FFP in Decompensated Chronic Liver Disease: Why It's Given (And Why It Shouldn't Be)
FFP is commonly given in decompensated chronic liver disease with portal hypertension and ascites based on the outdated assumption that elevated INR reflects bleeding risk—but current evidence demonstrates this practice is ineffective, potentially harmful, and should be avoided except in cases of active major bleeding. 1, 2
The Flawed Rationale Behind FFP Use
The traditional justification for FFP administration stems from a fundamental misunderstanding of coagulation in liver disease:
The INR was designed to monitor warfarin therapy, not assess bleeding risk in cirrhosis, and only measures select procoagulant factors (fibrinogen, factors II, V, VII, X) while ignoring anticoagulant proteins that are also reduced in liver disease 1, 3
Patients with cirrhosis have a "rebalanced" hemostatic system where simultaneous reductions in both pro- and anticoagulant factors result in normal or even prothrombotic states, despite abnormal conventional coagulation tests 1, 4
94% of patients with cirrhosis have normal or elevated thrombin generation capacity even when INR is prolonged, indicating preserved hemostatic function 5
Why FFP Doesn't Work
Multiple lines of evidence demonstrate FFP's ineffectiveness in cirrhosis:
FFP fails to normalize INR in most patients: Only 10-12.5% of cirrhotic patients achieve INR correction to <1.5 after standard FFP doses (2-4 units), because FFP contains both pro- and anticoagulant proteins in balanced proportions 1, 6
FFP minimally improves thrombin generation: Studies show only 5.7% median improvement in thrombin generation after FFP transfusion, and paradoxically worsens hemostatic capacity in 34% of patients 5, 7
No evidence of bleeding prevention: A Cochrane review found zero studies demonstrating that prophylactic FFP prevents bleeding during procedures in cirrhotic patients 1, 2, 3
Preprocedural FFP/platelet transfusion does not reduce hemorrhagic complication rates even when procedures are performed, as bleeding in liver disease relates more to portal hypertension and technical factors than coagulation defects 1
Significant Harms of FFP in Liver Disease
FFP transfusion carries potentially life-threatening risks that are particularly problematic in patients with portal hypertension and ascites:
Increased portal pressure from volume expansion (250-300 mL per unit) paradoxically increases bleeding risk in patients with varices and portal hypertension 1, 2, 3
Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related mortality 1, 2, 3
Transfusion-associated circulatory overload (TACO) occurs in up to 8% of transfusions with 5-15% mortality rate—especially dangerous in patients with ascites and compromised cardiovascular reserve 1, 2, 3
Infection transmission, allergic reactions (1:591 to 1:2,184 units), hemolytic reactions, and alloimmunization add further risk without demonstrated benefit 1, 2
When FFP IS Indicated in Liver Disease
The only evidence-supported indication for FFP in decompensated cirrhosis is active major bleeding:
Active major hemorrhage: FFP should be administered in balanced ratios with red blood cells (typically 1:1 or 1:1.5 ratio) until coagulation test results are available 2
Disseminated intravascular coagulation (DIC) with active bleeding or high bleeding risk, which represents a distinct pathophysiologic state from stable cirrhosis 1, 2
Therapeutic dose when genuinely indicated is 15 mL/kg (approximately 1,050 mL or 3-4 units for a 70 kg patient), not the 2-4 units commonly given 2, 8
Evidence-Based Alternatives
For procedures in patients with decompensated cirrhosis:
No routine correction is needed for most procedures including paracentesis, thoracentesis, and variceal ligation, even with elevated INR and thrombocytopenia 1
Viscoelastic testing (TEG/ROTEM) can guide management and has been shown to reduce blood product use from 100% to 17% without increasing bleeding complications 1, 3
For documented hypofibrinogenemia (<120 mg/dL), use cryoprecipitate or fibrinogen concentrate rather than FFP, as these are more effective and avoid volume overload 1, 2, 7
Prothrombin complex concentrates (PCCs) may be more effective at correcting PT/INR than FFP, though evidence in liver disease is limited and thrombotic risk exists 1, 3, 9
Critical Clinical Pitfalls to Avoid
Do not use INR alone to guide transfusion decisions in liver disease—it does not reflect true hemostatic balance and correlates poorly with bleeding risk 1, 3
Do not give prophylactic FFP simply because laboratory values are abnormal without active bleeding, as this increases harm without reducing bleeding risk 1, 2
Recognize that portal hypertension and technical factors predict bleeding better than coagulation tests in cirrhotic patients undergoing procedures 1
The large volume of FFP required (often >1,000 mL) to reach arbitrary INR targets makes this approach particularly dangerous in patients with ascites and compromised cardiovascular status 1, 2