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Old 09-06-2006, 06:26 AM   #13
yorkiegirl2
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Toluene/Dichlorophen
Toluene/dichlorophen anthelmintics (effective against ascarids, hookworms, and some tapeworms of dogs and cats) may cause adverse effects in healthy cats and dogs following oral administration of less than 1.5 times the recommended product dose [202]. Clinical signs usually are observed within 6 hours of dosing and include ataxia, aberrant behavior, mydriasis, vomiting, depression, muscle tremor, and hypersalivation. In this report, the four most common products associated with toxicosis in cats were Daltrek Tri-Wormer, De-Vos Control III Worm Caps, Zema Pulvex Multi-Purpose Worm Caps, and Vermiplex. In dogs, commonly involved products were Happy Jack's Trivermicide Worm Capsule, Farnam Triple Wormer, Zema Pulvex Multi-Purpose Worm Caps, Anchor Canine Wormer, and Performer Brand Dog Wormer. In most cases, clinical signs disappear within a few hours to a day with general supportive care.

Tricyclic Antidepressants
Tricyclic antidepressants (TCAs), a class of psychotherapeutic medications, are widely prescribed for human patients, thereby increasing the potential for accidental oral ingestion by companion animals [203]. Animals ingesting TCA in an amount exceeding 15 mg/kg are in grave danger. TCAs block re-uptake of biogenic amines (e.g., epinephrine), have anticholinergic (atropine-like) effects, and quinidine-like action on the cardiovascular system. Clinical signs in animals include hyperexcitement and vomiting followed by ataxia, lethargy, and muscular tremors. Bradycardia and cardiac arrhythmias should be anticipated in the later stages of the TCA toxic syndrome [203]. In a review of over 450 cases reported to the Illinois Animal Poison Information Center between 1985 and 1989, more than 7% of affected animals eventually died [203]. Initial therapy includes intubation, oxygen administration, enterogastric lavage, and activated charcoal via a stomach tube. Animals in a hyperactive state should receive diazepam (0.5 mg/kg IV or IM, repeated as needed, every 10 minutes for three doses), followed by activated charcoal (2 gm/kg, every 3 - 4 hours, PO) and a suitable cathartic, such as sorbitol (0.5 gm/kg, PO) or sodium sulfate (Glauber’s salts) at 0.25 gm/kg, PO. Magnesium sulfate (Epsom salts) is not recommended because of the TCS-induced decrease in GI motility. Intravenous sodium bicarbonate at 2 - 3 mEq/kg, over 15 - 30 minutes, should be given if acidosis, hypotension, tachycardia, or other cardiac abnormalities are noted. Blood pH should be maintained above 7.5.

Vincristine
Vincristine is a vinca alkaloid widely utilized in cancer chemotherapy. Its major clinical limitation is due to a drug induced sensory-motor neuropathy, the pathogenesis of which is poorly understood. In cats with experimental vincristine neuropathy, major pathological lesions were focal axonal swellings (giant axon formations) due to malaligned accumulations of neurofilaments and secondary paranodal demyelination [204]. These were primarily confined to the proximal portions of the peripheral nerves. Wallerian degeneration involved a small number of nerve fibers in the distal regions. Muscle spindles were affected and motor nerve conduction velocities were reduced by 30% [205]. We reported a vincristine-induced peripheral neuropathy in a 12 year old, female, Golden Retriever that received 16 weekly doses of vincristine (0.5 mg/m2) as part of a regimen for treatment of mycosis fungoides [206]. The dog was presented for sudden onset of a shuffling pelvic limb gait, intermittent collapse, and difficulty negotiating turns and stairs. Neurological examination revealed mild ataxia in the pelvic limbs, depressed pelvic limb postural reactions, and depressed patellar and pelvic limb withdrawal reflexes. Electromyographic testing revealed fibrillation potentials and positive sharp waves consistent with denervation. Sciatic motor nerve conduction velocity was decreased. Evoked muscle potentials were polyphasic and had reduced amplitude and prolonged duration. Severe nerve fiber degeneration, nerve fiber loss, and endoneurial fibrosis were seen in a nerve biopsy sample. The neuropathy improved after vincristine was discontinued. Results of a repeat nerve biopsy taken 10 weeks after cessation of vincristine administration showed fewer degenerating nerve fibers and presence of demyelination-remyelination. The dog appeared neurologically normal at this time. In people, vincristine-induced neurotoxicity is aggravated by itraconazole [207,208].

Zolpidem
Zolpidem is a nonbenzodiazepine hypnotic and sedative of the imidazopyridine class used for treating short-term insomnia in humans. The drug increases the frequency of chloride channel opening and inhibits neuronal excitation. A retrospective review of zolpidem ingestion in 33 dogs that were reported to the ASPCA Animal Poison Control Center between January 1998 and July 2000 revealed that ingested dosages ranged from 0.24 to 21 mg/kg [211]. Clinical signs reported included ataxia, hyperactivity, vomiting, lethargy, panting, disorientation, nonspecific behavior disorder, hypersalivation, tachycardia, tremors, apprehension, vocalization, weakness, and hyperesthesia. In most instances, clinical signs developed within 1 hour and typically resolved within 12 hours. Treatment includes induction of emesis within the first 1 to 2 hours (or gastric lavage), use of activated charcoal in conjunction with a catharctic, such as sorbitol, and fluid administration. Note that supportive treatment (e.g., phenothiazines or barbiturates) may be used to treat signs of stimulation and hyperactivity; however, the use of diazepam or other benzodiazepines should be avoided
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