Managing the coagulopathy of postpartum hemorrhage: an evolving role for viscoelastic hemostatic assays.

Postpartum hemorrhage (PPH) is usually caused by obstetrical complications but may be exacerbated by hemostatic impairment. Standard laboratory tests of coagulation often take too long to become available to inform treatment in a rapidly changing clinical situation. The role of point-of-care viscoelastic hemostatic assays (VHAs) in monitoring hemostatic impairment and guiding procoagulant blood product replacement during PPH is evolving, although these technologies are not available in most maternity units. We have used VHAs during PPH in our institution for the last 8 years and have developed a simple algorithm to direct blood component replacement. VHAs are useful for reassuring clinicians that hemostasis is adequate and that procoagulant blood products are not required and an obstetrical cause for bleeding needs to be sought. VHAs can be used to detect hypofibrinogenemia due to dilution or acute obstetrical coagulopathy and to guide fibrinogen replacement. The role of VHAs in guiding fresh frozen plasma infusion is less clear, but normal results suggest that fresh frozen plasma is not required. In this review, we describe 3 cases of postpartum hemorrhage to illustrate different hemostatic scenarios and discuss the controversies and evidence gaps related to each case.

Acute obstetric coagulopathy during postpartum hemorrhage is caused by hyperfibrinolysis and dysfibrinogenemia: an observational cohort study.

BACKGROUND: Postpartum hemorrhage (PPH) may be exacerbated by hemostatic impairment. Information about PPH-associated coagulopathy is limited, often resulting in treatment strategies based on data derived from trauma studies. OBJECTIVES: To investigate hemostatic changes associated with PPH. PATIENTS/METHODS: From a population of 11 279 maternities, 518 (4.6%) women were recruited with PPH ≥ 1000 mL or placental abruption, amniotic fluid embolism, or concealed bleeding. Routine coagulation and viscoelastometric results were collated. Stored plasma samples were used to investigate women with bleeds > 2000 mL or those at increased risk of coagulopathy defined as placenta abruption, amniotic fluid embolism, or need for blood components. Procoagulant factors were assayed and global hemostasis was assessed using thrombin generation. Fibrinolysis was investigated with D-dimer and plasmin/antiplasmin complexes. Dysfibrinogenemia was assessed using the Clauss/antigen ratio. RESULTS: At 1000 mL blood loss, Clauss fibrinogen was ≤2 g/L in 2.4% of women and 6/27 (22.2%) cases of abruption. Women with very large bleeds (>3000 mL) had evidence of a dilutional coagulopathy, although hemostatic impairment was uncommon. A subgroup of 12 women (1.06/1000 maternities) had a distinct coagulopathy characterized by massive fibrinolysis (plasmin/antiplasmin > 40 000 ng/mL), increased D-dimer, hypofibrinogenemia, dysfibrinogenemia, reduced factor V and factor VIII, and increased activated protein C, termed acute obstetric coagulopathy. It was associated with fetal or neonatal death in 50% of cases and increased maternal morbidity. CONCLUSIONS: Clinically significant hemostatic impairment is uncommon during PPH, but a subgroup of women have a distinct and severe coagulopathy characterized by hyperfibrinolysis, low fibrinogen, and dysfibrinogenemia associated with poor fetal outcomes.