Name of presentation

Practical
Hematology
Diagnosing
Coagulopathy
Wendy Blount, DVM
Practical Hematology
1. Determining the cause of anemia
2. Treating regenerative anemias
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3.
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6.
7.
8.
Blood loss
Hemolysis
Treating non-regenerative anemias
Blood & plasma transfusions in general practice
Determining the causing of coagulopathies
Treating coagulopathies in general practice
Finding the source of leukocytosis
Bone marrow sampling
Hemostasis
Primary hemostasis
– Platelets plug up damaged blood
vessels
• Von Willebrand Factor (vWF)
– Vasoconstriction
Secondary hemostasis
– Platelet plug organized by fibrin
– Fibrin generated by coagulation
cascade (factors)
Fibrinolysis
Coagulopathies
Poor Clotting
– Not enough hemostasis
– Problem with primary and/or
secondary hemostasis so that
clots do not form and stabilize
normally
Thromboembolic Disease
– Too much hemostasis
– Natural anticoagulants are
missing
– Or Fibrinolytics are missing
Signs of Bleeding
Primary hemostasis – small vessel
hemorrhage
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Immediate bleeding
Petechiae (except vWDz) - <3 mm
Ecchymoses
Bleeding from surfaces
• Nose, mouth
• Ocular - hyphema
• GI – hematemesis, melena, hematochezia,
hematuria
• repro
– Prolonged bleeding after injury or
surgery
Signs of Bleeding
• Secondary hemostasis
– Delayed bleeding after injury or surgery
– Bleeding into cavities
• Joints, pleural space, abdomen
• CNS
• Muscular hematomas
• Hemoptysis – can present as melena
– Blood coughed up, swallowed and digested
• Both primary and secondary
– Epistaxis
– Ecchymoses
– If severe 1o and 2o bleeding types blend
Assessment of Coagulation
1. Is bleeding appropriate to injury?
• Control arterial bleeding with
ligation
2. If not, assess coag status ASAP
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Platelet count
PT, PTT/ACT
BMBT
FDPs, D-dimers
Factor assays
Coagulation Tests
Primary hemostasis
• Platelet estimate
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Count platelets in 10 HPF (oil)
Divide by 10 to get average
Multiply by 15-20,000
8-15 platelets/HPF is adequate
• Automated platelet count
– Look at the feathered edge for
platelet clumping (cats!!)
– If clumping, get a new sample
– Use citrate (blue top) and count
immediately
Coagulation Tests
Primary hemostasis
• MPV – Mean Platelet Volume
– Increased in dogs when
immature platelets in circulation
– Indicates increased platelet pdxn
• DIC, vasculitis, chronic
hemorrhage
– Decreased with IMT - 50%
• Large, bizarre platelets
– Otter hound thrombocytopathia
– Cats with myeloproliferative
disease
Coagulation Tests
Primary hemostasis
• Platelet function tests
– Academia
– Must be performed within 2-3
hours of blood collection
Coagulation Tests
Primary hemostasis
• Buccal mucosal Bleeding Time (BMBT)
– Assesses primary hemostasis
– Prolonged if platelets <20,000/ul
– Rebleeding can indicate problems with
secondary hemostasis
– The only in clinic test that evaluates
vessel and platelet function
– Screen for vWDz in likely suspects
– Reasonable pre-operative estimate of
likelihood of surgical hemorrhage, if you
check for rebleeding
Coagulation Tests
Primary hemostasis
• How severe must Tpenia to cause
spontaneous bleeding?
– Can happen <50,000/ul
– More often <20,000/ul
• Splenomegaly of any kind can
result in thrombocytopenia
– Platelets sequestered in the
spleen, liver or lymph nodes
Coagulation Pathway
Coagulation Pathway
Coagulation Pathway
Coagulation Tests
Secondary hemostasis
• Partial thromboplastin time (PTT)
– Intrinsic and common pathways
– Heparin acts on intrinsic pathway
• Prothrombin time (PT)
– Extrinsic and common pathways
– PIVKA is a form of PT test
– PIVKA is not specific for rodenticide toxicity
• Factor 7 deficiency
• Common pathway - DIC, liver failure
• No clinical significance when PT/PTT are shorter
than normal
• PT <3 sec and PTT <5 sec prolonged may not
be clinically significant
Coagulation Tests
Secondary hemostasis
• Activated clotting time (ACT)
– Less sensitive version of PTT
• Intrinsic and common pathways
• Platelets as well
• Thrombocytopenia can elevate ACT by
<10%
• No such platelet effect on PTT
– Factors must be 5% of normal for ACT to be
elevated
• If ACT is increased, things are really
bad
Coagulation Tests
Secondary hemostasis
• Thrombin time (TT)
– Assesses fibrinogen activity
• Part of common pathway
Coagulation Tests
Fibrinolysis
• Fibrin degradation products (FDPs)
– AKA FSPs – fibrin split products
– Measure fibrinolysis
– High with clot formation and breakdown
over time
• DIC
• Chronic bleeding
• Hypercoagulable state
– Neoplasia
– Cushings Disease
– PLN, PLE
– IMHA
Coagulation Tests
Fibrinolysis
• D-dimers
– Measure fibrinolysis
– More specific for DIC than FDPs
– Normal D-dimers exclude DIC as
a diagnosis with 99.5%
confidence level
Anticoagulants
• Antithrombin III
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Produced by the liver
Activated by heparin
Modulates excessive coagulation
Consumed by coagulation
Lost with albumin – PLN, PLE
• Protein C (vitamin K dependent)
• Protein S (vitamin K dependent)
• TFPI – Tissue Factor Pathway Inhibitor
Coagulation Pathway –THAT’S Not ALL!!
Fibrinolysis
• tPA – tissue Plasminogen activator
converts plasminogen within the clot to
plasmin
• Plasmin breaks down fibrin clot
• So tPA promotes fibrinolysis, so that
clots are only temporary
• Urokinase and streptokinase work
similarly
• tPA, urokinase and streptokinase
are the “clot busters”
Excessive Fibrinolysis
• Enzymes prevent excessive
fibrinolysis which would lead to
rebleeding
• They break down the clot busters
– Alpha2-antiplasmin
• inactivates plasmin
– PA1-I: tPA-inhibitor1
• Inactivates tPA and uPA
• uPA – urokinase plasminogen activator
• FDPs and d-Dimers inhibit the
coagulation cascade by negative
feedback
Coags in Practice
Why do them at all???
– Patient shows signs of coagulopathy
• Excessive bleeding
• thrombosis
– Presurgical evaluation
• Patient predisposed to coagulopathy
• Procedure increases risk of bleeding
– Rodenticide toxicity suspected
– DIC suspected
– Genetic screening for breeding
– No expensive equipment for platelet
count, ACT, BMBT
– Can send out the rest
Coags in Practice
Platelet count
Partial thromboplastin time (PTT)
Prothrombin time (PT)
– Reference lab
– Human hospitals often
not calibrated for animals (Pluto)
– Synbiotics SCA 2000
• $2000-3000
– Idexx Coag Dx
Coags in Practice
Activated clotting time
– Reference labs
– Gray top tubes (other colors now)
• Diatomaceous earth (DE) or kaolin
– http://www.haemtech.com/ACT.htm
• Warming block or hand heat
• 2 ml whole blood in the tube immediately
• Invert once every 15-30 seconds
• First clot is the ACT
• Normal less than 2 minutes
– SCA 2000
– HESKA i-STAT
Coags in Practice
Coags in Practice
Coags in Practice
Coags in Practice
Buccal Mucosal Bleeding Time (BMBT)
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Simplate, Triplett, Surgicutt device
Lift the upper lip (gauze muzzle)
Remove the device safety tab
Place the device on the mucosa
Push the device trigger button
Dab dripping blood
every 15 seconds,
but don’t touch
the clot
Coags in Practice
Buccal Mucosal Bleeding Time (BMBT)
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When bleeding stops, you have BMBT
Normal is 2-4 minutes
5 minutes isn’t worrisome
Check the patient in 10-15 minutes for
rebleeding
– DON’T DO BMBT IF:
• Platelets <40,000/ul
• Petechiae are present
• ACT is increased
Coags in Practice
EVERY PRACTICE can have in
house PLATELET COUNT, ACT &
BMBT
EVERY PRACTICE can use a lab for
the rest
Coags in Practice
Tips for coag test sample handling
– Take blood from a peripheral vein
– Avoid cystocentesis if coagulopathy
– Holding the vein off for too long can
lead to platelet & fibrinolysis activation
– Multiple sticks can lead to the same –
you want a clean first stick.
– If you don’t get blood quickly, move to
another vein.
– Hemolysis and severe lipemia can
prevent accurate results
Coags in Practice
Tips for coag test sample handling
– 1 citrate:9 blood
• Vacuum tubes should autodraw
– Run platelet count immediately
– Run tests on whole citrated blood within
2 hours
– Centrifuge promptly to harvest plasma
for outside lab tests
• Freeze immediately in plastic or siliconized
glass tubes
• Ship frozen on dry ice
– May need special blue top clot tubes for
FDPs – ask lab
Coagulopathies - DDx
Disorders of primary hemostasis
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thrombocytopenia
thrombocytopathia
Von Willebrand Disease
vasculitis
Disorders of secondary hemostasis
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Congenital factor deficiencies
Liver disease (poor pdxn)
Vitamin K antagonism
Snake bite envenomation
Disorders of both
– Consumption – DIC, massive
hemorrhage
– Paraneoplastic coagulopathy
Thrombocytopenia - DDx
• Bone marrow disease – lack of production
• Consumption
– DIC
– Massive hemorrhage
• Destruction
– immune mediated
• Sequestration
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Splenomegaly
Hepatomegaly
Lymphadenitis, lymphangitis
vasculitis
Thrombocytopenia - DDx
Infectious Diseases
Multiple causes
• Viruses
– Canine – CDV, CHV,
CPV, CAV2
– Feline – FeLV, FIV,
panleukopenia, FIP
• Arthropod-Borne
– Ehrlichia spp.
– Babesia spp.
– Heamobartonella
spp.
• Arthropod-Borne
– Rickettsia spp.
– Leishmania spp.
– Cytauxzoon spp.
– Borrelia spp.
• Bacterial
– Sepsis
– Borrelia spp.
– Leptospira spp.
• Fungal
– Histoplasma spp.
– Candida spp.
Thrombocytopenia - DDx
Neoplasia
Multiple causes
• Marrow suppression
– Metastatic disease
– Hematopoietic
neoplasia
• Lymphoma
• Multiple myeloma
• leukemias
• DIC
– Hemangiosarcoma
– Inflammatory
mammary
carcinoma
• Vasculitis
• Cytotoxic drug therapy
– Azathioprine
– Chlorambucil
– Cyclophosphamide
– Doxorubicin
Thrombocytopenia - DDx
Drug Therapy
Multiple causes
• Impaired platelet pdxn
• Immune destruction
• Platelet dysfunction
Antibiotics
• Penicillin
• Chloramphenicol
• Sulfonamides
Antifungals
NSAIDs
• Ibuprofen
Cardiopulmonary drugs
• Procainamide
Cytotoxic drugs
• Azathioprine
• Chlorambucil
• Cyclophosphamide
• Doxorubicin
Estrogen
Methimazole
Immune Mediated Thrombocytopenia
• Primary – autoimmune
– Very rare in cats
– Dog breeds predisposed
• Same as IMHA
• Cocker spaniel
• Poodle
• Old English Sheepdog
– Diagnosis of exclusion
• Rule out other causes of Tpenia (normal
coags, normal BMBT unless <5K platelets)
• Rule out causes of secondary IMT
• Platelets <50,000/ul
• Increased megakaryocytes in the marrow
• Response to immunosuppressive therapy
Immune Mediated Thrombocytopenia
• Secondary – same as for IMHA
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infection
Drug therapy
Paraneoplastic
transfusion
• Anti-platelet antibodies
– Doesn’t distinguish between 1o & 2o IMT
– Sensitive for IMT
– But not very specific (many false negatives)
• Low MPV – microthrombocytosis
– MPV < 5.5 fL + platelets <20,000/ul is almost
always IMT (primary or secondary)
– But only 50% of dogs with IMT have this
combination of abnormalities
Breed Specific Thrombocytopenia
• Greyhounds
– Normal platelet count 150,00/ul
– Coags normal
– Remember greyhounds also predisposed to
von Willebrand Disease and Babesia
• Cavalier King Charles Spaniel
– Normal coags
– Normal platelets 25,000/ul-100,000/ul
– Giant platelets on blood smear
• CBC machines won’t count them
– Platelet mass usually normal
• Platelet mass = Platelet count x MPV
– Causes no clinical problems
Thrombocytopathia
• Platelet dysfunction
– hereditary
– acquired
• Acquired Thrombocytopathia
– Drugs
– Disease
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Anemia
Liver failure (plus factor deficiency)
Uremia (plus vasculitis)
DIC (plus consumptive coagulopathy)
Paraproteinemia
– Monoclonal gammopathy
– Ehrlichia, plasma cell myeloma
Thrombocytopathia - DDx
Drug Therapy
Antibiotics
• Beta lactams
– Carbenicillin
– cephalosporins
Antifungals
NSAIDs
• Aspirin
• Phenylbutazone
• Ibuprofen
• Naproxen
Cardiopulmonary drugs
• Aminophylline
• Verapamil
• Diltiazem
• Isoproterenol
• Propranolol
Dextran
Phenothiazines
CAUTION in pets with
thrombocytopenia,
undergoing surgery or
signs of coagulopathy
Thrombocytopathia
• Hereditary Thrombocytopathia
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Likely underdiagnosed
Otter hound, Great Pyrenees – thrombasthenia
Basset hound, Spitz
Persian cat – Chediak-Higashi
Cocker spaniel
Collie – cyclic neutropenia (stem cell defect)
– Boxer
– German shepherd
– Consider BMBT prior to major surgery
von Willebrand Disease
Most common canine hereditary coagulopathy in
dogs
• Does not occur in cats
• Clinical signs of primary hemostasis defect
– Mucosal hemorrhage, prolonged bleeding after
injury
– Petechiae are rare
– (Indy)
• von Willebrand Factor is not a coagulation
factor
– Made by the endothelium
– Acts as carrier protein for factor 8
– Severe vWDz can cause result in bleeding due
to lack of secondary hemostasis
von Willebrand Disease
• Three subtypes of vWDz
– Type 1 vWDz – most common – complex
genetics
• Mild to moderate bleeding
• Low plasma vWAg, normal multimer distribution
– Type 2 vWDz – simple recessive
• Moderate to severe bleeding
• Low vWAg, loss of high MW multimers
– Type 3 vWDz – simple recessive
• Severe bleeding
• Total lack of vWF
von Willebrand Disease
• Diagnosis
– Platelet count
• Normal (may be mildly low if hypothyroid)
– PT, PTT/ACT
• Normal (increased of Type 3)
– BMBT
• Type 1: 5-12 minutes
• Type 2&3: >12 minutes
– vWFAg assay
• carriers: 35-65%
• Type 1: 5-30% (clinical <15%)
• Type 2: 1-5%, no high MW multimers
• Type 3: <0.1%
von Willebrand Disease
Type 1 - mild
Airedale
Akita
Dachshund
Doberman
German shepherd
Golden retriever
Greyhound
Irish wolfhound
Manchester terrier
Pembroke Corgi
Poodle
Schnauzer
Sheltie
Type 2 - moderate
German shorthair
pointer
German wirehair
pointer
Type 3 - severe
Chesapeake Bay
Retriever
Dutch kooiker
Scottish terrier
Sheltie
DNA Tests
available for some
breeds
Less commonly:
Cocker spaniel
Spitz
Labrador retriever
Pit bull terrier
Rottweiler
Vasculitis – Clinical Signs
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Peripheral edema (dependent)
Proteinuria
Exudative skin lesions
Ascites, pleural/pericardial effusion
Necrosis of extremities
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Nose
Ear tips
Nail beds & toes
Tail tip
• hypoalbuminemia
Vasculitis - DDx
• Systemic inflammation
– Infection
• Bacterial – sepsis, Lepto, endocarditis,
pyelonephritis, pyometra, prostatitis, abscess
• Viral - FIP
• Fungal – systemic infection
• Parasitic – heartworm Dz, rickettsiae
– Immune mediated
• Primary – autoimmune
• neoplasia
– Uremia
• Infection of the blood vessels
– Rocky Mountain Spotted Fever
– Ehrlichia spp.
Vasculitis – Work-Up
• CBC, panel, lytes, UA
– Urine P:C ratio if proteinuria on dipstick
– Urine culture if dilute urine
– Anti-platelet-Ab if platelets <50,000/ul
• FeLV/FIV in cats, HWAg in dogs
• Chest x-rays
– Echo if murmur
– Blood culture if endocarditis
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Abdominal x-rays and/or ultrasound
Tick panel - RMSF, Ehrlichia, Borrelia
ANA
Definitive diagnosis of elusive vasculitis
is by skin biopsy
Vasculitis – Coags
• Platelet count
– <150,000/ul
– May see E platys in platelets, or morulae
from other species in WBC
• PT, PTT/ACT
– Normal
– ACT may be <10% prolonged if
thrombocytopenia
• BMBT
– Prolonged
Thrombocytosis
• Falsely increased platelets
– Lipid droplets in lipemic animals
– Small RBC – iron deficiency anemia
– Schistocytes
• IMHA
• DIC
• RBC fragility – congenital, liver disease
• Zinc toxicity
• Iron deficiency anemia
• Microangiopathy
– Sharp spikes on the platelet histogram and
low MPV make you suspect this
Coagulation Pathway - Hemophilia
Hemophilia
• See the chart
• Hemophilia A (Factor 8) and B (factor 9) are
sex linked recessives
– Most affected individuals are male
• Factor must be <5% for spontaneous
bleeding
• Secondary hemostatic defects
– Delayed bleeding, into cavities
• Often evident at a very young age
– Bleeding out from umbilicus
• Almost always evident prior to 2-3 years
Hemophilia
• Factor 7 deficiency
– increased PT and normal PTT
• Factor 10 deficiency
– increased PT and PTT
• Most of the rest increased PTT and normal PT
– Factor 11 and 12 (Hageman) deficiencies rarely cause
clinical bleeding
• There is a deficiency of all vitamin K dependent
factors in the Devon Rex
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2, 7, 9, 10
Causes severe bleeding
Increased PT and PTT
Long term vitamin K Tx can normalize
• Cockers and Kerry Blues can have prothrombin
deficiency
– Common pathway – increased PT, PTT/ACT, TT
Hemophilia
• Factor assays are diagnostic (Cornell)
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http://ahdc.vet.cornell.edu/coag/test/
Coag panels
individual tests
Submission form
• DNA Tests are available fro some defects in
some breeds
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www.vetgen.com
www.dog-dna.com
www.healthgene.com
www.optigen.com
Hemophilia
Vitamin K Antagonism
Vitamin K Antagonism
• Vitamin K1 found in green leafy vegetables
– phytonadione
• Vitamin K3 is found in drugs
– menadione
• Causes of Vitamin K deficiency
– Neonate born to malnourished mother
– Severe bacterial deficiency in ileum
– Decreased vitamin K absorption
• Bile duct obstruction
• Exocrine pancreatic insufficiency
• Lymphangiectasia
– Rodenticide toxicity is by far most common
Vitamin K Antagonism
• Disorder of secondary hemostasis
– Delayed bleeding, into cavities
– Signs begin 2-5 days after ingestion
Vitamin K Antagonism
• Diagnosis
– platelets
• Decreased if prolonged bleeding
• Usually ingested at least 3-4 days before
– PT elevated first for 12 hours or less
• Some say PIVKA elevated before PT
• PIVKA = procoagulant Proteins Induced by
Vitamin K Antagonism
– then PTT within 12-24 hours, then ACT
– FDPs and d-Dimers could be elevated with
chronic bleeding
– TT should be normal
– Send anticoagulant toxicology screen out
– Vitamin K therapy will not affect results
Vitamin K Antagonism
1st Generation
Coumadin
Warfarin
Pindone
Shorter half life
2nd Generation
Bromadiolone
Brodifacoum
Diphacinone
Longer half life
Lower incidence of
drug resistance
3rd Generation
Others
Longest half life
Heparin Toxicity
• Causes
– Iatrogenic
– Mast cell tumor degranulation
• Heparin prolongs PTT > PT
• Monitor PTT for heparin therapy for
thromboembolic disease
• INR is an even better monitor for coumadin
therapy
– International Normalization ratio
Liver Failure
• Define liver failure
– Significantly elevated bile acids
– Can’t be explained by prehepatic or posthepatic
icterus
• Prehepatic icterus (hemolysis)
• Posthepatic icterus (biliary obstruction)
• More than half of liver failure patients have at
least one abnormal coag test
• Only 2% of liver patients develop hemorrhage
• Concurrent coagulopathies
– Biliary obstruction can cause vit K deficiency
– DIC
• Disorder of secondary hemostasis
Liver Failure
• Diagnosis of coagulopathy due to liver failure
– Blood film
• Acanthocytes
• Target cells = leptocytes = codocytes
Liver Failure
• Diagnosis of coagulopathy due to liver failure
– Blood film
• Acanthocytes
• Target cells = leptocytes = codocytes
– Factor Assays
• Some say PIVKA most sensitive indicator for
risk of hemorrhage due to liver failure’
• PT and PTT elevated
• ACT elevated if severe
– BMBT
• Normal, then rebleeding if severe
– AT3, TT
• AT3 low, TT prolonged
Paraneoplastic Coagulopathy
• Thrombosis
– Iatrogenic
– Mast cell tumor degranulation
• Hemorrhage
– Thrombocytopenia
• inflammatory activation of platelets
• Microangiopathy
• Secondary IMT
• Chemotherapy induced bone marrow
suppression
– Thrombocytopathia
– DIC – HAS and inflammatory MGC
– Disruption of blood vessels by tumor invasion
Paraneoplastic Coagulopathy
• 2/3 of dogs with MGT have at least one
abnormal coag test
• Dogs with stage III or IV cancer are more
likely to have coagulopathy
• 83% of dogs taking chemo have at least one
abnormal coag test
• Only 20% of cats with neoplasia have
coaguloapthy
• LSA and HSA are commonly associated with
coagulopathy.
Chemo Drugs Affecting Coagulation
Marrow Suppression
• CCNU
• doxorubicin
• Bleomycin
• Cytosine arabinoside
• Melphalan
• Methotrexate
• Cisplatin, carboplatin
• Actinomycin D
Thrombocytosis
• Vincristine, vinblastine
Thrombocytopathia
• Melphalan
• vincristine
Factor Pdxn Suppression
• L-asparaginase
Vitamin K Antagonism
• Actinomycin D
Dysfibrinogenemia
• Melphalan
Increased fibrin
• Doxorubicin
• Daunorubicin
Snake Bite Coagulopathy
• Cause
– Toxins in the snake venom affect coagulation in many
ways
– The most common affect is lack of fibrin
– Lack of secondary hemostasis, though bleeding is
rare
• The Mojave rattler causes no coagulopathy
• Diagnosis
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Locate the snake bite injury
Decreased platelets
Prolonged PTT, PTT, ACT
Low fibrinogen
Elevated FDPs
d-dimers often normal
• True DIC can occur if toxicity is severe
Thrombocytosis
• > 800,000-900,000/ul platelets
• DDx
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Chronic blood loss
Paraneoplastic
Systemic inflammation
Primary bone marrow disease
Cushing’s Disease
Post-splenectomy
• Work-up (after CBC, panel, UA):
– Endoscopy, chest x-rays, abdominal US,
abdominal x-rays, fecal cytology
Thrombosis
• Hypercoagulable states
– IMHA
• 80% of dogs who died of IMHA had evidence of
thromboembolic disease on necropsy
– Hyperadrenocorticism
– Protein losing enteropathy and nephropathy
• AT3 is similar size as albumin
• AT3 level is a good assessment for risk of thrombosis
– AT3 60-75% at risk)
– AT3 <60% - grave prognosis
– Systemic amyloidosis
– Canine parvovirus
– Neoplasia – 30% have PTE
Thrombosis
• Symptoms of Thromboembolism
– Caused by ischemia of the organ affected
– PTE – pulmonary thromboembolism
• Acute dyspnea
– Renal artery
• Acute renal failure
– Jugular vein
• Swelling of the head
• Diagnosis
– Doppler ultrasound
– Angiography, venography
– Nuclear scans
Disseminated Intravascular
Coagulopathy (DIC)
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End result of systemic thrombosis
Rarely recognized in cats
Always secondary disease
Cause
– Any conditions of increased coagulation
– Systemic inflammation triggering thrombosis
– Hyperthermia is one of the causes that might
have a more favorable prognosis
• Two flavors
– Acute and uncompensated
– Chronic and compensated
Disseminated Intravascular
Coagulopathy (DIC)
Blood film
– Schistocytes (10% of the time)
Platelet count
– <150,000/UL
Partial thromboplastin time (PTT)
– prolonged
Prothrombin time (PT)
– Prolonged
Activated clotting time (ACT)
– Prolonged if severe
Disseminated Intravascular
Coagulopathy (DIC)
Fibrin degradation products (FDPs)
– increased
D-dimers
– increased
Antithrombin III
– Decreased (<75%)
Thrombin Time
– prolonged
Fibrinogen
– decreased
Ecchymoses/Petechiae Algorithm
Platelet count
Both prolonged
Low (next slide)
Normal or increased
FDPs, TT, AT3
PT, PTT/ACT
normal
VitK deficiency
One prolonged
BMBT
normal
Observe
Work up
vasculitis
vasculitis
or problem
resolving
prolonged
vWF assays
Work up vasculitis
platelet function
vWDz
Vasculitis
thrombopathia
•PT: congenital def. 7
early antiVitK
•PTT: congen def 8 9 11 12
severe vWDz - 8
heparin toxicity
Factor assays to Cornell
vWF assays
Rodenticide tox screen
or treat with VitK
Check for MCT
•All normal
Liver Failure
•TT prolonged
•AT3 low
Factor 10 deficiency
•All normal – blood to Cornell
prothrombin deficiency
•TT prolonged
Snake Bite
•FDP increased
•TT prolonged
•AT3 normal
Chronic Bleeding
•FDPs increased
Ecchymoses/Petechiae Algorithm
low platelet count
normal
50-150,000/ul
BMBT
normal
PT, PTT/ACT
<50,000/ul
ACT < 10 sec
prolonged
bone marrow
prolonged
platelet clumps
hyperlipidemia
Cavalier
mild vasculitis
mild rickettsial
Vasculitis
rickettsial dz
Some
thrombocytopathias
neoplasia
rickettsial dz
Aplasia
Infection
toxicity
Severe
platelet
problem
Both prolonged
FDPs, D-dimers, TT
Severe bleeding – platelet
consumption
•Advanced Vitamin K deficiency
DIC
•Increased FDPs, D-dimers, TT
Snake Bite
•Increased FDPs, TT
FDPs elevated
normal
Hypercoagulable state
1o or 2o IMT
Ecchymoses/Petechiae Algorithm
FDPs elevated
Platelets, PT, PTT, ACT, BMBT, D-dimers, TT, AT3 normal
Hypercoagulable state
Remember…..
Some animals will have multiple
coagulopathies simultaneously
•DIC
•Hypercoagulation
•Severe bleeding
•Vasculitis
•IMT
Epistaxis Algorithm
Onset
history of nasal
discharge
serosanguinous
to mucopurulent
acute onset
History of trauma?
hemorrhagic
no
check out local
processes
check blood pressure and
go to petechiaecchymoses algorithm
normal
normal
yes
supportive and
symptomatic
care, surgical
repair
Epistaxis – Local Processes
DDx
• Nasal foreign body
– Inhalation
– Reflux into caudal nasopharynx
• Infection
–
–
–
–
–
Chronic allergic rhinitis leading to 2o bacterial
Fungal
Viral
Parasites - Nasal mites, Cuterebra, Capillaria
Rickettsial infection
• Nasopharyngeal polyps
• Aneurysm or ruptured AV fistula
Epistaxis – Local Processes
DDx
• Neoplasia
– TVT
• Young animals
– Adenocarcinoma
– Sarcoma – melanoSA, chondroSA, fibroSA
– Lymphoma
• cats >dogs
• Young animals
• Dental disease
– Tooth root abscess
– Oronasal fistula
Epistaxis – Local Processes
Other signs of nasal disease
• Sneezing
• Reverse sneezing
• Gagging – caudal nasopharynx
• Pawing at face – rostral nasal cavities
• Melena, hemoptysis
Bilateral epistaxis
• Check out coagulopathy first
• Neoplasia can begin on one side, invade the
septum and eventually affect both sides
Epistaxis – Work Up
• CBC
– Iron deficiency anemia
– thrombocytopenia
• Profile
– Panhypoproteinemia indicates blood loss
– High globulins indicate chronic inflammation
• Neoplasia
• Chronic rhinitis
• Chronic infection – fungal, viral, bacterial, rickettsial
– Renal disease, Hepatic disease
– Hyperadrenocorticism – hypertension
– Triglycerides - hyperviscosity
• Cats - FeLV/FIV; Dogs – heartworm test
Epistaxis – Work Up
• UA
– Proteinuria – PLN, hypertension
– Confirm with urine protein:creatinine ratio
• Coags
– PT, PTT/ACT high
• Tests for DIC – FDPs, D-dimers, ATIII
• Factor Assays
– Normal PT/PTT, prolonged BMBT
• vWF Assays
• Platelet function tests
• Look for causes of vasculitis
• Blood pressure – if high
– T4/Free T4 in cats
Epistaxis – Work Up
• Imaging
– Chest x-rays
• Hemoptysis can present as epistaxis
– Nasal x-rays under sedation
– Dental x-rays if indicated
– CT is nice
• Nasal flush, rhinoscopy and biopsies
– Only if coagulopathy has been ruled out
– Culture is rarely helpful
• Exploratory rhinotomy if all else fails
Epistaxis – Supportive Care
•
•
•
•
Ice packs
Intranasal epinephrine
Cage rest
If coagulopathy or severe bleeding,
transfusion may be necessary
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