Bleeding - Oral Surgery Complications Flashcards
(61 cards)
1
Q
4 abnormalities that can increase bleeding risk?
A
- Vascular abnormalities.
- Platelet deficit - number.
- Platelet deficit - quality/ function.
- Clotting mechanism.
2
Q
How can you differentiate between bleeding due to a platelet problem vs due to clotting factor problem?
A
- Platelet issue would show PERSISTENT HEMORRHAGE FROM THE TIME OF INJURY/TRAUMA.
- Clotting factor issue would show HEMOSTASIS and later BLEEDING.
3
Q
How does bleeding due to PLATELET abnormalities usually present?
A
- SMALL (usually)
- Petichiae up to ecchymosis
- Usually SUPERFICIAL bleeds.
4
Q
How does bleeding due to CLOTTING abnormalities usually present?
A
- Likely to be DEEP ex. into JOINTS.
5
Q
What are the general values of platelets (normal and reduced) associated with different bleeding presentations?
A
- Normal: 150-450
- 50: PETECHIAL
- 20 to 50: PETECHIAL + ECCHYMOSIS.
- Less than 20: Melaena, haematamesis, haematuria
6
Q
What is melaena?
A
blood in stool
7
Q
what is hematemesis?
A
bloody vomit
8
Q
what is haematuria?
A
blood in urine
9
Q
4 HEREDITARY causes of increased bleeding risk?
A
- Hemophilia VIII and IX.
- Factor XIII
- vW disease
- Ehler danols
10
Q
What does vW affect? What is its effect?
A
Affects vW factor and thus PLATELET ADHESION - causes INCREASED BLEEDING.
11
Q
What is Ehler Danlos?
A
- Connective tissue disorder characterized by mutations in type 5 collagen which affects the INTEGRITY OF BLOOD VESSELS.
- Results in INCREASED BLEEDING RISK.
12
Q
How is the liver involved in the stopping bleeding?
A
- Hepatocytes are involved in the SYNTHESIS OF COAGULATION FACTORS.
13
Q
How can severe liver disease increase bleeding risk? (3)
A
- Deficiency in serum coagulation factors.
- Abnormal structure and function of fibrinogen.
- Impaired clearance of activated clotting factors and thus INCREASED FIBRONOLYSIS.
14
Q
How can alcoholism increase bleeding risk (2)?
A
- Can cause LIVER CIRRHOSIS which can affect COAGULATION FACTORS.
- ALCOHOL-INDUCED THROMBOCYTOPENIA (deficit in PLATELETS).
15
Q
How large is a petichiae?
A
Small 1mm hemmorhage.
16
Q
Where does ecchymosis usually present (3).
A
- Skin, epithelium of the nose, uterus.
17
Q
4 types of ACQUIRED increased bleeding risk?
A
- Medications
- Liver disease.
- Alcoholism.
- Hematological malignancy (lymphoma, leukaemia).
18
Q
10 conditions than in MH would raise suspicions for you if the patient is anticoagulae=ted/ antiplatelets.
A
- DVT.
- PE.
- IHD.
- Cardiac syndromes.
- AF.
- MI
- CVA (cerebro-vascular accident/ ischaemic stroke).
- TIA
- Surgical patients at risks of thromboembolism.
- Pregnancy.
19
Q
What are the 4 types of anticoagulants?
A
- Coumarins.
- Parenteral heparin.
- LMW heparin.
- Non Vit K (NOACs)
20
Q
what type of anticoagulant is warfarin
A
Coumarin
21
Q
What is the mode of action of apixaban, edoxaban and rivaroxaban?
A
Direct and reversible inhibitors of factor 10A.
22
Q
2 occasions LMW is useful?
A
- Pregnancy.
- Long periods of stasis in a hospital bed (ex. operating theater).
23
Q
5 types of parentral anticoagulants?
A
- Heparin sodium.
- LMW heparin.
- Dalteparin sodium.
- Enoxiparin.
- Tinzaparin.
24
Q
Hemodyalisis and heparin?
A
- Patients that undergo hemodyalisis may be heparinized the day of their dialysis.
- Can see them THE FOLLOWING DAY once the heparin effects have worn off.
25
What can long term use of heparin cause?
Can result in PLATELET DISORDERS.
26
5 antiplatelet drugs?
- Clopidogrel.
- Aspirin/ NSAIDs.
- Prasugrel
- Ticagrelor.
- Dipyridamole
27
What is the mode of action of aspirin?
- Irreversible inhibitor of cyclo-oxygenase.
- Ultimately affects arachidonic acid pathway.
28
4 NOACs?
- Rivaroxaban.
- Apixaban.
- Edoxaban.
- Dagibatran.
29
What is the mode of action of dagibatran?
- Direct thrombin (factor 2a) inhibitor.
30
What are coumarins (what is their mode of action)?
- Vitamin K antagonists.
- Affect the coagulaiton factors reliant on the Vitamin K carboxylase enzyme.
31
Wha does the Vitamin K carboxylase enzyme do?
- Adds a carboxyl group to these factors necessary for function.
32
What clotting factors do coumarins affect?
Clotting factors 2,7,9 and 10.
33
3 coumarins?
- Warfarin sodium.
- Acenocoumarol.
- Phenindione.
34
- INR of less than 4.
35
What do we do if INR is above 4?
Cannot proceed (blood less able to clot).
36
What do we do if INR is way below the therapeutic index?
Contact the prescriber - patient at risk of a thromboembolic event.
37
When does primary bleeding occur?
Intra operative from the soft/hard tissues.
38
What could prolonged primary bleeding indicate?
Platelet deficit.
39
What are the primary hemostatic mechanisms after vascular injury?
1. Vasoconstriction.
2. Platelet adhesion.
3. Platelet activation.
4. Platelet aggregation.
5. PRIMARY PLATELET PLUG.
40
Secondary hemostatic mechanisms?
Clotting cascade.
41
When is reactionary bleeding?
- Sometime after the primary platelet plus.
- Around 2-3 hours Post Op.
42
What is reactionary bleeding potentially associated with?
- LA wears off
- ALTHOUGH vasoconstrictor has a very short hald life (10 minutes).
- Likely FAILURE OF THE SECONDARY HEMOSTATIC MEASURES.
43
When does secondary bleeding occur? Why?
- up to 14 days post op.
- Due to INFLAMMATORY PROCESSES LINKED WITH LOCALIZED INFECTION.
44
Why does secondary bleeding occur?
Due to infection.
45
What do you suspect if reactionary bleeding is prolonged?
Platelet deficiency.
46
How do you stop primary bleeding in soft tissue (3)?
- Pressure.
- Suture.
- BIPP pack.
47
What is considered normal bleeding?
Stops 2-5 minutes post extraction.
- Stops with biting pressure or firm digital pressure.
48
How does crushing stop bleeding?
For BONY bleeds in cancellous bone, CRUSH any bleeding vessels by placing direct pressure.
49
What bleeds is electrocautery suitable for? What does it do?
- Not suitable for BONY bleeds but suitable for SOFT TISSUE BLEEDS.
- Uses electric current rhough the site which BURNS it.
50
8 methods to help hemostasis?
1. Pressure (immediate general).
2. Suture (pressure - immediate local).
3. Bone wax (bony bleed).
4. Crush (bony bleed).
5. Electrocautery (soft tissue).
6. Sodium Nitrate (soft tissue).
7. Hemostatic agents.
8. Antifibrinolytics (Tranexamic acid).
51
6 hemostatic agents?
- Gelatin
- Collagen
- Cellulose based.
- Adhesive (used extraorally).
- Topical thrombin.
- Antifibrinolytics (tranexamic acid).
52
What is tranexamic acid used for?
In patients with vW disease or other fibronolytic disorders.
53
What can we give to patients on warfarin to stop bleeding?
- Vitamin K.
- However there will be a rapid reversal and the patient will be very not anticoagulated. DO NOT DO ROUTINELY- ONLY AT TIMES OF NEED.
54
What is considered severe ongoing haemorrhage following XLA (5)?
- Mouth filling up with fresh blood.
- Biting pressure not useful.
- Having difficulty suctioning the blood.
- Cannot see.
- Patient anxious and spitting out blood.
55
4 bleeding instances to refer?
- Severe ongoing haemorrhage.
- Reached extent of capabilities (ex. suturing, pressure etc and bleeding still moderate).
- Decreased BP (100/60).
- Increased HR > 100bmp as both could indicate FLUID LOSS.
56
2 characteristics of severe fluid loss?
- Increased HR > 100bpm.
- Decreased BP: 100/60.
57
What causes a hematoma?
- Persistent arteriolar bleed once everything is closed up and there is no opportunity for the bleed to escape.
58
What is the treatment for a hematoma if caught early (2)?
- Empty using a WIDE SYRINGE.
- Open the surgical wound and allow blood to drainn.
59
What is the treatment for a hematoma if caught later (has formed gel-like mass)?
Incision and surgical removal.
60
What are 2 concerns with hematomas?
- Risk of bleeding.
- Source of severe infection.
- Bleeding into anatomic spaces (ex. FOM)
61
When do hematomas occur in dentistry (2)?
- Extraction of mandibular third molars.
- Surgical extraction of maxillary third molars.
