Page 515 - Problem-Based Feline Medicine

23 – THE BLEEDING CAT 507

● Note that idiopathic megakaryocytic hypoplasia Prognosis
and pancytopenia may be immune-mediated in ori-
Based on a limited number of cases, the prognosis is
gin. If there are any megakaryocytes present in the
good.
marrow biopsy, testing by immunofluorescence for
megakaryocyte-associated antibody should be per-
formed. ITP and immune-mediated megakary- VITAMIN K ANTAGONIST RODENTICIDES
ocytic hypoplasia are both uncommon but well- AND DRUGS
documented causes of thrombocytopenia in cats.
Whether or not concurrent immunologic attack on Classical signs
platelets and megakaryocytes is occurring in some
● Spontaneous or excessive internal or
cases is not known.
external bleeding.
● Note that FeLV infection may cause both
megakaryocytic hypoplasia and decreased platelet
lifespan.
Pathogenesis
In DIC a primary disease can usually be identified,
thrombocytopenia tends to be mild–moderate, and Vitamin K is normally obtained from the diet and intes-
there may be prolongation of PT, aPTT, and TT, tinal flora, and absorbed in the intestinal tract.
hypofibrinogenemia, increased FDPs, and red cell frag-
Vitamin K is essential for carboxylation of clotting
ments.
factors II, VII, IX and X. The uncarboxylated clotting
Splenomegaly as a cause of thrombocytopenia is prob- factors cannot bind calcium, a necessary step in clot
ably rare. If it is due to neoplasia it may be identified by formation.
splenic biopsy, but this does not rule out that thrombo-
Vitamin K is converted to inactive vitamin K-epoxide
cytopenia is due to secondary ITP. An increase in the
during the carboxylation process.
platelet count with prednisone treatment of a non-
hematopoietic neoplasm, e.g. hemangiosarcoma, gives The enzyme, epoxide reductase, converts vitamin K-
putative evidence that ITP is present. epoxide back to active vitamin K. This cycle conserves
vitamin K and precludes the need for daily intake.
Severe bleeding may result in mild thrombocytopenia.
In a series of cats with anti-coagulant rodenticide poi- Anti-coagulant rodenticides inhibit epoxide reduc-
9
soning, a platelet count as low as 58 × 10 /L (58 000/μl) tase preventing the re-cycling of vitamin K, such that
was noted. If severe bleeding is associated with mild hepatic stores become rapidly depleted, leading to coagu-
thrombocytopenia, it is more likely that the low platelet lopathy.
count is a result of, rather than the cause of, the bleeding.
There are numerous products classified chemically as
hydroxycoumarins (e.g. warfarin) and indandiones
Treatment (e.g. diphacinone). Second-generation products are
those effective against warfarin-resistant rats and are
Prednisone 2–4 mg/kg PO until platelet count is nor-
more potent. Potency is related to degree and duration
mal or stable (usually within one week). The dose is
of enzyme inhibition. The half-life of second-genera-
slowly tapered after 2 weeks with re-measurement of
tion products is much longer than warfarin.
platelet count.
Most toxicity data are based on other species or limited
If there is no response, then strategies used in dogs may be
data. As rules-of-thumb, single-dose oral LD for war-
tried, e.g. vincristine 0.02 mg/kg IV, cyclophosphamide 50
farin is 5–50 mg/kg, for diphacinone 15 mg/kg, and for
2
50 mg/m PO alternate days, cyclosporine 5 mg/kg
bromadialone and brodifacoum 25 mg/kg. Ten percent
PO bid.
of the LD is a rule-of-thumb to determine the mini-
50
If the cat is acutely weak from blood loss, a transfu- mum toxic dose. The lack of information is not a big
sion should be given (10–20 ml/kg whole blood), espe- concern since ingestion is rarely observed or quantifi-
cially if the PCV < 15. able with cats.