A 24-year-old woman, gravida 1 para 0, at 28 weeks gestation comes to the labor and delivery unit due to intense abdominal pain, vaginal bleeding, and absent fetal movement. Temperature is 36.7 C (98.1 F), blood pressure is 170/96 mm Hg, pulse is 108/min, and respirations are 22/min. Pulse oximetry shows 98% on room air. Physical examination shows a tense abdomen and a firm, tender uterus. Ultrasound shows a hematoma between the placenta and the uterine wall and no fetal cardiac activity. Laboratory results are as follows:
| Hemoglobin | 9.2 g/dL |
| Platelets | 60,000/mm3 |
| Aspartate aminotransferase (SGOT) | 12 U/L |
| Alanine aminotransferase (SGPT) | 24 U/L |
The patient is hospitalized for further management. Once hospitalized, she begins to experience bleeding from her gums and intravenous catheter sites. Blood is also noted in the urinary catheter. Vital signs are unchanged, and she reports no shortness of breath. Which of the following is the most likely underlying cause of this patient's hospital symptoms?
Show Explanatory Sources
This pregnant patient with new bleeding from the gums and catheter sites likely has disseminated intravascular coagulation (DIC), a life-threatening complication that can occur with postpartum hemorrhage, abruptio placentae, or amniotic fluid embolism. This patient has DIC due to abruptio placentae (ie, placental bleeding between the uterine wall and placenta), which results in premature placental separation, fetal hypoxia, and in severe cases, fetal demise. Patients with abruptio placentae typically have vaginal bleeding, uterine rigidity and/or tenderness, and contractions. Maternal hypertension (eg, preeclampsia) and tobacco use are risk factors.
Severe placental abruption (eg, retroplacental hematoma) causes decidual damage and ischemia, thereby triggering tissue factor release into the maternal circulation. Tissue factor, a procoagulant, then activates the extrinsic pathway of the coagulation cascade to cause excessive thrombin generation with formation of circulating platelet-fibrin microthrombi. As clotting factors and platelets are rapidly consumed, a consumptive coagulopathy (eg, thrombocytopenia, prolonged PT & aPTT) develops that results in profound bleeding, classically from mucosal surfaces and intravenous line sites.
(Choice A) Amniotic fluid embolism (AFE) introduces fetal antigens and tissue factor from the amniotic fluid into the maternal circulation, triggering a massive immune response and increased release of procoagulant factors that can lead to DIC. However, AFE typically causes maternal circulatory collapse with severe hypotension, making this diagnosis less likely in this patient.
(Choice B) An ascending polymicrobial infection of the endometrial lining (eg, postpartum endometritis) can cause uterine tenderness, vaginal bleeding, and sepsis, thereby precipitating DIC. However, patients typically also have fever and hypotension.
(Choice D) Acute fatty liver of pregnancy, characterized by microvesicular fatty infiltration of hepatocytes, can impair maternal hepatic function, reducing production of clotting factors and impairing clearance of fibrin degradation products, which may result in DIC. However, patients typically have elevated liver transaminases.
(Choice E) Complete uterine rupture through the endometrium, myometrium, and serosa can cause vaginal bleeding, abdominal pain, and fetal compromise. However, patients usually have had a prior uterine surgery and present with palpable fetal parts protruding through the disrupted uterine wall rather than a firm, tense uterus.
Educational objective:
Disseminated intravascular coagulation (DIC) can occur with abruptio placentae due to release of tissue factor, a procoagulant that activates the coagulation cascade, from the damaged decidua into the maternal circulation. DIC classically presents with thrombocytopenia and bleeding from mucosal surfaces (eg, gums) and intravenous line sites.