Bleeding Risk and Haemorrhage Flashcards

1
Q

What does the word haemorrhage mean?

A

Blood loss from a ruptured vessel

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2
Q

What are the 3 types of haemorrhage?

A

Primary
Reactionary
Secondary

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3
Q

Explain when the three types of haemorrhage occur

A

Primary haemorrhage = occurs due to injury such as laceration to tissues, inflammation, bone fractures.

Reactionary haemorrhage = due to the vasodilation of vessels after the LA vasoconstriction has worn off

Secondary haemorrhage = due to infection of the surface site causing erosion of small vessels leading to an increase in vascularity

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4
Q

What is haemostasis?

What are the two types of haemostasis?

A

Haemostasis = cessation of blood loss

Primary - platelet aggregation and platelet plug formation
Secondary - formation of insoluble fibrin by activated clotting factors

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5
Q

Give the 6 steps to haemostasis

A

1) Damage to vessels to exposed endothelium
2) Vascular constriction
3) Platelet plug formation
4) Coagulation cascade leading to production of thrombin
5) Fibrin clot formation
6) Fibrinolysis (degradation of the blood clot)

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6
Q

What is the coagulation process?

A

The process where blood changes from liquid to a gel to form a clot to stop loss from a vessel.

This occurs by activation, aggregation and adhesion of platelets and fibrin deposition.
This leads to a coagulation cascade which is a series of enzyme activated events which produce and lead to proliferation of fibrin.

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7
Q

What factor is first activated in the extrinsic clotting pathway?

A

factor 7

comes into contact with tissue factor at injury site

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8
Q

What happens during fibrinoylsis?

A

Enzymatic breakdown of fibrin in a blood clot.

This prevents the blood clot from growing and causing a problem.

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9
Q

What enzyme breaks down the fibrin clot?

A

Plasmin (made from plasminogen)

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10
Q

What happens if haemostasis is over or under active?

A

Over = stroke, myocardial infarction

Under = excessive bleeding after trauma/surgery

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11
Q

What are the 3 causes of excessive bleeding?

A
  • Defects in blood vessels
  • Defects in platelets
  • Defects in coagulation
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12
Q

Name some inherited and acquired causes of vascular defects

A

Inherited = hereditary hemorrhagic telangiectasia (blood vessels not formed properly), osteogenesis imperfects

Acquired = IgA vasculitis (inflammation of blood vessels)

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13
Q

Decrease in platelets is also another bleeding disorder called thrombocytopenia.
What are inherited and acquired factors which lead to this?

A

Inherited:

  • Von Willebrand disease (decrease in number and function)
  • Bernard- Soulier syndome

Acquired

  • HIV/AIDS
  • Chemotherapy
  • Liver disease
  • Renal failure
  • Bone marrow failure
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14
Q

How does anti-platelet therapy work?

A

By reducing platelet aggregation.
Commonly used on patients to prevent MI, stoke, TIA.

These drugs include aspirin, clopidogrel and dipyridamole.

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15
Q

What 4 measures can we do when extracting a tooth from a patient on anti-platelet drugs e.g. aspirin?

A

1) Stage multiple extractions
2) Local haemostatic measures
3) Longer postoperative monitoring
4) Morning appointments so patient can return if they are still bleeding

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16
Q

What are some inherited and acquired coagulopathies?

A

Inherited:

  • Haemophilia A and B
  • Von Williebrands disease

Acquired:

  • End stage liver disease
  • Renal disease
  • HIV/AIDS
  • Malabsorption (decrease in vitamin k)
  • Anti -coagulant drugs
17
Q

How does Warfarin work?

A

It is a Vitamin K antagonist so inhibits production of factor 2,7,9 and 10.
It is reversible.
It can interact with antibiotics such as metronidazole and erythromycin.

18
Q

How do direct acting oral anti-coagulants work?

A

They are factor 10a and thrombin 2 inhibitors.

Commonly used for preventing strokes or given to patients with atrial fibrillation.

19
Q

What types of patients with receive doses of heparin or clexane?

A

Patients who have kidney failure and are undertaking dialysis.

20
Q

How does a patient on warfarin affect our extraction?

A
  • INR < 4 within 24h of procedures
  • No NSAIDs given (increases bleeding risk)
  • Local haemostatic measures given
  • Delay INR if > 4
21
Q

For patients on direct oral anticoagulants, what do we do to allow them to have an extraction?

A

Dont take the morning dose and then take the normal pm dose.

22
Q

What do we do if a patient is on a combination of drugs?

A

Talk to GP, if not possible then refer to secondary care setting.

23
Q

What do we need to consider for safety of an extraction?

A
  • Is the surgery likely to cause bleeding? e.g. multiple teeth to extract
  • Take medical history and update at every appointment
  • Look at any hospital records
  • Talk to other teams about the patient
24
Q

If a patient is at high risk of bleeding, what measures do we take?

A
  • Liaise with GP
  • Plan treatment early in the day/week
  • Stage the treatment
  • Delay non-urgent procedures
  • Local haemostatic measures
  • Provide patient post operative advice and emergency contact details
25
Q

What can we do as dentists if a patient has secondary bleeding?

A
Give LA for vasoconstriction.
Curettage of socket.
Remove existing blood clot.
Local haemostatic measures.
Consider transexamic acid.
26
Q

How does transexamic acid work?

A
  • Antifibrinolytic agent that inhibits breakdown of fibrin clot
  • It inhibits fibrinolysis by inhibiting the activation of plasminogen to plasmin

It can be added to gauze or put in mouth wash.

27
Q

What happens if a patient has uncontrolled haemorrhage?

A
  • NHS 111
  • A and E
  • Patient needs to have blood tests to see why