An amniotic fluid embolism (AFE) is a very uncommon childbirth (obstetric) emergency in which amniotic fluid enters the blood stream of the mother, triggering a serious reaction, which results in cardiorespiratory (heart and lung) collapse and massive bleeding (coagulopathy). The rate at which it occurs is 1 instance per 20,000 births and it comprises 10% of all maternal deaths. This condition is unpredictable and no risk factors have been verified. Signs and symptoms
Amniotic fluid embolism is suspected when a woman giving birth experiences very sudden insufficient oxygen to body tissues, low blood pressure, and profuse bleeding due to defects in blood coagulation. Though symptoms and signs can be profound, they also can be entirely absent. There is much variation in how each instance progresses. Causes
AFE is very rare and complex. The disorder occurs during the last stages of labor when amniotic fluid enters the circulatory system of the mother via tears in the placental membrane or uterine vein rupture. Upon later analysis, fetal cells are found in the maternal circulation. When the fetal cells and amniotic fluid enter the bloodstream, reactions occur that cause severe changes in the mechanisms that affect blood clotting. Disseminated intravascular coagulation occurs and results in serious bleeding. The condition can also develop after elective abortion, amniocentesis, cesarean delivery, or trauma. Small lacerations in the lower reproductive tract are associated with AFE.According to one study, induction of labor may double the risk of AFE. However, other studies have refuted this claim.
Chromosomal translocation and extra chromosomes help create abnormally high activity of certain proto-oncogenes, which caused by these genetic abnormalities and include those encoding c-myc, HRAS, and vav. The activity of proto-oncogenes is not the only cellular function that is affected; tumour suppressor genes are affected by the chromosomal changes induced by mycoplasma, as well. Partial or complete loss of chromosomes causes the loss of important genes involved in the regulation of cell proliferation. Two genes whose activities are markedly decreased during chronic infections with mycoplasma are the Rb and the p53 tumour suppressor genes. Another possible mechanism of carcinogenesis is RAC1 activation by a small GTPase-like protein fragment of Mycoplasma. A major feature that differentiates mycoplasmas from other carcinogenic pathogens is that the mycoplasmas do not cause the cellular changes by insertion of their own genetic material into the host cell. The exact mechanism by which the bacterium causes the changes is not yet known. Partial reversibility of malignant transformationsThe malignant transformation induced by Mycoplasma species is also different from that caused by other pathogens in that the process is reversible. The state of reversal is, however, only possible up to a certain point during the infection. The window of time when reversibility is possible varies greatly; it depends primarily on the Mycoplasma involved. In the case of M. fermentans, the transformation is reversible until around week 11 of infection and starts to become irreversible between weeks 11 and 18. If the bacteria are killed using antibiotics (i.e.