Amniotic Fluid Embolism

An amniotic fluid embolism is a clinical syndrome of hypoxia, hypotension and coagulopathy, resulting from the entry of fetal antigens in the maternal circulation.

An amniotic fluid embolism is a rare obstetric emergency and is estimated at 2 to 6 of 100,000 pregnancies. They usually occurs during late pregnancy, but it can also end the first or second trimester of pregnancy occur.

An amniotic fluid embolism is a clinical syndrome of hypoxia, hypotension and coagulopathy, resulting from the entry of fetal antigens in the maternal circulation. An amniotic fluid embolism is a rare obstetric emergency and is estimated at 2 to 6 of 100,000 pregnancies. They usually occurs during late pregnancy, but it can also end the first or second trimester of pregnancy occur. Although estimates vary with respect. Mortality strong (about 20 to 90%), provides the syndrome clearly a significant risk, and of women who die suddenly during childbirth, an amniotic fluid embolism is one of the most likely causes (1). Survival depends on early diagnosis and immediate initiation of treatment. Note 1. Clark SL: amniotic fluid embolism Obstet Gynecol 123: 337-48, 2014. Pathophysiology The long-term amniotic fluid “embolism” means an essentially mechanical, obstructive disorder as occurs in thromboembolism or air embolism. However, since amniotic fluid is completely soluble in blood, it can cause any obstruction. In addition, the amounts of fetal cells and tissue debris that may accompany the amniotic fluid in the maternal circulation, is too small to hinder sufficient mechanical pulmonary vascular tree to cause a marked haemodynamic changes that occurs with this syndrome. Instead, is currently believed that exposure to fetal antigens during childbirth proinflammatory mediators activated trigger an overwhelming inflammatory cascade and release of vasoactive substances (eg. As noradrenaline), similar to the systemic inflammatory response syndrome (SIRS), which in sepsis and septic shock occurs. The inflammatory reaction caused organ damage, particularly to the lungs and the heart and triggers the coagulation cascade, leading to disseminated intravascular coagulation (DIC). The resulting maternal hypoxia and hypotension have deep negative effects on the fetus. As a maternal exposure to fetal antigens is probably pretty common during labor and delivery, it is not clear why only some women develop an amniotic fluid embolism. It is believed that various fetal antigens in variable amounts likely to interact with unknown maternal susceptibility factors. Risk factors Many factors are associated with an increased risk, but evidence is inconsistent. As with exposure to fetal antigens many risk factors are common, or at least much more likely than an amniotic fluid embolism, and there is no good pathophysiological knowledge about why only some women develop risk factors the syndrome. Nevertheless, the risk is generally appears to be increased by the following: cesarean section Advanced mother multiple pregnancy age Premature separation of placenta abdominal trauma placenta previa uterine cervical lacerations forceps delivery Polyhydramnios induction of labor symptoms and complaints An amniotic fluid embolism manifested usually during and shortly after labor and delivery. The first sign may be a sudden cardiac arrest. Other patients suddenly develop dyspnea and have tachycardia, tachypnea and hypotension. Respiratory arrest, with significant cyanosis, hypoxia and Lungenknistern often follows quickly. Coagulopathy manifests as bleeding from the uterus and / or sites of incisions and venous puncture. Uterine hHoperfusion caused uterine and fetal distress. Diagnosis Clinical Investigation exclusion of other causes, the diagnosis of amniotic fluid embolism is suspected when the classic triad developed during labor or immediately after childbirth: Sudden hypoxia hypotension coagulopathy The diagnosis is made clinically and by excluding other following causes: Sudden cardiac death in young women (z. B. coronary artery dissection, congenital heart disease) Acute respiratory insufficiency (pulmonary embolism, pneumonia) coagulopathy (eg sepsis, postpartum hemorrhage, uterine) at autopsy can be found fetal squamous cells and hair in the pulmonary circulation, but these findings do not confirm the Diagnosis. Fetal cells are sometimes found in patients who do not have the amniotic fluid embolism syndrome. Therapy Supportive treatment Treatment of amniotic fluid embolism is supportive. It involves the transfusion of red blood cells (as required to compensate for the blood loss) and fresh frozen plasma and clotting factors (as needed for reversing the coagulopathy) plus. Ventilation and circulatory support with inotropic drugs as needed. The recombinant factor VIIa should not be used routinely, but may be prescribed for women who continue to bleed heavily, even though they use other coagulation factors. An immediate surgical delivery does not appear to improve the outcome in mothers or deteriorate, but may be critical for fetal survival. Key points A amniotic fluid embolism occurs usually during labor and delivery and leads to a triad of hypoxia, hypotension and coagulopathy. The fault is not a mechanical embolic phenomenon, but is probably a biochemical reaction in which exposure to fetal antigens an overwhelming inflammatory response in the mother triggers the mortality is high, and patients need immediate aggressive respiratory and hemodynamic support and the replacement of coagulation factors , Immediate delivery is necessary for fetal survival, but does not seem to improve maternal Constitution or deteriorate.

Health Life Media Team

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