Internal Medicine: Haematology and Transfusion: Approach to Bleeding Flashcards

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1
Q

What needs to be assessed about a bleeding animal?

A

Quantify blood loss
* dog 80-90ml/kg
* cat 60-70ml/kg

Identify life threatening situations
* hypovolaemic shock
* Severe anaemia
* brain/pulmonary haemorrhage

Establish venous access and collect samples for tests
* PCV
* Blood smear
* Coagualation profile
* Biochem

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2
Q

How is a bleeding patient stabilised?

A
  • Control of haemorrhage- wound pressure
  • Fluid replacment/blood transfusion (>25% loss)
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3
Q

What are the stages to haemostasis?

A
  • Vessel injury
  • Vascular contraction
  • Primary haemostasis- endothelum, platelets, vonWillebrand factor
  • Secondary haemostasis- coagulation cascade, thrombin
  • Tertiary haemostasis- fibrinolysis- plasmin
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4
Q

What are clinical signs of primary haemostasis defects?

A

‘Small holes’

Due to lack of platelets/poor function

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5
Q

What are clinical signs of secondary haemostasis defects?

A

‘large holes’
* Results of deficiency in clotting factors
* Tend to present more acutely with life-threatening blood loss
* Subcutaneous or cavity bleeding
* Haematoma formation
* Pulmonary haemorrhage
* Haemarthrosis

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6
Q

What In-house lab tests can be done for a bleeding patient?

A
  • Haem
  • Biochem
  • Whole blood clotting time
  • Activated clotting time
  • Buccal mucosal bleeding time- if not thrombocytopenia
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7
Q

How can primary and secondary coagulation be differentiated?

A

Primary- test of platlet function or number
* manual platelet count
* mucosal bleeding time
* von Willebrand factor

Test of coagulation
* prothrombin time
* activates partial thromboplastin time
* Activated clotting time

Test of fibrinolysis
* fibrin degredation products
* D-dimers

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8
Q

What are disorders of primary haemostasis?

A

Thrombocytopenia
* platlets < 30x10^9/L

von Willebrand disease
Thrombocytopathia- very rare
Vasulcar disorders- very rare

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9
Q

What can cause thrombocytopenia?

A

Lack of production
* Bone marrow disorders
* Drug toxicosis

Increased consumption
* DIC
* Acute severe haemorrhage

Increased destruction
* Immune mediated: primary or secondary

Increased sequestration- splenic torsion

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10
Q

How can thrombocytopenia be inherited?

A

Inherited macrothrombocytopenia
Breed associated- sighthounds

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11
Q

What causes primary and secondary immune mediated thrombocytopenia?

A

Primary
* IgG binding to platelets
* results in their destrution

Secondary
* Drugs, infectious disease, neoplasia
* ABs most common
* Anaplasma, babesia, lepto, leishmania

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12
Q

What is used to diagnose immune mediated thrombocytopenia?

A
  • Full clin history- drugs, travel
  • Clinical and opthalmoloigcal exam
  • Haematology with blood smear
  • Biochem
  • Idexx 4DX snap- vector borne
  • Thoracic radiographs
  • Abdominal US
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13
Q

How is IMTP treated?

A

Secondary- treat underlying disease

Primary- glucocorticoids

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14
Q

When is platelet dysfunction suspected?

How is it treated?

A

Animals who bleed excessively despite normal platelet count and coagulation profile

Drug therapy
* NSAIDs, Aspirin, PBZ and many others

Occurs with hepatic disease, renal disease, hyperproteinaemias

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15
Q
  1. What can cause acquired von Willebrand disease?
  2. Where is vWF synthesised and stored?
A
  1. Severe aortic stenosis
  2. Endothelial cells
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16
Q

How is von Willebrand disease diagnosed and treated?

A
  • Buccal mucosal bleeding time increased
  • Antigenic test
  • Genetic testing

Tx
* Cryoprecipitate- whole blood, frozen plasma
* DDAVP- vasopressin- increases vWF release

17
Q

What are acquired and inherited disorders of secondary haemostasis?

A

Acquired
* vitamin K antagnoism- rodenticide
* toxicity
* liver disease
* DIC

Inherited disorders
* Haemophilia A- more common
* Haemophilia B

18
Q

What cause vitamin K deficincy?
Why does it cause secondary haemostasis?

A

Rodenticide most common- hepatic failure, decreased absorption

Involved in production/activation of factors II, VII, IX, X

19
Q
  1. What are the clinical signs of vit K deficiency
  2. How is it diagnosed?
  3. How is it treated?
A
  1. 2-5 days after ingestion, epistaxis, melaena, haematoma, haematuira, gingival bleeding
  2. Coagulation testing, PT/APTT
  3. Vit K therapy- 2-4 weeks, FFP transfusion in emergency
20
Q

What can cause DIC?

A
  • Infectious disease- septicaemia
  • Immune mediated disease
  • Neoplasia
  • Trauma
  • Heat stroke
  • Cardiac disease
  • Angiostronglyus vasorum
21
Q

What are lab abnormalities of DIC?

A
  • Prolonged clotting time
  • Reduced ATIII
  • Thrombocytopenia
  • Schistocytes
  • Increased FDPs/D-Dimers
  • Decreased fibrinogen
  • Poor prognosis
22
Q

What are D-dimers more indicative of in dogs?

A

Fibrinolysis in DIC