Interpretation Of A Coagulation Screen

Question 1

Intrinsic pathway

Answer 1

Factors: 12, 11, 9, 8

Question 2

Extrinsic pathway

Answer 2

Tissue factor and factor 7

Question 3

Vitamin K dependent clotting factors

Answer 3

2, 7, 9, 10 (+ proteins C/ S)

Question 4

Prothrombin Time (PT) and INR

Answer 4

Extrinsic pathway- TF added to blood to activate extrinsic pathway. PT is measured and then standardised with INR (0.8-1.2)

Only factor 7 involved in extrinsic pathway and Rare for it to be deficient. Factors that do affect PT/INR;

Warfarin, vitamin K deficiency
Liver disease
DIC

Question 5

APTT

Answer 5

Intrinsic pathway: activator added to blood to activate intrinsic pathway. Clotting time is between 30-50s

The APTT can be affected by;

Warfarin, vitamin K deficiency
Liver disease
DIC
Anything that affects factor 8 (haemophilia A/ VWD), factor 9 (haemophilia B), factor 11 (haemophilia C), or factor 12 (very rare)
Heparin

NB- anti-phospholipid syndrome can increase APTT (inactivates he phospholipid added in the laboratory)

Question 6

Bleeding time

Answer 6

Platelet function (affected by platelet quantity/ function)-and therefore aspirin
Also VWD
Rarely used in practice

Question 7

Fibrinogen

Answer 7

Acute phase protein
Low levels are due to increased consumption or decreased production

Low- DIC, liver disease, malnutrition

High- inflammation, malignancy, trauma, infection

Question 8

Vitamin K deficiency

Answer 8

Increased INR (PT)
Increased APTT
Low albumin
Normal bleeding time

Fat soluble vitamin (may be issues if fat malabsorption)
Affects factors 2,7,9,10 and thus the extrinsic and intrinsic pathways

Question 9

Liver failure and coagulation

Answer 9

Liver synthesis most clotting factors so failure can result in global deficiency affecting the intrinsic and extrinsic pathways

Platelets may be reduced due to hypersplenism

Question 10

Disseminated intravascular coagulation

Answer 10

Severe systemic illness- procoagulative state. Occludes small vessels

Thrombocytopenia
Increased PT/ INR
Increased APTT
Decreased fibrinogen (the fibrinogen has been used up in the intravascular clotting)
Increased D-dimer

Question 11

Warfarin

Answer 11

Reduces synthesis of vitamin K dependent factors and so affects the extrinsic and intrinsic pathways

Monitored by INR (from PT)- extrinsic

Reversed with vitamin K and PCC

Question 12

Heparin

Answer 12

Increases anti thrombin activity by enhancing its binding to factor Xa and thrombin

NB- LMWH is not allowed in reduced kidney function (cleared by kidneys) whereas unfractionated heparin is allowed (cleared by the liver)

All heparin reversed with protamine sulphate

Question 13

Haemophilia vs VWD

Answer 13

Haemophilia is characteristically more haemarthroses and muscle haematomas, whereas VWD is more platelet-deficiency-like bleeding eg. Petechaiea, menorrhagia, contact bleeding eg. Gums)

Question 14

Anti phospholipid syndrome

Answer 14

Anti phospholipid antibodies react against proteins that bind against plasma membrane phospholipids, resulting in arterial and venous thrombosis

Question 15

Mixing Study

Answer 15

Patient has prolonged PT or APTT redo the test with a 50:50 mixture of normal plasma.

If corrects- factor deficiency

If fails to correct- factor inhibitor

Question 16

If both APTT and PT are prolonged

Answer 16

Vitamin K deficiency, DIC, heparin overdose, factor X issue, liver failure

Question 17

Bleeding time in VWD

Answer 17

Increased as VWF is mainly involved in platelet adhesion (this is reduced)

Question 18

VWD

Answer 18

APTT- increased (factor 8)
PT- normal
Bleeding time- increased (platelets)

Question 19

Haemophilia

Answer 19

APTT- increased (factor 8 or 9)
PT- normal
Bleeding time- normal

Question 20

Coombs test

Answer 20

Direct or indirect
Looks for autoimmune causes of haemolytic anaemia ie. Human anti RBC antibodies

Question 21

Main Take Away

Answer 21

PT/INR assesses the EXTRINSIC pathway – since factor VII pathology is rare, it is better used as a measure of overall clotting. It will, therefore, be affected in anti-coagulant use (inc. WARFARIN/HEPARIN/DOAC’s), liver failure, and DIC

APTT assesses the INTRINSIC pathway – this, therefore, measures factors VIII (and vWF), IX, and XI. The most common causes of increased APTT are haemophilia A (VIII), B (IX), C (XI), and possibly von Willebrand’s disease (since vWF pairs with VIII)

Bleeding time – although no longer used formally – measures the formation of the platelet plug. This will be affected by platelet disorders like von Willebrand’s disease (vWF), Bernard-Soulier syndrome (GpIb), TTP, ITP, HUS, and thrombocytopaenia.

Total clotting derangement is rare, but the cause must be identified quickly (e.g. DIC, malnutrition, or liver failure).

Make sure to order complementary tests: FBC and LFTs can provide greater insight into a possible cause when correlated with the results of the coagulation screen. (mixing study etc. if corrects, factor deficiency, if doesn’t, inhibitor)