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

Lucy de Lloyd, Peter V Jenkins, Sarah F Bell, Nicola J Mutch, Julia Freyer Martins Pereira, Pilar M Badenes, Donna James, Anouk Ridgeway, Leon Cohen, Thomas Roberts, Victoria Field, Rachel E Collis, Peter W Collins* (Corresponding Author)

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)862-879
Number of pages18
JournalJournal of Thrombosis and Haemostasis
Issue number4
Early online date22 Dec 2022
Publication statusPublished - 1 Apr 2023

Bibliographical note

Funding information The study was funded by grants from The National Institute of Academic Anaesthesia, the Obstetric Anaesthetists' Association, and the Haemonectics Corporation. None of the grant-giving bodies played any role in study design, data collection, interpretation of results, or decision to publish. The study received support from Health Care Research Wales and Cardiff and Vale University Health Board Research and Development office. Health Care Research Wales NHS Research Time Award (2016–2019) and Sir Geraint Evans Cardiovascular Research Fund Award (2019) (P.V.J.).


  • coagulopathy
  • dysfibrinogenemia
  • fibrinogen
  • fibrinolysis
  • postpartum hemorrhage


Dive into the research topics of 'Acute obstetric coagulopathy during postpartum hemorrhage is caused by hyperfibrinolysis and dysfibrinogenemia: an observational cohort study'. Together they form a unique fingerprint.

Cite this