No. 14 1996
v
Cornell Feline Health Center
' Information Bulletin
Feline Hematology and Hemostasis Testing
M arjory Brooks, D .V .M .
Hematology is a broad discipline
encompassing disorders of both
cellular and fluid-phase components
of blood. This bulletin presents
overviews of the feline blood group
system and a diagnostic approach
to feline bleeding disorders.
neuram inic acid (NeuAc). A hy­
droxylase enzym e converts N euA c
to N euG c, an d it is hypothesized
th at blood-type A cats have this
enzym e w hereas blood-type B cats
lack the enzym e. In this m odel, one
theory for type AB is th at a m u ta ­
tion in the hydroxylase enzym e
causes less th a n total conversion of
N euA c to N euG c (figure 1).
Feline Blood Group
System
Blood g ro u p s are defined by the
presence of species-specific antigens
on the surface of re d blood cells.
C ats h ave a single blood g ro u p sys­
tem consisting of three blood types:
type A, type B, and the very rare type
AB. All cats h ave one of these three
types; th ere are no n egative or type
O feline cells.
The antigenic d eterm in an ts on
red cell m em branes responsible for
feline blood ty p es h av e been exam ­
ined in detail. The critical feature is
the specific form of neuram inic acid
p resen t on m em b ran e glycolipids.
Type A cells h ave th e N -glycolyl
(NeuGc) form of neu ram inic acid,
an d ty p e B cells h av e N -acetyl-
Figure 1
Blood Group Antigens
I
NeuAc
NeuG c
N euram inic Acid:
N euA c=N -acetyl
N euG c=N-glycol
T a b le 1
Predicted Offspring Blood Type
P a re n ta l B lo o d T y p e
(genotype)
J
Type A cell
(com m on)
Feline blood type is inherited as an
autosom al trait, w ith type A d o m i­
n an t to type B. All type B cats are
hom ozygotes (bb genotype), w h e re­
as type A cats are either ho m o zy ­
gotes (AA genotype) or h etero zy ­
gotes (Ab genotype).
C rosses b etw een tw o type B cats
are expected to pro d u ce only ty p e B
offspring. C rosses betw een tw o type
A cats, how ever, m ay pro d u ce b o th
type A a n d type B offspring. Table 1
lists the expected p ro p o rtio n of type
A an d type B kittens p ro d u c ed from
different m atings of type A an d type
B parents.
J
“norm al”
“variant”
hydoxylase . / T y p e B c e | | \ h y d r o x y l a s e
I
Inheritance of Feline Blood Types
Type AB cell
(rare)
O ffs p rin g B lo o d T y p e
(genotype)
I. type B x type B
(bb)
(bb)
all type B
(bb)
II. type B x type A
(bb)
(AA)
or
all type A
(Ab)
(bb)
(Ab)
III. type A x type A
(AA)
(AA)
1 type A : f type B
(Ab)
(bb)
all type A
(AA)
or
(AA)
(Ab)
(Ab)
(Ab)
or
all type A
(AA, Ab)
3 type A : 1 type B
(AA, Ab)
(bb)
2
Frequency of Feline Blood Types
Extensive surveys of blood type in
p u re b red and dom estic shorthair
(DSH) an d lo n g h air (DLH) cats have
been co n d u cted th ro u g h o u t the
U nited States. The p ro p o rtio n of
ty p e A a n d ty p e B cats varies in
different geographic locations and
w ith in certain p u re breeds. M ost
DSH a n d DLH are ty p e A; there is,
how ever, geographic variation. The
S outhw est a n d N o rth w est have the
highest p ro p o rtio n of type B in d i­
v id u als, w ith u p to 5 p ercent of the
DSH tested in C alifornia having
type B.
In co n trast to DSH, there is little
geographic v ariatio n w ith in p u re
breeds. V irtually all Siam ese are
ty p e A, w h ereas Rex cats an d British
S horthair cats h av e an alm ost even,
or 1:1, ratio of ty p e A to type B in d i­
viduals. The frequencies in other
breed s such as Persians, H im alayans, an d A byssinians fall som e­
w h ere betw een these tw o extrem es.
Clinical Importance of Feline
Blood Groups
M ost cats have antibodies directed
against foreign red-cell antigens.
These antibodies (hem olysins or
agglutinins) are n atu rally occurring,
presen t w h eth er or not the in d i­
v id u al has been transfused. The most
clinically severe incompatibility reac­
tions are caused by anti-A isoaggluti­
nins in blood-type B cats. Blood g ro u p
incom patibilities are responsible for
tw o different categories of clinical
disorders:
1. Transfusion reactions. Type B
cats tran sfu sed w ith type A cells are
at risk for im m ediate reactions char­
acterized by acute apnea, b rad y car­
dia, an d collapse. These reactions
are potentially fatal. In type B cats
w ith high titers of anti-A antibodies,
severe reactions occur after tran sfu ­
sion of v ery sm all volum es (<2-3
ml) of type A blood. H em olytic reac­
tions have also been described in
type B cats follow ing transfusion of
type A cells. Type A cats tran sfu sed
w ith type B blood are unlikely to
have a clinically severe reaction, b u t
the transfused B cells w ill have
shortened life sp an in com parison
w ith type-com patible cells.
2. N eonatal h em olysis. Type A
kittens born to type B queens are at
risk for neonatal isoerythrolysis
(NI), or hem olytic disease of n ew ­
borns. M aternal antibodies directed
against foreign red cell antigens are
tran sm itted to kittens in colostrum ,
an d clinical signs ap p e a r in the first
few days of life. These signs include
anem ia, icterus, pigm enturia, necro­
sis of tail a n d ear tips, w eakness,
failure to nurse, a n d death. Figure 2
presents a sam ple p edigree of a
type B fem ale b re d to type B an d
type A m ates. A ny type A kittens
p ro d u c ed in the type B to A m atings
are at risk for developing NI.
/
Figure 2
Sample Pedigree
Female type B bred to type B and type A males
Type B
Type B
Type A
Type A
3
Figure 3
Tube Agglutination Reactions
T y p e A c e lls r e a c t in g w it h a n t i- A a n t ib o d ie s
Summary of Key Points
1.
T he re is a sin g le blood group
system in cats: th e A B system .
2.
M ost D S H /D LH ca ts are type
A, but freq u e n cy of blood type
varies w id e ly in d iffe re n t pure
breeds.
3.
T ype A and typ e B cats have
n aturally o ccu rrin g an tib od ie s
a g a in st th e a lte rn a te red cell
type.
4.
T he m ost clin ica lly severe
rea ctio n s are caused by anti-A
a n tib od ie s fo u nd in type B cats.
5.
T ype A kittens born to typ e B
q u eens are at risk fo r neonatal
hem olysis.
6.
T here is no “ u n iversal" fe lin e
d o n or blood type.
7.
Blood Typing and Crossmatching
Blood ty p in g requires specific re­
agents, o r antisera, th at react in a
defined m an n er w ith red cell an ti­
gens. Feline ty p in g is accom plished
by setting u p reactions com bining
p atien t cells w ith reagents specifi­
cally d irected ag ain st either type A
or ty p e B cells.
T ype A cats h ave a strong ag g lu ­
tin atio n reaction w h en their cells are
com bined w ith anti-A antisera, b u t
th ere is no reaction w h en their cells
are m ixed w ith anti-B reagent. Type
B cells react only w ith anti-B re­
agent. B ack-typing is p erfo rm ed by
m ixing cells of k n o w n blood type
w ith p lasm a or seru m from the p a ­
tient. S erum from ty pe B cats show s
a stro n g ag g lu tin atio n reaction
w h e n m ixed w ith ty pe A cells, b u t
no reaction w ith ty p e B cells.
C rossm atching does no t require
special reagents, or k now ledge of a
cat's blood type. Cells from one cat
are m ixed w ith seru m from another
cat, a n d an y ag g lu tin atio n or
hem olysis is noted. A crossm atch
can be perform ed to detect incom ­
patibilities betw een blood donors
an d recipients, prospective m ates, or
a queen a n d h er kittens. The major
crossmatch is performed by mixing cells
from donor with serum from recipient.
A stro ng agglutination reaction in
the m ajor crossm atch is typical of
antibodies in a type B cat's serum
reacting to d o n o r type A cells (fig­
ure 3). This reaction denotes a seri­
ous incom patibility. A sim ple slide
agg lu tin atio n crossm atch test
sh o u ld be perform ed before each
transfusion w hen the blood type of
the recipient is unknow n.
Crossmatch technique: Place tw o
d ro p s of serum from recipient on a
glass slide, a d d one d ro p of d o n o r
blood an d m ix gently for 10-15
seconds. A fter 1 m inute, check for
gross or m acro-agglutination. A ny
agglutination reaction is a contra­
indication for proceeding w ith the
transfusion.
T ra n sfu se type A cats w ith type
A blood, tran sfu se w ith typ e B
cats w ith type B blood.
8.
C h e ck a m ajor crossm atch
(1 d ro p d o n o r blood m ixed with
2 d ro p s recipien t serum ) before
any tran sfu sio n b etw een cats
of unknow n blood type.
4
Diagnosis of Bleeding Disorders
B leeding is a com m on chief com ­
plaint. In each case, a defect or
break d o w n in one co m ponent of the
hem ostatic m echanism p re d o m i­
nates. The m ost successful approach
to m an ag in g these cases is based on
identifying w hich co m ponent of
no rm al hem ostasis is defective, an d
then p ro v id in g specific, as w ell as
sym ptom atic, treatm ent. N orm al
hem ostasis includes three basic
com ponents: blood vessels, p rim ary
hem ostasis (platelets a n d von
W illebrand factor), a n d secondary
hem ostasis (coagulation cascade).
Preliminary Evaluation:
Vessel Disorder versus
Bleeding Diatheses
The goal of initial ev alu ation is to
differentiate bleed in g from d a m ­
aged or d iseased blood vessels from
a system ic b leed in g d isorder, in­
volving either p rim ary or secondary
hem ostasis (figure 4). The principal
m eans of identifying vessel d iso r­
ders is inspection, either visually or
using ancillary diagnostics such as
endoscopy, rad io g rap h y , u ltra ­
sonography, CT scan, an d biopsy. In
certain cases, laboratory evaluation
to ru le o u t a p rim ary or secondary
hem ostatic d iso rd er is indicated
before invasive diagnostic inspec­
tion is perform ed.
Clinical signs of vessel d isorders
show different characteristics, d e ­
p en d in g on the size of d iseased or
dam ag ed vessels. Large-vessel d a m ­
age is accom panied by blood-loss
anem ia, w ith history a n d physical
exam ination revealing involvem ent
of a single or w ell-defined anatom ic
site. P rim ary causes of large-vessel
hem orrhage include traum atic or
surgical injury, erosion or infiltra­
tion from neoplastic, infectious, or
g ran u lo m ato u s lesions, an d vascular
anom aly or arteriovenous shunt.
Figure 4
Preliminary Evaluation
Bleeding Patient
Bleeding Diathesis
Large Vessel
Primary Hemostasis
Surgery
Trauma
Neoplasia
Infection
Granuloma
Vascular anomaly
Platelets
von Willebrand factor
Small Vessel
Vasculitis
infectious
immune
drug-induced
Degenerative
endocrine
collagen disorder
Secondary Hemostasis
Coagulation cascade
Sm all-vessel d iso rd ers (vasculopathies) rarely cause sufficient
blood loss to resu lt in anem ia. Vas­
culitis, or inflam m atory vessel d is­
ease, often involves m any organs,
causing m ultisystem ic signs. In­
volvem ent of cutaneous vessels
causes b ru isin g or ecchym oses, an d
ocular signs include uveitis and
retinitis. Specific differentials for
v ascu lo p ath y include inflam m atory
causes (feline infectious peritonitis,
toxoplasm osis, system ic lu p u s
erythem atosis, d ru g eruptio n ) an d
degenerative d isorders (hypercortisolism [producing fragile ves­
sels], intrinsic collagen defect).
Bleeding Diatheses:
Primary versus Secondary
Hemostatic Disorder
The com bination of clinical signs,
history, a n d screening tests w ill
differentiate p rim ary from second­
ary hem ostatic d iso rd ers in m ost
cases (figure 5).
P rim ary hem ostasis includes
interactions betw een the vessel w all
at the site of injury, platelets, an d
von W illebrand factor. The en d p o in t
of these interactions is form ation of
a platelet plug. A p latelet p lu g is
sufficient to control hem orrh ag e
from capillaries a n d sm all vessels.
D isorders of p rim ary hem ostasis
m ost typically cause petechiae and
m ucosal bleeding, as w ell as b leed ­
ing from sites of su rg ery or traum a.
S econdary hem ostasis includes
the reactions of the clotting factors
of the coagulation cascade. The e n d ­
p o in t of these reactions is form ation
of a fibrin clot. C lotting factors are
enzym es or coenzym es th at circu­
late in p lasm a in an inactive form .
The coagulation cascade acts like
a chain reaction, w ith sequential
activation an d am plification of the
factors, culm inating in the tran sfo r­
m ation of fibrinogen to fibrin. The
activation reactions are localized to
the site of vessel injury because they
5
Figure 5
Primary versus Secondary Hemostatic Disorders
Prim ary H e m o sta sis
S e c o n d a ry H e m o sta sis
Signs:
Signs:
mucosal hem orrhage
petechiae, bruising
hem atom a
Screening tests:
Screening tests:
coagulation panel
platelet count
von W illebrand factor
chem istry panel
C o a g u latio n D iso rd e rs
acquired (com m on)
inherited
von W illeb ra n d ’s
D ise a se (uncom m on)
Platelet D iso rd e rs (com m on)
T h ro m b o cy to p e n ia
T hrom bo pa th ia
decreased production
(bone m arrow disorder)
peripheral sequestration
(splenic disorder)
im m une destruction
underlying disease
urem ia
hyperproteinem ia
drug therapy
req u ire tissue an d p latelet p h o sp h o ­
lipids. Fibrin clot fo rm ation is
n eed ed to control h em o rrh ag e from
d am ag ed m ed iu m or large vessels.
The clinical signs of coagulation
d iso rd ers are h em ato m a form ation
(subcutaneous, in tram uscular), he­
m othorax, hem o p eritoneum , and
bleed in g from sites of su rg ery or
traum a.
Defects of Primary Hemostasis
Platelet d iso rd ers are classified as
eith er q u an titativ e defects (throm b­
ocytopenia) o r q u alitative defects
(throm bopathia). In alm ost all cases,
platelet d iso rd ers are acquired
rath er th an inherited.
T hrom bocytopenia is screened
for by exam ination of a stained
blood film u n d e r oil im m ersion.
Few er th an 5 to 10 platelets p er field
is indicative of throm bocytopenia
a n d should be confirm ed by platelet
count. T hrom bocytopenia is no t a
specific diagnosis, a n d fu rth er
evaluation to d eterm in e etiology is
indicated. T hrom bocytopenia re­
sults from one of three processes:
1. decreased p ro d u c tio n (bone m ar­
row disorder)
2. p erip h eral sequestration (splenic
disease, dissem inated intravascular
coagulation [DIC])
3. increased d estruction (im m unem ediated, DIC)
P roduction deficiencies are com ­
m on in cats, a n d resu lt from either
infiltrative or aplastic disorders.
Splenom egaly secondary to neo p las­
tic, infectious, o r hepatic disease
m ay cause sequestration a n d loss
of platelets from the vasculature.
Im m une-m ediated platelet d estru c­
tion is an uncom m on cause of
throm bocytopenia in cats. D iagnos­
tic w o rk u p to characterize th ro m ­
bocytopenia in cats m ay include
com plete blood count (CBC), chem ­
istry panel, bone m arro w asp iratio n
cytology, retro v iru s serology, ab ­
dom inal u ltraso u n d , a n d hepaticsplenic aspiration cytology.
T hrom bopathia occurs in associa­
tion w ith u n d erly in g m etabolic d is­
orders. The m ost com m on d iso rd ers
include u rem ia a n d h y p erp ro tein ­
em ia, a n d in these cases platelet
dysfunction m ay com plicate m an ­
agem ent a n d diagnosis of the p ri­
m ary disease process.
von W illebrand's disease (vWD)
is uncom m on in cats, b u t h as been
identified in p u re b red (H im alayan)
as w ell as D S H /D L H cats. Affected
cats h ad severe red u ctio n in plasm a
von W illebrand factor (vWF) con­
centration, a n d severe clinical signs
of spo n tan eo u s epistaxis, bleeding
from gingiva at sites of to o th e ru p ­
tion, a n d excessive hem o rrh ag e and
b ru isin g at sites of surgery.
Platelet count a n d coagulation
assays are norm al in vW D -affected
cats. A ssays u sed routinely to m ea­
sure canine (or hum an) vW F m u st
be a d a p te d or m odified to m easure
feline vW F, a n d each laboratory
m u st v alidate its assay an d develop
a norm al feline range.
Defects of Secondary Hemostasis
(Coagulation Disorders)
C oagulation d iso rd ers are caused
by either acquired or inherited defi­
ciency of one o r m ore clotting fac­
tors. C lotting factors are sy nthesized
in the liver, an d a subset of these
factors, the p ro th ro m b in g roup,
requires vitam in K for activation
after synthesis. Factors are con­
su m ed d u rin g the process of clot
form ation, a n d loss of localized clot
form ation, as in DIC, results in
depletion of factors.
6
Figure 6
Coagulation Screening Tests
aPTT
PT
Intrinsic System
Common System
Extrinsic System
Factors:
Factors:
Factors:
X II
X*
V II*
XI
V
tis s u e fa c to r
IX *
II*
V III
1
Factor I only:
TCT
f ib r in o g e n
Tests:
aPTT
= a c tiv a te d p a r tia l th r o m b o p la s tin tim e
PT
= p r o th r o m b in tim e
TCT
= t h r o m b in c lo ttin g tim e
Factors:
* = p r o th r o m b in g r o u p (II, V II, IX , X )
Figure 7
Differentiation of Coagulation Disorders
Acquired factor deficiencies
Acquired Factor Deficiencies
long aPTT
long PT
normal fibrinogen
long aPTT
long PT
low fibrinogen
/
Vitamin K deficiency
rodenticide toxicity
biliary obstruction
bowel disease
Liver failure
necrosis
cirrhosis
shunt
cholestasis
\
DIC
neoplasia
sepsis
trauma
Inherited Factor Deficiencies
long aPTT
normal PT
normal fibrinogen
/
Hemophilia
males affected
severe bleed
F. VIII or F. IX
deficiency
long aPTT
long PT
normal fibrinogen
long aPTT
long PT
low fibrinogen
\
Factor XII
deficiency
males and females
no clinical signs
C oagulation screening tests id en ­
tify abnorm alities in path w ay s, or
system s, w ith in the coagulation
cascade (figure 6). These tests are
based on in vitro form ation of a
fibrin clot. Factor deficiency or d y s­
function causes pro lo n g atio n of the
tim e for clot form ation, a n d these
tests are very sensitive to artifacts
in tro d u ced d u rin g sam ple collection
or processing.
Each testing laboratory sh o u ld
valid ate its assay technique, develop
norm al ranges for cats u sin g th at
technique, an d rep o rt a value for
feline control w ith each p atien t
tested. R outine screening tests of the
coagulation cascade (coagulation
panel or profile) consist of activated
p artial throm boplastin tim e (aPTT);
p ro th ro m b in tim e (PT); a n d fibrino­
gen or th rom bin tim e (TCT).
A severe factor deficiency is ru led
o u t if clotting tim es are norm al in all
three screening tests. P rolongation
of clotting tim e in one or m ore
screening tests is indicative of a
coagulation disorder, a n d the p a t­
tern of abnorm alities d ep e n d s on
w hich in d iv id u a l or g ro u p of factors
is involved. In d iv id u al clotting fac­
to r assays are then perform ed if a
m ore specific diagnosis is needed.
Prothrombingroup dysfunction
Devon Rex
Vitamin K-responsive
Fibrinogen deficiency
males and fem ales
uncommon
A cquired factor deficiencies (figure
7) are com m on a n d occur prim arily
as a re su lt of liver failure (p ro d u c­
tion defect), vitam in K deficiency
(activation defect), o r DIC (defect in
clot localization w ith secondary
factor d ep letio n an d system ic lysis).
Liver disease m u st cause hepatic
synthetic failure before clinically
significant red u ctio n in clotting fac­
tor p ro d u ctio n occurs. The diseases
m ost com m only accom panied by
coagulopathy include acute hepatic
necrosis, cirrhosis, portosystem ic
shunts, an d cholestatic liver disease.
V itam in K deficiency prev en ts
activation of the p ro th ro m b in g ro u p
of clotting factors. C om m on causes
of vitam in K deficiency include
anticoagulant rodenticide toxicity,
biliary obstruction, a n d infiltrative
bow el disease.
m
7
D issem inated in travascular co­
ag u latio n is trig g ered by w id e ­
sp read d am ag e to v ascular tissues,
p latelet aggregation, or intravascular release of tissue p hospholipids.
C linical d iso rd ers m ost com m only
associated w ith DIC include sepsis,
neoplasia (especially ly m p h o sar­
com a, m am m ary carcinom a, an d
m ast cell disease), an d severe
traum a.
3. D ysfib rin ogen em ia (long aPTT,
long PT, long TCT, low fibrinogen).
This is a rare defect in DSH caused
by either deficiency or dysfunction
of fibrinogen. Both m ales an d fe­
m ales are affected. S pontaneous
bleeding episodes are uncom m on,
b u t p rolonged bleeding occurs after
su rg ery or traum a.
Inherited factor deficiencies
1. G iger, U., Kilrain, C. G., Filippich,
L. J., an d Bell, K. 1989. Frequencies
of feline blood gro u p s in the U nited
States. /. Am. Vet. Med. Assoc.
195:1230.
In h erited factor deficiencies (figure
7) are caused by m u tatio n s in genes
coding for specific coagulation p ro ­
teins. N ew , sp o n tan eo u s m utations
can arise in an y p u re b red or D S H /
DLH cat. O nce a m u tatio n occurs,
the defect is m ost often p ro p a g ated
w ith in a b reed or line w h en asy m p ­
tom atic carriers are bred.
1. Intrinsic system defects (long
aPTT screening test).
a) H em ophilia is the m ost com m on
severe in h erited factor deficiency in
cats. The inheritance p attern is Xlinked recessive. H em ophilic m ales
in h erit an abnorm al gene from their
dam , an d express the bleeding ten­
dency. Fem ale carriers have one
no rm al an d one ab n o rm al gene and
are asym ptom atic. T here are tw o
form s of hem ophilia: hem ophilia A
= Factor VIII deficiency, and hem o­
philia B = Factor IX deficiency.
b) Factor XII deficiency is com m on
in D S H /D L H an d Siam ese cats. This
defect is n o t associated w ith a b leed­
ing tendency. P rolongation of clot
fo rm ation is an in vitro, no t an in
vivo p h enom enon. The inheritance
p attern is auto so m al recessive.
2. Intrinsic and extrinsic system
defects (long aPTT an d long PT
screening tests). P ro throm bin g ro u p
deficiency is a ra re coagulopathy
fo u n d in D evon Rex cats. The u n ­
derly in g defect causes abnorm al
vitam in K recycling an d red u ced
activity of all th e vitam in K d ep e n d en t factors. A dm inistration
of v itam in K corrects the bleeding
tendency.
Selected References
2. A ndrew s, G. A., C havey, P. S.,
Sm ith, J. E., an d Rich, L. 1992. Nglycolylneuram inic a n d N -acetylneuram inic acid define feline blood
g ro u p A an d B antigens. Blood
79:2485.
3. A uer, L., an d Bell, K. 1981. The
AB blood g ro u p system of cats.
Anim. Blood. Grps. Biochem. Genet. 12:
287.
4. G reen, R. A. 1989. H em ostatic
disorders: coagulopathies and
throm botic disorders. In: Textbook of
Veterinary Internal Medicine: Diseases
of the Dog and Cat. 3d. ed., ed ited by
5. J. Ettinger, 2246 pp. (Philadelphia:
W. B. S aunders Co.)
5. S lappendel, R. J. 1988. D issem i­
n ated intravascular coagulation. Vet.
Clin. North Am. Small Anim. Pract.
18:169.
Summary of Key Points
1.
b leeding due to da m a g e d or
diseased ve sse ls from a system ic
bleeding diathesis.
2.
coa g ulatio n panel (aP TT, PT, and
T C T or fibrinogen).
3.
ders.
4.
T hro m b o cyto p e n ia in cats is
m ore co m m o n ly caused by bone
m arrow ap la sia o r in filtration, or
sple n ic se q u estra tio n . Prim ary
im m u n e -m e d ia te d pla te le t d e ­
struction is uncom m on.
5.
C oa g u la tion fa cto r de ficie n cie s
cause pro lo n g a tio n in o ne or
m ore of th e co a g ulatio n s c re e n ­
ing tests. S p e cific fa cto r analysis
m ay be needed for de fin itive
diagnosis.
6.
A cq u ire d fa cto r deficie n cie s are
com m on, and are a sso cia ted w ith
m ultiple fa cto r d e ficie n cie s and
prolongation o f m ore than one
screening test.
7.
P rolongation of a P T T and PT,
w ith norm al T C T and fibrinogen,
is su g g estive of vitam in K d e fi­
ciency.
C o a g u lo pa th y due to liver fa ilu re
or DIC is a cco m p a n ie d by p ro lo n ­
gation of aPTT, PT, and TCT,
formerly affiliated with the New York
Diagnostic Laboratory. This association
P etechiae and m ucosal bleeding
are su g g estive of pla te le t d is o r­
8.
recently joined Cornell University's
P relim inary screening tests
sh o u ld include pla te le t co u n t and
The Comparative Hematology Section,
State Department of Health, has
Initial eva lu a tion of the patient
should a tte m p t to diffe re n tia te
and low fibrinogen.
9.
H e m op h ilia is th e m ost com m on
se ve re inherited coa g ulatio n
disorder. H e m ophilia A and B are
in trinsic system d e fe cts causing
long aPTT. M ales e xp re ss the
brings a new menu of tests and services,
readily accessible through the Diagnos­
tic Laboratory, to assist practitioners in
the diagnosis and management of feline
hematologic disorders.
b leeding te n de n cy, fe m a le s are
a sym p to m a tic carriers.
About
the Cornell Feline
Health Center
The ultim ate p u rp o se of the C ornell
Feline H ealth C enter is to im prove
the health of cats by developing
m eth o d s to p rev en t or cure feline
diseases a n d b y p ro v id in g continu­
ing education to veterinarians and
cat ow ners. The C ornell Feline
H ealth C enter is a nonprofit org an i­
zation su p p o rted prim arily by p ri­
vate contributions.
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C ornell Feline H ealth C enter
C ornell U niversity
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