Recurrent miscarriage syndrome (RMS) is characterized by recurrent spontaneous abortion. RMS is generally defined when a woman suffers one miscarriage and has a first order genetic relative with a miscarriage (mother or sister) or suffers two unexplained miscarriages.

There are many causes of RMS, including anatomical anomalies (about 10% of unexplained miscarriages), endocrine or hormonal abnormalities (about 15% of unexplained miscarriages), genetic / chromosomal abnormalities (about 10% of RMS and blood coagulation protein / platelet defects, which account for 50% - 60% of recurrent miscarriages. Many of these are treatable, leading to normal term pregnancy, if the clinician is astute and vigorously pursues a thorough evaluation of why the patient has suffered unexplained, spontaneous miscarriages.

There is not uniform agreement on how many spontaneous unexplained miscarriages constitute FWS; we generally pursue an evaluation for causation if a women has had two or more such events, or one event with a positive family history for unexplained miscarriage.

The coagulation protein and platelet defects associated with fetal wastage include Factor XIII and Factor XII defects, dysfibrinogenemia, antiphospholipid syndrome including both anticardiolipin antibodies (ACLA) and lupus anticoagulant (LA), plasminogen defects, other fibrinolytic system defects such as elevated plasminogen activator inhibitor, Type 1 (PAI-1) or low tissue plasminogen activator (t-PA), congenital protein S defects, Prothrombin 20210A and Sticky Platelet Syndrome.

Bleeding defects (rare) lead to inadequate fibrin-induced implantation of the fertilized ovum into the decidua. However thrombotic defects (extremely common), including antiphospholipid syndrome, plasminogen defects, fibrinolytic system defects, some cases of dysfibrinogenemia, Sticky Platelet Syndrome and other hypercoagulable blood protein/platelet defects leading to accelerated clotting are associated with thrombosis of the early placental blood vessels, precluding viability of the implanted ovum or fetus.

The diagnosis of fetal wastage syndrome due to blood coagulation protein/platelet defects is made by noting two or more unexplained spontaneous abortions, usually in the first trimester and a high index of suspicion, followed by appropriate clinical and laboratory evaluation. We have reported our experience, including prevalence and management, in women with fetal wastage syndrome due to blood protein/platelet defects.

Treatment Program:

All patients found to have a blood protein/platelet defect associated with fetal wastage syndrome via hypercoagulability and thrombosis (thrombosis/vasculitis) of placental vessels are treated with appropriate antithrombotic therapy and followed very carefully. Our success rate for normal term delivery, using the antithrombotic program designed at the Center, is currently greater than 98%.

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