| Amniotic fluid embolism | |
|---|---|
 | |
| Intravascular squames are present in this example of amniotic fluid embolism. | |
| Specialty | Obstetrics  |
| Risk factors | Advanced maternal age, history of pre-eclampsia, uterine rupture, fetal distress |
| Frequency | 1 in 20,000 births |
Anamniotic fluid embolism (AFE) is a life-threatening childbirth (obstetric) emergency in whichamniotic fluid enters the blood stream of the mother, triggering a serious reaction which results in cardiorespiratory (heart and lung) collapse and massive bleeding (coagulopathy).[1][2][3] The rate at which it occurs is 1 instance per 20,000 births and it comprises 10% of all maternal deaths.
Amniotic fluid embolism is suspected when a woman giving birth experiences very suddeninsufficient oxygen to body tissues,low blood pressure, and profuse bleeding due todefects in blood coagulation.
The signs and symptoms of amniotic fluid embolism can vary from one individual to another but involve systemic involvement of multiple organ systems. Often, a patient may present with a cough due to the release ofbradykinin, an inflammatory marker released during times of pain and which causes ananaphylactoid reaction.[4] The cough may then progress todyspnea and shortness of breath or difficulty breathing due to the vasoconstriction of the pulmonary arterioles making it more difficult for air to flow through.[4][5] This decreased air flow will lead to the decrease of oxygen being delivered to the tissues to offload carbon dioxide from the blood. The heart will try to compensate by speeding up and causingtachycardia or a fast heart rate in the mother. The fetus will respond to the changes in the mother if still in labor by exhibiting tachycardia and decelerations in thefetal heart rate tracing. It will then register as a lowpulse oximetry reading when performed by the health care staff and will result inhypoxia.[5]
Most commonly patients will experiencehypotension or low blood pressure due to the widespread inflammation and anaphylaxis occurring.[5]
As the amniotic fluid builds up in the lungs, the patient may begin to exhibit signs of pulmonary hypertension due to the fluid blocking the blood flow of the lungs and decreasing the oxygen.[4] As the amniotic fluid embolism progresses the final stage before cardiovascular collapse involves hemorrhaging or large volume blood loss.[5] This leads to the over activation of thecoagulation cascade creating an over production of blood clots with the inability to be broken down resulting in DIC ordisseminated intravascular coagulation.[4][5]
There are several posited ways that have been positioned to cause amniotic fluid embolism. The first of which involves the thought that a combination or one of the following that include a difficult labor, aplacenta that is abnormal and trauma to the abdomen through acaesarean section or other surgical tools dissipates the barrier that exists from the maternal fluid to the fetal fluid.[5][6] The disruption then causes a buildup ofhydrostatic pressures andoncotic pressures leaking the fetal fluid into the maternal circulation.[5][7] This fluid is then carried through the veins to thesuperior vena cava to the right atrium and on to the right ventricle eventually entering thepulmonary artery and disseminating through thepulmonary circuit.[5][7] This causes the fluid of thealveoli of the lungs to build up and cause increased pressures that put extra work on the heart. This leads to pulmonary hypertension causingright ventricular heart failure which leads tocardiovascular collapse.[5][7][6]
The second school of thought is that a series of inflammatory markers in amniotic fluid causes a widespread inflammatory activation in the blood throughout the maternal circulation.[5][7] This causes intense pulmonary vasospasm leading to dysregulation of the pulmonary circulation causing failure in the systemic circulation. This school of thought is supported by a study which showed that amniotic fluid can activatecomplement.[8] Additionally, another study showed activity levels ofC1 esterase inhibitor, a key regulator of thecomplement system, are significantly decreased in amniotic fluid embolism patients compared with control women.[9]
Furthermore, amniotic fluid contains further elements such as tissue factor and other clotting factors that lead to a hypercoagulable state or consistent development and formation of blood clots in the body with the inability to be broken down.[4] This hypercoagulable state is amplified by the decreasedC1 esterase inhibitor levels as this protein is the primary inhibitor ofFactor XIa andFactor XIIa in theclotting cascade, and deficiency has been shown to be associated with an increased risk ofvenous thromboembolism.[10][11] This leads to the sequelae ofDIC ordisseminated intravascular coagulation.[5][7] The DIC in amniotic fluid embolism is often associated withhyperfibrinolysis, which is likely to be due to elevatedtissue plasminogen activator (tPA) and decreased totalthrombin-activatable fibrinolysis inhibitor (TAFI).[12]
It is also supposed thatendothelin a potent vasoconstrictor is upregulated during the course of the amniotic fluid embolism in the maternal circulation. This endothelin acts in an antagonistic fashion to blood vessels causing intensevasoconstriction.[5] This leads to super tight vessels that cut off the blood supply to the lungs and heart resulting incardiorespiratory collapse.[5][7]
The occurrence of amniotic fluid embolism is not readily defined as it is a spontaneous event and has not set progression. However, it is most known to occur alongside a cesarean section delivery, a difficult vaginal birth and hours after delivery has been completed.[5][13]
Some risk factors for amniotic fluid embolism include:
The method by which labor is induced seemingly plays a role in the risk for amniotic fluid embolism as well.[4] Induction with vaginal prostaglandin E2 was seen as significantly increasing the relative risk for the emergence of amniotic fluid embolism on a laboring mother.[5][4]
Overall, however, any method of induction for labor including surgical induction, artificial rupture of membranes oroxytocin is seen as increasing the risk of amniotic fluid embolism in labor.[4]
Male fetuses and fetuses of low birth weight also present an increased risk to mothers.[7]
In order to diagnose amniotic fluid embolism, there are a few important factors that must be present:
In order to diagnose an amniotic fluid embolism, an arterial blood gas (ABG) must be taken immediately to determine the acid-base status. The ABG should demonstrate a low PH and increased PCO2 levels consistent with a respiratory acidosis. Continuous pulse oximetry readings as well will determine the level of hypoxia and what the oxygen requirements are.[5]
Coagulation studies should also be collected. Special attention should be paid to the PT (prothrombin time) and the PTT (partial thromboplastin time). If coagulation factors are being used, the PT will be prolonged and the PTT may be normal or prolonged.[5][4]
A type and screen should also be ordered in case there needs to be blood products transfused in the event of an hemorrhage.[5]
There are several biomarkers that are said to be able to determine if AFE will occur or has occurred, including:[5][4][13]
When dealing with a patient with amniotic fluid embolism, stabilizing the patient is the first line of action. If the patient is in need of oxygen, oxygen delivered via a high flow rebreather mask should be given. If a patient is unstable and unable to receive oxygen via the high flow rebreather mask or nasal cannula, then steps should be taken to support the patient via endotracheal tube and placed on a ventilator.[13][6]
A patient at risk of cardiovascular compromise due to late stage vasodilation of the blood vessels should be givenphenylephrine to vasoconstrict the arteries and raise the blood pressure to prevent persistent hypotension[13] Due to the nature of AFE being an anaphylaxis-like reactionepinephrine should be given as well.[5][7][13]
If hemorrhage occurs, the transfusion ofpacked red blood cells is given promptly to prevent further complications.[5][7] In the case of DIC, recombinant activated factor VIIa is a quick way to address this issue. Serine proteinase inhibitor FOY and Aprotinin have also been used to treat DIC in AFE.[13]
The successful use of heparin in these cases could be attributable not only to it being ananticoagulant useful in the treatment of DIC, but also due to its ability to enhancec1 esterase inhibitor activity thereby reducingcomplement activation and inflammation.[14][15] A case report published in 2015 also documented the successful use of c1 esterase inhibitor concentrate in the treatment of amniotic fluid embolism.[16]
A case report on Amniotic Fluid Embolism published in theA & A Practice Journal in 2020 has revealed that whenmilrinone is administered as an aerosol, selective pulmonary vasodilation occurs without significant changes[17] in mean arterial pressure or systemic vascular resistance; and if used immediately after Amniotic Fluid Embolism, inhaled milrinone may mitigate the pulmonary vasoconstriction.[18][19]
Amniotic fluid embolism is very uncommon and the rate at which it occurs is 1 instance per 20,000 births. Though rare, it comprises 10% of all maternal deaths.[2]
This rare complication has been recorded seventeen times prior to 1950. The complication was originally described in 1926 by J. R. Meyer at theUniversity of São Paulo.[20][21] A 1941 case study of eight autopsies of pregnant women who died suddenly during childbirth byClarence Lushbaugh and Paul Steiner enabled widespread recognition of the diagnosis within the medical community, and was eventually republished as a landmark paper in theJournal of the American Medical Association.[21][22]
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