Most Likely Cause of Prolonged PT with Normal aPTT in Cirrhosis
The prolonged PT in this patient is most likely due to chronic liver disease (cirrhosis) causing decreased hepatic synthesis of vitamin K-dependent clotting factors, though this laboratory abnormality does not predict bleeding risk and should not be routinely corrected. 1
Understanding the Laboratory Pattern
Why PT is Prolonged but aPTT is Normal
Cirrhosis causes decreased synthesis of all liver-derived coagulation factors, but the PT (which measures factors II, V, VII, and X) becomes abnormal earlier than aPTT because factor VII has the shortest half-life (4-6 hours) and is most sensitive to hepatic dysfunction. 1, 2
The normal aPTT (28.2 seconds) indicates the intrinsic pathway remains functional, suggesting that factors VIII, IX, XI, and XII are adequate—this pattern is typical of early-to-moderate liver disease rather than severe consumptive coagulopathy. 1, 3
Isolated prolonged PT with normal aPTT in the setting of cirrhosis is the most common pattern seen in chronic liver disease, occurring in approximately 35% of patients with coagulation abnormalities. 3
Why This is NOT a Bleeding Disorder
The PT/INR does not predict bleeding risk in cirrhosis because it only measures procoagulant factors and ignores the simultaneous decrease in anticoagulant proteins (protein C, protein S, antithrombin) that rebalances hemostasis. 1, 4
Studies demonstrate that thrombin generation remains normal in cirrhotic patients despite prolonged PT, and adding fresh frozen plasma does not improve thrombin generation even though it shortens PT. 5, 2
The INR was specifically designed and validated only for monitoring warfarin therapy, not for assessing bleeding risk in liver disease, making its interpretation in cirrhosis fundamentally flawed. 4, 6
Alternative Diagnoses to Exclude
Vitamin K Deficiency
Vitamin K deficiency is the most common cause of isolated prolonged PT (occurring in 10% of cases) and must be considered, especially given the patient's chronic heart failure and potential malabsorption or poor nutrition. 3
However, vitamin K deficiency would be expected to show some aPTT prolongation as factors II, IX, and X (which affect aPTT) are also vitamin K-dependent, making pure cirrhosis more likely with completely normal aPTT. 7, 8
A trial of vitamin K (10 mg subcutaneously or intravenously) can be diagnostic: if PT corrects within 6-8 hours, vitamin K deficiency was contributory; if no correction occurs, hepatic synthetic dysfunction is the primary cause. 7
Disseminated Intravascular Coagulation (DIC)
DIC is unlikely given the normal aPTT, normal platelet count (401 × 10³/µL), and normal fibrinogen (407 mg/dL)—DIC would cause prolongation of both PT and aPTT with thrombocytopenia and fibrinogen <100 mg/dL. 1
DIC in cirrhosis requires rapid changes in coagulation parameters (hours to days) and evidence of multiorgan failure, neither of which is described in this stable outpatient presentation. 1
Clinical Management Recommendations
What NOT to Do
Do not administer fresh frozen plasma (FFP) to correct the PT/INR prophylactically—this practice is not supported by evidence, does not reduce bleeding risk, and exposes patients to transfusion reactions, volume overload, and TRALI. 1, 4
Do not delay necessary procedures based solely on prolonged PT—the PT does not predict procedural bleeding risk in cirrhosis, and arbitrary PT cutoffs lack validity. 1, 4
Do not assume the easy bruising is due to coagulopathy—studies show no difference in PT/aPTT between cirrhotic patients with and without minor bleeding (bruising, epistaxis). 1
What TO Do
Identify and treat the underlying cause of bleeding if present: in cirrhosis with upper GI bleeding, the cause is typically portal hypertension (varices, portal hypertensive gastropathy) or mechanical vascular injury, not intrinsic coagulopathy. 4, 9
Consider a trial of vitamin K 10 mg subcutaneously or intravenously to exclude vitamin K deficiency as a contributing factor, particularly given the heart failure and potential for malabsorption. 7
Reserve hemostatic interventions for massive bleeding with consumptive coagulopathy, defined as fibrinogen <100 mg/dL or platelet count <50 × 10³/µL with active bleeding—neither of which applies to this patient. 4
If invasive procedures are planned, consider viscoelastic testing (TEG/ROTEM) for more comprehensive hemostatic assessment, though even these tests have not been proven to predict procedural bleeding. 1, 4, 6
Key Clinical Pitfalls to Avoid
The "rebalanced hemostasis" concept in cirrhosis means that decreased procoagulants are offset by decreased anticoagulants, and thrombocytopenia is compensated by elevated von Willebrand factor—making standard coagulation tests poor predictors of actual bleeding risk. 1, 2
Heart failure can worsen hepatic congestion and synthetic function, potentially contributing to the prolonged PT through "cardiac cirrhosis" or hepatic congestion. 1
The easy bruising is likely multifactorial (vascular fragility, minor trauma, possible platelet dysfunction) rather than evidence of severe coagulopathy requiring correction. 1