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Bleeding disorders - Coggle Diagram
Bleeding disorders
immune-mediated thrombocytopenia (primary)
one of the most common causes of acquired bleeding in dogs
IMT results from binding of antibodies to the platelet surface + the premature clearance of these stimulated platelets by the mononuclear phagocytic system
secondary IMT occurs in association with neoplasia, viral or bacterial infections, or disease such as systemic lupus erythematous and rheumatoid arthritis. It may also be associated with administration of various drugs
any drug has potential to cause IMT, most common are antibiotics particularly sulphonamides and cephalosporins
neoplasia associated via several mechanisms e.g. increased platelet consumption 2ry to a bleeding tumour or DIC, splenic sequestration, decreased platelet production due to myelophthisis
breed predisposition
cocker spaniels
GSDs
old english sheepdogs
poodles
more common in females and middle aged
Diagnosis
exclude other causes of thrombocytopenia
decreased production
bone marrow disease
drugs
infection
haemophagocytic syndrome
secondary IM thrombocytopenia
infection
neonatal alloimmune thrombocytopenia
neoplasia
systemic lupus erythematosus
transfusion reaction
increased utilisation/non-immune destruction
DIC
haemolytic-uraemia syndrome
microangiopathic destruction
septicaemia
snake venom
chronic/severe haemorrhage
coagulopathy
neoplasia
vasculitis
canine adenovirus-1
canine herpes virus
dirofilariasis
ehrlichiosis
FIP
neoplasia
polyarteritis nodosa
rocky mountain spotted fever
septicaemia
systemic lupus erythematosus
sequestration
hepatomegaly
sepsis
splenomegaly
chronic infection
haematoma
IMHA
neoplasia (hemangiosarcoma/oma, mast cell, mets)
portal hypertension
splenic torsion
splenitis
systemic lupus erythematosus
sudden onset of anorexia, lethargy, weakness, pallor, bruising, epistaxis or other forms of mucosal or surface bleeding (esp after stressors e.g. surgery, kennelling, oestrus, parturition) is suggestive of primary IMT
approx 20% of dogs concurrent IMHA
confirmed based on the response to corticosteroid therapy
normalisation of platelet count 7-10 days of initiating therapy
this reduces the rate of sequestration of stimulated platelets. It will not differentiate between primary and secondary forms of IMT
Treatment
cage rest to minimise risk of trauma
glucocorticoids
inhibit macrophage induced sequestration of antibody stimulated platelets, reduce antibody prodcution, increase capillary resistance to haemorrhage and in some patients stimulate platelet production
oral prednisolone (2mg/kg every 12h)
monitor platelets weekly and continue treatment until count returned to normal (1-several weeks) depending on patient
then taper drug over an equal period of time
some must remain on tx to prevent recurrence
dogs with recurrent disease and cases unresponsive to glucocorticoids have been treated with drugs such as vincristine
reduces platelet phagocytosis by macrophages and stimulates thrombopoiesis
also cyclophosphamide and synthetic androgen danazol
or by surgical removal of the spleen
primary IMT is rarely diagnosed in cats and oral prednisolone not as effective in dogs, consider dexamethasone, cyclosporine and chlorambucil
Anticoagulant rodenticide toxicity (vitamin K deficiency)
first generation anticoagulant warfarin
short half life 12 h
relatively low toxicity in target species
repeated or massive exposure required to cause clinical bleeding in dog
second generation coumarin derivatives (bromadiolone and brodifacoum) and indandione rodenticides (pinion and diaphacinone)
more potent
longer lasting effects (half life 4-6 days)
more completely bound to plasma proteins and have an enhanced tendency to accumulate in hepatic tissue
most likely via secondary poisoning through ingestion of killed target species
inactivate vitamin K enzyme and prevents carboxylation of vitamin K dependent coagulation proteins and cannot lead to fibrin formation
clinical signs
onset delayed for several days post exposure while the concentrations of the vitamin K dependent clotting factors become depleted
may be non-specific if internal bleeding
depression
weakness
pallor
dyspnoea
abdominal swelling
sudden death
anaemia
external haematomas
bruising
excessive bleeding from venipuncture sites or other sites of injury
epistaxis
haematemesis
haematochezia
melaena
haematuria
lameness
diagnosis
coagulation screening tests unlikely to reveal abnormalities until at least 36-72 hours post-exposure
pro-thrombin time generally prolonged first (36-48h)
factor VII has the shortest half life (approx. 6h)
partial thromboplastin time and activated clotting time usually prolonged to 48-72 hrs post exposure
Proteins induced by vitamin K antagonism (PIVKA) can be detected by some labs, usually cleared within 12h of administration of vitamin K, collect samples before vitamin K therapy
other possible confirmatory tests:
quantification of vitamin K epoxide concentrations and determination of the specific anticoagulant in blood, liver +/- stomach
treatment
supportive to correct hypovolaemia and coagulopathy
fresh blood or plasma will help correct the hypovolaemia and enhance haemostasis by restoring depleted clotting factors
vitamin K1 (5mg/kg) loading dose subcutaneously at multiple sites
followed by s/c or oral doses (1.25-2.5mg/kg) at 8-12hr intervals for as long as necessary until toxin metabolised or excreted
duration of tx depends on anticoagulant, 1 week tx may be undertaken initially
PT + PTT must be checked 48-72h after cessation of vitamin K1 tx
if prolonged indicates residual toxic effect and need for continued vitamin K 1 tx
hypo coagulable patients at increased risk of internal haemorrhage so monitor condition and minimise physical activity
Dissminated intravascular coagulation
develops 2ry to 1ry disease which in some way damages the vasculature or releases procoagulant tissue factors or other activators into the general circulation
potential causes
neoplasia
infectious disease
shock
heat stroke
envenomation
acute inflammatory processes
categorised as acute or chronic, localised or generalised
peracute
(hypercoagulable) stage
may be no overt signs of bleeding or only non-specific signs consistent with organ dysfunction
coagulation screening tests may be normal or decreased and platelet concentration may be normal
acute
excessive bleeding tendency becomes apparant
consumptive phase
bleeding from any/all body orifices
bruise easily
ooze excessively from venipuncture sites or other sites of tissue trauma
platelet count and fibrinogen concentration decrease as these haemostat factors are consumed
all coagulation screening tests (ACT, PTT, PT and TCT) become prolonged as clotting factors are depleted due to excessive consumption +/- degradation
FDPs may accumulate and become detectable in plasma if their rate of production exceeds the liver's ability to clear them from the blood
these contribute to the hypocoagulable state as they exert both anticoagulant and anti platelet effects
chronic
continuous low grade activation of the haemostat mechanism with few if any clinical signs of bleeding
platelet and FDP concentrations and coagulation screening tests may be normal (if replacement balances consumption) or abnormal
clinical signs
signs reflected micro thrombosis of vasculature are harder to recognise than signs associated with extensive failure of the haemostatic mechanism
often recognised well advanced into haemorrhagic phase by this stage the syndrome is increasingly difficult to control or reverse
treatment
early recognition and intensive therapy
the causal agent or underlying disease must be identified and corrected or removed before any form of therapy likely to be successful
promote capillary blood flow and oxygenation
IV dextran or hydroxyethyl starch solutions (10-15ml/kg) can provide the fluid and colloid properties necessary to improve tissue perfusion and hopefully re-establish organ function
fresh blood/plasma
replace haemostatic components that have been depleted
provide fluid and oncotic components
heparin therapy
potent inhibitor of activated clotting factors
anticoagulant by enhancing the activity of antithrombin III
most likely effective in early stage of DIC
before the plasma antithrombin III concentration decreases
paradoxical syndrome
over activation of a normal body defence mechanism designed to produce a blood clot (haemostatic response) ultimately leads to clinical condition characterised by a tendency to bleed. Patients may die from either thrombotic or haemorrhagic complications before the underlying cause can be identified and eliminated
Hepatic failure
liver responsible for synthesising most pro and anti-coagulant factors and plays a central role in haemostasis
vitamin K deficiency can result from liver disease and it can exacerbate coagulation factor deficiency
aside from 1ry tx for liver disease, supportive care in cases of haemorrhage secondary to liver failure can include vitamin K1 therapy and plasma transfusions
Von Willebrand disease
hereditary
classification
type 1
low plasma VWF conc
mild to moderate bleeding tendencies
full array of VWF multimers
type 2
variable reduction in plasma VWF concentrations
absence of high molecular weight VWF multimers
moderate to severe bleeding tendencies
type 3
complete absence of plasma VWF
severe bleeding tendency
prompts for investigation
mucosal surface bleeding
excessive bleeding following surgery or trauma in a dog with abnormal platelet count, prothrombin time and activated partial thromboplastin time
diagnosis
buccal mucosal bleeding time
over 4 mins in a dog with a platelet count over 100,000/mcL and PCV >30% is suggestive of VWS , thrombopathia or rarely vasculopathy
quantitative or qualitative VWF assay
DNA testing
measurement of plasma VWF:Ag concentration
treatment
control spontaneous e.g. epistaxis, haematuria or trauma/surgery induced bleeding
prophylactic treatment based off case by case basis
Desmopressin
synthetic analogue to the neurohypophyseal hormone vasopressin
blood component therapy
feline uncommon but still important differential