Why bleeding happens
Blood thinners reduce clot formation. This helps prevent stroke (e.g., atrial fibrillation) and treat/prevent clots (DVT/PE). The trade-off is higher risk of bleeding—especially from the GI tract, urinary tract, and after trauma.
Key concept: “Bleeding risk” is not one thing—dose, kidney function, interacting drugs, and recent procedures all matter.
Highest-risk situations
- Prior major bleed (GI bleed, intracranial hemorrhage)
- Recent surgery or invasive procedure
- History of falls or head injury risk
- Kidney impairment (many DOACs are partly renally cleared)
- Liver disease, alcohol misuse
- Concomitant antiplatelets/NSAIDs
- Uncontrolled hypertension
Warfarin vs DOACs (practical differences)
Warfarin (vitamin K antagonist)
- Requires INR monitoring; many food/drug interactions
- Bleeding risk rises with supratherapeutic INR
- Reversal often includes vitamin K + PCC in emergencies
DOACs (apixaban, rivaroxaban, dabigatran, edoxaban)
- No routine INR monitoring; fewer food interactions
- Still significant drug interactions (CYP3A4/P-gp)
- Specific reversal agents exist for some (see below)
Reversal agents (overview): Dabigatran → idarucizumab. Factor Xa inhibitors (apixaban/rivaroxaban/edoxaban) → andexanet alfa in selected settings; clinicians may use PCC depending on scenario and local protocols.
Bleeding risk scores (used by clinicians)
Clinicians may use scoring systems (e.g., HAS-BLED) to identify modifiable risks and guide closer follow-up. A “high score” usually means: treat blood pressure, avoid interacting drugs, reduce alcohol, manage anemia/ulcers—rather than automatically stopping anticoagulation.
If you want a patient-friendly overview: focus on modifiable risks and warning signs rather than the numeric score.