinant factor VIIa after amniotic fluid embolism and disseminated intravascular coagulopathy". Int J Gynaecol Obstet. 87 (2): 178–9. doi:10.1016/j.ijgo.2004.08.007. PMID 15491576.

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