Thrombotic microangiopathy (TMA) is a pathology that results in thrombosis in capillaries and arterioles, due to an endothelial injury. It may be seen in association with thrombocytopenia, anemia, purpura and kidney failure. The classic TMAs are hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. Other conditions with TMA include atypical hemolytic uremic syndrome, disseminated intravascular coagulation, scleroderma renal crisis, malignant hypertension,
antiphospholipid antibody syndrome, and drug toxicities, e.g. calcineurin inhibitor toxicity. Signs and symptoms
The clinical presentation of TMA, although dependent on the type, typically includes: fever, microangiopathic hemolytic anemia (see schistocytes in a blood smear), kidney failure, thrombocytopenia and neurological manifestations. Generally, renal complications are particularly predominant with Shiga-toxin-associated hemolytic uremic syndrome (STx-HUS) and atypical HUS, whereas neurologic complications are more likely with TTP. Individuals with milder forms of TTP may have recurrent symptomatic episodes, including seizures and vision loss. With more threatening cases of TMA, and also as the condition progresses without treatment, multi-organ failure or injury is also possible, as the hyaline thrombi can spread to and affect the brain, kidneys, heart, liver, and other major organs. Cause
The specific cause is dependent of the type of TMA that is presented, but the two main pathways that lead to TMA are external triggers of vascular injury, such as viruses, bacterial Shiga toxins or endotoxins, antibodies, and drugs; and congenital predisposing conditions, including decreased levels of tissue factors necessary for the coagulation cascade.
This can lead to death of the baby or other complications. Historically, the rate of fetal death in the setting of cord prolapse has been as high 40%. However, these estimates occurred in the context of home or births outside of the hospital. When considering cord prolapses that have occurred in inpatient labor and delivery settings, the rate drops to as low as 0-3%, though the mortality rate remains higher than for babies without cord prolapse. The reduction in mortality for hospital births is likely due to the ready availability of immediate cesarean section. Many other fetal outcomes have been studied, including Apgar score (a quick assessment of a newborns health status) at 5 minutes and length of hospitalization after delivery. While both measures are worse for newborns delivered after cord prolapse, it is unclear what effect this has in the long-term. Relatively large studies that have tried to quantify long-term effects of cord prolapse on children found that less than 1% (1 in 120 studied) had a major neurologic disability, and less than 1% (110 in 16,675) had diagnosed cerebral palsy. Epidemiology
Rates of umbilical cord prolapse ranges from 0.1 to 0.6% of all pregnancies. This rate has remained stable over time. A recent study estimates 77% of cord prolapses occur in singleton pregnancies (where there is only one baby). In twin pregnancies, cord prolapses occur more frequently in the second twin to be delivered, with 9% in the first twin and 14% in the second twin. References


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