Amniotic fluid embolism (AFE) is an extremely rare, but life-threatening obstetric emergency characterized by sudden cardiorespiratory collapse and disseminated intravascular coagulation followed by severe coagulopathy and refractory resuscitation, altered mental status, disseminated intravascular coagulation (DIC), renal, neurologic, and pulmonary complications that affect pregnant women shortly before, during, or immediately following labor and childbirth. It is one of the catastrophic complications of pregnancy in which amniotic fluid, fetal cells, hair, or other debris enters the maternal pulmonary circulation, causing cardiovascular collapse.
Most instances occur during labor. In this disorder, it is hypothesized that a pregnant woman has a severe, allergic reaction to amniotic fluid or other fetal material such as fetal cells, which enter the mother’s bloodstream. Amniotic fluid is contained within the amniotic sac. This fluid supports, cushions, and protects a developing fetus. Amniotic fluid embolism is unpredictable and no risk factors have been identified. AFE can cause a severe, rapid decline in the mother’s health. For years, some researchers believed that the amniotic fluid and fetal cells cause an obstruction within the mother’s blood vessels, but now most researchers believe that the mother’s immune system reacts to the amniotic fluid and fetal cells causing an overwhelming immune system response, which ends up harming the mother and the fetus. Breathing problems, cardiac arrest, and excessive bleeding are some of the life-threatening complications that can occur. Researchers and physicians do not fully understand why amniotic fluid or fetal cells entering the mother’s bloodstream causes this reaction in some women. Amniotic fluid embolism is a medical emergency that develops suddenly and rapidly and can be fatal. Early recognition and prompt supportive treatment are essential.
An amniotic fluid embolism (AFE) is a very uncommon childbirth (obstetric) emergency in which amniotic fluid enters the bloodstream of the mother to trigger a serious reaction. This reaction then results in cardiorespiratory (heart and lung) collapse and massive bleeding (coagulopathy). The setting for amniotic fluid embolism (AFE) is a disruption of the placenta-amniotic interface with the subsequent entry of amniotic fluid and fetal elements (such as hair, meconium, squama, and mucin) into the maternal circulation. Portals of entry may include the placental attachment, the cervical veins, or uterine surgical incisions. Upon entering the pulmonary arterial tree, intense pulmonary vasoconstriction occurs. This may be associated with concomitant bronchoconstriction. The hemodynamic result is acute pulmonary arterial obstruction, dilatation of the right ventricle and the right atrium, and significant tricuspid regurgitation. The right ventricular enlargement causes the intraventricular septum to bow into the left ventricle creating obstruction and systolic dysfunction, further raising pulmonary artery pressure and decreasing cardiac output. Hypoxemia and hypotension lead to sudden cardiovascular collapse.
Symptoms
The signs and symptoms of amniotic fluid embolism often develop rapidly. Nonspecific symptoms including headaches, chest pain, cough, sweating, nausea, and vomiting have been reported as early signs. Other common initial symptoms include difficulty breathing or shortness of breath (dyspnea), abnormally rapid breathing (tachypnea), low blood pressure (hypotension), an abnormally rapid heartbeat (tachycardia), bluish discoloration of the skin and mucous membranes due to a lack of oxygen (cyanosis) in the blood, and a deficiency in the amount of oxygen reaching the tissues of the body (hypoxia). There may be rapidly high blood pressure in the blood vessels of the lungs (pulmonary hypertension) and sudden narrowing of blood vessels (vasospasm).
The suspicion of AFE is suggested by the sudden appearance of dyspnea, dysphoria, hypotension, cardiovascular collapse, and coagulopathy following some action during the peripartum period-, e.g., active labor, rupture of membranes, vaginal delivery, or cesarean section.
Breathing problems can progress to acute respiratory failure a severe, life-threatening complication where damage and fluid leakage into the lungs makes breathing difficult or impossible. Some affected women experience increasing cardiac rhythm abnormalities, low blood pressure, shock, and/or the abrupt loss of heart function despite no underlying heart disease (cardiac arrest). Cardiac arrest can cause gasping breath, no breathing, or complete unresponsiveness in the affected individual. Affected women may experience an altered mental status including anxiety or confusion, seizures, or coma.
Most women develop a condition called disseminated intravascular coagulation (DIC). In DIC, blood clotting factors, specialized proteins that help the blood clot, are used up or broken down. Without these clotting factors, an affected woman cannot create blood clots to stop bleeding. There may be bleeding from the uterus and puncture sites, such as the site of an intravenous needle or an epidural catheter. In rare instances, severe bleeding (hemorrhaging) may be the first sign of amniotic fluid embolism.
Amniotic fluid embolism might develop suddenly and rapidly. Signs and symptoms might include:
- Symptoms are acute dyspnea, cough, hypotension, cyanosis, fetal bradycardia, encephalopathy, acute pulmonary hypertension, coagulopathy etc.
- Sudden shortness of breath
- Excess fluid in the lungs (pulmonary edema)
- Sudden low blood pressure
- Sudden failure of the heart to effectively pump blood (cardiovascular collapse)
- Life-threatening problems with blood clotting (disseminated intravascular coagulopathy)
- Bleeding from the uterus, cesarean incision, or intravenous (IV) sites
- Altered mental statuses, such as anxiety or a sense of doom
- Chills
- Rapid heart rate or disturbances in the rhythm of the heart rate
- Fetal distress, such as a slow heart rate, or other fetal heart rate abnormalities
- Seizures
- Loss of consciousness
Doctors may note a condition called nonreassuring fetal status. This term means that the fetus is not doing as well as would normally be expected. The fetus may not be getting enough oxygen and there may be an abnormally slow heart rate. Nonreassuring fetal status is an assessment of fetal health given late in the pregnancy or during delivery. If an AFE occurs during pregnancy, the infant must be expeditiously delivered as a life-saving measure for both the mother and fetus.
Causes
Amniotic fluid embolism is a condition that occurs because there is a systemic reaction similar to that found in an allergic response to amniotic fluid or fetal cells or fetal tissue debris by the pregnant mother. The amniotic fluid and other material enter the mother’s bloodstream, most likely due to small tears in the lower part of the uterus, the part of the cervix that forms a canal connecting the vagina to the uterus (endocervix), or because of damage or abnormality affecting the placenta. The cervix is the narrow passage that forms the lower end of the uterus. The placenta is the organ that joins or connects the developing fetus to the mother. The placenta allows the transfer of oxygen and nutrients from the mother to the fetus.
How amniotic fluid or fetal cells cause an allergic reaction in some women and not others are not completely understood. Originally, researchers believed that amniotic fluid had an embolic effect, which means that the amniotic fluid formed clots (emboli) in the mother’s blood vessels, most likely the blood vessels of the lungs. That is where the disorder’s name, amniotic fluid embolism, came from. While amniotic fluid or fetal cells may contribute to some mechanical obstruction, amniotic fluid dissolves in fluid (soluble) and the fetal cells or tissue debris that can also enter the mother’s blood are usually too small an amount to cause a clot to form. Researchers now believe that this is an immune-mediated disorder and that the symptoms are caused by the mother’s immune system, which reacts to the amniotic fluid or fetal cells as foreign substances. This immune response causes an overwhelming inflammatory response in the mother’s body that damages healthy tissue and structures, which ultimately is believed to cause the signs and symptoms. The process more closely resembles anaphylactic shock than it does an embolic event.
Although many potential risk factors have been discussed, no risk factors for amniotic fluid embolization have been conclusively proven to increase a woman’s risk of developing this disorder. Most studies have been inconsistent or contradictive regarding risk factors. The onset of amniotic fluid embolism cannot be predicted or anticipated by doctors nor can the disorder be prevented.
The following signs and symptoms are indicative of possible AFE:[rx,rx]
Acute dyspnea or sudden, agitation, sudden chills, shivering, sweating, coughing and anxiety are common premonitory symptoms. Labored breathing and tachypnea may occur:[rx]
-
Cough: This is usually a manifestation of dyspnea.
-
Altered mental status.
-
The rapid decline in pulse oximetry values or sudden absence or decrease in end-tidal carbon dioxide may be apparent.
-
Hypotension: Hemodynamic compromise quickly follows these prodromal signs. Hypotension is the most common presenting sign and symptom (100%). Blood pressure may drop significantly with the loss of diastolic measurement. Some researchers postulate that an acute anaphylactoid reaction may play a part in the development of cardiovascular collapse.[rx]
-
Cyanosis: Ventilation-perfusion mismatching as a result of pulmonary vascular constriction at the onset of AFE may explain sudden hypoxia and respiratory arrest. As hypoxia/hypoxemia progresses, circumoral and peripheral cyanosis and changes in mucous membranes may manifest.
-
Fetal bradycardia: In response to the hypoxic insult, fetal heart rate may drop to <110 bpm. If this drop lasts for 10 min or more, it is bradycardia. A rate of 60 bpm or less over 3-5 min may indicate terminal bradycardia.
-
Encephalopathy associated with AFE is thought to be secondary to hypoxia and includes a spectrum of symptoms ranging from altered mental state to seizures. Tonic-clonic seizures are seen in 10-50% of patients.
-
Uterine atony: Uterine atony usually results in excessive bleeding after delivery.
-
Acute pulmonary hypertension and vasospasm result in right ventricular failure, hypoxia, and cardiac arrest. Pulmonary hypertension and right heart strain/failure may be the result of physical amniotic fluid debris in the pulmonary vasculature result from circulating pulmonary vasoconstrictive mediators. Proposed explanations include myocardial failure in response to sudden pulmonary hypertension, a direct myocardial depressant effect of humoral mediators in amniotic fluid, deviation of the intraventricular septum due to right ventricular dilation, and/or ischemic myocardial injury from hypoxemia.[rx] If one survives this initial insult, then the pulmonary hypertension is generally not sustained and may be replaced with left ventricular failure and pulmonary edema. Increased pulmonary artery pressure has not been consistently reported probably because this finding may be short-lived. When cardiac pressures are measured early in the process, pulmonary and right ventricular pressures have been found to be elevated.[rx,rx]
-
Coagulopathy or severe hemorrhage: Coagulation disorders are a prominent feature of amniotic fluid syndrome. DIC is present in more than 83% of patients with AF. The onset can occur as quickly as 10-30 min from the onset of symptoms or may be delayed by as long as 4 h.[rx,rx] Whether coagulopathy is primarily a consumptive process or due to massive fibrinolysis is controversial. Amniotic fluid contains tissue factor that acts as a procoagulant and may account for coagulopathy. Tissue factor binds with Factor VII and activates the extrinsic coagulation pathway. Alternatively, coagulopathy may be related to fibrinolysis due to increased levels of plasminogen activation inhibitor 1 in amniotic fluid.[rx,rx]
Diagnosis
A diagnosis of amniotic fluid embolism is based upon the identification of characteristic clinical symptoms only. To date, there are no diagnostic assays, imaging studies, or pathologic markers that have been validated for the diagnosis of AFE. Standard laboratory turnaround times for important clotting parameters such as prothrombin time, partial thromboplastin time, clotting factor analysis, and fibrinogen tend to be excessive. The use of viscoelastic tests such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM), when done at the bedside (point of care) by a trained specialist, offers the capability of a minute to minute evaluation of fibrinogen level, platelet count, and function, as well as evaluation of the entire extrinsic clotting pathway.
- Initial diagnostic evaluation should include continuous pulse oximetry and arterial blood gas (ABG) measurements to determine the degree of hypoxemia. Decreased pH.Decreased PO2 .Increased PCO2 levels. Base excess increased. Blood type and screen in anticipation of the requirement for a transfusion.
- ABG levels are expected changes consistent with hypoxia/hypoxemia.
Serial complete blood counts and coagulation studies should be sent to follow trends and detect early coagulopathy.CBC with platelets. PT is prolonged because clotting factors are used up. Values are institution-specific, but intervention is indicated when the PT is 1.5 times the control value PTT may be within the reference range or shortened.Prothrombin time (PT) and activated partial thromboplastin time (aPTT). If available, the fibrinogen level should be monitored.
Hemoglobin and hematocrit levels should be within reference ranges. Thrombocytopenia is rare.
- Chest radiograph posteroanterior and lateral findings are usually nonspecific. The chief radiographic abnormalities in AFE are diffuse bilateral heterogeneous and homogeneous areas of increased opacity, which are indistinguishable from acute pulmonary edema.
- A 12-lead electrocardiogram may show tachycardia, ST-segment and T-wave changes, and findings consistent with right ventricle strain.
- A lung scan may demonstrate some areas of reduced radioactivity in the lung field.[rx]
- Increased serum tryptase, urinary histamine concentrations, and significantly lower complement concentrations suggest an anaphylactoid process.[rx,rx,rx,rx] Tryptase is a serine protease with a half-life of several hours. Although the specific function of tryptase in anaphylaxis is unknown, with a half-life measured in hours instead of the minutes of histamine, the protein has proven useful in the diagnosis of anaphylaxis.[rx]
- Decreased serum levels of C3 and C4 complement had sensitivities between 88% and 100% and a specificity of 100%.[rx]
- More studies are also needed to determine the utility of both monoclonal TKH-2 antibodies and zinc coproporphyrin as rapid diagnostic markers.[rx,rx]
- Few studies have evaluated the diagnostic accuracy of serum sialyl Tn (STN), a fetal antigen present in meconium and amniotic fluid, detected through the use of TKH-2 monoclonal antibody. TKH-2 reacts with meconium and mucin and stains the lung tissue in those with AFE. For serum levels >50 U/ml, the sensitivities varied between 78% and 100%, and the specificities were between 97% and 99%.[rx,rx,rx,rx]Few authors reported a significantly high serum level of STN antigen in the AFE cases as high as 110.8 ± 48.1 U/ml for AFE versus 17.3 ± 2.6 U/ml for control). In few cases reports in the literature reported that intravascular fetal material in the uterus can be used to confirm a diagnosis of AFE in situations where AFE is prevented by ligation of the uterine artery.[rx,rx]
- Bedside transesophageal echocardiography may aid early diagnosis by showing acute pulmonary vasoconstriction, right ventricular dilation, and a collapsed left ventricle with a leftward deviation of the intraventricular septum.[rx,rx] However, rapid access to transesophageal echocardiography is probably not available in many obstetric units.
Clinical Testing and Workup
Laboratory tests are nonspecific (a complete blood count, coagulation profile, arterial blood gases, cardiac enzymes, and electrolytes). The white blood cell count may be elevated and, depending on the presence of DIC, the hemoglobin and hematocrit values will be low. The laboratory manifestations of DIC include prolonged prothrombin and partial thromboplastin times, with decreased fibrinogen levels. Thrombocytopenia is a rare finding. Cardiac enzymes may be elevated, and arterial blood gases may show hypoxemia. The electrocardiogram may show tachycardia, with a right ventricular strain pattern in the early stage and ST and T wave abnormalities. Cardiac arrhythmias or asystole can be seen with severe cardiovascular collapse. Pulse oximetry may reveal a sudden drop in oxygen saturation. The chief radiographic abnormalities in AFE are diffuse bilateral heterogeneous and homogeneous areas of increased opacity, which are indistinguishable from acute pulmonary edema from other causes. Transesophageal echocardiography may demonstrate severe pulmonary hypertension, acute right ventricular failure with a leftward deviation of the interatrial and interventricular septum, and a cavity-obliterated left ventricle during the early phase of AFE
A chest x-ray may show fluid in the lungs, a prominent pulmonary artery, or enlargement of the heart (cardiomegaly). An electrocardiogram, an echo or echocardiography, is a test that uses high-frequency sound waves to create pictures of the heart. This test can show right heart strain and abnormalities of the heart rhythm as well as dysfunction of the right or left upper chamber of the heart (ventricular dysfunction). A finding on echocardiography that is specifically characteristic of AFE is right heart strain followed by elevated pulmonary pressures and resultant left-sided failure. An electrocardiogram can also measure the electrical activity of the heart and can reveal abnormal electrical patterns.
Transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) is essential to the diagnosis. If stability is acquired, TEE is preferred. Significant findings of AFE are right ventricle dilatation, hypokinesis, and overload, tricuspid regurgitation, and right atrial enlargement. Early cardiac thrombi may be detected in the enlarged right ventricle or right atrium. Highly associated with this syndrome is the bowing of the intraventricular septum into the left ventricle, creating left ventricular obstruction and systolic dysfunction. The echocardiographic appearance of this bowing resembles the letter ‘D.’ Blood should be obtained immediately for urgent type and crossmatch, complete blood count, comprehensive metabolic panel, and a full coagulation panel to include platelets, prothrombin time, partial thromboplastin time, bleeding time, fibrinogen, d-dimer, and fibrin degradation products (FDPs).
Sometimes, doctors would take a sample of pulmonary blood to look for the fetal squamous cells, which were believed to be covered with white blood cells called neutrophils and fetal debris like fetal tissue or cells. This was once considered diagnostic of amniotic fluid embolism but is no longer considered conclusive evidence of the disorder as this finding is not specific to this disorder.
Besides basic investigations lung scan, serum tryptase levels, serum levels of C3 and C4 complements, zinc coproporphyrin, serum sialyl Tn etc are helpful in establishing the diagnosis.
Treatment
Amniotic fluid embolism is a medical emergency. Treatment is aggressive and supportive. A team of specialists is required to treat affected individuals. This team will include specialists in treating pain and in managing the care of a patient before, during, and after surgery (anesthesiologists); physicians who specialize in pregnancy, childbirth, and a woman’s reproductive system (obstetricians); obstetricians who specialize in maternal and fetal health (maternal-fetal medicine specialists); physicians who specialize in the diagnosis and treatment of blood disorders (hematologists); and physicians who specialize in the treatment of critically ill patients (intensivists). Treatment is mainly supportive, but exchange transfusion, extracorporeal membrane oxygenation, and uterine artery embolization have been tried from time to time.
General
-
Maintaining vital signs. The initial goal is the rapid correction of maternal hemodynamic instability, which includes a correction of hypoxia and hypotension, for preventing the additional hypoxia and subsequent end-organ failure.[rx]
-
Oxygenation and Control of the airway with tracheal intubation and administration of 100% O2 with positive pressure ventilation should be performed as soon as possible.
-
Fluid resuscitation is imperative to counteract hypotension and hemodynamic instability. Treatment of hypotension includes optimization of preload, with rapid volume infusion of isotonic crystalloid and colloids solutions. Although both can restore blood volume in ongoing hemorrhage, transfusion of packed red blood cells is necessary to restore oxygen-carrying capacity.[rx]
-
Correcting coagulopathy — Blood and blood products, including fresh frozen plasma (FFP), platelets and cryoprecipitate, must be available and administered early in the resuscitation phase of AFE. If platelets are <20,000/μL, or if bleeding occurs and platelets are 20,000-50,000/μL, transfuse platelets at 1-3 U/10 kg/day.
- Administer FFP to normalize the PT.[rx,rx,rx,rx]
-
If fibrinogen level is <100 mg/dL, administer cryoprecipitate. Each unit of cryoprecipitate raises the fibrinogen level 10 mg/dL.
-
Arterial catheterization should also be considered for accurate arterial blood pressure monitoring and frequent blood sampling.[rx]
Pharmacological
Vasopressors and inotropic support are generally needed to varying degrees in AFE. Central venous access should be established for vasopressor infusion and monitoring. The choice of the vasopressor drug depends on the clinical scenario.[rx,rx,rx,rx]
-
Epinephrine may be the first-line agent of choice as it is used in other anaphylactoid reactions, in addition to the α-adrenergic vasoconstrictor effects.
-
Phenylephrine, a pure α-1 agonist, is often an excellent choice early in the treatment of AFE because at that time point systemic vasodilation is the most prominent circulatory abnormality.
-
Inotropic support like dopamine or noradrenaline may be ideal agents because of the additional β-adrenergic effects, which improve cardiac function.
-
Vasopressin may be used as primary therapy or as an adjunct to other inotropic therapies and has the benefit of sparing the pulmonary vasculature from vasoconstriction, especially at low doses. In the face of right heart failure, milrinone or other phosphodiesterase inhibitors should be considered.[rx,rx]
-
Digoxin: acts directly on the cardiac muscle and conduction system. Digoxin causes an increase in force and velocity of systolic contraction, a slowing of the heart rate, and decreased conduction velocity through the AV node.
-
Hydrocortisone: Because AFE is more similar to an anaphylactic reaction, steroids that mediate the immune responses are recommended.
-
Oxytocin: Most commonly used uterotonic. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.
-
Methylergonovine (Methergine): Acts directly on uterine smooth muscle, causing a sustained tetanic uterotonic effect that reduces uterine bleeding.
-
Carboprost tromethamine: Prostaglandin is similar to F2-alpha (dinoprost), but has a longer duration and produces myometrial contractions that induce hemostasis at the placentation site, which reduces postpartum bleeding
-
The successful use of recombinant factor VIIa (rfVIIa) has been reported.[rx] although it has also been associated with massive intravascular thrombosis.
-
Aprotinin has also been effective in reducing hemorrhage with AFE.
The general sequence of vasopressors support starts with dopamine, dobutamine, or epinephrine, but may be switched to norepinephrine for persistent hypotension. Vasopressin may be added at this point to augment cardiac output. Ideal management is to maintain mean arterial pressure (MAP) of more than 65 mmHg, a cardiac index of more than 2 L per meter square, an adequate urine output of 40-50 ml/hr, and a PaO2/FiO2 ratio of more than 250. Ventilation using inhaled nitric oxide assists in reducing RV afterload. Sildenafil is utilized for its pulmonary arterial vasodilatation. Extracorporeal membrane oxygenation (ECMO) has been used successfully for refractory cardiogenic shock secondary to amniotic fluid embolus. Any patient who remains in persistent cardiopulmonary collapse should have femoral arterial and venous 4 Fr sheaths placed in anticipation of ECMO.
The management of the coagulopathy (DIC) of AFE has classically been to empirically administer units of packed red blood cells (pRBCs), fresh frozen plasma (FFP), and platelets in a 1:1:1 ratio until bleeding is controlled. Cryoprecipitate contains concentrated clotting factors, including factor VIII, von Willebrand factor, and fibrinogen. It is also given to maintain fibrinogen levels of more than 200 mg/dl. Tranexamic acid is given for fibrinolysis. Algorithms derived from these measurements dictate the appropriate administration of cryoprecipitate, fibrinogen, prothrombin complex concentrates, platelets, FFP, pRBCs, and tranexamic acid (TXA). Anecdotal reports in the literature cite the use of rivaroxaban, a factor Xa inhibitor, as successfully reversing the DIC of AFE. Other anecdotal reports suggest the use of ketorolac to inhibit thromboxane, which activates platelets in AFE. Besides, ondansetron has been utilized to block serotonin receptors in the lung. Serotonin is thought to be a potent pulmonary vasoconstrictor.
Obstetrical management must include the rapid evacuation of the fetus, usually by cesarean section. The Society for Maternal-Fetal Medicine recommends this for all fetuses over 23 weeks gestational age. Ongoing resuscitation of the mother in the obstetrical operating room with an anesthesiologist or critical care provider running the cardiovascular resuscitation must go on during the extraction of the infant. It is recommended to shift the gravid uterus to the left, therefore, relieving aortocaval compression. This multidisciplinary team must be able to initiate neonatal resuscitation and should include a neonatologist because the majority of these infants are born with a low Apgar score. The infant will likely need rapid suctioning, intubation, and vascular access. The obstetrician may elect several different procedures to alleviate the ongoing uterine hemorrhage. Uterine artery ligation or embolization has been documented with some success. Circumferential B-Lynch, Hayman, or Pereira compression sutures have been utilized to compress the atonic uterus and staunch bleeding. However, in the setting of massive hemorrhage and an atonic uterus, the best course is an emergency hysterectomy.
Initially, physicians will work to stabilize a woman’s breathing and heart function. If an affected woman is unconscious, they may receive cardiopulmonary resuscitation (CPR). An affected woman may receive supplemental oxygen to make up for a lack of oxygen in the blood or tissues. This can require the insertion of a breathing tube to help with breathing and the use of a machine to assist with breathing (mechanical ventilation).
Immediate delivery of the fetus is required for the health of the fetus. Decreasing the aortocaval compression may improve maternal resuscitation.
Psychosocial support for the entire family is essential as well. Some women survive amniotic fluid embolism with no long-term complications of the condition. However, there is a risk of long-term complications including neurological problems because of a lack of oxygen to the brain.
A Practice Journal in 2020 has revealed that when milrinone is administered as an aerosol, selective pulmonary vasodilation occurs without significant changes[rx] in mean arterial pressure or systemic vascular resistance; and if used immediately after Amniotic Fluid Embolism, inhaled milrinone may mitigate the pulmonary vasoconstriction
Investigational Therapies
Researchers are studying whether specific biomarkers for amniotic fluid embolism may be identified and used to help with diagnosis. Biomarkers are substances that can be detected and measured in a person and when detected at certain levels indicate a specific disorder or condition is or may be present. More research is necessary to determine whether there are specific biomarkers that can be used to detect amniotic fluid embolism.
Several other treatment methods have been discussed in the medical literature that have been tried in individual patients or small series of patients. Due to the rarity of the disease, there are no treatment trials that have been tested on a large group of patients. More research is necessary to determine the long-term safety and effectiveness of various treatments for amniotic fluid embolism proposed in the medical literature.
The AFE Foundation along with the Baylor College of Medicine maintains an international patient registry of women with amniotic fluid embolism. In collaboration with Wayne State University, a biorepository of samples from women and their offspring is being collected to further understand this elusive disease. A registry is a special database that contains information about individuals with a specific disorder or group of conditions. The collection of data about rare disorders may enable researchers to increase the understanding of such disorders, expand the search for treatments, and accelerate clinical trials into specific treatment options
References
Amniotic Band Syndrome
