Management of GI Bleeding in Cirrhosis with Elevated INR
Vitamin K should NOT be administered to patients with cirrhosis and elevated INR presenting with gastrointestinal bleeding, as it does not improve the INR or reduce bleeding risk in this population. 1
Why Vitamin K is Ineffective in Cirrhotic Coagulopathy
The elevated INR in cirrhosis reflects decreased hepatic synthesis of clotting factors, not vitamin K deficiency. 1 Key evidence demonstrates:
- Subcutaneous vitamin K administration does not modify coagulation parameters in cirrhosis 1
- Oral or subcutaneous vitamin K fails to improve INR in patients with cirrhosis 1
- A retrospective study of 276 hospitalized cirrhotic patients found vitamin K administration had no impact on INR reduction (AOR = 1.17; 95% CI = 0.66-2.08; P = 0.59) or bleeding events (AOR = 4.90; 95% CI = 0.56-43.0; P = 0.15) 2
- A multicenter study of 370 cirrhotic patients with upper GI bleeding showed vitamin K did not reduce 30-day rebleeding rates (16.5% with vitamin K vs 5.5% without) 3
Critical caveat: Intravenous vitamin K can transiently correct INR in cholestatic liver disease only, but this effect does not apply to cirrhosis from other etiologies. 1
Initial Management Algorithm for Variceal Bleeding
Immediate Resuscitation (First 30 Minutes)
- Restrictive transfusion strategy: Transfuse packed red blood cells only when hemoglobin <7 g/dL, maintaining target of 7-9 g/dL 1, 4
- Liberal transfusion (targeting hemoglobin 9-11 g/dL) increases portal pressure, rebleeding, and mortality, particularly in Child-Pugh A and B patients 1, 4
- Start vasoactive drugs immediately (octreotide in the US) before endoscopy 1
- Initiate antibiotic prophylaxis with ceftriaxone 1g IV every 24 hours for maximum 7 days 1
What NOT to Correct
Do NOT attempt to correct the INR with fresh frozen plasma (FFP) or recombinant factor VIIa, as: 1
- Only 14% of cirrhotic patients achieve complete INR correction with FFP 1
- FFP does not modify thrombin generation despite shortening INR 1
- FFP carries significant risks including transfusion-associated circulatory overload and transfusion-related acute lung injury 1
- Randomized trials of recombinant factor VIIa showed no clear benefit 1
- INR is not a reliable indicator of coagulation status or bleeding risk in cirrhosis 1, 5
Endoscopic Management
If hemostasis is achieved with portal hypertension-lowering drugs and endoscopic treatment, correction of hemostatic abnormalities is NOT indicated 1
Only if local measures fail to control hemorrhage should correction of hemostasis be considered on a case-by-case basis 1
Management of Non-Variceal GI Bleeding in Cirrhosis
For bleeding from non-portal hypertensive causes: 1
- First-line: Address bleeding with local measures and/or interventional radiology procedures 1
- Second-line: If local measures fail, address contributing factors (renal failure, infection/sepsis, anemia) 1
- Last resort: Correction of hemostatic abnormalities can be considered case-by-case only after other measures fail 1
Role of Viscoelastic Testing
Thromboelastography (TEG) should be used when available to guide transfusion decisions, as it: 1
- Reduces blood product use without increasing bleeding or mortality 1
- Provides more accurate assessment of hemostatic status than INR or platelet count 6
- In a randomized trial of 96 cirrhotic patients with nonvariceal bleeding, TEG-guided strategy resulted in only 26.5% receiving all three blood components versus 87.2% in standard care (P<0.001), with no difference in bleeding control or mortality 6
Common Pitfalls to Avoid
- Do not assume elevated INR equals bleeding risk: INR and APTT do not predict procedural or spontaneous bleeding in cirrhosis 1
- Do not withhold necessary procedures based on INR alone: Traditional hemostatic tests cannot predict procedural bleeding risk 1
- Do not use tranexamic acid in variceal bleeding: Antifibrinolytic agents should not be used in active variceal bleeding 1
- Do not overtransfuse: Liberal transfusion increases portal pressure and worsens outcomes 1, 4
- Do not assume cirrhotic patients are "auto-anticoagulated": They have rebalanced hemostasis with both pro- and anticoagulant deficiencies 7