In most women with fetal death, spontaneous labor eventually ensues, most often within 2 weeks; however, the psychological stress imposed by carrying a dead fetus usually prompts induction of labor at the time of discovery that the fetus is dead. This also obviates the dangers of coagulation defects that may subsequently develop. Undoubtedly, the advent of more effective methods of labor induction (see Chapter 22) has enhanced the desirability of early delivery.
A potentially ominous complication of delayed delivery following fetal death is the development of gross disruption of the maternal coagulation mechanism. Such disruption rarely develops less than 1 month after fetal death. However, if the fetus is retained longer, about 25 percent of women develop coagulopathy. The consumptive coagulopathy is presumably mediated by thromboplastin from the dead products of conception entering into the maternal circulation.
Consideration should also be given to the cause of the fetal demise. In the setting of antecedent trauma or other history concerning for abruption, the risk of maternal coagulopathy at the time of diagnosis is very high, and assessment of coagulation studies is mandatory.
Typically the fibrinogen concentration falls to levels that are normal for the nonpregnant state, and in some cases it falls to potentially dangerous concentrations of 100 mg/dL or less. The rate of decrease commonly found is demonstrated in Figure 31-1. Simultaneously, fibrin degradation products are elevated in serum. The platelet count tends to decrease in these instances, but severe thrombocytopenia is uncommon even if the fibrinogen level is quite low. Although coagulation defects may correct spontaneously before evacuation, this is unusual and happens quite slowly.
FIGURE 31-1 Slow development of maternal hypofibrinogenemia following fetal death and delayed delivery. (From Pritchard JA: Fetal death in utero. Obstet Gynecol 14:573, 1959, with permission.)
Correction of coagulation defects has been accomplished using low doses of heparin—5000 U two to three times daily—under carefully controlled conditions in women with an intact circulation. Heparin appropriately administered can block further pathological consumption of fibrinogen and other clotting factors, thereby slowing or temporarily reversing the cycle of consumption and fibrinolysis. Such correction should be undertaken only if the patient is not actively bleeding and with simultaneous steps to effect delivery after correction of the patient’s coagulation status.
FETAL DEATH IN MULTIFETAL PREGNANCY
Demise of a single twin after 20 weeks of gestation occurs in approximately 5 percent of twin pregnancies. It is uncommon that an obvious coagulation derangement develops in multifetal pregnancy complicated by death of at least one fetus and survival of another. Those cases that do develop a coagulopathy tend to occur in monochorionic gestations with vascular anastomoses. The surviving twin has an extremely high risk of cerebral palsy and other neurological impairment in these cases due to rapid changes in fetal hemodynamics. These changes occur at the time of cotwin demise, and pursuing delivery thereafter does not mitigate the potential impairment.
For further reading in Williams Obstetrics, 23rd ed.,
see Chapter 35, “Obstetrical Hemorrhage” and 39, “Multifetal Gestation.”