Page 840 - Clinical Small Animal Internal Medicine

808 Section 8 Neurologic Disease

aspiration pneumonia. Recumbent nursing care, which Drug‐Induced Neuromuscular Blockade
VetBooks.ir includes frequent turning, good padding to prevent Certain drugs have been shown to induce NMJ blockade
decubital ulcers and bladder care, is essential for a good
in veterinary medicine although most reports are
recovery and to avoid secondary complications. Oral
antibiotics are of no benefit, unless toxico‐infectious experimental, with very few documented clinical cases.
The most commonly associated antibiotics are amino-
botulism is suspected and in that case penicillins or glycosides, lincomycin, penicillamine, polymyxins, and
metronidazole would be indicated. Administration of tetracyclines. The mechanism of action in aminoglycoside
C. botulinum antitoxin needs to be type specific and NMJ blockage is presynaptic inhibition of ACh release as
would not be beneficial unless a specific type C‐antitoxin a result of blocked calcium influx. There is also blockage
were available. The antitoxin administration only helps of calcium influx on the postsynaptic membrane. The
to inactivate circulating unbound toxin and not toxin degree of transmission impairment with aminoglyco-
already fixed at the site of neuromuscular junction sides depends on the specific drug and the balance
damage so, depending on the timing of administration, between the pre‐ and postsynaptic effects. The most
it could be too late in the course of the disease to use. potent effects, in descending order, are from neomycin,
Complete recovery is possible with proper care and kanamycin, amikacin, gentamicin, and tobramycin.
should occur within 1–3 weeks. Dogs with aspiration Penicillamine has been documented to cause an immune‐
pneumonia and respiratory paralysis may have a more mediated MG in people. Polymyxins have their most
guarded prognosis depending on severity and the ability profound effect on the postsynaptic membrane by acting
to obtain respiratory support.
as a noncompetitive nondepolarizing agent. Tetracyclines
have the proposed effect of chelating calcium ions and
Postsynaptic Disorders thereby depressing the effect of ACh on the postsynaptic
muscle fiber.
Organophosphate and Carbamate Toxicity It is important to remember that these drugs can
Organophosphates (OP) and carbamates are commonly potentiate neuromuscular blocking agents used during
used compounds found in many pesticides and insecti- surgical procedures or may worsen or unmask preexist-
cides. They are long‐acting anticholinesterases that ing disorders of neuromuscular transmission. The use of
irreversibly bind acetylcholinesterase (AChE) in nervous these agents should be avoided in the treatment of other
tissue and muscle, allowing accumulation of ACh to cause neuromuscular disorders such as MG patients. Other
continuous cholinergic stimulation. This occurs in cen- drugs that have a reported effect on neuromuscular
tral, muscarinic, and nicotinic cholinergic synapses, transmission are antiarrhythmic agents, phenothiazines,
resulting in clinical signs that include autonomic over- methoxyflurane, magnesium, and the antiprotozoals
stimulation (salivation, lacrimation, urination, defecation) chloroquine and quinine. Methimazole has been docu-
and neuromuscular dysfunction. A delayed OP‐induced mented to cause a reversible drug‐induced autoimmune
polyneuropathy has also been described. Clinical toxicity MG in hyperthyroid cats.
in veterinary medicine is usually associated with inappro-
priate or accidental dosing, with cats being more suscepti-
ble to these compounds than dogs. Historical information Black Widow Spider Envenomation
is imperative to reaching the diagnosis. The black widow spider (Lactrodectus spp.) has a
Although serum cholinesterase concentrations can be
measured, the results are usually not available in a timely worldwide distribution. The most potent component
of its venom is the purified fraction B known as alpha‐
fashion so a presumptive diagnosis based on history and latrotoxin. The toxin causes a massive release of neuro-
clinical signs is enough to begin treatment. transmitter and loss of synaptic vesicles. The synaptic
Clinical signs of OP intoxication are usually dominated
by the autonomic effects, but neuromuscular signs vesicle loss is caused by increased fusion and docking of
the synaptic vesicles with the plasma membrane and
include a stiff rigid gait, muscle tremors, and fascicula- inhibition of new vesicle formation.
tion (except for fenthion). The cat appears to be more susceptible to envenoma-
Treatment for these toxicities consists of reducing fur-
ther exposure or absorption by bathing or gastric lavage tion and the clinical signs usually occur within the first
eight hours. There are fine muscle tremors, muscle
as appropriate. Atropine sulfate can be titrated to effect spasticity, abdominal rigidity, pain, and profound flac-
to counteract the parasympathetic signs. Pralidoxime cid muscle weakness. Hypertension and electrolyte
chloride (2‐PAM or protopam chloride) and pralidoxime abnormalities may also occur.
mesylate (P2S) can be used in OP toxicity but not in Treatment consists of administering the appropriate
carbamate toxicity (except for aldicarb). These oxime antivenin and supportive care. A rapid response to the
reactivators cause release the bound AChE from the antivenin is reported in people.
OP compound.