ETIOLOGY AND RISK FACTORS

Amniotic fluid embolism is taken into consideration an unpredictable and unpreventable occasion with an unknown cause. AFE may also arise in healthful women for the duration of labor, at some stage in cesarean section, after abnormal vaginal delivery, or at some stage in the 2^nd trimester of pregnancy. It can also arise as much as forty eight hours postdelivery. It also can arise throughout abortion, after abdominal trauma, during the amnioinfusion. [4] AFE has additionally been said following intrauterine injection of hypertonic saline to set off abortion. [11][12]

Identified risk factors include: Older maternal age, Multiparity, Intense contractions for the duration of labor, Abdominal trauma, Cesarean section, Induction of labor, Previous placenta, Eclampsia, Multiple pregnancy, Tears with inside the uterus or cervix. Early separation of the placenta from the uterus wall. [13][14]

Epidemiology

The occurrence of amniotic fluid embolism (AFE) is expected at 1 case according to 8000 to 30, 000 pregnancies. The actual incidence isn't always recognized because of erroneous analysis and now no longer reporting the nonfatal cases. In Germany, AFE became the main reason of demise at some point of parturition in 2011. [15]AFE is diagnosed because the main direct reason of maternal mortality in Australia from 1 in 8000 to one in 80, 000 deliveries. In the UK, the expected prevalence is 1: 9 consistent with ten thousand to 7. 7 in line with ten thousand births. [16]

PATHOPHYSIOLOGY

The placing for amniotic fluid embolism (AFE) is a disruption of the placenta-amniotic interface with the following access of amniotic fluid and fetal factors (along with hair, meconium, squama, and mucin) into the maternal flow. Portals of access may also consist of the placental attachment, the cervical veins, or uterine surgical incisions. Upon getting into the pulmonary arterial tree, severe pulmonary vasoconstriction takes place. This can be related to concomitant bronchoconstriction. The hemodynamic end result is acute pulmonary arterial obstruction, dilatation of the proper ventricle and the proper atrium, and giant tricuspid regurgitation. The proper ventricular expansion reasons the intraventricular septum to bow into the left ventricle developing obstruction and systolic dysfunction, in addition elevating pulmonary artery strain and reducing cardiac output. Hypoxemia and hypotension cause surprising cardiovascular crumble. Normally, pregnancies are procoagulant, to start with, having elevated degrees of clotting elements X, IX, VIII, von Willebrand element (VWF), and tissue component pathway inhibitor (TFPI). The creation of amniotic fluid and fetal factors cause inflammatory mediators together with platelet-activating element, tissue necrosis aspect-alpha (TNF-alpha), interleukin-six, interleukin-one, phospholipase A2, endothelin, plasminogen activators, thromboplastins, and supplement elements. The coagulation cascade and fibrinolytic structures are for that reason activated. Amniotic fluid withinside the maternal move turns on platelet element III, stimulates platelet aggregation, and turns on clotting element Xa. The superimposed pathologic activation of the coagulation and fibrinolytic pathways create a intense coagulopathy. Disseminated intravascular coagulation (DIC) happens in about 80% of sufferers with AFE. This can be instant on the time of the cardiopulmonary crumble or delayed. Bleeding can be extreme, unrelenting, and fatal. Amniotic fluid and fetal factors also are recognised to infiltrate the uterus, inflicting excessive uterine atony, which in addition exacerbates the hemorrhage. Autopsies on girls succumbing to AFE display pulmonary edema, amniotic issue emboli with inside the lungs, and alveolar hemorrhage. Myocardial infarction, acute renal failure from acute tubular necrosis, and cerebral infarctions also are found. [17][18][19][20][21]

CLINICAL SYMPTOMS

The signs and symptoms are frequently unexpected. The providing signs and symptoms of AFE contain many organ systems. Clark proposed a biphasic version of the hemodynamic effects of AFE. The preliminary reaction is acute pulmonary high blood pressure and vasospasm main to proper ventricular failure, hypoxia, and cardiac arrest. Hankins et al. validated in a goat version that injecting 2. five ml/kg of homologous amniotic fluid IV multiplied proper coronary heart and systemic vascular resistance. They additionally verified that the presence of meconium turned into had to produce left coronary heart failure and hypoxia. The following symptoms and symptoms and signs and symptoms are indicative of viable AFE [8][22][23][24]Acute dyspnea or unexpected, agitation, unexpected chills, shivering, sweating, coughing and tension are not unusual place premonitory signs. Labored respiration and tachypnea can also additionally arise Cough: This is mostly a manifestation of dyspnea. Altered intellectual status. Rapid decline in pulse oximetry values or unexpected absence or lower in end-tidal carbon dioxide can be apparent. Hypotension: Hemodynamic compromise speedy follows those prodromal symptoms and symptoms. Hypotension is the maximum not unusual place providing signal and symptom (100%). Blood stress may also drop extensively with the lack of diastolic measurement. Some researchers postulate that an acute anaphylactoid response can also additionally play a element with inside the improvement of the cardiovascular collapse. Cyanosis: Ventilation-perfusion mismatching due to pulmonary vascular constriction on the onset of AFE might also additionally provide an explanation for surprising hypoxia and respiration arrest. As hypoxia/hypoxemia progresses, circumoral and peripheral cyanosis and adjustments in mucous membranes might also additionally manifest. Fetal bradycardia: In reaction to the hypoxic insult, fetal coronary heart fee might also additionally drop to < a hundred and ten bpm. If this drop lasts for 10 min or extra, it's far a bradycardia. A charge of 60 bpm or much less over 3-five min may also imply a terminal bradycardia. Encephalopathy related to AFE is idea to be secondary to hypoxia and consists of a spectrum of signs starting from altered intellectual kingdom to seizures. Tonic-clonic seizures are visible in 10-50% of sufferers. Uterine atony: Uterine atony typically outcomes in immoderate bleeding after delivery. Acute pulmonary high blood pressure and vasospasm effects in proper ventricular failure, hypoxia, and cardiac arrest. Pulmonary high blood pressure and proper coronary heart strain/failure can be the end result of bodily amniotic fluid particles with inside the pulmonary vasculature end result from circulating pulmonary vasoconstrictive mediators. Proposed factors encompass myocardial failure in reaction to unexpected pulmonary high blood pressure, an immediate myocardial depressant impact of humoral mediators in amniotic fluid, deviation of the intraventricular septum because of proper ventricular dilation, and/or ischemic myocardial harm from hypoxemia. If one survives this preliminary insult, then the pulmonary high blood pressure is normally now no longer sustained and can be changed with left ventricular failure and pulmonary edema. Increased pulmonary artery strain has now no longer been continuously said likely due to the fact this locating can be short-lived. When cardiac pressures are measured early with inside the method, pulmonary and proper ventricular pressures were determined to be elevated. Coagulopathy or excessive hemorrhage: Coagulation issues are a distinguished function of the amniotic fluid syndrome. DIC is found in extra than 83% of sufferers with AFE. The onset can arise as fast as 10-30 min from the onset of signs and symptoms or can be behind schedule through so long as four hours. [25] Whether the coagulopathy is basically a consumptive procedure or because of large fibrinolysis is controversial. Amniotic fluid consists of tissue issue that acts as a procoagulant and might account for the coagulopathy. Tissue thing binds with Factor VII and turns on the extrinsic coagulation pathway. Alternatively, the coagulopathy can be associated with fibrinolysis because of improved stages of plasminogen activation inhibitor 1 in amniotic fluid.

DIAGNOSIS

1. Initial diagnostic assessment have to consist of non-stop pulse oximetry and arterial blood gas (ABG) measurements to decide the diploma of hypoxemia. ABG stages: Expect adjustments constant with hypoxia/hypoxemia. Decreased pH. Decreased PO2. Increased PCO2 degrees. Base extra elevated.

2. Serial whole blood counts and coagulation research have to be despatched to observe tendencies and discover early coagulopathy. CBC with platelets. Hemoglobin and hematocrit ranges must be inside reference ranges. Thrombocytopenia is rare. Prothrombin time (PT) and activated partial thromboplastin time (aPTT). PT is extended due to the fact clotting elements are used up. Values are organization precise, however intervention is indicated while the PT is 1. five instances the manage value. aPTT can be inside reference variety or shortened. If to be had, fibrinogen degree have to be monitored.

3. Blood kind and display in anticipation of the requirement for a transfusion.

4. Chest radiograph posteroanterior and lateral findings are commonly nonspecific. The leader radiographic abnormalities in AFE are diffuse bilateral heterogeneous and homogeneous regions of improved opacity, which can be indistinguishable from acute pulmonary edema.

5. A 12-lead electrocardiogram may also display tachycardia, ST-phase and T-wave adjustments, and findings steady with proper ventricle strain.

6. Lung test may also exhibit a few regions of decreased radioactivity withinside the lung field. [4]

7. Increased serum tryptase, urinary histamine concentrations and appreciably decrease supplement concentrations endorse an anaphylactoid process. Tryptase is a serine protease with a half-lifestyles of numerous hours. Although the precise feature of tryptase in anaphylaxis is unknown, with a half-lifestyles measured in hours in place of the mins of histamine, the protein has tested beneficial withinside the prognosis of anaphylaxis. [13][26][27].

8. Decreased serum ranges of C3 and C4 supplement had sensitivities among 88% and 100% and a specificity of 100%. [12]

9. More research also are had to decide the application of each monoclonal TKH-2 antibodies and zinc coproporphyrin as speedy diagnostic markers[28].

10. Few research have evaluated the diagnostic accuracy of serum sialyl Tn (STN), a fetal antigen found in meconium and amniotic fluid, detected via using TKH-2 monoclonal antibody. TKH-2 reacts with meconium and mucin and stains the lung tissue in people with AFE. For serum stages > 50 U/ml, the sensitivities numerous among 78% and 100% and the specificities among 97% and 99%. Few authors stated a enormous excessive serum degree of STN antigen withinside the AFE instances as excessive as 110. 8 ± 48. 1 U/ml for AFE as opposed to 17. 3 ± 2. 6 U/ml for manage). In few case reviews withinside the literature pronounced that intravascular fetal cloth withinside the uterus may be used to verify a analysis of AFE in conditions wherein AFE is avoided through ligation of uterine artery. [7][12][29][13][24]

11. Bedside transesophageal echocardiography may also resource early analysis through displaying acute pulmonary vasoconstriction, proper ventricular dilation, and a collapsed left ventricle with leftward deviation of the intraventricular septum. [30][31] However, speedy get right of entry to to transesophageal echocardiography might be now no longer to be had in lots of obstetric units.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of amniotic fluid embolism consists of obstetric, nonobstetric, and anesthetic etiologies[7][12].

Anaphylaxis.

Aortic dissection.

Cholesterol embolism.

Myocardial infarction.

Pulmonary embolism.

Septic shock

Air embolism.

Eclamptic convulsions and coma.

Convulsion from the poisonous response to nearby anesthetic drugs.

Aspiration of gastric contents.

Hemorrhagic shock in an obstetric patient.

MANAGEMENT

⇐ Предыдущая 1 234 5 Следующая ⇒