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SMALL ANIMAL > 4.3.5: Haemostatic disorders - Bleeding disorders > Flashcards

4.3.5: Haemostatic disorders - Bleeding disorders Flashcards

1
Q

Clinical signs of primary haemostatic disorders

A
  • Petechiae/ecchymoses are common
  • Bleeding from mucus membranes
  • Often more than one site of bleeding
  • Prolonged bleeding at sites of injury
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2
Q

Clinical signs of secondary haemostatic disorders

A
  • Petechiae/ecchymoses are rare
  • Deep or cavity bleeds; can bleed from mucus membranes
  • Sometimes single site of bleeding
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3
Q

A puppy comes in bleeding from the mouth where its new teeth are coming through. What type of haemostatic disorder are you suspicious of?

A

Primary haemostatic disorder (bleeding from mm common)

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4
Q

Compare the clinical signs of primary vs secondary haemostatic disorders

THIS IS IMPORTANT

A
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5
Q
A

Hyphaema

Bleeding into the anterior chamber of the eye

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6
Q
A

Haematoma after jugular sample. This dog had rodenticide toxicity.

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7
Q
A

Petechiae
Small pinprick haemorrhages
Tiny vessels bleed into the skin and mucus membranes

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8
Q
A

Ecchymoses
Haemorrhage under the skin.
5p coin size or bigger.

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9
Q

If you need to take blood from an animal but you are suspicious of a coagulopathy, what should you do?

A

Take blood from a leg (not jugular), put on a pressure bandage afterwards, and watch carefully.

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10
Q

Name of this test and how it helps us differentiate between petechiae and allergies

A

Diascopy
* Microscope slide is pressed against the lesion to see if it blanches
* If it blanches (positive result) = erythema secondary to vasodilation. e.g. allergies
* If it does not blanche (negative result) = bleeding into the skin e.g. petechiae

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11
Q

What named factor is involved in primary haemostasis and what does it do?

A

Von Willebrand Factor
Acts as the “glue” sticking platelets to each other and to the subendothelial matrix on a damaged vessel

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12
Q

Broad causes of primary haemostatic disorders

A
  • Thrombocytopaenia
  • Thrombocytopathia
  • vWF deficiency
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13
Q

What tests can you do to diagnose a primary haemostatic disorder?

THIS IS IMPORTANT

A
  • Platelet count
  • Buccal mucosal bleeding time
  • vWF antigen test
  • Platelet function assays
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14
Q

Causes of thrombocytopaenia

A
  1. Defective platelet production
  2. Accelerated platelet removal
  3. Platelet sequestration or loss
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15
Q

Examples of diseases that could cause defective platelet production and therefore thrombocytopaenia

A
  • Bone marrow neoplasia e.g. leukaemia
  • Drug/chemical/toxin-induced bone marrow suppression
  • Bone marrow infections esp. viral and rickettsial
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16
Q

Examples of diseases that could cause accelerated platelet removal and therefore thrombocytopaenia

A
  • Immune-mediated thrombocytopaenia (IMTP) –> most common!
  • Consumption in microangiopathic conditions e.g. DIC
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17
Q

Examples of diseases that could cause platelet sequestration or loss and therefore thrombocytopaenia

A
  • Splenomegaly/vascular pooling
  • Acute ongoing haemorrhage
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18
Q

What type of anaemia is observed here? How do we know this?

A

Regenerative anaemia
There are spherocytes and reticulocytes visible

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19
Q

How can IMTP be categorised?

A

Immune mediated thrombocytopaenia
* Primary = idiopathic
* Secondary = drug-induced/secondary to infection or neoplasia

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20
Q

IMTP signalment

A
  • Young to middle aged, female dogs are over-represented
  • Breeds: Cocker Spaniels, miniature/toy poodles, Old English sheepdogs
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21
Q

IMTP treatment

A
  • Treat any underlying disease
  • Whole blood transfusion can be justified if life-threatening bleeding, but it typically doesn’t significantly raise platelet count
  • Long-term treatment centres around immunosuppression
  • Splenectomy has had variable results but could be considered in refractive cases
  • Patient will require ongoing monitoring
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22
Q

IMTP prognosis

A
  • Can be good: 10-15% mortality, 10-40% relapse
  • Negative prognostic indicators: melaena, high BUN
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23
Q

Thrombocytopathia

A

any kind of abnormal platelet function.
* Can be congenital or acquired.
* Clinical signs similar to thrombocytopenia, but platelet count is normal

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24
Q

Causes of thrombocytopathia

A
  • Inherited thrombopathias
  • Drug induced defects of platelet function e.g. several drugs including NSAIDs
  • Platelet dysplasia (=neoplasia)
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25
Q

Diagnosis of thrombopathia

A
  • Normal platelet counts but prolonged BMBT
  • Normal levels of vWF
  • Platelet function tests/assays

To a certain degree it is often a diagnosis of exclusion.

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26
Q

Thrombopathia treatment

A
  • No specific therapy
  • Platelet transfusions are not possible
  • Withdraw any drugs e.g. NSAIDs
  • Treat symptomatically e.g. blood transfusions if marked anaemia
27
Q

von Willebrand’s Disease (vWD)

A
  • Most common inherited bleeding disorder in dogs
  • Affects wide range of dog breeds; rare in cats
  • Can be classified as Type I, II and III
28
Q

Clinical signs of vWD

A
  • Typical of a primary haemostatic defect: mucosal haemorrhage, cutaneous bruising, prolonged bleeding from wounds
  • Occasionally more profound bleeding occurs:
  • Epistaxis
  • Haematuria
  • GI haemorrhage
  • Prolonged oestral bleeding
  • Gingival bleeding at tooth eruption reported
29
Q

Diagnosis of vWD

A
  • Platelet count is normal (check first using a blood smear)
  • BMBT is a useful screening test (severe forms of vWD >12 min)
  • vWF antigen test
  • Genetic testing is available: can classify as clear/carrier/affected
30
Q

Treatment of vWD

A
  • Plasma transfusion - in severe cases
  • Cryoprecipitate
  • Transfuse red cells (if oxygen carrying capacity compromised)
  • Type I: desmopressin to stimulate release of vWF from endothelial cells. Will not work in Type II and III.
31
Q

Example of breed prone to vWD

A

Dobermann

32
Q

Primary haemostasis

A

formation of a platelet plug. When a vessel is injured, platelets adhere to collagen; vWF is needed for this.
* Involves platelets, endothelial cells, vWF, thrombin, collagen

33
Q

Secondary haemostasis

A

=formation of a fibrin clot under the influence of clotting factors specifically thrombin; stabilisation of the platelet plug.
* Involves fibroblasts, platelets, endothelial cells, leukocytes
* Involves Factors II, VII, IX, X, XI
* Also involves non-enzymatic coagulation factors e.g. tissue factor, Factor V and VIII

34
Q

1

A

aPTT

35
Q

2

A

ACT

36
Q

3

A

PT

37
Q

Which factor has the shortest half-life and so will disappear first?

A

Factor VII

38
Q

If your patient has a very high PT, but APTT is not so high, what are you suspicious of?

A

This patient has eaten rat poison until proven otherwise
* This occurs because Factor VII (shortest half life) has disappeared first
* This is part of the extrinsic and common pathway, which PT tests
* aPTT tests the intrinsic and common pathways; the intrinsic pathway does not involve Factor VII, hence the aPTT result is not very high yet

39
Q

If fibrinogen is low, what does this suggest?

A

The patient is making a lot of clots and has used it all up

40
Q

Factor 1 is also known as

A

fibrinogen

41
Q

What is fibrinogen? Where is it made and how? Why might it be high/low?

A

Fibrinogen: a.k.a. Factor 1, the final factor into the coagulation cascade. It is a soluble plasma glycoprotein synthesised by the liver.
* Fibrinogen is converted by thrombin into fibrin during blood coagulation
* Fibrinogen will be elevated in any form of inflammation (it is an acute phase protein) -> this elevation takes 24-48hrs and often occurs before other clinical signs
* Low levels of fibrinogen = systemic activation of the clotting system has occured and there has been consumption of clotting factors

42
Q

What is produced from the breakdown of fibrinogen?

A

FDPs are produced from the breakdown of fibrinogen
Their presence indicates a pro-thrombotic state

43
Q

Why might fibrinogen be increased?

A
  • Elevated in inflammation
  • Indication of DIC
  • Potential bleeding/ making lots of clots
44
Q

Why might fibrinogen be decreased?

A
  • Viral and bacterial infection
  • Kidney disease
  • Traumatic injuries, surgery
  • Cancer
  • Heart disease
  • Canine pregnancy, post-abortion
  • DIC (due to consumption)
  • Liver failure
45
Q

How does rodenticide toxicity impact the coagulation cascade?

A
  • Vitamin K is an essential cofactor to the function of Factor II, VII, IX, and X
  • If there is low Vitamin K, fibrin formation is defective (i.e. rodenticide toxicity = rubbish secondary haemostasis)
  • Warfarin and rodenticides cause relative vitamin K deficiency because they inhibit Vitamin K reductase which is needed for recycling of Vitamin K to its active form
46
Q

Clinical signs of rodenticide toxicity

A
  • Clinical signs mimic coagulation factor deficiencies
  • Spontaneous haemorrhage into body cavities
  • SC haematomas
  • Prolonged bleeding from wounds
47
Q

Clinical signs of failure of secondary haemostasis

A
  • Deep or cavity bleeds
  • Mucus membranes may bleeding
  • Sometimes single site of bleeding
  • Haematomas are common

Petechiae / ecchymoses are rare in secondary haemostasis

48
Q

Diseases of secondary haemostasis

A
  • Congenital: haemophilia
  • Acquired: Vitamin K antagonism (coumarin/ rodenticide toxicity), hepatic disease
49
Q

Tests of secondary haemostasis

THIS IS IMPORTANT

A
  • Activated clotting time (ACT) : modification of APTT, assess intrinsic and common pathways. Less sensitive, good screening test.
  • Prothrombin time (PT): a.k.a. OSPT, measures extrinsic and common pathways.
  • Activated partial thromboplastin test (APTT): useful screen for intrinsic and common pathways.
  • Thrombin clot time (TCT) : direct measure of the function of fibrinogen.
  • Fibrinogen is converted into fibrin during coagulation.
  • Whole blood clotting time (WBCT)
  • Specific factor assays
50
Q

What does ACT measure?

A

ACT: activated coagulation time
* Modification of APTT
* Tests intrinsic and common pathways
* Requires patient platelets and calcium
* Less sensitive than APTT
* Good quick in-house screening test

51
Q

What does prothrombin time measure and what are the normal intervals for dogs and cats?

A

Prothrombin time (PT)
* Measures activity of extrinsic and common pathway factors
* Prolonged time = due to a deficiency of any one factor
* Normal dog = 7-10s
* Normal cat = 7-10s

52
Q

What does APTT measure and what are the normal intervals for dogs and cats?

A

Activated partial thromboplastin time
* Useful screen for intrinsic and common pathways
* Prolonged due to a deficiency of any single factor
* Intervals depend on machine used
* Normal dog = 12-20s
* Normal cat = 12-22s

53
Q

What does TCT and what does an abnormal result indicate?

A

Thrombin clot time
* Direct measure of the function of fibrinogen
* Prolonged TCT indicates decreased clot formation and will occur if there is a deficiency in/ abnormal fibrinogen

54
Q

What does WBCT measure and what are the normal intervals?

A

Whole blood clotting time (WBCT)
* Crude measure of the intrinsic and common pathways
* Will also be increased if thrombocytopaenia is present
* Normal dog = 3-13 mins
* Normal cat = 8 mins

55
Q

What do specific factor assays measure and when would you use them?

A

Specific factor assays
* Measure the level of some individual clotting factors
* Used in the investigation of inherited coagulation disorders

56
Q

What are the two forms of haemophilia and how will you diagnose them?

A

Haemophilia A
* Sex-linked inherited, affects males
* Patient suffer spontaneous, life-threatening bleeding episodes
* Deficiency of Factor VIII (essential to intrinsic pathway)
* Results in prolonged APTT
* Confirm with specific Factor VIII assay

Haemophilia B
* Sex-linked inherited
* Deficiency of Factor IX
* Clinically identical to Factor VIII deficieny as both at same point in pathway
* Confirm with specific Factor IX assay

57
Q

Treatment of haemophilia

A
  • Pain relief (care with drugs)
  • Restrict movement
  • Fresh plasma/ FFP/ whole blood can be considered for serious bleeding
  • Often animal will experience small bleeds which are contained by anatomical structures e.g. haemarthrosis
58
Q

How long does it take rodenticide toxicity to have an effect?

A

1-2 days
Can take as long as 1 week

59
Q

Diagnosis of rodenticide toxicity

A

Initially PT/ OSPT is prolonged
Later APTT also increases

60
Q

Treatment of rodenticide toxicity

A
  • Decontamination of the GIT esp if consumption in last few hours: emesis, gastric lavage, enema, activated charcoal etc.
  • Specific therapy: Vitamin K (injectable or oral) for weeks to months
  • PT promptly returns to normal with treatment but will increase if treatment withdrawn too early
61
Q

True/false: advanced liver disease is a major differential that should be ruled out in cases of suspected coagulopathies.

A

True
* Many clotting factors and their inhibitors are synthesised in the liver
* Vitamin K dependent factors are also activated in the liver
* In cases of coagulopathy due to liver disease, there is elevation of both PT and APTT
* In liver disease, factors go down, and coagulation times go up.

62
Q

True/false: if you suspect advanced liver disease, taking a biopsy is a good first step to confirm your suspicions.

A

False
* They may bleed from the biopsy
* Test liver enzymes and coags first before you make the patient bleed out

63
Q

What are some good general principles for management of a patient with either a pimary or secondary coagulopathy?

A
  • Avoid injections, but if you have to, go for SC over IM
  • Vitamin K is like injecting oil, so supplement orally within 7 days of toxicity if you can
  • Minimise invasive procedures
  • Handle gently - they will bleed. Sedate if required to avoid further trauma.

SMALL ANIMAL (90 decks)

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