Ifeanyichukwu Ifechidere: Rebalanced Haemostasis in Liver Disease
Ifeanyichukwu Ifechidere, Specialist Biomedical Scientist at Sheffield Teaching Hospitals NHS Foundation Trust, shared a post on LinkedIn:
“A patient with liver disease has:
- Prolonged PT/INR
- Low fibrinogen
- Thrombocytopenia
So naturally… everyone assumes they’re ‘auto anticoagulated.’
Right?
Not necessarily.
Because one of the most misunderstood concepts in coagulation is this:
Patients with liver disease can bleed And clot.
And if you work in haemostasis long enough, you eventually realise:
- The coagulation profile in liver disease is not simply ‘hypocoagulable.’
- It’s rebalanced haemostasis.
This changes everything.
Yes — the liver produces most clotting factors.
So in liver disease:
PT/INR may become prolonged
Factor levels decrease
Platelets may fall
But here’s what many people overlook:
Natural anticoagulants also decrease:
- Protein C
- Protein S
- Antithrombin
At the same time:
- Factor VIII increases
- von Willebrand factor increases
Meaning?
The haemostatic system is no longer ‘normal’ —
but it may still remain balanced enough to clot.
This is why some patients with severe liver disease:
- Bleed during procedures
And - Develop portal vein thrombosis in the same admission
Sounds contradictory… until you understand rebalanced haemostasis.
And this is where coagulation scientists become essential.
Because if we interpret PT/INR in liver disease the same way we interpret it in warfarin therapy…
we risk misunderstanding the patient completely.
A prolonged INR in liver disease does Not reliably predict bleeding risk.
Read that again.
This is why blindly correcting coagulation numbers without clinical context can sometimes do more harm than good.
As biomedical scientists, our role is not just to report abnormalities.
It’s to understand:
- What the test reflects
- What it does Not reflect
- And how physiology changes the meaning of the result
Because in liver disease…
the coagulation system isn’t broken in one direction.
It’s walking a fragile tightrope between bleeding and thrombosis.”
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