APPROACH TO

COAGULATION DISORDERS
Dr.K.Pavithran, MD, DM
Assistant Professor,Dept of Hematology
Medical College Hospital
Trivandrum-695011, India
 Clinical approach
1. Is the bleeding significant ?
2. Local Vs Systemic ?
3. Platelet Vs Coagulation disorder ?
4. Inherited Vs Acquired ?
 Laboratory Approach
1. Demonstration of the defect
2. Identification of the defect(s)
3. Assessment of severity
4. Consequential studies eg. carrier detection
5. Monitoring of treatment
 Screening Tests
1. Platelet count & morphology
2. Bleeding Time
3. Clotting Time
4. Prothrombin Time
5. Activated Partial Thromboplastin Time
6. Thrombin Time
 Collection of blood sample
1. Minimum circulatory stasis
2. Clean venous puncture
3. Proper anticoagulant
4. Proportion of blood to anticoagulant
5. Separation of plasma and storage
6. Effect of stress, pregnancy, drugs
7. Effect of PCV on the proportion of plasma
to anticoagulant
 Prolonged PT/APTT
• Coagulation factor deficiency/inhibitor
• Test plus control plasma - 1:1
• Repeat PT/APTT
• > 50% correction
– Yes - Factor deficiency
– No - inhibitor

timed incubation
abnormally increasing no change
specific inhibitor Lupus Anticoagulant
 HMWK VII
XII
PK
XI
APTT IX PT
VIII
X

PT -  V
II
APTT, TT, PLC - N I TT

* Factor VII deficiency

* Anticoagulant therapy
 HMWK VII
XII
PK
XI
APTT IX PT
VIII
X

APTT -  V
II
PT, TT, PLC - N I TT

* Factor deficiency
* vWD
* Inhibitors
* Heparin therapy
Mixing tests with APTT
APTT of test plasma +
Aged plasma Adsorbed plasma Diagnosis

No correction Corrected VIII

Corrected No correction IX

Corrected Corrected XI,XII

Prolonged APTT, BT
von Willebrand’s disease
Ristocetin Induced Platelet Agglutination
VIII:C
vWF:Ag
vWF multimeric analysis
Type 1 - Partial deficiency of vWF
2A - Absence of large and interm. multimers
2B - Absence of large multimers
2M- multimers normal, pl. function 
2N -  affinity for FVIII
3 - severe deficiency of vWF
 HMWK VII
XII
PK
XI
APTT IX PT
VIII
X

PT, APTT -  V
II
TT, PLC - N I TT

* Common Pathway Factor deficiency

* Vitamin K deficiency
* Oral anticoagulant therapy
* Liver disease
Mixing tests with PT

PT of test plasma +
Aged plasma adsorbed plasma Diagnosis

Corrected Not corrected X

Not corrected Corrected V

Not corrected Partial II

 HMWK VII
XII
PK
XI
APTT IX PT
VIII
X

PT, APTT, TT -  V
II
PLC - N I TT

* Hypo / dysfibrinogenemia
* Heparin
* Liver disease
* Systemic hyperfibrinolysis
 HMWK VII
XII
PK
XI
APTT IX PT
VIII
X
APTT, PT,TT all  V
PLC - low II
I TT

* DIC
- FDP
- D-dimer
- Fibrin monomer
 HMWK VII
XII
PK
XI
APTT IX PT
VIII

PT, APTT- 
X
V
TT - N II
PLC -  I TT

Massive transfusion
with stored blood
 HMWK VII
XII
PK
XI
APTT IX PT
VIII
X

PT, APTT,TT-N V
II
PLC -  I TT

Thrombocytopenia
Pseudo vs True
Bone marrow biopsy to differentiate
 production
 destruction
 PT, APTT, TT, PLC - Normal
• Factor XIII deficiency • Platelet function
• Thrombasthenia – BT
– congenital – clot retraction
– drug induced – 1 minute platelet count
– aggregation
• Disorders of vascular
hemostasis • Tourniquet test
• Factor XIII - clot
solubility
 Asymptomatic Patient
Routine screening tests shows
prolonged APTT

– Inhibitor - lupus anticoagulant

– Factor XII deficiency
– Mild congenital factor deficiency
 Antiphospholipid Antibody Syndrome
Criteria by Branch and Silver 1996

• Clinical • Laboratory
– Recurrent abortion – IgG/IgM anticardiolipin Ab
– Recurrent venous – Lupus anticoagulant
thrombosis • Diagnosis
– Recurrent arterial
– 1 clinical + 1 lab criteria
thrombosis
– Lab result must be positive
– Persistent
on at least 2 occasions
thrombocytopenia
more than 3 months apart
– Livedo reticularis
 Lupus Anticoagulant
• Kaolin clotting time
• Dilute Russel’s viper venom time
• Platelet neutralization test
• Tissue thromboplastin inhibition test