Dental management of haemostatic problems

Question 1

Methods of creating an intravascular solid

Answer 1

Coagulation - soluble proteins to insoluble proteins involving two potential pathways (intrinsic and extrinsic), using enzymes
Platelets - portions of cells. work together with coagulation factors in layers

Question 2

Coagulation cascade

Answer 2

Subendothelial tissue (tissue factor) --extrinsic pathway i.e. outside the vessel (PT/INR)--> final common pathway
Negatively charged molecules from endothelial trauma (phospholipid) + factor --intrinsic pathway i.e. inside the vessel (contact activation -APTT)--> final common pathway
Final common pathway polymerising fibrinogen to fibrin
Prothrombin time (PT/INR) measures extrinsic pathway and final common pathway
Activated partial thromboplastin time (APTT) measures intrinsic pathway and final common pathway

Question 3

Measuring coagulation

Answer 3

Blood collected in CITRATE
-this chelates Ca2+
-Ca2+ is clotting factor IV; required for both intrinsic and extrinsic pathways
In lab, an excess of Ca2+ is added to overcome citrate and then other things are added to activate either extrinsic or intrinsic pathway

Question 4

Probthrombin time

Answer 4

Tissue factor added to blood sample in lab, and time how long to clot
Measures EXTRINSIC PATHWAY
Also, will measure final common pathway
Factors I, II VII, X

Question 5

Importance of factors II, VII, X

Answer 5

Warfarin inhibits factors II, VII, IX, X

So warfarin increases prothrombin time

Question 6

INR

Answer 6

Ratio -patient’s PT: normal PT
Under specific laboratory conditions
Used to assess Warfarin’s effect

Question 7

What does an INR of 2 mean?

Answer 7

Px’s extrinsic pathway of coagulation is twice as long under specific lab conditions
NOT that it takes twice as long for patient’s blood to clot - intrinsic pathway and platelets not taken into account

Question 8

APTT

Answer 8

Activated Partial Thromboplastin Time
Phospholipid, silica & Ca2+ added to sample
Time how long to clot formation
Measures INTRINSIC PATHWAY and also final common pathway
I, II, V, VIII, IX, X, XI, & XII
-Warfarin affects APTT (inhibits factors VIII and IX)
-haemophilia is VIII or IX deficiency (APTT would be elevated)

Question 9

Important causes of haemostatic problems

Answer 9

Congenital bleeding disorders
Acquired bleeding disorders
-medical conditions
-drugs

Question 10

Important congenital disorders

Answer 10

Haemophilia (increased APTT)
- A – factor VIII
- B – factor IX
Von Willebrand’s 
-not a coagulation factor
- shortage of VWBF
- important in platelet adhesion (increased bleeding time (marker of platelet function)
- a.k.a. factor VIIIVWF (factor VIIIc) binds to factor VIII to stop breakdown in the blood (increased APTT)

Question 11

Medical conditions causing haemostatic problems

Answer 11

Liver
Kidney
Cardiac (due to drugs…)
Cancer (due to drugs or myelosupression -condition in which bone marrow activity is decreased)
ITP, ITTP - you can get thrombocytopenia idiopathically

Question 12

Why does liver disease cause haemostatic problems

Answer 12

Liver important for production of MOST coagulation factors
NOT the same as Vitamin K-dependent coagulation factors
However, ALL Vitamin K-dependent coagulation factors ARE produced by the liver
-cancer (including metastases)
-cirrhosis/ jaundice
-paracetamol overdose -PT is marker of failing liver

Question 13

Why can kidney cause haemostatic problems

Answer 13

Not an easy explanation
Is related to platelet function and not number
Prolonged bleeding time
Also will be heparinised (anticoagulant) during dialysis

Question 14

Drugs to know

Answer 14

Important ones to know:
- Warfarin
- Aspirin
- Clopidogrel
- Heparin
New drugs coming into play: ‘NOACs’ - new oral anticoagulants
- Dabigatran ( direct thrombin inhibitor)
- Rivaroxaban (direct activated factor X)

Question 15

Aspirin

Answer 15

Highly first pass metabolised by liver
-liver recognises it as drug, metabolises it and excretes it
Therefore main therapeutic effect needs to be within hepatic portal vein before reaching liver
Reason for efficacy is IRREVERSIBLE INACTIVATION of COX within platelets
Lasts the life of the platelet so if px was coming in for tooth out it would not help taking it the day before
Reversal requires 7 days of discontinuation (enough new platelets)

Question 16

Simplified arachidonic acid pathway

Answer 16

Arachidonic acid –> leukotrienes (attracts white blood cells - leukocytes)
Arachidonic acid –COX1,2,3–> Thromboxane A2 (TXA2) and Prostaglandins/ prostacyclins
TXA2 –> platelet aggregation
Prostaglandins/ prostacyclins –> pain and gastric regulation (side effect of aspirin is gastric ulcers)

Question 17

Warfarin

Answer 17

–> Vit K Epoxide reductase
Vit K Epoxide –Vit K Epoxide Reductase–> Vit K
Vit K –> Vit K Epoxide causes inactive factors (2,7,9,10, protein C, protein S) –> active factors and vice versa

Question 18

Heparin

Answer 18

Binds to and activates Antithrombin III

• inhibitor of factor X and factor II, which converts fibrinogen to fibrin
• given to pxs sitting in hospital after operation to prevent deep vein thrombosis

Question 19

Clopidogrel

Answer 19

P2Y12 inhibitor
P2Y12 is an important receptor on platelets
P2Y12 involved in platelet aggregation and linking to the fibrin meshwork

Question 20

Dental management of haemorrhage

Answer 20

Avoid it in first place
Standard measures
Further measures

Question 21

Avoiding haemorrhage

Answer 21

Warfarinised patient
- check INR within 72hrs of procedure
- INR <4
- avoid ID blocks where possible
Antiplatelets (aspirin, clopidogrel, dipyridamole)
- monotherapy – continue as planned
- multiple (e.g. Aspirin + Clopidogrel) - no evidence of increased bleeding risk, but may consider hospital-based treatment
Haemophilia/ VWB
- Liase with haematologist
- DDAVP
- Recombinant factor VIII/ IX
- mild may need no preoperative 			  management
- Tranexamic acid

Question 22

Types of haemorrhage

Answer 22

Primary
– as soon as tooth is removed
– will be due to bleeding disorder or local cause
Reactionary
– not immediate, but within 48hrs of extraction
– ETOH, exercise, heat, anaesthetic wearing off
Secondary
- approximately 1 week after surgery, due to infection

Question 23

Standard measures to achieve haemostasis in any tooth

Answer 23

firm pressure/ bite on gauze

• compress socket
• post-op instructions (reactionary haemorrhage)

Question 24

Further measures to achieve haemostasis in any tooth

Answer 24

Bone - haemostatic pack in socket

Gingivae - suture

Question 25

Packing

Answer 25

Sugicel

• resorbable oxidised cellulose
• helps clot form

Question 26

Gelatin sponge

Answer 26

• absorbs up to 45 times own weight in blood

- pressure tamponades bleed

Question 27

Suturing

Answer 27

Will compress gingival blood supply, stemming soft tissue bleed
Will act to preent haemostatic pack from falling out

Question 28

Ongoing bleed

Answer 28

Tranexamic aci
May need reversal of anticoagulant (if possible)
-warfarin -omit/ vitK
-heparin -omit/ protamine sulphate
Need to weigh up against risks of thrombosis, and actually very rarely done where INR has been correctly check pre-op
Accept very small amount of oozing for few days if known bleeding disorder

Question 29

Ongoing bleed of unknown cuase

Answer 29

Coagulation screen/ bleeding time
Full blood count (platelets)
Factor assay

Question 30

Reversal of warfarin’s effect?

Answer 30

Give them vast excess of Vit K in emergency

Question 31

Reversal of heparin’s effect?

Answer 31

Protamine sulphate (from salmon semen) - given subcutaneously