Which condition is associated with an increased risk for DIC in pregnancy, as noted in fetal-mortality complications?

Study for the NCLEX Pregnancy at Risk Test. Use flashcards and multiple choice questions with hints and explanations to prepare. Get ready to excel on your exam!

Multiple Choice

Which condition is associated with an increased risk for DIC in pregnancy, as noted in fetal-mortality complications?

Explanation:
Disseminated intravascular coagulation in pregnancy is most commonly prompted by exposure to tissue thromboplastin from nonviable fetal tissue. When a fetus dies and is retained in utero (dead fetus syndrome), thromboplastic material is released into the maternal circulation, triggering widespread activation of the coagulation cascade. This leads to consumption of platelets and clotting factors, causing both clot formation and a tendency to severe bleeding as the system becomes exhausted. That scenario—a second pregnancy with a dead fetus—creates a strong risk for DIC because the ongoing release of thromboplastic material sustains the coagulopathy. In contrast, mild preeclampsia without severe features does not typically provoke DIC; a large infant delivered recently isn’t a classic trigger; and a moderate blood loss after delivery without additional complications doesn’t reliably initiate DIC. The key concept is that the dead fetus in utero provides a continuous source of tissue thromboplastin, driving DIC unless the source is removed and the coagulation system is supported.

Disseminated intravascular coagulation in pregnancy is most commonly prompted by exposure to tissue thromboplastin from nonviable fetal tissue. When a fetus dies and is retained in utero (dead fetus syndrome), thromboplastic material is released into the maternal circulation, triggering widespread activation of the coagulation cascade. This leads to consumption of platelets and clotting factors, causing both clot formation and a tendency to severe bleeding as the system becomes exhausted. That scenario—a second pregnancy with a dead fetus—creates a strong risk for DIC because the ongoing release of thromboplastic material sustains the coagulopathy.

In contrast, mild preeclampsia without severe features does not typically provoke DIC; a large infant delivered recently isn’t a classic trigger; and a moderate blood loss after delivery without additional complications doesn’t reliably initiate DIC. The key concept is that the dead fetus in utero provides a continuous source of tissue thromboplastin, driving DIC unless the source is removed and the coagulation system is supported.

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