doctors who specialize in amniotic fluid embolism

There must be a pressure gradient that favors transfer of fluid from the uterus into the systemic circulation. The first historic idea is that a disorderly labor, abnormal placentation, surgical trauma, or any other breach of the barrier between maternal blood and amniotic fluid forces the entry of amniotic fluid into the systemic circulation and results in a physical obstruction of the pulmonary circulation. There are two theories regarding the pathogenesis of AFE. In 1995, Clarke suggested that the syndrome arose from an immune rather than the embolic process. Urinary histamine has also been used to diagnose anaphylaxis as a small percentage of histamine is excreted into the urine, unmetabolized. Tryptase is released by mast cells along with histamine when they degranulate in response to IgE cross-linking on the cell surface in the presence of antigen.

Benson suggested that this hypothesis can be established by testing women acutely ill with AFE for serum tryptase. Attwood in 1956 suggested anaphylaxis as a mechanism of AFE. The pathophysiology of AFE is not completely understood but various theories have been published. In some women, AFE may lead to a mild degree of organ dysfunction while in others it may lead to coagulopathy, cardiovascular collapse, and death. The process is similar to anaphylaxis than to embolism, so also termed as anaphylactoid syndrome of pregnancy because fetal tissue or amniotic fluid components are not universally found in women who present with signs and symptoms attributable to AFE. Recent evidence suggests that the occurrence of AFE is not a consequence of the “simple” mechanical respiratory obstruction, but a humoral effect causing anaphylactoid reactions or complement activation. However, the condition is exceedingly rare, and the exact pathophysiology is still unknown. It was first reported by Meyer in 1926, and the syndrome was first described by Steiner and Lushbaugh in 1941. The maternal prognosis after amniotic fluid embolism is very poor though infant survival rate is around 70%.Īmniotic fluid embolism (AFE) is one of the most catastrophic complications of pregnancy in which it is postulated that amniotic fluid, fetal cells, hair, or other debris enters the maternal pulmonary circulation, causing cardiovascular collapse. Treatment is mainly supportive, but exchange transfusion, extracorporeal membrane oxygenation, and uterine artery embolization have been tried from time to time. 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. Clinical signs and symptoms are acute dyspnea, cough, hypotension, cyanosis, fetal bradycardia, encephalopathy, acute pulmonary hypertension, coagulopathy etc. The presenting signs and symptoms of AFE involve many organ systems. Possible historical cause is that any breach of the barrier between maternal blood and amniotic fluid forces the entry of amniotic fluid into the systemic circulation and results in a physical obstruction of the pulmonary circulation. The pathophysiology of AFE is not completely understood. It can also occur during abortion, after abdominal trauma, and during amnio-infusion. It may also occur up to 48 hours post-delivery. Etiology largely remains unknown, but may occur in healthy women during labour, during cesarean section, after abnormal vaginal delivery, or during the second trimester of pregnancy. Amniotic fluid embolism (AFE) is one of the catastrophic complications of pregnancy in which amniotic fluid, fetal cells, hair, or other debris enters into the maternal pulmonary circulation, causing cardiovascular collapse.

Doctors who specialize in amniotic fluid embolism