Hemostasis Pt. 1 Flashcards
(45 cards)
Components of Normal Hemostasis (3)
- Blood vessel
- Adequate platelet mass & function
- Adequate plasma coagulation factor levels & function
Hemostatic tests for intrinsic pathway
ACT, PTT
Hemostatic tests for extrinsic pathway
PT
What causes hemorrhage?
- blood vessel, platelet, and coagulation factor causes
Blood vessels
* Damage (e.g., trauma)
* Inflammation (vasculitis)
Platelets
* Reduced number (<50,000/uL; especially < 20,000)
* Impaired function
Coagulation factors
* Reduced levels
* (Impaired function)
Primary Hemostatic Defect; clinical signs? what are they due to?
- Clinical signs due to lack of platelet plug
- Widespread cutaneous & mucosal petechiae / ecchymoses:
- Gingival bleeding
- Epistaxis
- Hematuria
- Hematemesis / melena / hematochezia
- Hematoma after venipuncture
Secondary Hemostatic Defect; clinical signs?
- Clinical signs:
- Hemothorax
- Hemoabdomen
- Hemarthrosis
- Epistaxis
- Hematemesis / melena / hematochezia
- Large ecchymoses
- Petechiae typically not observed
what are primary and secondary hemostasis?
Hemostasis has two phases: primary and secondary hemostasis. In primary hemostasis, platelets aggregate to form a plug at the site of an injured blood vessel. While these platelets are aggregating, coagulation, or secondary hemostasis starts.
pre-surgery plan for breeds at risk of vWD?
- Pre-anesthetic CBC & mini-chemistry panel (liver/kidneys)
- Buccal mucosal bleeding time
- vWf: Ag level
Von Willebrand Disease - what does VWF circulate with, and what does it do? is this a common disorder?
- VWF circulates with factor VIII
- Promotes platelet-endothelial interaction
- Most common inherited hemostatic disorder in dogs
types of VWD and definitions
Type 1 VWD:
- Most common
- Reduction in all multimers of VWF
Type 2 VWD:
- Reduction in high molecular weight multimers
Type 3 VWD:
- Virtual absence of any VWF
VWD Clinical Signs
- Spontaneous hemorrhage, especially mucosal
- Severity highly variable
> Signs might only be seen after trauma - Petechial hemorrhage uncommon
Diagnosing VWD - helpful tests and what they mean?
- BMBT not specific for VWD
> Even when normal can still be at risk for bleeding - VWF Antigen Test
> Reported as a percentage of “normal”
> Normal range is 70-180% - VWF deficient:
> <50% = VWD carrier or affected
=> <35% = usually affected
> 50-69% = borderline (VWD carrier or normal) - VWF Function (collagen binding assay)
> Preliminary studies: appears to correlate well with bleeding risk
> Longer turnaround vs Antigen test - DNA test
> Often used to identify carriers (breeding stock)
> Does not correlate with risk of bleeding
Peri-Operative Risk management for dog with VWD?
- Pre-operative transfusion options
> Cryporecipitate plasma transfusion
: Concentrated source of VWF, Factor VIII (to stabilize existing VWF), fibrinogen
> Fresh frozen plasma
: VWF and all coagulation factors - DDAVP (Desmopressin)
> Stimulates VWF release
> Helps for 2-4 hours in some affected dogs
> Useful adjunct to plasma
> 1 microgram/kg SQ, 30 min prior to
surgery
> No additional benefit in repeated dosing
VWD Patients: Pre-Surgical Planning
- what do we do for dogs with low VWF titre but no previous bleeding episodes & normal BMBT
- Consider giving only DDAVP pre-op
- (Might not need plasma but ideal to have it in the clinic just in case)
how can we treat a VWD patient in the case of trauma or other factors causing excessive bleeding?
- DDAVP injection
- Cryoprecipitate or fresh frozen plasma transfusion
- +/- RBC replacement if marked hemorrhage
- Compression and other hemostatic techniques
Prognosis for VWD
Mild to moderate cases Type I (majority):
* Good prognosis
* Client education
* Treatment of trauma, pre-surgical care needed
other platelet conditions aside from VWD
- Immune mediated thrombocytopenia
- Platelet function disorders uncommon
> Often inherited, breed-related
Top differential diagnosis for petechial hemorrhage, mucosal bleeding
- Immune mediated thrombocytopenia
Types of hereditary Secondary Hemostatic Defects
- Hemophilia A, B
- Other factor deficiencies
Types of acquired Secondary Hemostatic Defects
- Liver dysfunction
- Toxicity (Vitamin K antagonism)
- Disseminated intravascular coagulation (DIC)
- Others
mechanism of Anticoagulant Rodenticide Toxicity
Inhibits recycling of Vitamin K1 from vitamin K1 epoxide reductase
- Vitamin K antagonism = lack of production of factors II, VII, IX, X
> FVII has shortest half-life, affected first - Several types of anticoagulant rodenticides exist, variable half-life
> Warfarin (and Similar 1st generation Anticoagulants): ~7 days
> Bromadiolone: ~14 days
> Brodifacoum (& Other “Super Warfarins”): 3-4 weeks
Clinical Signs of anticoagulant rodenticide toxicity and timing
- Develop 3-5 days following ingestion
- Common clinical signs:
- Dyspnea, coughing
- Exercise intolerance
- Hematomas
- Hematemesis, melena
- Hematuria
- Pale MMs
- Signs secondary to bleeding in other locations
Diagnosing Rodenticide Toxicity - common tests and findings
- Prolongation of PT, PTT, ACT
> PT prolonged first - CBC findings:
> May see anemia, mild thrombocytopenia
Radiographs - Radiographs
> Thoracic or abdominal effusions
Less Common Tests for Rodenticide toxicity
PIVKA:
* Proteins induced by vitamin K antagonism
* Levels will be increased
* Not widely available
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Definitive diagnosis requires serum levels (or tissue levels, stomach contents)
* Rarely performed
