Related Experiment Video
Updated: Mar 6, 2026
11:59
In Vivo Real-Time Study of Drug Effects on Carotid Blood Flow in the Ovine Fetus
Published on: April 28, 2023
669
Using antifibrinolytics in the peripartum period - concern for a hypercoagulable effect?
H K Ahmadzia1, E L Lockhart2, S M Thomas3
1Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, Duke University, Durham, NC, USA.
Journal of Neonatal-Perinatal Medicine
|March 18, 2017
Summary
Antifibrinolytic agents like tranexamic acid do not appear to increase clotting in healthy or obese pregnant women. Further research is needed to confirm the safety of these agents in preeclamptic pregnancies.
Area of Science:
- Obstetrics and Gynecology
- Hematology
- Pharmacology
Background:
- Antifibrinolytic agents are used to manage hemorrhage.
- Concerns exist regarding their potential to increase peripartum venous thromboembolism risk.
Purpose of the Study:
- To investigate the in vitro impact of tranexamic acid and ɛ-aminocaproic acid on clotting properties during pregnancy.
Main Methods:
- Rotation thromboelastometry was used to measure maximum clot firmness (MCF) and clotting time (CT).
- Blood samples from healthy pregnant, obese pregnant, preeclamptic pregnant, and non-pregnant women were analyzed with varying concentrations of antifibrinolytics.
Main Results:
- Healthy pregnant women exhibited significantly higher MCF compared to non-pregnant controls.
- In vitro addition of tranexamic acid or ɛ-aminocaproic acid did not significantly alter MCF or CT in healthy pregnant, obese pregnant, or non-pregnant women.
- Preeclamptic women showed increased MCF with antifibrinolytic agents compared to baseline.
Conclusions:
- Pregnancy is characterized by a hypercoagulable state.
- In vitro, antifibrinolytic therapy does not seem to exacerbate clotting in most pregnant populations.
- The safety of antifibrinolytics in preeclampsia warrants additional investigation.
Related Concept Videos
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
2.2K
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
2.2K
01:29Venous Thrombosis III: Interprofessional Care
428
Venous thrombosis requires effective prevention and treatment strategies to improve patient outcomes and reduce potential complications.Prevention StrategiesHealthcare providers must prioritize preventing venous thromboembolism (VTE) for all adult patients upon admission. Interventions depend on bleeding and thrombosis risk, medical history, current medications, diagnoses, planned procedures, and patient preferences. Patients on bed rest should change positions every two hours and, if not...
428
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
2.6K
Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
2.6K
01:20Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
1.4K
Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
1.4K
01:16Clot Retraction and Fibrinolysis
9.7K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
9.7K
01:20Extrinsic and Intrinsic Pathways of Hemostasis
14.3K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
14.3K