Page 1128 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Nervous system 1103

VetBooks.ir or normal saline and administered at 75 mg/kg/day 10.56
i/v, divided into three doses. A therapeutic protocol
of 4 days treatment, 2 days off and 4 days treatment
should be followed. The days between treatments
allow for equilibration of the lead out of the bone and
other body stores so that it is available for chelation.
Concurrent intravenous fluid therapy is preferred
because it facilitates excretion of the water-soluble
chelate and also aids dehydrated animals. The effec-
tiveness of the chelation therapy can be evaluated
by changes in the lead concentrations of urine and
blood. Blood levels should be stable below 0.2 ppm
following treatment, whereas urinary concentrations
are expected to increase 2–30 times above baseline
during treatment. The blood concentration should
be checked within 2 weeks of final chelation and if it Fig. 10.56
has rebounded to exceed 0.35 ppm, a second course Rattlesnake bite
of chelation therapy is recommended. Thiamine on the nares of a
therapy (1 mg/kg i/v) is also used in ruminants with mare in Arizona,
lead poisoning and has proved an effective adjunc- USA.
tive treatment with EDTA. The nature of the pro-
tective effect of thiamine is unclear. Supportive care
should also be instituted while patients are undergo- the skin of the prey, so envenomation is extremely
ing chelation therapy. Identification of lead toxicosis uncommon. When it occurs, there is an initial
in a horse should prompt an environmental investi- period of excitement and hyperaesthesia, followed
gation to identify the source of contamination. by generalised weakness. Snakebites are not usually
fatal to adult horses but can be fatal in young foals.
Prognosis Treatment includes supportive care, tetanus prophy-
The prognosis is good if chelation therapy is started laxis, broad-spectrum antimicrobials and local treat-
and the animal’s lead levels decrease. ment of wounds (Fig. 10.56).

SNAKEBITE TICK PARALYSIS

Bites from a wide variety of venomous snakes have Definition/overview
been reported in horses. Most reports involve snakes Tick paralysis is a rare condition in horses. It causes
from the families Crotalidae (pit vipers) and Elapidae progressive, ascending LMN paralysis.
(cobras). The majority of venomous snakebites in
North America are inflicted by rattlesnakes, cop- Aetiology/pathophysiology
perheads and water moccasins. These usually cause The ticks Ixodes bolocyclus and Dermacentor andersoni
local effects, with swelling and oedema at the bite have a toxin present in their saliva that can cause neu-
site. Usually the head and muzzle are affected, but romuscular junction dysfunction. Ixodes paralysis has
bites can occur in other areas such as the limbs. The been reported in horses in Australia. Dermacentor is
venom of members of the family Elapidae is mainly a cause of tick paralysis in a variety of animal species
neurotoxic, with minimal local effects. This family in North America; however, its role in equine disease
includes cobras, mambas and coral snakes. These is less clear. Inhibition of acetylcholine release at the
snakes, however, frequently require prolonged con- neuromuscular junction results in signs of gener-
tact (30 seconds or longer) to work the venom into alised flaccid paralysis.