1. Diseases of the Cardiovascular and Hemolymphatic System
Disease
(other name)
Brief description Epidemiolog
y
Brief pathogenesis Clinical signs Lesions Diagnosis &
Differential Diagnosis
Treatment &Control,
Prevention(CP)
Congestive Heart
Failure
The heart is unable to maintain
circulatory equilibrium at rest
and congestion of the venous
circuit occurs.
Rare in
horses.
Develops when the
compensatory
mechanism of the heart
reaches their physiologic
limit and the heart is
unable to cope with the
circulatory requirement
at rest.
LEFT: inc. rate and depth
of respiration at rest,
cough, presence of moist
crackles, and inc dullness.
RIGHT: inc. heart rate,
edema, anasarca, ascites
hydrothorax and
hydropericardium.
Pulmonary
congestion,
edema (left).
Anasarca,
ascites,
hydrothorax,
hydropericardi
um, and
enlargement
and
engorgement
of liver
(right).
Based on the findings of
the clinical signs on
physical; examination.
Echocardiography
Auscultation
Diuretics, Venesecton,
Digoxin( 7mg/100kg-loading
dose) (3.5mg/100kg-maintanance
dose)
CP: Rest or avoidance of violent
exercise.
Acute Heart
Failure
Sudden loss of consciousness,
falling with or without
convulsions, severe pallor of the
mucosa and either death or
complete recovery from the
episode.
Excessive tachycardia
(short diastolic period,
ventricular fibrillation
(no contraction and
blood ejection fr heart.
Leads to precipitate fall
in minute volume of the
heart and severe degree
of tissue anoxia.
Dyspnea, staggering and
falling, death follows
within second or minutes
after 1st
appearance of sign
is seen, marked pallor of
mucosa.
Engorgement
of visceral
veins,
pulmonary
congestion,
and early
pulmonary
edema.
Heart examination Not practicable due to short
course of disease.
Intracardiac injection of very
small doses of adrenalin may be
used.
Peripheral
circulatory failure
Occurs when cardiac output is
reduced because of the failure of
venous return to the heart.
Depression, weakness,
listeleness, inc heart rate,
falls in temp to below
normal.
No lesions. Diagnosed when there is
circulatory failure but
no detectable cardiac
abnormality.
D.D: severe toxemia
Hematogenic failure: fluid
replacement
Shock; plasma Dehydration:
isotonic fluids
Hemorrhage: whole blood
Myocardial disease,
myocardial
asthenia,
cardiomyopathy
Manifested by dec. power of
contraction resulting in
reduction of cardiac reserve.
Few animals
develop
myocardial
failure
without
severe
underlying
valvular heart
disease.
Myocardial fibrosis
and/or myocardial
function may be affected
by systemic disease such
as septicaemia. Drugs,
toxins and electrolyte
disturbances may also
result in arrhythmias
and/or poor myocardial
function.
Dec exercise tolerance, inc
heart rate and heart size
Discrete
abscesses,
areas of
inflammation
in the
myocardium,
pallor of
muscle,
petechial or
linear
hemorrhage,
and flabby
heart, thin
walled and
shows patches
Bacteriological and
virological
examinations,
toxicologic and
nutritional analyses or
examination of the
environment
D.D: Diaphragmatic
hernia, mediastinal
abscess and tumor.
Cardiac dilatation of
myocardial asthenia:
INC and DEC audibility
of heart sounds
Corticosteroids
Vit E and selenium,
Digoxin and
Frusemide
Anti-arrythmic drugs
CP: Rest

2. Diseases of the Cardiovascular and Hemolymphatic System
of shrunken,
tough fibrous
tissue.
Valvular disease Interferes with the normal flow
of blood through the cardiac
orifices causing murmurs and in
severe cases,CHF.
Degenerative
valve disease
(DVD) is seen
in geriatric
horses and
also horses as
young as 10
years of age.
Murmurs and palpable
thrills are caused by
turbulence and eddying
in blood flow and
possibly also by the
vibrations produced by
abnormally directed flow
impinging on the heart
and vessel walls.
Decreased cardiac output,
Exercise intolerance,
Cough, Increased heart rat
Stenosis of the
aortic valve,
insufficiency
of the aortic
valve, stenosis
and
insufficiency
of the
pulmonary
valve,
insufficiency
of the left and
right
atrioventricula
r valve, and
stenosis of the
right or left
atrioventricula
rvalves.
Recognition of an
endocardial murmur.
No specific treatment.
endocarditis Inflammation of the
endocardium may interfere with
the ejection of blood from the
heart by causing stenosis of the
valves.
May arise from
implantation of bacteria
onto the valves from the
bloodstream or by
bacterial embolism of the
valve capillaries. It is
also a common sequel on
valve that are subject to
flow-associated stressas
the result of congenital
cardiac defects.
Subacute: persistent
pyrexia, weight loss,
lethargy, depression,
lameness, septic/
nonspecific arthritis
Acute: severe pyrexia,
depression, reluctance to
move, edema, jugular
filling.
Shrunken
valves,
distorted and
thickened
along edges.
Mass in the
valve orifice.
Phonocardiography,
echocardiography
Blood culture
D.D: Any and all causes
of chronic inflammation
and antigenic
stimulation
Antibiotics (erythromycin)
Penicillin (50 000 IU/kg IV qid)
combined initially with
gentamicin.
CP: Using an antimicrobial mouth
wash to prevent bacterial infection
Treatment of any infection with
antibiotic therapy, especially in
case of patients who already
suffer from an existing heart
condition or have artificial heart
devices implanted

3. Diseases of the Cardiovascular and Hemolymphatic System
pericarditis Inflammation of the pericardial
sac.
Pericarditis
appears to be
much less
common in
the UK than
in the USA.
This may be
because
pericarditis is
sometimes
associated
with pleuro-
pneumonia,
which is more
common in
animals
transported
long distances
overland
between two
climatic
extremes.
In early stages, it is
accompanied by
hyperemia and the
deposition of fibrinous
exudate which produces
a friction rub when the
pericardium and
epicardiumrub together
during cardiac
movement.
Pain, avoidance of
movement, abduction of
the elbows, arching of the
back and shallow
abdominal respiration.
(Early stages).
Fibrinous pericarditis:
marked muffling of the
heart sounds, tachycardia,
distention of the jugular
veins, and subcutaneous
edema of the ventral body
wall.
Hyperemia of
the pericardial
lining and a
deposit of
fibrin, gas
may be
present,
embolic
abscesses.
Electrocardiography
Echocardiography
Radiography
Clinical pathology
Antibacterial treatment of the
specific infection.
Broad spectrum antibiotics
(sulfonamides) for non-specific
treatment.
Ventricular septal
defect
Subaortal defect occurring high
in septum at the pars
membranaceae.
in one large
study of
congenital
heart disease
in dogs, a
prevalence of
0.68% was
noted;
common
defects
included
patent
ductusarterios
us (PDA,
28%),
pulmonic
stenosis
(20%),
subaortic
stenosis
(14%),
persistent
right aortic
Shunting of blood from
left ventricle into the
right ventricle outseen
tracts due to the higher
pressure of the left
ventricle, blood shunted
into the right ventricle is
recirculated thru the
pulmonary vessels and
left cardiac chambers,
which cause dilatation of
these structure.
Lassitude, failure to grow
well, and dyspnea.
Echocardiography,
catheterization,
indicator dilation
techniques
D.D: Tricuspid
regurgitation(adult).
Foal
Tricuspid dysplasia.
Other congenital
defects.
No practical correction.
Surgery, pulmonary artery
banding, therapy.

4. Diseases of the Cardiovascular and Hemolymphatic System
arch (8%),
and
ventricular
septal defect
(7%).
Left
atrioventricularval
vular
regurgitation(
LAVR)
Systolic murmur, severe
dyspnea, tachypnea,
cough, flaring of the
nostrils.
Acute: profuse, frothy,
blood-stained discharged
from nose
Fibrous
thickening
Echocardiography
Spectral and color film
Doppler
Ultrasound
D.D: Chordal rupture,
acute pulmonary edema,
acute bronchospasm
No treatment.
Right
atrioventricualrVal
vularregurgitation
(RAVR)
Secondary consequence of
generalized cardiac failure
resulting from LAVR or
bacterial endocarditis.
Echocardiography
Doppler ultrasound
Aortic valvular
regurgitation
Backflow of blood from the
aorta into the left ventricle due
to insufficiency of the aortic
semilunar valve.
Causes include idiopathic
valvular degeneration,
rheumatic fever,
endocarditis,
myxomatous
degeneration, congenital
bicuspid aortic valve,
aortic root dilatation or
dissection, and
connective tissue or
rheumatologic disorders.
Murmurs, regurgitation Nodules,
bands plaques,
fenestrations,
holes in the
margin of the
valve cusps,
Combination of
auscultation, palpation
of peripheral pulses, M-
mode, two dimensional,
and Doppler
echocardiography.
No specific treatment
Aortic and
pulmonic Stenosis
Marked narrowing of its orifice.
Either minor disruption of
valvular structure that do not
reduce the cross sectional area
of the valve but cause
disturbance of flow during
systole.
peripheral or ventral
edema
Echocardiography
Cardiac catheterization.
Tricuspid atresia/
atrial septal defect
Consistent opening of the
interatrial septum, which allows
blood to shunt from the atrium
with the greater pressure.
Blood shunts from the
left atrium to the right
atrium, causing a volume
overload of the right
sided chambers.
Poor growth rate, lethargy,
severely limited exercise
tolerance, cyanosis, and
intense pan systolic shunt
type of murmur.
Blood gas analysis,
echocardiography,
contrast studies,
angiocardiography,
electrocardiography,
catheterization
D.D: Tetralogy of Fallot
myocarditis Active inflammation of the heart
muscle thatmaybe parasite, viral
or bacterial in origin.
Myocardial disease is
often suspected when an
arrhythmia develops after
Exercise intolerance,
dyspnea in exertion, gallop
sound, arrhythmia,
Cellular
infiltrate-
devoid
Enzymology,
echocardiography
X-rays, EKG's, and
echocardiograms
CP: Preventative strategies to

5. Diseases of the Cardiovascular and Hemolymphatic System
an infectious disease,
such as strangles or
influenza. When the
heart muscle becomes
inflamed, it loses
strength and contracts
less forcefully. The
bacteria Streptococcus
equi is the chief cause of
myocarditis.
neutrophils. reduce the likelihood of heart
disease are, so far, limited to
avoiding in-breeding, not
breeding animals with known
congenital defects of any kind,
and not breeding horses that have
acquired a heart disorder
relatively early in life, as this may
indicate a strong genetic
component (with increased
susceptibility in offspring).
Ionophore toxicity This type of intoxication
involves specific feed additives
used as growth-promoting
agents in cattle and as
coccidiostats in poultry and
other birds. Horses are highly
susceptible.
.
Death is possible less
than 24 hours after
ingestion. Horses
surviving the initial
intoxication, or horses
with chronic exposure,
may show progressive
signs of congestive heart
failure due to irreparable
cardiac muscle damage,
as well as poor growth
and poor weight gain. A
number of cases of
sudden death in the
weeks or months after
intoxication have been
reported
Acute: abd. Pan, diarrhea,
severe dyspnea
Per acute: inc swelling
with inc urine output,
hypovolemic shocks
Sub-acute: depression,
reduce feed intake, cardiac
arrhythmias, tachycardia,
hyperventilation
Chronic: unthriftiness,
cardiac dysfunction,
reduced exercise
intolerance.
Toxic tubular
nephritis and
hepatitis,
paleness,
subcutaneous
and
pulmonary
edema,
congestion
and
hemorrhage,
inc pleural,
abdominal,
and
pericardial
fluid.
Ionophore poisoning is
diagnosed by
identifying ionophore
content in the stomach.
Thin-layer
chromatography is used
to make this
identification and can be
used to link ionophores
to feed products.
No specific treatment for
ionophorepoisoning is known, but
supportive care includes oral
administration of activated
charcoal in acute cases to block
intestinal absorption. Although
treatment success is rare,
aggressive fluid therapy supports
cardiac and kidney function, and
correction of electrolyte
abnormalities with supplemental
potassium is advised.
CP: Because most
ionophorepoisonings involve
contaminated or poorly mixed
feeds, it's imperative that horse
owners deal with reputable feed
companies and that quality
assurance programs be in place
and enforced in all mills that
produce equine nutritional
product
Pericardial effusion Effusive pericarditis results in
right-sided CHF when the
pressure within the pericardium
rises so that it exceeds that
within the heart, restricting
diastolic filling of the cardiac
chambers.
The low-pressure RA is
the first chamber to
collapse under the
pressure of the intra-
pericardial fluid. This
limits venous return. The
increase in filling
pressure leads to venous
congestion and the
limited preload means
that cardiac output
cannot be raised to meet
Triad of tachycardia,
muffled heart sounds, and
venous hypertension.
Auscultation,
echocardiographic
examination,
pericardiocentesis
D.D: Pleural disease
Pericardiocentesis
Anti-inflammatory therapy
CP: Controlling inflammation and
sepsis.

6. Diseases of the Cardiovascular and Hemolymphatic System
any increased demands.
The greater the pressure
within the pericardium,
the higher the pressure
required to fill the RA
and ventricle. The rate at
which the effusion
develops also affects the
severity of the condition,
because the pericardium
can stretch to
accommodate larger
volumes of fluid if it
accumulates slowly. If an
acute effusive episode
occurs, the fibrous sac
will have little time to
dilate and intra-
pericardial pressure will
be high.
HEMOLYMPHATIC DIISEASES
Blood Loss
Anemia/Hemorrha
gic Anemia
Results from decrease
circulating blood volume and
associated hypovolemic shock.
Severe hemorrhage usually is
due to loss of vascular integrity
which may result from
iatrogenic or accidental trauma
or from erosion of vessel walls
by neoplastic or parasitic lesion
Common causes of external
hemorrhage caused by large
vessel rupture include castration
complication or accidental
trauma.
Epistaxis due to nasal surgery or
guttural pouch mycosis
Hemophilia
Major effects of
hemorrhage are loss of
blood volume, loss of
plasma proteins and
erythrocytes. If rate of
blood is rapid the loss of
circulating blood volume
results to peripheral
circulatory failure and
anemic anoxia results
from loss of erythrocytes.
Tachycardia, tachypnea,
pale mucous membranes,
prolonged jugular filling.
Progressive exercise
intolerance, muscular
weakness and collapse
Decreased organ perfusion
can cause oliguria and
ileus
Extreme
pallor of all
tissues and a
thin watery
appearance of
blood
Physical examination to
discern clinical signs of
hemorrhage and to
differentiate them from
other signs of
abdominal, thoracic or
musculoskeletal
diseases.
Auscultation,
percussion, centesis and
percutaneous
ultrasonography are
useful ancillary
diagnostic aids.
Diagnostic work-up like
platelet count and
clotting process
D.D: Shock and
dehydration
External hemorrhage is controlled
with direct pressure or large
vessel ligation
Surgical intervention to identify
and control sides of internal
hemorrhage.
Use of anti-fibrinolytic agents
epsilon-aminocaproic acid and
tranexamic acid is used to treat
post-partum uterine artery
hemorrhage
IV administration of 0.37%
formaldehyde to treat
uncontrolled hemorrhage.
IV crystalloids solution should be
administered at 40-60ml/kg to
provide cardiovascular support.
Administration of hypertonic
saline and colloid solution
Whole blood transfusion
Hemolytic Anemia
Equine infectious A retroviral disease Retroviruses contains Acute form = fever, Thrombocyto Coggins test which is an No vaccine available

7. Diseases of the Cardiovascular and Hemolymphatic System
Anemia characterized by chronic
episodic and hemolytic anemia
RNA-directed DNA
polymerase which gives
virus the ability to
incorporate into host
genome of infected
macrophage
It is transmitted through
transfer of blood by
interrupted feeding of
arthropods like horse
flies and deer flies can
also be transferred
through use of blood
contaminated
instruments. Tran’s
placental transfer can
happen.
The virus is tropic for
macrophage and act like
‘Trojan Horse’ providing
latency after viral
replication particles are
released from the
macrophage into
surrounding extracellular
milieu thus introducing a
cycle of viral
amplification within the
host
Hyperplasia of
lymphoreticular system
and
hyperhemoglobulinemia
develop. Hemolysis is
considered to result from
immune complex
attachment to RBC via a
viral hemagglutinin with
subsequent extravascular
removal of cells by the
mononuclear phagocytic
system.
depression,
thrombocytopenia that is
clinically represented by
mucosal petechiation
Chronic form (more than
30 days) = anorexia,
ventral edema, episodic
fever spikes, abdominal
pain, ataxia, abortion or
infertility
penia during
acute phase
with anemia
and icterus
developing
during sub
acute to
chronic phases
of disease
Leucopenia
with
lymphocytosis
and
monocytosis
Hyperglobulin
emia, increase
serum liver
enzyme
activities and
proteinemia
may develop
agar gel
immunodiffusion assay
ELIZA
CP: Absolute attention to
restriction of blood transfer or
blood-related material
Isolation of no less than 200 yards
from other horses and double
screening in a stable environment
Babesiosis caused by intraerythrocytic
protozoan parasite of genus
Babesia

8. Diseases of the Cardiovascular and Hemolymphatic System
it is tick borne transmitted and
causes intravascular hemolysis
Phenothiazine
Poisoning
Oxidants like phenothiazines,
onions or wilted red maple
leaves damage erythrocyte
Causes hemoglobin to
become denatured with
subsequent disulfide
bond formation.
Oxidized hemoglobin
forms precipitates called
Heinz bodies. These cell
change result in
increased fragility of
cells with subsequent
intravascular hemolysis
Oxidative damage causes
increase permeability of
membrane, thereby
altering ion transport
mechanism and osmotic
gradient.
Tissue hypoxia secondary
to methynoglobinemia
Fever, tachycardia,
tachypnea, lethargy,
intense icterus,
hemoglobinuria with
characteristic brown
coloration of skin and
mucous membrane
Anemia, increase mean
corpuscular hemoglobin,
free plasma hemoglobin,
anisocytosis, increased
RBC fragility, variable
presence of Heinz bodies,
neutrophilia
Hyperkalemia,
hyperglycemia, metabolic
acidosis
Laboratory evidence of
oxidative damage
Reducing fragility of erythrocyte,
maximizing oxygenation
Maintaining venal perfusion
Providing supportive care
Activated charcoal (8-24mg/kg up
to 2.2kg PO)
Ascorbic acid to maintain cellular
a-tocopherol in reduced form and
as scavenger of free radicals
Oxygen
Isoerythrolysis in
foals/ Neonatal
Isoerythrolysis
develops when there are blood
group incompatibilities between
the mare and foal, particularly
when the foal has the Aa or Qa
red cell antigens and the mare
does not.
The mare becomes
sensitized to the foal’s
alloantigen and
alloantibodies are
concentrated in
colostrum. When the
affected foal ingest
colostrum within 24
hours of birth , the
hemolysitc antibody is
absorbed along with
other immune globulins
and hemolytic anemia
develops
foals may die within 24
hours of life or may
develop signs 24-96 hours
after colostrum ingestion
=== tachypnea, depression, icterus and progressively developing anemia
anemia,
elevated
icterus index,
increase total
serum
bilirubin
concentration,
hemoglobinuri
a and
biliribinuria
Direct Coomb’s test
provides a presumptive
diagnosis of NI
Direct
Immunofluorescence
assay using cytometry
supportive care, particularly
placement of foal in quiet,cool
environment,. Blood transfusion
in severe anemia
Autoimmune
Hemolytic Anemia
Primarily idiopathic condition or
secondary to infection, drug
administration or neoplasia
Primary IMHA (autoimmune
hemolysis) results from loss of
self-tolerance and is relatively
rare
Secondary IMHA results from
adherence of cross-reacting
Production of
autoantibodies to red
cells, resulting in
increased destruction of
red cells by
lysiserythrophagocytosis.
The primary antibodies
involved are IgGangIgM.
Extravascular hemolysis
Spherocytes may be
present in cytology of
peripheral blood smear
Agglutination will
suggest surface bound
antibody
Direct and indirect
Coombs test
Whole blood transfusion
Antimicrobial therapy is required
when sepsis is confirmed
Immunosuppressive therapy may
be considered
Administration of Dexamethasone
at 0.05 to 0.2mg/kg IV at 24 hour

9. Diseases of the Cardiovascular and Hemolymphatic System
antibodies to erythrocyte surface
antigen
The presence of these molecules
on RBC causes intravascular
destruction by complement
activation (IgM-mediated)-or
most commonly extravascular
removal of macrophage
Toxin exposure due
to snake bites from
rattle snakes
Piriplasmosis A tick-borne disease of horses
resulting from infection with
protozoan Babesiacaballi and
theileriaequi.
Babesiacaball
i is
transmitted
transovarially
from one tick
generation.
Vector of
theileriaequi
is
dermacentorni
tens which
transfer the
protozoa
horizontally.
Apparent in first 1-4 weeks
of infection and include
fever, depression anorexia,
weakness, ataxia,
lacrimation, mucoid
discharge, chonosis,
icterus, hemoglobinuria
and potentially death
Observation of
parasitized erythrocytes
with giemsia stained
blood smears
Isolation of the
organism from blood or
serology
Complement fixation
test or indirect
fluorescent antibody test
PRC
Administration of imidocarb to
reduce parasite load
Equine Ehrlichiosis Caused by rickettsial organism
(Erhlichiaequi)
Fever, depression,
petechiae, ventral edema,
ataxia with reluctance to
move
Granulocytopenia, anemia,
thrombocytopenia are
detected on hematology
Indirect Fluorescent
antibody test
PRC
Should be differentiated
with
purpurahemorrhagica,
equine viral arthritis and
encephalitis
Supportive care with NSAIDS
therapy,
Lower limb sweat wraps
IV oxytetracycline for clearance
Anemia Secondary
to Inadequate
Erythropoiesis
Anemia of Chronic
Disease
Can be caused by chronic
suppurative processes, radiation
injury, poisoning bracken,
thrichlorethylene-extracted soy
Pleuropnemonitis
Internal abscessation
Peritonitis
Chronic organ failure
Presence of a chronic
disease process
accompanied by a mild
to moderate, non-
Related to eliminating the
underlying disease condition and
to ensuing that the anemia is not
caused by blood loss or hemolysis

10. Diseases of the Cardiovascular and Hemolymphatic System
bean meal, arsenic,
phenylbutazone causes
depression of bone marrow
Immune-mediated or
granulomatous disease
Neoplasia
Chronic viral disease such
as Equine infectious
Anemia
regenerative,
normochromic and
normocytic anemia.
Serum ion and total iron
binding capacity is
decreased can be
demonstrated by normal
serum Ferritin
concentration or
positive Prussian blue
stain for marrow iron.
Nutritional
Deficiency
Inadequate erythropoiesis
caused by dietary inadequacy.
Vitamin B12 and folic acid are
important cofactors in
erythrocyte maturation. Can also
be caused by copper, cobalt and
iron deficiency
Iron-deficiency anemia is
diagnosed on the basis of
hypoferritemia,
hypoferremia, normal to
increased total iron-
binding capacity and
detection o decreased iron
stores in examination of
bone marrow aspirates
Supplementation with iron
Thrombocytopenia Caused by reduced platelet
production, abnormal platelet
distribution, and increased
consumption or decreased
platelet survival
It causes altered hemostasis due
to insufficient phospholipid
substrate for coagulation
proteins. The platelet plug
localizes activated clotting
factors and maintains vascular
integrity, thus spontaneous
hemorrhage from developing
Hemorrhagic diathesis
caused by small vessels
bleeding and represented
by petechiation, although
ecchymosis of the ocular,
oral, nasal or vaginal
mucous membranes may
be observed.
Epistaxis, hyphema,
microscopic hematuria or
spontaneous hemorrhage
may develop when the
platelet concentration falls
below 10,000/ul
Confirmation of a
decreased platelet count
(<100,000/ul)
Identification of
surface-associated IG
molecules on peripheral
platelets using direct
immunofluorescence
and flow cytometry
D.D: DIC,
bone marrow disease or
IMTP should be
suspected
No treatment available for
primary bone marrow
megakaryocyte hypoplasia
Whole blood or platelet rich
plasma transfusion
Dexamethasone (0.05-0.1mg/kg
IV) to decrease Fc binding,
phagocytic removal and antibody
production
Hemostatic
Diseases
Can be inherited or acquired
The most common acquired
coagulation disorders in the
hoses are Immune mediated
Vasculitis and disseminated
intravascular coagulation.
Unexpected bleeding after
minor trauma or surgery
Petechial, and ecchymoses,
hyphema, epistaxis,
melena, hematoma, and
hemorrhage
Hemarthrosis,
hemoabdomen, and
Recognition of clinical
signs and basic
laboratory test
Performing platelet
count
Measurement of
activated partial
thromboplastin time

11. Diseases of the Cardiovascular and Hemolymphatic System
hemothorax can occur
Clinical signs associated
with hypercoagulation
include jugular vein
thrombosis or
thromboembolic disease
that affects the GIT,
pulmonary, renal, and
cerebral or the digital
vasculature
(APTT; intrinsic and
common pathways),
fibrin degeneration
products concentration
and fibrinogen
Hemophilia A
(Factor VIII
Deficiency)
Caused by a deficiency of factor
VIII and is the most common
inherited coagulation disorder
Only occur in
males and
their life
expectancy is
short (6
months to 3
years)
presence of unexpected,
recurrent hemorrhage in
a young male with an
abnormally prolonged
APTT and reduced
factor VIII:C activity
administration of fresh plasma
can temporarily replace the
clotting factor deficiency but the
effect only last for hours to days
Von Willebrands
Disease
Caused by quantitative or
qualitative defects in von
Willebrand factor. This result in
a defect in platelet plug.
epistaxis and bleeding
from skin or mucous
membranes after mild
trauma or surgery
specific assays for
vWF= ELIZA
Prekallikrein
Deficiency
A contact factor that becomes
activated when plasma interacts
with a negatively charged
surface that initiates the intrinsic
coagulation cascade
minimal to excessive
hemprrhage after castration
Protein C
deficiency
It results in hypercoagulable
state of horses
recurrent venous
thrombosis, nephrolithiasis
and severe renal disease
Acquired
Coagulation
Disorder
Disseminated
Intravascular
Coagulation
Most common hemostatic
dysfunction in horse
Acquired process in which
activation of coagulation causes
widespread fibrin deposition in
the microcirculation resulting in
ischemic damage to tissues.
Hemorrhagic diathesis occurs as
a result of consumption of
procoagulants or
hypersensitivity of fibrinolysis
In DIC, antithrombin III
and protein C become
depleted as a result of
overzealous activation of
coagulation. This results
in excessive, unchecked
thrombin and clot
formation, which in turn
activates plasmin. FDPs
are formed when plasmin
degrades fibrin. As the
FDPs begin to
accumulate in the
Range from mild
thrombosis and ischemic
organ failure to petechiae
and hemorrhage
Petechial or ecchymotic
hemorrhages of the
mucous membranes or
sclerae, epistaxis,
hyphema, and melena can
occur
Hypoperfusio
n and
microvascular
thrombosis
lead to focal
or widespread
tissue damage
and
culminates in
colic,
laminitis, and
signs of renal,
pulmonary
Presence of clinical sigs
– thrombocytopenia,
prolonged APTT and
PT, and increase in FDP
concentration
Intravenous fluid therapy to
maintain tissue perfusion and
combat shock.
If septic process is present,
antimicrobials are indicated
Minimizing the effects of
entotoxemia may attenuate the
disease process.
Flunixinmeglumine will mitigate
the detrimental effects of
eicosanoids
Fresh plasma therapy is indicated
with severe hemorrhage

12. Diseases of the Cardiovascular and Hemolymphatic System
circulation, they
contribute to the
coagulopathy by
inhibiting thrombin
activity and by causing
platelet dysfunction
and cerebral
disease
Warfarin and
Sweet Clover
Toxicosis
Horses may develop
hemorrhagic diathesis after
consumption of warfarin for for
therapeutic reasons like
treatment of thrombophlebitis
and navicular disease,
rodenticides, or moldy sweet
clover
Sweet clover hay or silage that
is improperly cured can contain
dicumarol
Dicumarol and warfarin
competitively inhibit
vitamin K, which is
essential for the
production of clotting
factors II, VII, IX, X.
Hematomas, hematuria,
epistaxis, and ecchymoses
of mucous membranes
Based on history of
exposure and laboratory
data.
Clinical pathology
reflects prolonged PT
first because the plasma
half-life of factor VII is
shorter than the other
clotting factors.
Discontinuation of the drug
Treatment with vitamin K
Polycythemia/
erythrocytosis
Is an increase in RBC mass.
Relative polycythemia or
hemoconcentration, is common
in horses and occurs when
plasma volume is decreased
because of conditions such as
dehydration or endotoxemia.
Splenic contraction may cause
transient polycythemia
Absolute polycythemia indicates
an increased red cell mass in the
absence of plasma volume
change.
Primary absolute polycythemia
occurs when red cell mass
increase without concurrent
increase in erythropoietin
concentrations
Lethargy, weight loss, and
mucosal hyperemia
Increased blood viscosity
impairs oxygen delivery to
tissues when packed Cell
Volume exceeds 60%.
Abnormal pigmentation,
epistaxis, tachycardia, and
tachypnea
Based on the
measurement of
persistently increased
PCV, hemoglobin
concentration and red
blood cell count in the
face of normal plasma
volume.
Phlebotomy is indicated when the
PCV remains persistently above
50%. 10 to 20 ml of blood/kg are
removed and replaced by an equal
volume of balanced polyionic
fluid.
Lymphoproliferati
ve and
Myeloproliferative
Disorder
1. Lymphom
a
A general term denoting
malignant transformation of
lymphoid cells, but is often used
in equine medicine in place of
the term lymphosarcoma which
is the malignant transformation
of lymphoid cells into solid
tumors
Lymphoid leukemia denotes
Decreased appetite,
depression, weight loss,
fever, lymphadenopathy
and dependent edema
Numerous
lymphoma
tumor
locations
include
peripheral and
internal lymph
nodes, spleen,
liver, kidneys,
Physical examination
through transrectal
abdominal palpation and
careful thoracic
auscultation and
percussion.
Observation of the
neoplastic cells in
aspirates or biopsy
Immunosuppressive
glucocorticoid therapy may be
palliative for steroid-responsive
malignancies and may also
suppress immune-mediated
sequelae including hemolytic
anemia and thrombocytopenia
Use of multiple-agent induction
protocol in horses with

13. Diseases of the Cardiovascular and Hemolymphatic System
malignant transformation of
lymphoid cells within the bone
marrow
Etiology unknown
intestines,
heart, lung
nasopharynx,
eye and
adnexia
skeletal
muscle, skin,
reproductive
organs and
central and
peripheral
nervous
systems.
specimens of lymph
nodes and other masses
or in centesis, samples
of body cavity fluids,
bone marrow aspirates,
or peripheral blood
lymphoma. Cytosine arabinose,
chlorambucil, prednisone are
used.
2. Plasma
Cell
Myeloma
Plasma cells are terminally
differentiated B-cell
lymphocytes
Malignant transformation can
result in 3 categories tumors:
chronic B cell Lymphocytic
leukemia, B-cell lymphoma, and
plasma cell tumors
Limb edema, ataxia,
lameness, epistaxis,
lymphadenopathy, weight
loss, and anorexia
Secondary infections
commonly involve the
lower respiratory or
urinary tract may develop
Anemia and
hyperglobulin
emia are
common
abnormal
laboratory
findings.
Definitive diagnosis is
based on th
demonstration of bone
marrow plasmacytosis
Skeletal survey
radiographs of the long
bones and cervical
vertebrae and
biochemical tests to
detect renal or hepatic
involvement.
Most horses die or are euthanized
within 4 months of developing
clinical signs.
Melphalan, prednisone, and
cyclophosphamide areused
3. Myeloid
Leukemia
Characterized by medullary and
extramedullary proliferation of
bone marrow constituents
including the erythroid,
granulocytic, monocytic and
megakaryocytic cell series
Occurs in
ages ranged
from 10
months to 16
years and in
both genders
Ventral and peripheral
edema, petechial, weight
loss, depression, and
enlarged lymph nodes
Thrombocytopenia and
anemia can occur
Bone marrow
examination
Cytosine arabinose based o a low-
dose protocol
The aim of this therapy is to
promote terminal differentiation
of the neoplastic cell line and
diminish clonal expansion

14. Diseases of the Cardiovascular and Hemolymphatic System
Vasculitis An inflammation and necrosis of
blood vessel walls, can affect
any size, location or type of
vessel in any age, breed or sex
of horses.
The mechanism of issue
damage in immune-
mediated vasculitis is
thought to be caused by a
type III hypersensitivity
reaction in which soluble
immune complexes are
deposited in blood vessel
walls in areas of
increased vascular
permeability. Activation
of complement by
immune complexes
releases complement and
other compounds that are
chemotactic for
neutrophils. Proteolytic
enzymes released by
infiltrative neutrophils
directly damage vessel
walls
Edema of the skin and
subcutaneous tissue, distal
extrimities, face, and
ventral abdomen
Serum leakage, and
crusting may occur
Necrosis of
affected areas
result in
ulceration and
or sloughing
of the skin
Mucous
membranes
and sclerae
are often
hyperemiv
and have
multiple
petechiae and
ecchymoses
Definitive diagnosis is
made from the history,
clinical signs and skin
biopsy results
Histopathologic
findings of
hypersensitivity
vasculitis are infiltration
of neutrophils, the
presence of neutrophil
nuclear debris and
fibrinoid necrosis of
affercted dermal vessels
Direct
Immunofluorescence
test
Removing the antigenic stimulus,
suppressing the immune-response,
reducing vessel wall inflammation
and providing supportive care.
Systemic glucocorticoids are
warranted because
purpurahemorrhagica and other
undefined vasculitides are most
likely immune-mediated
Splenomegaly may occur for many reasons
relating to neoplasia, equine
infectious anemia,
salmonellosis, and rarely
anthrax
primary spleenomegaly may
also occur as a result of
cogestion secondary to spleenic
cirrhosis, cardiac failure, or
active sequestration of
erythrocytes