Evaluation of Coagulopathies

Last updated: April 6, 2026, 6:50 PM Pacific Time (PDT)

Interactive bedside framework for prolonged PT/INR, prolonged aPTT, combined coagulation-test abnormalities, and DIC-pattern labs. Start by asking whether the problem is isolated or combined, then sort factor deficiency, liver disease, vitamin K deficiency, anticoagulant effect, inhibitor physiology, and consumptive coagulopathy.

Interactive diagnostic assistant

Activate the assistant to re-rank likely coagulopathy mechanisms from entered data.

Coagulation pattern PT / INR (PT roughly 11-13.5 sec, INR about 0.8-1.2)
aPTT (roughly 25-35 sec)
Fibrinogen (mg/dL, ref about 150-400)
Platelets (k/uL, ref about 150-450)

History and bedside clues Active bleeding, oozing, or procedure-related hemostasis concern Cirrhosis, acute liver injury, or chronic liver disease context Warfarin or vitamin K antagonist exposure Heparin exposure or contaminated line-draw concern DOAC exposure or recent anticoagulant use Sepsis, shock, malignancy, trauma, or obstetric DIC-risk setting Personal or family history suggesting congenital factor deficiency Thrombosis history or antiphospholipid / inhibitor concern

Other labs

Core labs

Mixing study (correction expected with factor deficiency)
D-dimer / FDP (typically low or undetectable when normal)
Hemoglobin (g/dL, ref about 12-17 depending on sex)
Liver enzymes / bilirubin context

Optional labs

Factor VIII / lupus anticoagulant context
Factor V / vitamin K pattern context
Creatinine (mg/dL, ref about 0.6-1.3)
Hemolysis / schistocyte context (normally absent)

Free-text entries are interpreted automatically when they look prolonged, low, high, corrected, uncorrected, elevated, or clearly abnormal.

Likely mechanisms

Likely diagnoses from entered data

This is a simplified teaching assistant for bedside coagulation reasoning. Major bleeding, severe DIC concern, or urgent procedure planning still requires immediate clinical judgment and treatment planning.

Flowchart

Step 1

Decide whether the abnormality is isolated PT/INR, isolated aPTT, or combined

That first split usually narrows the differential quickly before you chase rare factor patterns.

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Step 2

Use the mixing study and consumption markers when available

Correction points toward factor deficiency; failure to correct raises inhibitor, lupus anticoagulant, or anticoagulant-effect physiology.

Isolated PT / INR prolongation

Common

Warfarin effect or vitamin K deficiency

A common first branch when INR is up more than aPTT.

Synthetic

Liver synthetic dysfunction

Think factor production failure when the liver story fits.

Isolated aPTT prolongation

Factor

Intrinsic factor deficiency

Congenital or acquired factor deficiency usually corrects on mixing.

Inhibitor

Heparin effect, lupus anticoagulant, or acquired inhibitor

No-correction patterns and thrombosis history matter here.

Both PT and aPTT prolonged

Production

Liver failure, severe vitamin K deficiency, or multiple-factor deficiency

Combined prolongation often means broader factor loss or impaired synthesis.

Drug

Anticoagulant effect or mixed anticoagulant exposure

Heparin, warfarin, DOACs, or combinations can all distort the pattern.

Consumption / DIC-pattern branch

Consumptive

DIC or acute consumptive coagulopathy

Low fibrinogen, thrombocytopenia, high D-dimer, and shock or sepsis should pull you here quickly.

Re-check

Sample, heparin contamination, or lab-artifact issues

Unexpected coagulation panels sometimes reflect the tube more than the patient.

Teaching pearl: isolated PT, isolated aPTT, and combined prolongation are different bedside problems. The branching becomes much simpler once you commit to that first split.