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Year 3 MOD > Clinical Pathology- Haematology: Approach to Bleeding Patient and Transfusion Medicine > Flashcards

Clinical Pathology- Haematology: Approach to Bleeding Patient and Transfusion Medicine Flashcards

(54 cards)

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1
Q

If a patient arrives and is bleeding how should you approach the animal?

A

Attempt to quantify blood loss

Identify life threatening situation- hypovolaemic shock, severe anaemia, brain or pulmonary haem

Establish venous access and collect samples for test

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2
Q

How can the patient be stablilised?

A

Control of haemorrhage- pressure

Fluid replacement:
Volume replacement crystalloid if hypovolaemic
‘shock rates’ recomend a bolue of 1/5-1/4 animals blood volume
Blood transfusion if significant anaemia

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3
Q

Briefly describe the process of haemostasis?

A

Vessel injury

Vascular contraction- primary plug

Primary haemostasis- endothelium, platelets, von willebrand

Secondary haemostasis- coagulation cascade resulting in generation of thrombin

Tertiary haemostasis- fibrinolysis- plasmin

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4
Q

What is needed for primary haemostasis?

A

von Willebrand factor

platelets

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5
Q

What are clinical signs of primary haemostasis defects?

A

‘Small holes’

due to lack of platelets/poor platelet function

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6
Q

What are clinical signs of secondary haemostasis defects?

A

Result of deficiency in clotting factors

Tend to present more acutely with life-threatening blood loss

Subcutaneous or cavity bleeding

Haematoma formation

Pulmonary haemorrhage

Haemarthrosis

‘Large holes’

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7
Q

What in house tests can be used to test for primary and secondary haemostasis disorders?

A

Haematology- smear examination and platelet estimation

Biochemistry

Whole blood clotting time- uncommon

Activated clotting time- uncommon

Buccal mucosal bleeding time

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8
Q

Where should thepatient be venepunctured if worried aboiut haemostasis disorders?

A

Cephalic/Saphenous vein

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9
Q

What tests can be used to differentiate between primary and secondary haemostasis disorders?

A

Primary coagulopathy- test platelet function or number:
manual count, buccal mucosal bleeding time, von Willebrand factor

Test of coagulation:
Prothrombin time
Activated partial thromboplastin time
Activated clotting time- rarely used
Test specific factor levels

Test of fibrinolysis- fibrinogen degredation products, D-dimers

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10
Q

How much blood can healthy animals usually lose?

A

15-25% of blood

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11
Q

What disorders of primary haemostasis are there?

A

Thrombocytopenia

von Willebrands disease

Thrombocytopathia- v rare

Vascular disorders- v rare

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12
Q

What can cause thrombocytopenia?

A

Most common cause

Lack of production- bone marrow disorders, drug toxicosis

Increased consumption- DIC, acute severe haemorrhage

Increased destruction- immune mediated- primary/secondary

Increased sequestration- splenic torsion

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13
Q

What are the two types of inherited thrombocytopenia?

A

Inherited macrothrombocytopaenia- CKCS, norfolk and cairn terriers

Breed-associated thrombocytopenia- Sighthounds with lower platlet counts

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14
Q

What is the difference between primary and secondary immune mediated thrombocytopenia?

A

Primary- IgG binding to platlets resulting in their destruction, marked thrombocytopenia

Secondary- secondary to drugs, infectious disease or neoplasia, antibiotics most common

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15
Q

How is IMTP diagnosed?

A

Full clinical history- including drugs and travel history

Full clinical exam including opthalmological exam

Haematology with blood smear evalutation

Biochemistry +/- urinalysis

Thoracic radiographs

Abdominal ultrasound

Idexx 4DX SNAP

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16
Q

How is IMTP treated?

A

Secondary- treat underlying disease or discontinue offending drug

Glucocorticoids mainstay of therapy for primary disease:
regulator of gene expression, effects humoral and cell-mediated immune system

Whole blood transfusions can provide short-term haemostasis despite a negligible increase in platelet count post-transfusion

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17
Q

What is platlet dysfunction and what can cause it?

A

Animals who bleed excessively despite normal platelet count and coagulation profile

Causes:
Drug therapy
von Willebrands disease
Hepatic disease
Renal disease
Hyperproteinaemias
Bone marrow neoplasia

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18
Q

What is von Willebrands disease?

A

Deficiency of von Willebrand factor- inherited, acquired with severe aortic stenosis

vWF is synthesised and stored by endothelial cells- vital for platelet adherence

Mucosal surface bleeding or excessive bleeding following surgery

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19
Q

How is von Willebrands disease treated?

A

Cryoprecipitate- rich in VII, fibrinogen and vWF, whole blood or fresh plasma

DDAVP- 1-desamino-8-D-arginine vasopressin increases vWF release

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20
Q

What causes disorders of secondary haemostasis?

A

Deficiency of clotting factors

Inherited uncommon- haemophilia A/B

Usually acquired- vitamin K antagonism (deficency), severe liver disease, DIC

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21
Q

What can cause vitamin K deficiency?

A

Most commonly caused by ingestion of vitamin K antagonists- rodenticides

Other causes- hepatic failure, decreased absorption

Vit K involved in production/activation of factors II, VII, IX, X

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22
Q

What are the clinical signs, diagnosis and treatment of vitamin K deficiency?

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A

Clinical Signs:
typically 2-5 days after ingestion- epitaxis, melaena, haemoptysis, haematoma, eccymoses, haematuria, gingival bleeding, haemoabdomen, haemothorax

Diagnosis- clinical history, signs, coatulation testing

Treatment- vit K therapy, not IV, recommended for 2-4 weeks, FPP transfusion in emergency

23
Q

What does DIC stand for and what does it cause?

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A

Disseminated intravascular coagulation

Widespread activation of coagulation leads to thrombosis and multiorgan failure

24
Q

What are the common underlying casues of DIC?

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A

Infectious disease, immune mediated, neoplasia, trauma, heat stoke, cardiac disease, parasites, toxicity

25
What can cause acute DIC?
Presentation with thrombotic disease Haemorrhage Thrombosis Multiorgan failure Metabolic acidosis
26
What are the lab abnormalities of acute DIC and how is it treated?
Lab abnormalities: Prolonged clotting times, reduced ATIII, thrombocytopenia, schistocytes, increased FDPs/D-dimers, decreased fibrinogen- poor prognosis Treatment- treat underlying cause, plasma, heparin, whole blood
27
What are FDPs and what causes their increase?
Fibrinogen degredation products Increased- DIC, thrombotic disease, reduced hepatic clearence
28
What are D-dimers more sensitive indicators of and why?
D-dimers are more senstitive indicators of fibrinolysis in canine DIC because they are specific for breakdown of cross linked fibrin
29
What is PT and aPTT?
PT- prothombin aPTT- activated partial thromboplastin time- blood coagulation test
30
Can you fill in the following table?
31
When should a patient be given a blood transfusion?
Based on clinical signs- signs of reduced oxygen delivery- taccycardia, lethargy, collapse, weakness Transfuse dogs with PCV 15-20% and cats of 10-15%
32
How long does it take PCV to decrease after acute haemorrhage?
Lag period of 24 hours
33
What decides what blood product should be used?
Replace like with like Haemorrhage there is equal loss so whole blood preferred
34
35
What blood product should be used with blood loss, haemolysis and coagulopathy?
Blood loss- fresh whole blood or packed red cells Haemolysis- packed red cells Coagulopathy- fresh frozen plasma, regular plasma, cryoprecipitate
36
What different blood transfusion products are availible and what are its constituents?
Whole blood- 35% RBC, 65% plasma Packed red cells- 60-80% RBCs, plasma 40-20% Fresh frozen plasma- 99.9% I-XI clotting factors and vWF Regular plasma- 99.9%- II, VII, IX, X clotting factors
37
What is the UK blood bank and how does it work?
Charity that provides all blood products and equipment as well as guidance Can deliver 24/7- cost depends on distance Provide cross match with IDEXX No feline or platelet products
38
Within how long does fresh whole blood need to be used?
Within the first 24-48 hours following collection After this there is a decrease in liable clotting factors and the product becomes whole blood with 21 day shelf life 6 hours after colleciton there is no platelets in blood
39
How long is fresh frozen plasmas shelf life?
Centrifuged blood within 6-8 hours, contains clotting factors 1 year shelf life
40
What information needs to be known about patients blood types before infusion?
Ideally give type-specific in dogs as it has a longer life span If in doubt or an emergency give dogs DEA -ve In cats it is imperative that type specific blood is given as can lead to acute haemolytic transfusion reactions Not necessary for adminstration of plasma products
41
Why does blood type of patients usually need to be known?
RBCs have different antigens If a patient has a specific antigen it will not have antibodies against that protein If they do it will cause RBC haemolysis
42
Why can dogs be given any blood in an emergency but cats cannot?
Dogs rarely have naturally occuring auto-antibodies so will rarely have an acute haemolytic transfusion reaction- auto-antiboides are usually produced 3-5 days after transfusion- the first one is free Cats do have naturally occuring auto-antibodies, non-matched blood causes acute haemolytic reaction
43
What antigen is found on the surface of canine RBCs? How is this used for typing?
DEA, the only one we can type is the DEA 1 system Typing: * DEA 1-ve recieving DEA 1+ve blood for the first time will develop delayed haemolytic transfusion reaction * DEA 1+ve dogs reciving DEA 1-ve blood for the first time will not have any DEA 1 antigens giving longer lifespan of RBCs
44
How is cats blood typed?
In cats the main RBC antifen is the A/B system where A is autosomal dominant to B All B cats have auto-antibodies for A Not all cats have auto-antibodies for B
45
What are the different ways blood can be tested?
Gold standard is testing in an external lab- there is rarely time though Most common methods are rapid vet-card method and alvedia cassette method Cassette method easier to interpret and autoagglutination does not need to be ruled out
46
What is cross matching?
Cross matching looks for reactions between red blood cell antigens and antibodies in the donor and recipient Performed by mixing two bloods and looking for evidence of haemolysis
47
What is major and minor cross matching?
Major- looks for the presence of auto-antibodies in plasma Minor- looks for the presence of auto-antibodies in donors plasma against recipients RBCs
48
How much blood should be tansfused to the patient?
Restrictive transfusion target- 21-25% PCV just as good as liberal 35-40% Use formulas as a rough guide Round up to the nearest bag/cat Wide variation in post-transfusion PCV
49
How should transfusion be administered?
IV/IO All administered slowly to prevent transfusion reactions Consider equipment and ability to monitor patient Maintaining sterility is vital Must be fiven through transfusion set with in-line filter Dogs better drip-by-drip, cats a syringe 0.5-1ml/kg/hr for first 30 mins 4-6ml/kg/hr thereafter only flush IV with saline No access to food
50
What should be monitored for a transfusion?
Monitoring for signs of transfusion reactions during and after Monitor HR, RR, rectal temp Watch for anaphylaxis, uticaria, nausea, vomiting
51
What haemolytic transfusion reactions can occur?
Type II with varying degrees of severity Severe acute haemolytic reactions- obvious- tachycardia, tachypnoea, pyrexia, haemolysis of serum, haemoglobinuria Mild delayed haemolytic reactions- slow removal of RBCs by monocytic phagocytic syndrome
52
What respiratory transfusion reactions can occur?
Increase in respiratory rate- common but could be stress or disease TRALI- transfusion induced acute respiratory distress syndrome TACO- transfusion related cardiovascular overload- cats or patients with cardiac/renal disease
53
How should transfusion reactions be managed?
If reaction suspected stop transfusion If in doubt, temporarily stop and and restart at slower rate If cause cannot be found symptomatic treatment should be administered
54
What non-heamoltyic transfusion reactions can occur?
Most common is non-haemolytic pyrexia and anaphylaxis Reactions vary from tachycardia, tachypnoea, and pyrexia but can also be uticaria

Year 3 MOD (42 decks)

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