Page 511 - Problem-Based Feline Medicine

23 – THE BLEEDING CAT 503

Adequate fluid therapy to promote microvascular cir- ● Resistance to hematoxins may in part reflect
culation, but not excessive fluid therapy, which will cats playing with, and subsequently being bitten,
promote edema and bleeding. by smaller snakes (thus receiving less venom),
and/or only cats with mild–moderate envenomation
If clinically bleeding, transfuse to replace platelets
surviving long enough to be presented to a veteri-
and/or clotting factors and anti-thrombin III with fresh
narian.
whole blood, platelet-rich plasma, or fresh/fresh-frozen
plasma, 10–20 ml/kg. Venoms from Elapidae snakes (e.g. Australian tiger
snake and brown snake, North American coral snakes,
Heparin therapy is controversial.
Indian cobras) are predominantly neurotoxic, although
● It is recommended because, although bleeding is
procoagulants and myolysins may cause significant
clinically more obvious, thrombosis causes most
complications.
of the organ damage.
● Signs include areflexic dilated pupils, dysphagia
● The goal is to block microvascular thrombosis
(salivation), dyspnea (respiratory paralysis),
while not aggravating bleeding.
hindlimb ataxia and flaccid quadriplegia.
● In cats with fulminant DIC, doses of 50–200 units/kg
● Local reaction to the bite wound may be minimal.
SC q 6–8 h have been recommended; 75–100 units SC
● Although neurologic signs predominate, cats with
q 8 h is used most often. The dose may be incubated
tiger or brown snake bites may have significant dis-
for 30 minutes in the blood product prior to transfu-
turbances of hemostasis.
sion to activate antithrombin III, although the value of
– Potent procoagulants, especially in the brown
this practice is unproven. An initial goal is prolonga-
snake venom, act as prothrombin converters,
tion of the ACT or aPTT to 1.5–2 times the mean
resulting in consumption of fibrinogen.
value of normal range or aPTT control value.
– 10–30% of cats show evidence of hemostatic
● It should not be used in cats with subclinical, subacute
abnormalities. Typical signs include non-clotting
or chronic DIC, unless thromboembolism is present.
blood, prolonged coagulation times (ACT typ-
– If thromboembolism is present, an initial dose of
ically 180–240 s), continuous bleeding from
200 units/kg SC q 6–8 h is recommended.
wounds and venepuncture sites, hematemesis
and hematuria.
Prognosis
Venoms from Viperidae (e.g. common adder in Britain
The prognosis is largely determined by the primary
and continental Europe, Vipera palaestina in the
disease.
Middle East) are predominantly hematoxic, although
Acute diffuse DIC has a very poor prognosis. some have neurotoxic properties.
● Edema ± bleeding/bruising around the bite is
typical, but is not predictive of systemic toxicosis.
SNAKE BITE ENVENOMATION* ● Widespread bleeding is uncommon with bites from
the common adder and V. palaestina, but may occur.
Classical signs
Venoms from Crotalidae (e.g. North American rattle-
● Bite wound on cranial half of body ± local snakes, copperhead, cottonmouth, and South American
swelling or bleeding (Viperidae, fer-de-lance and bushmaster) are predominantly hema-
Crotalidae). toxic, although some (e.g. Majove rattlesnake, Asian
● Paresis/paralysis or bleeding tendency habu snake) are potent neurotoxins.
depending upon species of snake. ● Severe regional swelling may occur surrounding
the bite from massive extravasation of plasma and
red cells, but local reaction is not predictive of sys-
Clinical signs
temic toxicosis.
Cats are believed to be less likely to be bitten by most ● Hypotension may result from pooling of blood in
snake species than dogs, and to be more resistant to lungs and thoracic vessels.
hematoxins. ● Widespread bleeding may occur.