Coagulation Profile Interpretation


 Standard Coagulation Tests 

Test

Pathway / What It Measures

Factors Assessed

Normal Value

Clinical Use / Where Important

PT (Prothrombin Time)

Extrinsic + Common pathway

VII, X, V, II, I

11–14 sec

Warfarin monitoring, liver disease, vitamin K deficiency

INR

Standardized PT

Same as PT

0.8–1.2 (normal)

Therapeutic: 2–3

Warfarin monitoring

aPTT

Intrinsic + Common pathway

XII, XI, IX, VIII, X, V, II, I

25–35 sec

Heparin therapy, hemophilia

Platelet Count

Primary hemostasis

Platelets

150,000–450,000/µL

Bleeding risk, DIC

Bleeding Time (BT)

Platelet function + vascular integrity

Platelet adhesion/aggregation

2–7 min

vWD, platelet dysfunction (rarely used now)

Clotting Time (CT)

Whole blood clot formation (intrinsic pathway)

All intrinsic factors

5–11 min (Lee-White method)

Obsolete test; severe factor deficiency

Activated Clotting Time (ACT)

Whole blood clot time after activator

Intrinsic + common

90–120 sec

High-dose heparin monitoring (cardiac surgery, ECMO)

Fibrinogen

Final substrate for clot formation

Factor I

200–400 mg/dL

DIC, liver failure, massive transfusion

D-dimer

Fibrinolysis (cross-linked fibrin breakdown)

Degraded fibrin fragments

< 0.5 µg/mL (FEU)

DIC, VTE rule-out

Thrombin Time (TT)

Fibrinogen → fibrin conversion

Fibrinogen

14–18 sec

Heparin effect, dysfibrinogenemia


 Stepwise Approach to Interpretation

STEP 1: Check Platelet Count

  • ↓ Platelets → primary hemostasis problem
  • Normal platelets + bleeding → think coagulation defect


STEP 2: Look at PT and aPTT Pattern

🔷 Pattern 1: Isolated Prolonged PT

Causes:

  • Early vitamin K deficiency
  • Warfarin therapy
  • Early liver disease
  • Factor VII deficiency

Mechanism:

  • Factor VII has shortest half-life (~6 hrs)

High-yield point:
PT rises first in liver failure.


🔷 Pattern 2: Isolated Prolonged aPTT

Causes:

  • Hemophilia A (Factor VIII deficiency)
  • Hemophilia B (Factor IX deficiency)
  • Heparin therapy
  • Lupus anticoagulant
  • Severe vWD (low VIII)

Clinical differentiation:

  • Bleeding → hemophilia
  • Thrombosis → lupus anticoagulant


🔷 Pattern 3: Both PT and aPTT Prolonged

Causes:

  • Advanced liver disease
  • DIC
  • Vitamin K deficiency (late)
  • Massive transfusion
  • Severe factor deficiencies (X, V, II, fibrinogen)

This suggests common pathway involvement.


🔷 Pattern 4: Normal PT & aPTT with Bleeding

Think:

  • Platelet dysfunction (uremia, antiplatelets)
  • vWD
  • Mild factor XIII deficiency
  • Connective tissue disorders


5️⃣ Mixing Study Interpretation

Why Perform Mixing Study?

To differentiate:

  • Factor deficiency
  • Inhibitor presence

Method:

Mix patient plasma 1:1 with normal plasma.

Interpretation:

Result

Meaning

Corrects

Factor deficiency

Does not correct

Inhibitor present

Common inhibitors:

  • Lupus anticoagulant
  • Factor VIII inhibitor
  • Heparin contamination

7️⃣ Thrombin Time (TT)

Prolonged in:

  • Heparin therapy
  • Dysfibrinogenemia
  • Severe liver disease
  • DIC

If TT prolonged but reptilase time normal → heparin effect.


8️⃣ Fibrinogen Interpretation

Normal: 200–400 mg/dL

Low in:

  • DIC
  • Liver failure
  • Massive transfusion

High in:Fibrinogen is an acute phase reactant.

  • Acute phase response
  • Pregnancy
  • Inflammation


9️⃣ D-Dimer Interpretation

Elevated in:

  • DIC
  • PE
  • DVT
  • Sepsis
  • Post-op
  • Trauma

Important:High sensitivity, low specificity.

Never diagnose VTE on D-dimer alone in ICU.


🔟 Massive Transfusion Coagulopathy

Triad:

  • Dilutional thrombocytopenia
  • Hypofibrinogenemia
  • Factor depletion

Lab:

  • ↑ PT
  • ↑ aPTT
  • ↓ Platelets
  • ↓ Fibrinogen


🔵 Activated Clotting Time (ACT)

What it is:

  • Whole blood bedside test
  • Uses surface activator (celite/kaolin)
  • Used in high-dose heparin states

Where Important:

  • Cardiac surgery
  • ECMO
  • Cardiopulmonary bypass
  • Interventional cardiology

Therapeutic Targets:

  • Cardiac surgery: > 400–480 sec
  • ECMO: 180–220 sec (institution dependent)

ACT is unreliable at low heparin levels → use aPTT or anti-Xa instead.


🔵 Clotting Time (CT)

Old Lee-White method.

Measures:

  • Time for whole blood to clot in glass tube.

Limitations:

  • Poor reproducibility
  • Replaced by PT/aPTT

Rarely used today.


🔵 Bleeding Time (BT)

Measures:

  • Platelet function
  • vWF interaction
  • Capillary integrity

Prolonged in:

  • Thrombocytopenia
  • vWD
  • Uremia
  • Aspirin use

Now replaced by:

  • Platelet function analyzer (PFA-100)
  • Aggregometry



6️⃣ Disease-Specific Patterns

 Disseminated Intravascular Coagulation (DIC)

Lab Pattern:

  • ↓ Platelets
  • ↑ PT
  • ↑ aPTT
  • ↓ Fibrinogen
  • ↑ D-dimer
  • Schistocytes

Mechanism:
Consumption of clotting factors + secondary fibrinolysis.


 Liver Disease

Lab Pattern:

  • ↑ PT (early)
  • ↑ aPTT (late)
  • ↓ Fibrinogen (late)
  • ↓ Platelets (hypersplenism)
  • Elevated INR

Important concept:Rebalanced hemostasis — both pro and anti-coagulant factors reduced.

 Vitamin K Deficiency

Causes:

  • Malnutrition
  • Obstructive jaundice
  • Antibiotics
  • Newborn

Lab:

  • ↑ PT first
  • Later ↑ aPTT

Corrects with vitamin K.



 von Willebrand Disease

Entity:
von Willebrand disease

Lab:

  • Normal PT
  • Normal or ↑ aPTT
  • Normal platelet count
  • ↑ Bleeding time

Mechanism:
vWF stabilizes factor VIII.


 Antiphospholipid Syndrome

Entity:
Antiphospholipid syndrome

Lab:

  • ↑ aPTT
  • No correction on mixing
  • Thrombosis clinically

Paradox:
Prolonged clotting time but hypercoagulable.