11/13/24, 7\:31 PM Guide | Coagulation screen interpretation

Coagulation screen interpretation

Table of contents

Introduction

The coagulation screen is an important diagnostic test, yet is notorious for misinterpretation. In order to make the coagulation
screen easier to interpret, it is important to understand the physiology of what is being assessed.

Why do we perform this test?

The main reasons for performing a coagulation screen are\:
To con
To monitor the coagulation status of a patient on long/short term anti-coagulants.
To assess a patients coagulation status prior to surgery.
To assess the synthetic function of the liver.

How does coagulation work?

The coagulation screen assesses the function of the clotting cascade and the body's ability to create a platelet plug. First, we
shall look at how platelets work.

Platelets

In response to vascular injury, the following steps lead to a platelet plug\:
1. von Willebrand's Factor (vWF) adheres to the vascular injury.
2. vWF then binds to GpIb receptors on surrounding platelets.
3. After binding, the ADP (P2Y12) receptor on the platelet is activated leads to increased expression of GpIIb/IIIa.
4. These newly expressed receptors then
Now, let’s look at how the clotting cascade works.

Clotting cascade

The clotting cascade is comprised of many di
intrinsic pathway, the extrinsic pathway, and the combined pathway.
Key features of each pathway are shown below.
Intrinsic pathway
The intrinsic pathway is activated by contact with a damaged surface and goes as follows\:
F a c t o r X I I → F a c t o r X I → F a c t o r I X ( + F a c t o r V I I I + v W F ) → C o m m o n p a t h w a y
Extrinsic pathway
The extrinsic pathway is activated by the release of tissue factors and goes as follows\:
F a c t o r V I I → C o m m o n p a t h w a y
Combined pathway
The combined pathway then proceeds the intrinsic/extrinsic pathways and goes as follows\:
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F a c t o r X ( + F a c t o r V ) → F a c t o r I I → F a c t o r I ( + F a c t o r X I I I → F i b r i n m e s h )
The diagram below should help put all of this into context.
Coagulation cascade [1]
How are clots later dissolved?
Fibrin clots can then be dissolved through a separate pathway whereby plasminogen becomes its activated form, plasmin, via
tPA. This plasmin then breaks down the

Tests

There several components to the coagulation screen, some of the core parts and what they mean are covered below.

PT/INR (12-13 seconds/0.8-1.2)

The prothrombin time (PT) is a measure of the time taken for blood to clot via the extrinsic pathway (a good way to remember
is that you ‘Play Tennis OUTSIDE’ therefore PT is EXTRINSIC).
International normalised ratio (INR) is a standardised version of this test, commonly used with patients on anticoagulants.
Since the only factor in the pathway is VII (which is rarely de
factor synthesis or consumption.
This test can be a
levels.

APTT (35-45 seconds)

The activated partial thromboplastin time (APTT) is a measure of the time taken for blood to clot via the intrinsic pathway (a
good way to remember, following PT, is that you ‘Play Table Tennis INSIDE’ therefore PTT is INTRINSIC).
Like with PT, APTT time will be a
liver failure, vitamin K de
APTT, however, can indicate issues with factors VIII (and vWF), IX, and XI speci
The main conditions that could result in an abnormal APTT include\:
Haemophilia A (VIII – X-linked recessive)
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Haemophilia B (IX – X-linked recessive)
Haemophilia C (XI – autosomal recessive)
von Willebrands disease (as vWF pairs up with factor VIII)
N o t e \: a n t i- p h o s p h o l i p i d s y n d r o m e c a n c a u s e a h i g h A P T T d e s p i t e b e i n g a d i s o r d e r t h a t c a u s e s c l o t s , p h o s p h o l i p i d u s e d i n A P T T .
d u e t o i t i n a c t i v a t i n g t h e

Bleeding time (1-6 minutes for

Whilst no longer formally used due to its rather barbaric nature, bleeding time assesses overall platelet function and levels. It
is therefore worth noting the time it takes for a patient to stop bleeding from any cuts.
As such, platelet speci
Some examples of such disorders that will increase bleeding time include\:
von Willebrand's disease (vWF de
Bernard-Soulier syndrome (GpIb de
Glanzmann thrombasthenia (GpIIb/IIIa de
TTP/ITP/HUS/DIC
Thrombocytopaenia

Thrombin time (10-15 seconds)

This is a test of how fast
In cases of a prolonged time, the cause is either a synthetic issue or consumption issue.
Similar to prolonged PT, this can be due to DIC, liver failure, malnutrition, abnormal

Extra tests

Further tests can be ordered to work out the exact pathology. These can provide levels of speci
thrombophilia screens, ADAMTS13 (for TTP) and many more – however, some of these can only be ordered at the request of a
haematologist.
It is also worth ordering a full blood count (to assess platelet levels), liver function tests (to assess for general liver function
abnormalities), albumin (to assess the liver’s synthetic function/malnutrition) and D-dimer.

Patterns of common coagulopathies

Platelet
Condition PT/INR APTT BT
count
Vitamin K de
Warfarin use
↑ ↑- -
Haemophilia A/B/C - ↑- -
von Willebrand's
disease
- -/↑ ↑-
Notes
D i
c o n d i t i o n s , s o a h i g h v a l u e m a y b e n o r m a l f o r t h e p a t i e n t ( e .g.
A F , v a l v e r e p l a c e m e n t s , e t c )
S y m p t o m s o f ‘ c l o t t i n g’ d i s o r d e r s \: h a e m a r t h r o s i s , m u s c l e
h a e m a t o m a s , p r o l o n g e d b l e e d i n g a f t e r d e n t a l s u r ge r y
S y m p t o m s o f ‘ p l a t e l e t’ d i s o r d e r s \: p e t e c h i a e , b l e e d i n g ( e .g . g u m s ) , m e n o r r h a g i a
b r u i s i n g , c o n t a c t
DIC ↑ ↑ ↑ ↓
T o t a l c o a g u l o p a t h y , p r i m a r y c a u s e m u s t b e t r e a t e d , gi v e
p l a t e l e t s a n d c l o t t i n g f a c t o r s
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ITP/TTP/HUS - - ↑ ↓
L a c k o f P T / A P T T d e r a n g e m e n t i s a go o d d i
N E V E R g i v e p l a t e l e t s t o t h e s e p a t i e n t s

E

All anticoagulants (warfarin, heparins, NOACs) will increase the PT/INR and the APTT; this should, therefore, be considered
when interpreting results. Patients on warfarin will have a speci
replacements, etc), it is, therefore, a good idea to get a medical history from the patient.
Antiplatelets, such as clopidogrel (P2Y12 inhibitor) and aspirin, will also cause derangement. These, however, will cause an
increase in the overall bleeding time but won’t a

Key points

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 a
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 a
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 identi
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.

References

Texts

1. Hall, J. & Guyton, A. G u y t o n a n d H a l l t e x t b o o k o f m e d i c a l p h y s i o l o gy ( 1 3 t h E d i t i o n ) . (Saunders Elsevier, 2011).
2. Wilkinson, I., Raine, T. & Wiles, K. O x f o r d h a n d b o o k o f c l i n i c a l m e d i c i n e ( 9 t h E d i t i o n ) . (Oxford University Press, 2010).
3. Le, T., Bhushan, V., Sochat, M., Petersen, M. & Micevic, G. F i r s t A i d f o r t h e U S M L E S t e p 1 2 0 1 9 . (McGraw-Hill Education, 2019).
4. Rang, H. P., Dale, M., Flower, R. J. & Henderson, G. R a n g a n d D a l e’ s p h a r m a c o l o g y ( 8 t h E d i t i o n ) . (Elsevier/Churchill Livingstone,
2016).

Images

1. Dr Graham Beards. Coagulation pathway. Licence\: [CC BY-SA 3.0]. Available from\: [LINK].
Source\: geekymedics.com
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