International journal of obstetric anesthesia · 2026
Hyperfibrinolysis and reduced functional fibrinogen in haemorrhagic caesarean delivery: a secondary analysis of the TRACES trial evaluating fibrinogen kinetics following fibrinogen concentrate or plasma infusion.
СтатьяРандомизированное исследованиеМногоцентровое исследованиеНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hureau Maxence, Lanoiselée Julien, Ollier Edouard, Abraham Emilien, Denys Bérangère, Bouthors Anne-Sophie
Аннотация
INTRODUCTION: Postpartum haemorrhage-induced coagulopathy is marked by early fibrinogen depletion and, in acute obstetric coagulopathy, by hyperfibrinolysis and fibrinogenolysis. It remains unclear that exogenous fibrinogen concentrate is similarly susceptible to plasmin-mediated degradation. This secondary analysis of the TRACES trial assessed fibrinogen restoration kinetics after fibrinogen concentrate administration during postpartum hemorrhage.
METHODS: The TRACES trial was a multicentre, randomised, double-blind, placebo-controlled study investigating tranexamic acid dosing in haemorrhagic caesarean delivery. For this analysis, only patients receiving fibrinogen concentrate were included. All laboratory and clinical data were re-timestamped relative to the first fibrinogen concentrate administration. Hyperfibrinolysis (HF) was defined by fibrinogen < 300 mg/dL, D-dimer ≥ 50,000 ng/mL and plasmin-antiplasmin complexes ≥ 2,000 ng/mL at any time point. Fibrinogen restoration trajectories were compared between cases with HF and No HF.
RESULTS: Among 151 patients, 34 received fibrinogen concentrate. Five met HF criteria. Despite receiving higher fibrinogen concentrate doses, HF patients showed significantly impaired fibrinogen restoration (p < 0.01), with an initial rise followed by early decline. HF status was also associated with increased blood loss during postpartum hemorrhage.
DISCUSSION: These exploratory findings support the hypothesis that exogenous fibrinogen may undergo plasmin-mediated cleavage in acute obstetric coagulopathy, leading to restoration failure and highlight the hypothesis of fibrinogenolysis.
CONCLUSION: Hyperfibrinolysis markedly impairs fibrinogen concentrate-mediated fibrinogen restoration during postpartum haemorrhage. Dedicated pharmacokinetic-pharmacodynamic studies are needed to optimise fibrinogen supplementation and hemostatic strategies.
METHODS: The TRACES trial was a multicentre, randomised, double-blind, placebo-controlled study investigating tranexamic acid dosing in haemorrhagic caesarean delivery. For this analysis, only patients receiving fibrinogen concentrate were included. All laboratory and clinical data were re-timestamped relative to the first fibrinogen concentrate administration. Hyperfibrinolysis (HF) was defined by fibrinogen < 300 mg/dL, D-dimer ≥ 50,000 ng/mL and plasmin-antiplasmin complexes ≥ 2,000 ng/mL at any time point. Fibrinogen restoration trajectories were compared between cases with HF and No HF.
RESULTS: Among 151 patients, 34 received fibrinogen concentrate. Five met HF criteria. Despite receiving higher fibrinogen concentrate doses, HF patients showed significantly impaired fibrinogen restoration (p < 0.01), with an initial rise followed by early decline. HF status was also associated with increased blood loss during postpartum hemorrhage.
DISCUSSION: These exploratory findings support the hypothesis that exogenous fibrinogen may undergo plasmin-mediated cleavage in acute obstetric coagulopathy, leading to restoration failure and highlight the hypothesis of fibrinogenolysis.
CONCLUSION: Hyperfibrinolysis markedly impairs fibrinogen concentrate-mediated fibrinogen restoration during postpartum haemorrhage. Dedicated pharmacokinetic-pharmacodynamic studies are needed to optimise fibrinogen supplementation and hemostatic strategies.