Clinical Pathology- Haematology: Approach to Bleeding Patient and Transfusion Medicine Flashcards
If a patient arrives and is bleeding how should you approach the animal?
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
How can the patient be stablilised?
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
Briefly describe the process of haemostasis?
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
What is needed for primary haemostasis?
von Willebrand factor
platelets
What are clinical signs of primary haemostasis defects?
‘Small holes’
due to lack of platelets/poor platelet function
What are clinical signs of secondary haemostasis defects?
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’
What in house tests can be used to test for primary and secondary haemostasis disorders?
Haematology- smear examination and platelet estimation
Biochemistry
Whole blood clotting time- uncommon
Activated clotting time- uncommon
Buccal mucosal bleeding time
Where should thepatient be venepunctured if worried aboiut haemostasis disorders?
Cephalic/Saphenous vein
What tests can be used to differentiate between primary and secondary haemostasis disorders?
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
How much blood can healthy animals usually lose?
15-25% of blood
What disorders of primary haemostasis are there?
Thrombocytopenia
von Willebrands disease
Thrombocytopathia- v rare
Vascular disorders- v rare
What can cause thrombocytopenia?
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
What are the two types of inherited thrombocytopenia?
Inherited macrothrombocytopaenia- CKCS, norfolk and cairn terriers
Breed-associated thrombocytopenia- Sighthounds with lower platlet counts
What is the difference between primary and secondary immune mediated thrombocytopenia?
Primary- IgG binding to platlets resulting in their destruction, marked thrombocytopenia
Secondary- secondary to drugs, infectious disease or neoplasia, antibiotics most common
How is IMTP diagnosed?
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
How is IMTP treated?
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
What is platlet dysfunction and what can cause it?
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
What is von Willebrands disease?
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
How is von Willebrands disease treated?
Cryoprecipitate- rich in VII, fibrinogen and vWF, whole blood or fresh plasma
DDAVP- 1-desamino-8-D-arginine vasopressin increases vWF release
What causes disorders of secondary haemostasis?
Deficiency of clotting factors
Inherited uncommon- haemophilia A/B
Usually acquired- vitamin K antagonism (deficency), severe liver disease, DIC
What can cause vitamin K deficiency?
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
What are the clinical signs, diagnosis and treatment of vitamin K deficiency?
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
What does DIC stand for and what does it cause?
Disseminated intravascular coagulation
Widespread activation of coagulation leads to thrombosis and multiorgan failure
What are the common underlying casues of DIC?
Infectious disease, immune mediated, neoplasia, trauma, heat stoke, cardiac disease, parasites, toxicity
What can cause acute DIC?
Presentation with thrombotic disease
Haemorrhage
Thrombosis
Multiorgan failure
Metabolic acidosis
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
What are FDPs and what causes their increase?
Fibrinogen degredation products
Increased- DIC, thrombotic disease, reduced hepatic clearence
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
What is PT and aPTT?
PT- prothombin
aPTT- activated partial thromboplastin time- blood coagulation test
Can you fill in the following table?
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%
How long does it take PCV to decrease after acute haemorrhage?
Lag period of 24 hours
What decides what blood product should be used?
Replace like with like
Haemorrhage there is equal loss so whole blood preferred
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
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
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
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
How long is fresh frozen plasmas shelf life?
Centrifuged blood within 6-8 hours, contains clotting factors
1 year shelf life
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
