Page 546 - Problem-Based Feline Medicine

538 PART 8 CAT WITH ABNORMAL LABORATORY DATA

Primary immune-mediated thrombocytopenia is rare in The fundus of the eye and mucous membranes of the
cats, but treatment is as discussed for hemolytic anemia mouth, vulva and penis are good places to evaluate for
(see appropriate section). evidence of hemorrhage.
Clinical signs are usually consistent with where the pri-
FACTOR ABNORMALITIES (SECONDARY mary bleeding is occurring and the primary disease
HEMOSTATIC DEFECTS)** resulting in hemorrhage.

Ingestion of vitamin K antagonistic rodenticides may
Classical signs
be known.
● Anemia.
Cats with hepatic insufficiency usually have other
● Evidence of hemorrhage at more than one
clinical signs like weight loss, anorexia, polyuria/poly-
site involving fundus of the eye, mucous
dipsia.
membranes of the mouth, vulva, and penis,
and skin including ears. Cats with cholestasis commonly have other clinical
● Dyspnea, coughing, hemothorax or findings like weight loss, anorexia and icterus.
hemoabdomen.
DIC is a syndrome induced by other diseases; clinical
findings are consistent with the primary disease.
Pathogenesis If severe enough to cause spontaneous hemorrhage,
hemophilia usually presents in younger cats.
Factor abnormalities can be divided into decreased
amounts (liver disease, DIC, hemophilia, cholestasis,
warfarin toxicity) or decreased function of coagula- Diagnosis
tion factors (circulating anti-coagulants like heparin).
Activated clotting time (ACT; normal < 65 seconds)
Hepatic insufficiency leads to decreased production can be used in clinical settings to assess the intrinsic
of procoagulants. and common coagulation pathways. Factor VII is the
only factor deficiency not screened by the activated
Hepatic cholestasis results in absence of vitamin K
clotting time (extrinsic pathway), but factor VII
and failure to convert factors II, VII, IX and X to
hemophilia is rare and so the ACT is an excellent
active coagulants.
clinical screening test for factor deficiencies.
DIC results in factor consumption Thrombocytopenia < 50 000 platelets/μl can prolong
the ACT by up to 10–15 seconds due to lack of
Hemophilia is the congenital lack of a factor or factors.
platelet phospholipid.
Warfarin toxicity results in vitamin K antagonism and
The activated partial thromoplastin time and pro-
the resultant failure to convert factors II, VII, IX and X
thrombin time as well as specific assessment of differ-
to active coagulants.
ent factors or proteins induced by vitamin K absence
Increased amounts of circulating anticoagulants are or antagonism are performed on citrated plasma; sam-
most common with mast cell tumors (heparin) or ples should be collected and stored prior to starting
DIC (fibrinogen degradation products). treatment.

Clinical signs Treatment

Most bleeding disorders will have evidence of hemor- Treatment varies with the disease, but frequently
rhage in more than one site. includes administration of fresh whole blood transfu-
sion if life-threatening hemorrhage is occurring.
Decreased amounts or function of coagulation factors
usually results in bleeding into body cavities like the Frozen plasma can be used to supply coagulation fac-
chest and peritoneal cavity. tors if red blood cells or platelets are not needed.