|
 
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| REVIEW ARTICLE |
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| Year : 2015 | Volume
: 5
| Issue : 1 | Page : 3-8 |
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Amniotic fluid embolism
Girendra Sadera1, Bharathram Vasudevan2
1 Consultant, Critical Care and Anaesthesia, Wirral University Teaching Hospital, NHS Foundation Trust, Upton, Wirral, United Kingdom
2 Department of Anaesthesiology, All India Institute of Medical Sciences, New Delhi, India
| Date of Web Publication | 15-Apr-2015 |
Correspondence Address:
Upton Girendra Sadera
Consultant, Critical Care and Anaesthesia, Wirral University Teaching Hospital, NHS Foundation Trust, Upton, Wirral, CH49 5PE
United Kingdom
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2249-4472.155192
Amniotic fluid embolism (AFE) is a rare complication of pregnancy carrying a high mortality rate. The exact pathogenesis of the condition is still not known. Diagnosing AFE needs a high suspicion as it is essentially a clinical diagnosis of exclusion. Patients with AFE are best-managed in a critical care unit by a multidisciplinary team and management is largely supportive. This review compiles the currently available information on AFE. Keywords: Amniotic, embolism, fluid, pregnancy
How to cite this article:
Sadera G, Vasudevan B. Amniotic fluid embolism. J Obstet Anaesth Crit Care 2015;5:3-8 |
| Introduction | |  |
Amniotic fluid embolism (AFE) is an uncommon complication of pregnancy with a high mortality rate, making it one of the leading direct causes of maternal mortality in developed countries. [1] Although the first case of amniotic fluid entering the maternal circulation was published in 1926 by Meyer, [2] it was recognized as a distinct clinical entity only in 1941 when Steiner and Lushbaugh made a detailed description of the syndrome based on their autopsy findings. They postulated that pulmonary embolism by amniotic fluid was the reason for death in eight women who died unexpectedly during labor. [3] Despite being known for so many years now, it remains a medical mystery even today with no consensus on the exact pathogenesis of the syndrome. There is a recent surge of research to find novel biomarkers which can help in predicting and diagnosing AFE. This article aimed to provide a comprehensive review of the available knowledge on AFE.
| Epidemiological Data | | |
The reported incidence of AFE varies widely among different studies, as is the reported mortality rates. The wide variation is due to the absence of universally accepted diagnostic criteria, varied clinical presentations and rarity of the condition. Frati et al. recently compared nine studies and arrived at a mean incidence of 5.5/100,000 deliveries (range 2-15.2) and a mean case fatality rate of 24.8% (range 13.3-48%). [4] The incidence of AFE in UK is about 2/100,000 maternities. [5]
World Health Organization defines maternal death as death of a woman during pregnancy or within 42 days after pregnancy due to causes related to pregnancy or aggravated by it. [6] Maternal deaths can be divided into direct or indirect based on the etiology. A direct death is one resulting from obstetric complications of the pregnant state (example: Preeclampsia), while an indirect death is due to an associated disease which may be aggravated by physiological effects of pregnancy (example: Pre-existing cardiac disease). AFE is one among the top five leading causes of direct obstetric deaths in developed countries. Busardo et al. examined seven different national registries and concluded that fatal cases of AFE amounted to a mean of 12.8% (range 4.7-24.3%) of maternal deaths. [7] It was the leading cause of maternal mortality in the Japanese registry while it was among the top five in other registries. [7] The mortality rate due to AFE in UK is 0.33/100,000 (2010-2012). [6] It is the fifth leading cause of direct obstetric death in UK after thromboembolism, sepsis, hemorrhage, and preeclampsia/eclampsia. [6]
| Risk Factors | | |
Many risk factors have been associated with AFE, but causality has not been proved for most of them though a consistent association has been observed with older maternal age and medical induction of labor. [1] According to data from the UK and Ireland, confidential enquiries into maternal deaths and morbidity 2009-2012 labor induction or augmentation was done in six out of eleven women who died of AFE in 2009-12 and three out of eleven had uterine hyper-stimulation. [6] The associated risks are mentioned in [Table 1]. [8],[9],[10],[11],[12] Instrumental delivery, caesarean delivery, cervical trauma or uterine rupture may be the result of attempting to deliver the fetus after an AFE and may not be causative. [8] Some authors are of the opinion that uterine stimulation is the least likely time for amniotic fluid to come into contact with the maternal circulation, thereby questioning the causative role of uterine stimulation. [13] Thus, no significant risk factor has been proved yet to change the current obstetric practice. The risk of recurrence of the condition is also not known, though there are a few reports of successful subsequent pregnancies. [14]
| Pathogenesis | | |
Exposure of the maternal circulation to amniotic fluid or fetal antigens is universally accepted as a prerequisite for AFE to occur. This can occur through one of the three routes - uterine trauma sites, endocervical veins or placental attachment site. [14] Minor uterine trauma occurs at the time of normal labor as well as instrumental or cesarean delivery. The exact mechanism underlying the occurrence of AFE after this exposure is still not known.
Historically, AFE was thought to be caused due to mechanical obstruction of pulmonary vessels by amniotic fluid embolus consisting of fetal squames, vernix caseosa, lanugo hair, trophoblasts, fetal gut mucin, and bile stained meconium. But this could not explain the entire clinical manifestations of the syndrome. Moreover, this mechanism could not be proved in animal studies. [15],[16]
At present, AFE is thought to result from an immune-mediated mechanism, given its similarity to septic shock or anaphylactic shock. It results from an abnormal immunological response of the mother following exposure to fetal antigens leading to the release of various pro-inflammatory mediators. [13] Clark et al. even proposed to rename the syndrome as "anaphylactoid syndrome of pregnancy," [11] though it was not widely accepted. The exact immunological mechanism is still unknown. Amniotic fluid itself contains various vasoactive and prothrombotic substances such as platelet activating factor, interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF α), leukotrienes C4 and D4, endothelin, tissue factor, arachidonic acid, and others which when released into the maternal circulation can lead to vasoconstriction, bronchoconstriction and coagulation. [17] An anaphylactic mechanism is supported by studies showing increased mast cell degranulation [18] and refuted by studies that failed to show a rise in serum tryptase levels. [19] Complement activation as the primary mechanism has been proposed. [20] The levels of complement factors C3 and C4 have been found to be reduced in patients with AFE. Furthermore, mast cells can be secondarily activated after complement activation. Platelet aggregation and neutrophil activation are also other mechanisms proposed for the release of inflammatory mediators that ultimately lead to the clinical syndrome. [17]
The reason for activation of the coagulation cascade is incompletely understood. Tissue factor in amniotic fluid and apoptotic amniotic cells may initiate the coagulation cascade, but it is still doubtful if the small quantities of these factors could lead on to the disseminated intravascular coagulation (DIC) picture that is seen in AFE. [13]
Recently, an integrated mechanism was proposed. According to this theory, activation of the coagulation cascade can lead to microthrombi in pulmonary vessels and add on to the mechanical obstruction by amniotic fluid components. This, along with the various inflammatory mediators like leukotrienes can cause the complete picture of the syndrome. [21] An overview of the pathogenesis of AFE is shown in [Figure 1].
| Clinical Features | | |
About 70% of cases occur during labor, 19% during cesarean section, and 11% after delivery in the immediate postpartum. [22] There have been reports of delayed AFE occurring up to 48 h after delivery. [14] There are also reports of cases occurring after second-trimester abortions, amniocentesis, blunt abdominal trauma, abdominal surgeries, dilatation and evacuation, and intrapartum amnioinfusion with normal saline. [23],[24]
The classical form of AFE presents as a sudden onset respiratory distress followed by a sudden cardiovascular collapse. This is followed by cardiac arrest and/or coagulopathy. [13] The signs and symptoms in this early phase include dyspnea, desaturation, hypotension, cardiac arrhythmias, seizures, loss of consciousness, bleeding, and cardiac arrest. [13] Fetal hypoxia and bradycardia are almost universal if AFE occurs prior to delivery. Premonitory symptoms of tingling, numbness, restlessness, and agitation have been described and are thought to occur from early hypoxia. [9] The cause of cardiac arrest can be hypoxia, direct myocardial suppression or excessive bleeding. [11] Lung injury and acute respiratory distress syndrome (ARDS) are seen in the late phase. Multiple organ dysfunction and hypoxic brain damage are common in those who survive the initial cardiac arrest. Infants born to these mothers are at risk for hypoxic ischemic encephalopathy and cerebral palsy. [25]
In the atypical form, coagulopathy manifesting as severe bleeding occurs in the absence of cardiopulmonary manifestations. [13] Uterine atony can additionally contribute to the hemorrhage.
Studies utilizing transesophageal echocardiography have found that the cardiac abnormalities in AFE are biphasic - an early transient phase of intense pulmonary vasoconstriction, pulmonary hypertension, and right ventricular failure, and a late phase of left ventricular dysfunction leading to hypotension and cardiogenic pulmonary edema. [14]
Tsunemi et al. attempted to classify 136 cases of AFE into three subtypes:
- Classical subtype with early respiratory distress and hypoxia,
- Anaphylactoid subtype with early cardiac dysfunction and arrhythmias and
- DIC subtype with coagulopathy.
They found considerable overlap of features in many patients. The DIC subtype carried a lesser mortality when compared with the classical subtype which was associated with a higher incidence of sudden death. [26]
| Diagnosis | | |
Amniotic fluid embolism is essentially a clinical diagnosis and a diagnosis of exclusion as there is no available laboratory test to confirm the diagnosis. The classical triad of respiratory distress, cardiovascular collapse, and coagulopathy makes it easy to diagnose the classical form. [13] Different national registries have their own entry criteria but share common features involving the classical triad along with a criterion to describe the timing of occurrence of the syndrome. [11],[25] Other similar conditions need to be excluded before a diagnosis of AFE is made [Table 2]. [6],[14],[27],[28] The UK Obstetric Surveillance System diagnostic criteria for AFE are given in [Table 3]. [10]
| Laboratory Tests | | |
There is no confirmatory laboratory test available at present for diagnosing AFE. Earlier, demonstration of fetal tissues in maternal blood by aspiration through the distal port of a pulmonary artery catheter was considered confirmatory. But it is now known that it's not specific for AFE. [13] Many biomarkers are presently under study, and some are available commercially. [29] Their clinical use is doubtful and not recommended routinely. Some of the currently available biomarkers are discussed below.
TKH2 is a monoclonal antibody against Sialyl Tn (STN) antigen. Immunohistochemical staining using TKH2 antibody can help in detecting meconium and the amniotic fluid mucin in lung secretions. [30]
Sialyl Tn is a known antigen in meconium and amniotic fluid mucin. Detection of STN in maternal serum can act as a diagnostic evidence for amniotic fluid in maternal circulation. [30]
Zinc coproporphyrin-1 (ZnCP-1) is a known component in meconium and fetal urine. The maternal plasma levels of ZnCP-1 have been found to be high in patients with AFE. It can be detected by high-performance liquid chromatography and can act as a sensitive diagnostic tool. [31]
Levels of complement factors C3and C4 are decreased in patients with AFE while serum mast cell tryptase has been found to be high. [29] Measuring the levels of these proteins can play a useful role. Levels of other nonspecific factors found to be high in amniotic fluid include IL-6 and 8, TNF α soluble receptor.
Insulin-like growth factor binding protein-1 (IGFBP-1) is a protein synthesized in the decidua. Normally, its level in amniotic fluid is approximately 150 times more than in maternal plasma. [32] Higher levels in maternal plasma can point towards AFE. A combination of maternal serum IGFBP-1, alpha-fetoprotein, and fetal fibronectin has been postulated as a confirmatory test for AFE. [33]
Other adjuvant laboratory tests can help in exclusion of other conditions and also help in the management. These are listed in [Table 4]. [14]
| Management | | |
Management of AFE is supportive, and thus a final diagnosis is not required to manage these patients. Supportive management based on the pathophysiological changes should be started as soon as signs and symptoms arise and should not wait for laboratory tests. These patients are ideally managed in an intensive care setting by a multi-disciplinary team.
In the event of cardiac arrest, cardiopulmonary resuscitation (CPR) should be done according to advanced cardiac life support guidelines with special consideration to pregnancy. Left lateral displacement of the uterus or left lateral tilt should be done to relieve aortocaval compression and hands should be placed higher up on the chest during chest compressions.
Hypoxia and respiratory distress are to be managed with 100% oxygen. Early intubation and mechanical ventilation are to be considered. [34] The level of respiratory support needed will depend on the severity of presentation. [35] Early intubation can help preventing aspiration, the risk of which is higher in pregnant women. A difficult airway is to be anticipated given the physiological changes in pregnancy, and appropriate preparedness is necessary. [36] Mechanical ventilation should follow lung protective strategy protocol as these patients are at risk for ARDS. [35]
Hemodynamic instability needs to be treated with careful volume expansion, vasopressors and inotropes. Invasive arterial pressure monitoring, central venous, and pulmonary artery catheters can help in the management. Echocardiography helps in assessing the cardiac status and guiding fluid therapy. [35] Noninvasive advanced hemodynamic and cardiac output monitors may be helpful. Intraaortic balloon counter pulsation, cardiopulmonary bypass, and extracorporeal membrane oxygenation have all been used with reported success in cases of AFE. [37],[38],[39],[40],[41] These modalities may be tried when available in the event of worsening cardiopulmonary status not responding to other treatment modalities.
Transfusion of blood products forms the cornerstone of treating coagulopathy. Massive blood transfusion protocol needs to be initiated. [42] Damage control resuscitation in the form of packed cells, plasma, and platelets in the ratio of 1:1:1 is recommended by some in cases of uncontrolled hemorrhage. [43] Transfusion of fresh frozen plasma (FFP) should be done at an initial rate of 15 mL/kg body weight. Severe hypofibrinogenemia (<1 g/L) persisting after FFP transfusion may be treated with fibrinogen concentrates or cryoprecipitate. Fibrinogen assessments are recommended as they correlate with the severity of bleeding, with fibrinogen levels <2 g/L predicting more severe bleeding. [42] Repeated monitoring of coagulation status is necessary and point-of-care devices like thromboelastometry are especially useful Thromboelastometric measurements can help in early detection of a hypercoagulable or a hyperfibrinolysis state and can direct therapy with FFP, factor concentrates and tranexamic acid. [44] The role of heparin and factor VIIa are controversial and should be used with caution.
Treatment of uterine atony is equally important to control bleeding. Initially, uterine massage and drugs such as oxytocin, methylergometrine, and carboplast can be tried. Uterine tamponade, manual exploration, and uterine artery embolization may be helpful in some cases. Hysterectomy as an early resort is recommended to remove the main source of bleeding especially when there are no experienced personnel to perform the less definitive procedures. [6]
Isolated case reports of successful management of AFE with other treatment modalities such as inhaled nitric oxide, inhaled prostacyclin, aprotinin, exchange transfusion, continuous hemodiafiltration, cell salvage, and pulmonary thromboembolectomy have been published. [45],[46],[47],[48],[49],[50] The extent of their usefulness in AFE is uncertain.
| Perimortem Caesarean Delivery | | |
Perimortem cesarean delivery in cases of maternal cardiac arrest is vital in resuscitation of the mother and also in saving the fetus. Royal College of Obstetricians and Gynaecologists guideline states that perimortem cesarean section should be done in cases of maternal collapse where return of spontaneous circulation does not occur after 4 min of effective CPR and the fetus should be delivered within 5 min of arrest. The viability of the fetus is not a matter of concern in such cases. It should be done then and there without shifting the patient to operating room. [36] In the case of cardiopulmonary instability without overt cardiac arrest, the role of cesarean section is controversial. The mother may not tolerate stress of surgery. If not delivered, the fetus is at risk for hypoxia and intrauterine death. The decision needs to be made on a case to case basis. [27]
| Conclusion | | |
Amniotic fluid embolism remains a clinical diagnosis of exclusion and management is only supportive. There is no clearly proven risk factor to predict or prevent its occurrence. Though the mortality rate has decreased over the years due to better resuscitation and critical care, [35] it still remains high at 12.8%. [7] An encouraging light of hope is the recent increase in research to find the exact pathogenesis of this condition and also to discover clinically relevant biomarkers that can help in earlier diagnosis and prompt treatment.
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[Figure 1]
[Table 1], [Table 2], [Table 3], [Table 4]
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