Download PowerPoint - Hemolysis

Practical Hematology
Hemolytic Anemia
Wendy Blount, DVM
February 2017
Practical Hematology
1. Blood Loss Anemia
2. Hemolysis
3. Non-Regenerative Anemias
4. Bone Marrow Disease
5. Transfusion Medicine
6. Cases
7. Polycythemia
8. Coagulopathy
9. Central IV Lines
10. Leukophilia
11. Leukopenias
12. Splenic Disease
Hemolysis
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Normal lifespan of the RBC
• 100-120 days in dogs
• 70-80 days in cats
Causes of shortened RBC lifespan
• Premature RBC removal (more common)
• Extravascular hemolysis
• In the liver, spleen & bone marrow
• May be triggered by antiRBC Ab
• Intravascular RBC destruction
• May be triggered by antiRBC Ab
• Or complement
• membrane permeability changes
• Enzyme deficiency or malfunction
Hemolysis
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Clin Path Changes with EV hemolysis, in
addition to low PCV
• hepatosplenomegaly
• Increased serum bilirubin
• yellow to orange serum
• Bilirubinuria
• yellow-orange urine
• Small amounts bilirubin made by
normal canine kidneys
• Always pathologic in the cat
Hemolysis
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Clin Path Changes with IV hemolysis
• Increased serum Hb
• amber to red serum
• Increased serum bilirubin (higher)
• Yellow to orange serum
• Depleted plasma haptoglobin
• Hb breaks into 2 dimers that bind to
plasma haptoglobin
• Hemoglobinuria
• red-brown urine (port wine)
• Distinguish from hematuria
• Few RBC on sediment
• Myoglobinuria rare in small animals
Hemolysis
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Signs of Hemolysis (vs. Blood Loss)
• Jaundice
• Gingiva and sclera first
• Then skin
• Plasma Proteins
• High with hemolysis
• Low with external blood loss
• Pigmenturia
• Bilirubinuria
• Hemoglobinuria in dogs
• Hburia not always present in cats who
are hemolyzing
Hemolysis
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Signs of Hemolysis (vs. Blood Loss)
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Autoagglutination
• Indicates immune mediated hemolytic
anemia (IMHA)
Checking for Autoagglutination
1. Gross autoagglutination
• 1 drop saline and 1 drop blood
on the slide
2. Microscopic AutoAg – wet mount
• 5:1 saline to blood, coverslip
• Dilute until you can see RBC with
space between them
• Stacks of poker chips is
Rouleaux – dilute more
• Piles of poker chip winnings
(stuck to each other) is AutoAg
Checking for Autoagglutination
Checking for Autoagglutination
3. Microscopic AutoAg – stained
smear
• Look in the monolayer
Checking for Autoagglutination
4. Saline Wash
• Blood mixed with saline 3:1 to 5:1
• Centrifuge and remove supernatant
1-5 times
• Then dilute for a microscopic wet
mount
Causes of Hemolysis
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Inherited RBC defects
IMHA (primary or secondary)
Transfusion Reaction
Neonatal Isoerythrolysis
Infection
• Mycoplasma haemofelis
• Cytauxzoon felis, Leishmania spp
• Babesia canis, Babesia gibsoni
• Bartonella hensalae
• Leptospira interrogans spp
• Ehrlichia spp & other rickettsiae
Hypophosphatemia
Causes of Hemolysis
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Toxicity
• Methemoglobinemia (Tylenol® - cats)
• Heinz body anemia
• Zinc and copper toxicity
• Naphthalene
• Onion, garlic, broccoli
• Propylene glycol
• Snake bite (viper), Hymenoptera sting
Drugs
• Cats – propylthiouracil, methimazole
• Dogs – levamisole, Carprofen, sulfas,
cephalosporins
Causes of Hemolysis
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Membrane lipid abnormalities
• Severe liver disease
• Have seen it with advanced
hyperadrenocorticism
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Microangiopathy/Angiopathy
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Myeloproliferative disease
Whitney Orlando
Boerne TX
Immune Mediated Hemolytic Anemia
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Causes of secondary autoimmune IMHA
• Neoplasia
• Lymphoma, myeloma, others
• Chronic infection
• Viral – FeLV, FIV, FIP, URI
• Bacterial – Leptospira,
Hemobartonella/Mycoplasma, Bartonella,
Clostridium, Streptococcus, Staphylococcus
• Parasitic – Babesia, Leishmania, HWDz,
Ehrlichia, Hookworms
• Drug induced
• TMPS, cephalosporins, penicillin
• methimazole
• Vaccination – within 2-4 weeks
• Toxicity
• Bee sting, anti-venin
Immune Mediated Hemolytic Anemia
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Syndromes associated with primary
autoimmune IMHA
• Autoimmune diseases
• SLE – systemic lupus erythematosis
• Polyendocrine disorder
• hypothyroidism
• Diabetes mellitus
• Addison’s disease
• Genetic predisposition
• American cocker spaniel (33%)
• English Springer Spaniel
• Old English sheepdog
• Irish Setter, Poodle, Dachshund
IMHA is the most common cause of hemolytic
anemia in dogs
Most common causes of HA in cats:
FeLV, Hemobartonella/Mycoplasma
Methimazole
Chronic inflammation
IMHA + IMT =
Evan’s Syndrome
Look for underlying causes prior to embarking
on long term, expensive therapy
Clinical Signs of IMHA
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Vomiting or diarrhea are the most
common chief complaints
Fever
Hepatosplenomegaly, lymphadenopathy
Followed by clinical signs of anemia
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Signs of hemolysis
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Weakness, lethargy, pallor, etc.
Icterus and pigmenturia
Signs of thromboembolic Disease
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Dyspnea – PTE
Swelling of head or limbs (vein thrombosis)
Lab Abnormalities of IMHA
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Icterus and pigmenturia - hemolysis
Neutrophilia (often >100,000/ul)
• May have degenerative left shift
• Bone marrow with both erythroid and
myeloid hyperplasia
Thrombocytopenia
• If Evan’s Syndrome (<25,000/ul)
• Or DIC (any thrombocytopenia)
ALT and SAP usually elevated
• Even prior to corticosteroids
Spherocytes on blood smear
Abnormalities associated with underlying
disease
Spherocytes
Spherocytes
• Two-thirds of dogs with IMHA have
them in large numbers
• Small in size, hyperchromic, no central pallor
• Also seen with PRCA
• Can be present in smaller numbers with
other causes of hemolytic anemia
• Hypophosphatemia
• Zinc toxicity
• Microangiopathy
• Heartworm disease
• hemangiosarcoma
• Spherocytes are a canine phenomenon
• SPHEROCYTES ARE THE MOST
RELIABLE INDICATOR OF IMHA
IMHA can Appear Nonregenerative
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Acute/peracute onset
• 1 week needed for regenerative response
Antibodies can be directed against RBC
precursors in the bone marrow (NRIMHA)
If autoagglutination is present without a
regenerative response, do a bone marrow
• Autoimmune bone marrow disease
• Bone marrow neoplasia (LSA)
• Ehrlichia, FeLV
Animals with NRIMHA must be
aggressively transfused
Treating IMHA
• Monitoring
• PCV at least BID at first
• IMHA can vary from mild to life
threatening
• Platelets SID to QOD
• Look for ITP and DIC
• Treat the underlying cause
• All treated with doxycycline 5-10 mg/kg
PO/IV BID x 3 weeks
• Withdraw any drugs with might be
causing IMHA
Treating IMHA
• Supportive care
• Rehydrate and maintain hydration
• Avoid overzealous IV fluid therapy
• Transfuse packed cells, or whole blood
if DIC
• Little evidence that transfusion worsens
IMHA
• Alloantibodies don’t trigger autoantibodies
• Autoagglutination makes reading crossmatches difficult (wash RBC)
• Use universal donor blood - DEA 1.1
negative DOGS
• Oxyglobin can decrease need for blood
• More effective when used earlier
• Administer/dispense Cerenia® to
control vomiting
Treating IMHA
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Specific Therapy – immunosuppression
1. Corticosteroids
• Prednisone 1-2 mg/lb/day
• Dexamethasone 0.15-0.3 mg/lb
QOD
Pros
• Works quickly (3-7 days)
• cheap
Cons
• Many familiar side effects
• Often not suitable for long term (years)
• hypercoagulability
Treating IMHA
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Specific Therapy – immunosuppression
2. Azathioprine 1 mg/lb SID x 2 weeks,
then QOD
• Takes 10-14 days to kick in – start
early in severe cases
Pros
• Usually well tolerated
• Affordable (<$50-100 a month)
Cons
• Though side effects are rare, they can
be severe
• Delayed onset of activity
Treating IMHA
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Specific Therapy – immunosuppression
3. Cyclosporine 5 mg/lb/day
• Titrate dose based on blood levels
• Increase up to 20 mg/kg/day
• Trough target 100-500 ng/ml
Pros
• Steady state within 48 hours
• No bone marrow suppression (serial
CBCs not necessary)
Cons
• Expensive (hundreds a month)
• GI side effects, hypercoagulability
• Cancer and opportunistic infections?
Treating IMHA
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Specific Therapy – immunosuppression
4. Mycophenolate 5-10 mg/lb PO or IV
BID
• severe bone marrow suppression
in people if given w/ azathioprine
Pros
• Generally well tolerated
• Cheap (<$40 a month)
• Rapid onset of action
Cons
• GI side effects can be severe
• May need to be compounded for small
dogs ($$)
• Not well studied in dogs, unknown in
cats
Treating IMHA
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Specific Therapy – immunosuppression
5. Cyclophosphamide 200 mg/m2 weekly
• PO or IV
• Can divide PO over 2-4 days
• Given no more than 4x
Pros
• ????
Cons
• No studies support positive outcome
• Associated with increased risk of death
• Because it is used in most severe
cases??
Treating IMHA
Desperation Drugs
6. Danazol 5 mg/lb PO SID
• Specifically for ITP
• Expensive
• Possible hepatotoxicity
• Fluid retention is possible
7. Leflunomide (Arava®) 4 mg/kg PO SID
• Plasma trough 20 ug/ml
• Expensive
• Pharmacist may have apoplexy
over the proposed dose
Treating IMHA
Desperation Drugs
8. IV Immunoglobulin to block antiRBC
• Human IVIG 0.5 g/lb x 2 days
• Short lived response
• Expensive
• Hypersensitivity reaction can be severe
9. IV vincristine to release platelets from bone
marrow
• 0.02 mg/kg IV once
Treating IMHA
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Splenectomy
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Use only as a last resort – can be effective
when unresponsive to medications, or side
effects are unacceptable
Efficacy may be temporary
• Relapse is possible
May result in death if there is an underlying
undiagnosed infections
• Babesia spp.
Permanent and irreversible
immunosuppression results
• May be no more severe than long term
drugs
• But drug side effects are potentially
reversible when stopped
Treating IMHA
Antithrombotic therapy
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Heparin 50U/kg SC TIC while hospitalized
Clopidrogel (Plavix®) 1-3 mg/kg/day, as long
as disease is active
Low dose aspirin – 0.5 mg/kg/day PO
• One study shows safety with
immunosuppressive corticosteroids
Melatonin may help??
• VIN internists are convinced it is *very* helpful
• It modulates cytokines (both immunosuppressing
and immunoenhancing), as well as suppressing
inflammation
• Can aid in preventing relapse
• lifetime supplementation to prevent relapse
• 1-4 mg per dog per day
Treating IMHA
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Continue each drug for at least 2-3 days
before increasing dose or adding another
drug
evidence of response
• Stabilized or rising PCV
• Resolution of or less autoagglutination
• Fewer spherocytes, reticulocytes
• Falling bilirubin & WBC
Continue immunosuppressive
corticosteroids (1 mg/lb/day) for at least 2
weeks before decreasing
• 2 mg/lb/day for no longer than 2 weeks
• Longer can risk GI ulceration
• If regenerative anemia relapses while still
on high dose pred, consider GI bleeding
Treating IMHA
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Wean off immunosuppressive drugs
over 3-6 months *after hemolysis has
stopped*
• May take 6-12 months, or never
happen
• Change one drug at a time
• Not more often than q2-3 weeks
• Not more than 1/3 to ¼ of dose
require to control hemolysis
• Reduce drug only when PCV stable
for 2 weeks
• The faster hemolysis is controlled, the
faster the weaning process
• Wean drugs causing most side effects
first
Treating IMHA
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Treat sequellae
• Fractionated heparin (Fragmin®), or
coumadin if thromboembolic disease
• Plasma 5-10 ml/lb daily for DIC
• Watch carefully for GI ulceration and
treat promptly
• No drugs are proven to decrease risk
of GI ulceration
• Dogs more often die of sequellae of
disease or side effects of treatment
treatment than anemia per se
• Jugular catheters can result in
thrombosis
• Euthanasia due to expense of
prolonged treatment is not uncommon
Treating IMHA
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Treating relapses
• Wean slowly and carefully to prevent
relapse
• Each episode can be more difficult to
treat than the last
• Taper more gradually with each
successive successfully treated
relapse
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Preventing relapse
• Consider never vaccinating the dog
again (skipping rabies is illegal)
• Cytopoint® ??? (Anti IL-31)
• Prevent relapse of underlying cause
IMHA Prognosis
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1/3 easy to treat, 1/3 difficult to treat, 1/3
die no matter what you do
Negative prognostic indicators
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Bilirubin >10 mg/dl – grave prognosis
Rapid drop in PCV (10-15% in one day)
Non-regenerative response after 1-2 weeks
Intravascular hemolysis
• hemoglobinuria
IMHA Prognosis
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1/3 easy to treat, 1/3 difficult to treat, 1/3
die no matter what you do
Negative prognostic indicators
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Bilirubin >10 mg/dl – grave prognosis
Rapid drop in PCV (10-15% in one day)
Non-regenerative response after 1-2 weeks
Intravascular hemolysis
• hemoglobinuria
Persistent autoagglutination
Thromboembolic complications
General condition of the patient
Not the first episode (relapse)
Non-compliant owner
Shih tsu or cocker spaniel
Cold Hemagglutinin Disease
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Antibodies bind to RBC at relatively lower
temperatures
Occlude capillaries, resulting in ischemic
necrosis
Signs of cold agglutination disease
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Skin necrosis at the extremities
Ears, nose, tail tip, nail beds
Diagnosis - Cold agglutinin antibody titer
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Depend only on a lab accustomed to
performing these tests
Inherited Hemolytic Disorders
Seldom diagnosed
Could explain unresponsive
IMHA
Hyperkalemia with IV hemolysis
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Some dog breeds keep
NaKATPase in their RBC
Normal RBC have low K and
high Na
RBC of these dogs have the
reverse
Akita, Shiba Inu, Asian mongrels
Inherited Hemolytic Disorders
Stomatocytosis - nonpathogenic
• Overhydrated cup-shaped
macrocytes
• Slit-like central pallor
• Chondrodystrophic Malamutes
• Schnauzers
Inherited Hemolytic Disorders
Congenital spherocytosis
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golden retrievers
Inherited Hemolytic Disorders
PFK Deficiency (phosphofructokinase)
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PFK important to anaerobic glycolysis
RBC have no nucleus or mitochondria
Hemolytic crises with exercise and
exertional myopathy
Stress induced hyperventilation and
respiratory alkalosis
• This worsens PFK activity
Splenomegaly, anemia + icterus
English Springer & Cocker Spaniels
• Also whippets and mixed dogs
Dx - DNA test for some breeds
• enzymatic PFK test for the rest
• Decreased DPG
• All affected pets do not have the
exact same mutation
Inherited Hemolytic Disorders
PK Deficiency (pyruvate kinase)
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PCV 10-30%, splenomegaly
Marked regeneration
• Retics as high as 95%
No spherocytes (EV hemolysis)
Myelofibrosis and osteosclerosis of
bone marrow at 1-3 years of age
Die of anemia or liver failure due to
hemosiderosis at 3-5 yrs. of age
Splenectomy and prednisone do not
help dogs, but help cats
Basenji’s, Westies & more
DNA tests for many breeds
• Autosomal recessive
PK enzyme activity test for others
Inherited Hemolytic Disorders
Familial non-spherocytic hemolytic
anemia
• Poodles and beagles
• Similar presentation to PK Deficiency in
poodles
• Not as severe in beagles
• No hemosiderosis, myelofibrosis or
osteosclerosis
Congenital Osmotic Fragility
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Recurring anemia, splenomegaly
lymphocytosis, hyperglobulinemia,
hemosiderosis
Abyssinian and Somali cats
Also seen in Siamese and DSH
Pred and splenectomy and reduce
phagocytosis or damaged RBC
David Waters
Boerne TX
Infection Associated Hemolysis
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Direct infection of the RBC by organism
Indirect hemolysis by inflammatory
mediators
• Systemic inflammation causes shortened
RBC lifespan in cats
• Secondary IMHA
• FeLV
• Some bacteria produce hemolysins
• Lepto, Clostridium, Strep, Staph
Cytauxzoon felis
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Carried by ticks
Two life forms
• Schizonts and then merozoites in the
tissue macrophages
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Piroplasms in the RBC
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Enlarging tissue histiocytes cause venous
obstruction, ischemia and organ failure
Merozoites infect the RBC
Parasitemia is late stage disease
Do serial blood smears
Rapid illness progressing to death in one
week (diagnosed on necropsy)
• Fever, anemia, icterus, pigmenturia,
dyspnea, hepatomegaly, splenomegaly,
lymphadenopathy
Cytauxzoon felis
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Used to be considered uniformly fatal
Leukocytosis, or Leukopenia with left
shift due to tissue necrosis
Anemia may appear non-regenerative
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Not enough time for regenerative response
Some cats do survive with aggressive
supportive care
carrier state is possible
PCR is available
Cytauxzoon felis
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Treatments
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Transfusion or Oxyglobin
Heparin 100-200 U/kg SC TID for presumptive
DIC
Imidocarb 2-5 mg/kg IM, repeat in 4-7 days
aggressive supportive care
Atovaquone 15 mg/kg PO TID + azithromycin 10
mg/kg PO SID (atovaquone >$1000)
Diminazine 2 mg/kg IM – 2 doses 3-7 days apart
(not approved in the US)
Cytauxzoon felis
Mycoplasma-Hemobartonella
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Large (more pathogenic) and small types
– hemoplasma mollicutes
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Mycoplasma haemofelis
Mycoplasma haemominutum (aka Candidatus M
haemominutum)
Mycoplasma haemocanis – rare cause of disease
in splenectomized or immunosuppressed dogs
Opportunistic - 50% FeLV or FIV positive
Splenomegaly common
PCR is available and a good test, but
presence of organism does not always
result in disease
Make smears immediately after capillary
blood collection 9 (ear prick)
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Organisms detach with time
Organisms released every 1-2 days
Mycoplasma-Hemobartonella
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Treatment
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Doxycycline 5 mg/kg PO BID x 3 weeks
Enrofloxacin 5 mg/kg PO SID x 3 weeks
Both in refractory cases
Prednisone 1-2 mg/lb/day x 2 weeks, then
taper for secondary IMHA
Hemobartonella vs Cytauxzoon
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Hemobartonella is epicellular
Cytauxzoon is intracellular
Cytauxzoon in macrophages
Hemobart – marked regeneration
Cytauxzoon – organ failure
Eve Gerome
Bonham TX
Babesia canis
Babesia gibsoni
Babesia
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Carried by ticks - Babesia canis, Babesia gibsoni,
Babesia felis (resembles Cytauxzoon)
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Endemic in greyhound and pit bull kennels
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Transmitted by transfusion
Severe hemolytic anemia, fever, shock and
multiple organ failure
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Puppies more susceptible, carriers possible
Transmitted by dog bites and tick bites
Thrombocytopenia and leukocytosis
Lymphadenopathy, splenomegaly
Secondary IMHA causes more hemolysis than the
organism does directly
PCR, IFA and ELISA are available
Prednisone 1-2 mg/lb/day x 2 weeks, then
taper for secondary IMHA
Methemoglobinemia
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Heme is oxidized from ferrous to ferric so that
it can’t bind and transport oxygen
Cats are especially susceptible
• more sulfhydryl groups on their hemoglobin
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Drugs
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Also they are glucuronyl transferase is deficient
Benzocaine containing skin products and sprays
Acetaminophen
Phenazopyridine (urinary tract analgesic)
Dyspnea, cyanosis, ataxia, coma, death
Facial edema and GI signs with Tylenol
Diagnose with “spot test”
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Put drop of affected EDTA blood on white paper
towel next to control blood
Control will turn red, metHb blood stays brown
Heinz Body-Membrane Injury Anemia
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Denatured hemoglobin forms Heinz
bodies
Pale staining with Wright’s stain
Dark staining with NMB or BCG
Cats are especially susceptible
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more sulfhydryl groups on their
hemoglobin to oxidize
Feline spleen is not efficient at removing
Heinz bodies
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<10% Heinz bodies can be normal in cats
10-50% RBC affected – moderate HBA
>50% RBC affected – marked HBA
Heinz bodies in dogs usually pathologic
Heinz Body-Membrane Injury Anemia
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Foods
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Onion**, garlic
Broccoli
propylene glycol – semi moist foods
Drugs/Supplements
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Acetaminophen, phenacitin (cats)
benzocaine
Methionine (cats)
Phenothiazines (cats)
VitaminK3
Propofol – not on successive days
**Onions ingestion is the most common
cause of Heinz body anemia in dogs
Heinz Body-Membrane Injury Anemia
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Chemicals
• naphthalene – moth balls and toilet
cleaner
• Zinc hardware and pennies (since 1983)
• Serum zinc > 5 ppm (plastic tubes)
• Copper
• phenols
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Metabolic Disease
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Diabetic ketoacidosis
Heinz Body-Membrane Injury Anemia
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Treatment
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Remove the oxidative agent
antioxidants
• Methylene blue 0.4 mg/lb slowly IV
• N-acetylcysteine 64 mg/lb initial dose
then 32 mg/lb TID x 7 treatments (PO
or IV)
• Mucomyst is preferred for Tylenol
toxicity
• Vitamin C, vitamin E
Transfusion with packed cells
• Oxygen not all that helpful without
transfusion
• Blister cells
• Helmet cells
• keratocytes
• Pyknocytes
• Cell membrane tags
• Eccentrocytes
• Clear areas in cat RBC are most likely
oxidized hemoglobin
Hypophosphatemia
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Hemolysis can occur when phosphorus falls
below 2.5 mg/dL
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Causes of severe hypophosphatemia
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Likely to occur when < 1.0-1.6 mg/dL (dog)
Cats more sensitive <2.0-2.5 mg.dL
DKA – diabetic ketoacidosis
Hepatic lipidosis
Refeeding syndrome
Phosphate binder overdose (AlOH)
Supplement phosphorus when feeding
anorectic cats, or treating DKA
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IV – potassium phosphates (chart)
• Watch for hypocalcemia
PO when eating and stable – most foods contain
plenty of phosphorus
• Dilute tube feeding diets with skim milk
Zinc and Copper Toxicity
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Severe IV hemolysis
Signs in addition to anemia, icterus,
leukocytosis, spherocytes, pyknocytes
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GI signs – vomiting and diarrhea
Diagnosis
Zinc and Copper Toxicity
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Severe IV hemolysis
Signs in addition to anemia, icterus,
leukocytosis, spherocytes, pyknocytes
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Diagnosis
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GI signs – vomiting and diarrhea
GI foreign body on imaging
Increased serum Zn (>2 mg/kg)
Dogs with copper storage disease can suffer
from hemolytic anemia if excessive copper is
suddenly released from the liver
Angiopathy, Microangiopathy
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Schistocytes
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Destruction of RBC as they move through
damaged blood vessels
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Triangular or helmet shaped RBC fragments
Shear Force Destruction - Endocarditis, Caval
Syndrome, Thrombosed IV catheter
Microangiopathy - Liver or Splenic Disease,
Hemangiosarcoma, Vasculitis, cold agglutinin
disease
RBC destruction - Hemolytic-uremic syndrome,
DIC
RBC Membrane Fragility – FeLV, liver disease
Schistocytes are also seen with osmotic
fragility
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Liver disease, iron deficiency, water intoxication,
congenital, zinc toxicity
Work-Up for Hemolytic Anemia
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CBC with reticulocyte count
General Health profile with electrolytes
Urinalysis with sediment
FeLV/FIV for cats, occult HWTest for dogs
Fecal
Check for autoagglutination
Blood smear cytology
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Chest and abdominal x-rays
Abdominal US
• Aspirates of spleen, liver, lymph nodes if
enlarged
Coag panel if thrombocytopenic or
critically ill
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Work-Up for Hemolytic Anemia
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Secondary tests – as indicated by
symptoms
• DNA or enzyme activity tests if congenital
hemolytic anemia is suspected
• Tick panel
• PCR, IFA, culture
• antibody titers
• Thyroid panel
• ANA – support diagnosis of IMHA
• Antiplatelet antibodies if
thrombocytopenic
COOMBS TEST IS NOT ON THIS LIST
Why Not Coombs Test?
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30-40% false negatives
Almost as many false negatives
Test results almost never change
what you are doing
COOMBS TEST IS NOT ON THIS LIST
Acknowledgements
Chapter 2: The Complete Blood Count, Bone
Marrow Examination, and Blood Banking
• Douglass Weiss and Harold Tvedten
• Small Animal Clinical Diagnosis by Laboratory
Methods, eds Michael D Willard and Harold
Tvedten, 5th Ed 2012
Chapter 3: Erythrocyte Disorders
• Douglass Weiss and Harold Tvedten
• Small Animal Clinical Diagnosis by Laboratory
Methods, eds Michael D Willard and Harold
Tvedten, 5th Ed 2012
Acknowledgements
Chapter 59: Pallor
• Wallace B Morrison
• Textbook of Veterinary Internal Medicine, eds
Stephen J Ettinger and Edward C Feldman, 6th
Ed 2003
Cytauxzoon
• Linda Shell, ACVIM
• Veterinary Information Network – Associate
Challenging Anemia Cases
• Crystal Hoh, ACVIM
• Heart of Texas Veterinary Specialty Center
• CAVMA CE
Acknowledgements
Canine Babesiosis
• Linda Shell, ACVIM
• Veterinary Information Network – Associate