Problem-oriented Approach

to Anemia in the Horse

What is anemia?
What is anemia?
Decreased proportion of RBC in blood
Decreased oxygen-carrying capacity
Objective 1.
How do you know anemia is present?
Objective 2.
RECOGNITION OF ANEMIA
How do you know anemia is
present?
1. Mucous membrane color
1. pallor
2. Icterus (look in sclera)
2. Exercise intolerance
3. Decreased PCV, Hb, RBC count

Objective 2.
Objective 2.

Packed cell volume < 30%
RBC count < 6 x 10
6
/uL
Hemoglobin < 10.0 g/dl
1/3 of PCV
LABORATORY DEFINITION
Objective 2.
How can you tell Mechanisms of
your patient is anemia?
WHAT CAUSES ANEMIA IN HORSES?
If you can determine the mechanism, you can
rule out most of the causes
(blood loss, hemolysis, inadequate production)
Objectives 3.
Blood loss (regenerative)
Hemolysis (regenerative)
Inadequate production (non-regen

Regenerative vs. non-regenerative
Horses are different.. do a bone
marrow evaluation (dont have retics
released from BM)

MECHANISMS OF ANEMIA
Objective 3.

Take history
Perform physical exam
Perform CBC
Evaluate leukogram & proteins
Evaluate biochemical panel
APPROACH TO DIAGNOSIS
Objective 5.
Perform bone marrow analysis (if not obvious you have
anemia)
Analyze urine (if chronic renal dz, glomerulonephritis w/
protein loss)
Test feces for occult blood
Measure serum iron and TIBC
Perform Coggins test
Perform Coombs test
Do other things

APPROACH TO DIAGNOSIS (CONT)
Objective 5.
What are the causes of anemia in horse?

Piroplasmosis
Trypanosomiasis
Equine infectious anemia

1) INFECTIOUS CAUSES OF ANEMIA
Objectives 3 and 4.
Piroplasmosis
biliary fever
Babesia caballi and Babesia equi
intra-erythrocyte protoza
tick-borne
certain species of ticks
not airborne and not direct contact
B. equi causes more severe disease
Piroplasmosis
Clinical signs
vague generalized signs
fever, depression
icterus, anemia (d/t hemolysis from parasitemia)
Edema (in distal limbs)
hepatomegaly, splenomegaly
colic
ecchymosis of 3rd eyelid
Piroplasmosis
Diagnosis
serology (complement fixation test is approved test
in US)
o C-ELISA and PCR better than complement fixation
tests
o visualization of organism in erythrocytes
Piroplasmosis
Treatment
variable success
repeated treatment often required
imidocarb
Berenil, Ganaseg
phenamidine isethionate
12 HR OLD MULE FOAL
One differential is piroplasmosis not most likely in LA, but on your listcan do
serology, look at smears, send sample in for PCR
Trypanosomiasis
several species produce disease in horses;
Vague signs - fever, cachexia, anemia, CNS signs
and death
Dx based on observation of organism in blood
smear or serology
"swamp fever"
retrovirus similar to AIDS
limited to horses, donkey, mules
persistent viral infection for life
virus infects macrophages
new variants repeatedly emerge
EQUINE INFECTIOUS ANEMIA

Wild onion
Phenothiazine drug not really available
Red maple
Water
Drugs

All tend to cause hemolysis

2) TOXIC CAUSES OF ANEMIA
Objective 3.
Wild Onion Intoxication
Allium canadense
n-propyl disulfide = toxic principle
usually unpalatable = but if not much else to eat or
if randomly like
Wild Onion Intoxication
Clinical signs:

Tend to cause hemolysis
Pallor/icterus, hemoglobinemia (pink serum),
hemoglobinuria
petechia
pigment nephrosis (if lots of blood going through urine)
anemia
Heinz bodies
Wild Onion Intoxication
Diagnosis:

plant identification and evidence of ingestion
typical clinical signs
Heinz bodies
absence of other erythro oxidants
Heinz bodies
NMB heinz bodies look
like blue dots and RBC look
clear
Phenothiazine Toxicity
anthelmintic drug rarely used
toxicity idiosyncratic toxic dose varies
debilitated animals more susceptible
Phenothiazine Toxicity
Clinical signs (same as wild onion):

anemia,
hemoglobinemia,
hemoglobinuria
Heinz bodies
Phenothiazine Toxicity
Treatment:

no specific antidote
transfusion
supportive treatment
avoid future exposure
hematincs not necessary or beneficial all lysed
hemoglobin still in body so more blood really not very useful
Red Maple Toxicity
Acer rubrum
leaves and bark contain toxic principal
wilted leaves
Red Maple Toxicity
Two clinical syndromes
marked methemoglobinemia and few Heinz
bodies
high mortality
large numbers of Heinz bodies and no
methemoglobinemia
low mortality
Red Maple Toxicity
Clinical signs (same as other toxic causes) :
icterus, hemoglobinemia, hemoglobinuria
petechia
pigment nephrosis
anemia
Heinz bodies
Red Maple Toxicity
Treatment
remove toxic agent
blood transfusions (some become v. anemic 10-15%)
sodium ascorbate IV
new methylene blue NOT effective (used in cattle,
but not effective in horses)
supportive therapy (fluids, corticosteroids)
stall rest
Red Maple Toxicity
Prognosis (can base on lab work)
no methemoglobinemia -- favorable
methemoglobinemia -- poor




Often idiopathic
Internal abscesses and other chronic infections such as EIA
Often Coombs test positive
reagents are equine specific
Neonatal isoerythrolysis

3) IMHA

(2) Chronic draining wounds
granulating wounds
venous fistulas
gastric ulcers, colonic ulcers - occult blood
urethral defects - urethroscopy
GI neoplasia


BLOOD LOSS ANEMIA
GI ULCERATION
PHENYLBUTAZONE TOXICITY
(3) Parasitism
internal parasites - strongyles - fecal exam
external parasites - lice, mosquitoes, ticks

BLOOD LOSS ANEMIA
(4) Bleeding defects
hemophilia A
idiopathic thrombocytopenia
coumarin toxicity
DIC

BLOOD LOSS ANEMIA
1. Iron deficiency
Chronic blood loss
Chronic malabsorption syndrome
2. Copper deficiency
3. B12/cobalt deficiency
4. Protein deficiency
5. Over supplementation (Vitamin A, others)
6. Anemia of chronic disorders
7. Drug induced
Bone marrow suppression
8. Neoplasia

PRODUCTION
FAILURE/SUPPRESSION
Microcytic, hypochromic anemia
decreased marrow iron stores
decreased serum iron
GI problem - prevents absorption
chronic external blood loss
IRON DEFICIENCY ANEMIA
Uncommon
injectable iron compounds usu. not indicated
Somewhat hazardous b/c anaphylactic rxns
molybdenum can interfere w/ iron and copper
metabolism
IRON DEFICIENCY ANEMIA

Decreased serum iron
Decreased serum ferritin content best indicator of
iron status
Normal or increased iron binding capacity

IRON DEFICIENCY ANEMIA
affects iron metabolism
molybdenum can interfere w/ Cu metabolism
too much copper can produce anemia (similar to
Wilsons disease)
Cu, iron, molybdenum can all be measured in feed and
blood to see if imbalanced


COPPER DEFICIENCY
Cobalt needed for GI flora to make B12
synthesized in LI
malabsorption can cause deficiency
too much cobalt can lead to anemia
Horses hardly ever cobalt deficient, but given to
stimulate appetite

B12/COBALT DEFICIENCY
Proteins needed to form hemoglobin and
other structures of RBCs
starvation or other systemic disease can
interfere with availability of substrates

PROTEIN DEFICIENCY
secondary to chronic (1 mo +) purulent
infections or parasitism
neutrophilia
hyperfibrinogenemia
marrow iron stores increased
serum iron decreased all iron goes to BMjust
cant recycle it
5) ANEMIA OF CHRONIC
DISORDERS/INFECTION
6) DRUG-INDUCED BM SUPPRESSION
drugs reported to cause
suppression
chloramphenicol
phenylbutazone
Dipyrone NSAID
not on market anymore
sulfonamides


estrogens
Arsenicals
streptomycin
erythropoietin
neoplastic cells replace normal BM
compete for substrates
RBCs more fragile and susceptible to lysis
7) MYELOGENOUS LEUKEMIA
May result from any of the mechanisms
discussed.
Search for site/type of tumor

OTHER NEOPLASIA
CASE STUDIES
Take history
Perform physical exam
Perform CBC
Evaluate leukogram & proteins
Evaluate biochemical panel
APPROACH TO DIAGNOSIS
Objective 5.
Perform bone marrow analysis
Analyze urine
Test feces for occult blood
Measure serum iron and TIBC
Perform Coggins test
Perform Coombs test
Do other things

APPROACH TO DIAGNOSIS (CONT)
Objective 5.
Objective 5.
Whiskey, 12 yo FE QH
Age/signalment
Diet/nutrition
Anthelmintic program
EIA status
Trauma/hemorrhage
Recent transport/import
Medications
Recent disease
Cohort disease
HISTORY
Age/signalment
Diet/nutrition
Anthelmintic program
EIA status
Trauma/hemorrhage
Recent
transport/import
Medications
Recent disease
Cohort disease
HISTORY
icterus
ectoparasites
hemorrhages
epistaxis
swollen joints
fever

weight loss
musculoskeletal or
neurologic deficits
urine color
edema
PHYSICAL EXAM
Always at least some minimum
form of restraint required.
Minimum restraint required: halter
and lead rope
A PE should never be attempted
without a halter and lead rope in
place with someone holding the
horse.
Never wrap lead around your hand,
arm or any other body part
Never tie a horse unless you know it
is accustomed to being tied.

PHYSICAL RESTRAINT:

PHYSICAL RESTRAINT:

PHYSICAL RESTRAINT:

The general examination should
start with the observation of the
horse from a distance in order to
detect abnormalities that might be
obscured by handling and restraint.
PHYSICAL RESTRAINT:

Mucous membranes are examined for moistness,
icterus, hyperemia, cyanosis, pallor, ulceration, and
petechia. Capillary refill time is also evaluated at
this time by blanching the mucous membranes.
The retropharyngeal lymph nodes are
not readily palpated in the normal
animal but may be if enlarged. The
facial artery is palpated at the ventral
aspect of the mandible.
The thyroid gland is frequently
palpable in older horses and
should not be confused for a
lymph node (P). The left jugular
vein is then occluded and palpated
to evaluate jugular fill and to
examine for thrombophlebitis.
The heart is then ausculted in
three locations on the left
cranial ventral thorax: over the
pulmonic, aortic, and mitral
valves.

The normal resting heart rate
of the horse is 28-42 BPM.
The hand is then run down the
forelimb to evaluate
temperature of the distal
extremities if cardiovascular
shock is a concern and also to
palpate temperature of the
hoof and evaluate digital pulses
if laminitis is a concern.
FIRM, UPWARD PRESSURE IS THEN PLACED ON THE VENTRAL
THORAX ON MIDLINE TO EVALUATE FOR VENTRAL EDEMA.


A discussion of auscultation of the thorax and abdomen is included in
the focused examination of the respiratory and gastrointestinal tracts
respectively.
TEMPERATURE
THE HEALTHY HORSE
Sign Normal
Temperature 99.5
o
F to 101.5
o
F
Heart rate 30-45 bpm
Respiratory rate 8-20 breaths per minute
Mucous membranes Pink
Capillary refill time 1-2 seconds


Most resting horses have rectal temperatures of 98.0-101.5 F.
Examination is then continued on the left side for visual
inspection of the integument and auscultation of the abdomen
and thorax, as noted in the focused physical examination.
In the general examination, the right side of the heart is then
ausculted, the right jugular vein is occluded, and the right side
of the head and neck are visually examined.
As one can see, this general physical examination can be easily
performed in just a few minutes, yet it can provide important
information that would otherwise be easily missed.
THE LATERAL THORACIC VEIN
AND CEPHALIC VEIN (ARROWS)
ARE PROMINENT ON THIS
BELGIUM MARE, BUT FOR SOME
HORSES, THE LATERAL
THORACIC VEIN IS DIFFICULT TO
FIND.
TO COLLECT A SMALL AMOUNT OF
BLOOD FROM THE TRANSVERSE
FACIAL VEIN, A NEEDLE IS INSERTED
THROUGH SKIN, JUST BELOW THE
FACIAL CREST, ON A LINE
PERPENDICULAR TO THE FACIAL
CREST DRAWN FROM THE MEDIAL
CANTHUS OF THE EYE.
TO COLLECT A LARGE AMOUNT OF BLOOD FROM THE TRANSVERSE
FACIAL VEIN, 20-GA, 1.5 IN NEEDLE WITH A SYRINGE ATTACHED IS
INSERTED BELOW THE FACIAL CREST UNTIL THE POINT OF THE
NEEDLE STRIKES BONE. THE PLUNGER OF THE SYRINGE IS GENTLY
RETRACTED, AS THE NEEDLE IS SLOWLY WITHDRAWN, UNTIL THE
SYRINGE BEGINS TO FILL WITH BLOOD.
icterus
ectoparasites
hemorrhages
epistaxis
swollen joints
fever

weight loss
musculoskeletal or
neurologic deficits
urine color
edema
PHYSICAL EXAM
CBC
Serum biochemistry
Urinalysis
Feces for occult blood
Coggins test
Bone marrow analysis
Iron, TIBC
Coombs test
others
LABORATORY EXAM (MDB)
PCV = 22%, Hb = 7 g/dl
TPP = 4.2 g/dl
WBC = 11,000 / uL
Segs = 9,500 / uL

LAB ABNORMALITIES
CBC
Serum biochemistry
Urinalysis
Feces for occult blood
Coggins test
Bone marrow analysis
Iron, TIBC
Coombs test
others
LABORATORY EXAM (MDB)
Weight loss
Chronic draining wound
Anemia
Hypoproteinemia
Neutrophilia


PROBLEMS IDENTIFIED:
???
Blood loss anemia
2 Iron deficiency
[2 Protein deficiency ?]

ANEMIA