Methylphenidate toxicosis in dogs: 128 cases (2001-2008).

OBJECTIVE: To determine clinical signs and outcomes of methylphenidate hydrochloride (MPH) toxicosis in dogs; to assess effects of amount (ie, dose) and formulation (immediate or extended release) of ingested MPH on onset, duration, and severity of clinical signs; and to describe management of MPH intoxication. DESIGN: Retrospective case series. ANIMALS: 128 dogs with MPH toxicosis or exposure. PROCEDURES: Data from an Animal Poison Control Center (APCC) database from November 1, 2001, to November 30, 2008, were reviewed. Records of dogs were searched for APCC classifications of confirmed (n = 71) or suspected (39) MPH toxicosis; dogs (18) that ingested MPH but did not develop clinical signs of toxicosis were also included. Signalment, dose, clinical signs, treatment, and outcome were evaluated. RESULTS: Clinical signs of toxicosis were reported in 107 of 128 (84%) dogs that ingested MPH; these included hyperactivity in 42 (33%), tachycardia in 27 (21%), vomiting in 19 (15%), agitation in 16 (13%), and hyperthermia in 13 (10%). Doses ranged from 0.36 mg/kg (0.164 mg/lb) to 117.0 mg/kg (53.18 mg/lb). Severity of clinical signs was not strongly associated with dose. More severe and prolonged clinical signs were associated with ingestion of extended-release formulations of MPH; 3 dogs that consumed these formulations (doses, 10.2 mg/kg [4.64 mg/lb], 15.4 mg/kg [700 mg/lb], and 31.1 mg/kg [14.14 mg/lb]) died. Favorable outcomes were reported for most (31/34 [91%]) dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Ingestion of even small amounts of MPH can cause severe clinical signs in dogs. Monitoring and supportive care are recommended regardless of dose.

Acute hepatic failure and coagulopathy associated with xylitol ingestion in eight dogs.

CASE DESCRIPTION: 8 adult dogs were evaluated for treatment of lethargy and vomiting after ingestion of xylitol, a sugar alcohol used as a sweetener in various products. CLINICAL FINDINGS: In addition to vomiting and lethargy, 5 of the dogs had widespread petechial, ecchymotic, or gastrointestinal tract hemorrhages. Common clinicopathologic findings included moderately to severely high serum activities of liver enzymes, hyperbilirubinemia, hypoglycemia, hyperphosphatemia, prolonged clotting times, and thrombocytopenia. Necropsies were performed on 3 dogs and severe hepatic necrosis was found in 2. In the third dog, histologic examination revealed severe hepatocyte loss or atrophy with lobular collapse. TREATMENT AND OUTCOME: Treatments varied among dogs and included IV administration of fluids; plasma transfusions; and, if indicated, administration of dextrose. Three dogs were euthanatized, 2 dogs died, 2 dogs made a complete recovery, and 1 dog was recovering but was lost to follow-up. CLINICAL RELEVANCE: Although xylitol causes hypoglycemia in dogs, hepatic failure after ingestion has not previously been reported. Because an increasing number of consumer products contain xylitol, clinicians should be aware that ingestion of xylitol can have serious, life-threatening effects.

Acute renal failure in dogs after the ingestion of grapes or raisins: a retrospective evaluation of 43 dogs (1992-2002).

A review of records from the AnTox database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center identified 43 dogs that developed increased blood urea nitrogen concentration, serum creatinine concentration, or both as well as clinical signs after ingesting grapes, raisins, or both. Clinical findings, laboratory findings, histopathological findings, treatments performed, and outcome were evaluated. All dogs vomited, and lethargy, anorexia, and diarrhea were other common clinical signs. Decreased urine output, ataxia, or weakness were associated with a negative outcome. High calcium x phosphorus product (Ca x P), hyperphosphatemia, and hypercalcemia were present in 95%, 90%, and 62% of the dogs in which these variables were evaluated. Extremely high initial total calcium concentration, peak total calcium concentration, initial Ca x P, and peak Ca x P were negative prognostic indicators. Proximal renal tubular necrosis was the most consistent finding in dogs for which histopathology was evaluated. Fifty-three percent of the 43 dogs survived, with 15 of these 23 having a complete resolution of clinical signs and azotemia. Although the mechanism of renal injury from grapes and raisins remains unclear, the findings of this study contribute to an understanding of the clinical course of acute renal failure that can occur after ingestion of grapes or raisins in dogs.

Clinical syndrome associated with zolpidem ingestion in dogs: 33 cases (January 1998-July 2000).

Zolpidem is a nonbenzodiazepine hypnotic of the imidazopyridine class that is used to treat insomnia in humans. Zolpidem binds selectively to the benzodiazepine omega-1 receptor and increases the frequency of chloride channel opening, which results in inhibition of neuronal excitation. A retrospective study was conducted of zolpidem ingestion in dogs that were reported to the ASPCA Animal Poison Control Center (APCC) between January 1998 and July 2000. Data analysis included amount ingested, clinical effects, and time of onset of signs. Thirty-three reports of zolpidem ingestion in dogs (ranging in age from 5 months to 16 years) were evaluated. Approximate ingested dosages ranged from 0.24 to 21 mg/kg. Clinical signs reported included ataxia (18 dogs; 54.5%), hyperactivity (10 dogs; 30.3%), vomiting (7 dogs; 21.2%), and lethargy (5 dogs; 15.2%), as well as panting, disorientation, nonspecific behavior disorder, and hypersalivation (4 dogs each sign; 12.1%). Other signs reported include tachycardia, tremors, apprehension, vocalization, hypersalivation, weakness, and hyperesthesia. In 85% percent of reports, clinical signs developed within 1 hour and usually resolved within 12 hours. Although central nervous system (CNS) depression is reported as a primary effect of zolpidem in humans and would also be expected in dogs, information obtained from this study indicates that some dogs may exhibit a paradoxical excitation reaction. This effect appears to vary among individual dogs.

General toxicologic hazards and risks for search-and-rescue dogs responding to urban disasters.

In large-scale disasters, it is not always possible to identify every potential toxic agent to which SAR dogs may be exposed. However, an understanding of the basic means by which dogs may be exposed to toxic agents can aid veterinarians in determining basic risks for particular SAR sites and allow veterinarians to institute general preventive measures (eg, frequent eye washes) to minimize exposure. Discussions with public health and other authorities on-site may aid in identifying site-specific risks for SAR dogs. Finally, ensuring that SAR dog handlers are aware of basic risks, precautions, and decontamination measures is essential, as handlers are the first line of defense in preventing illness or injury to SAR dogs as they work a disaster area.

Newer antidotal therapies.

Although the availability of an antidote for a toxic agent does not take away the primary responsibility of the clinician to manage the patient's clinical signs, the use of antidotes in appropriate situations can result in a more rapid recovery with potentially fewer long-term complications. Recent advances in pharmacology and molecular biology have resulted in the development of new and safer antidotal therapies for the management of toxicosis. The progress in immunotoxicotherapy over the last two decades continues and may ultimately lead to an era when the clinical toxicologist has a vast array of antibody fragments available for use with specific toxic agents. Development of specific pharmacologic antagonists for other agents should also enable the clinician to more reliably manage toxicoses. In spite of all these potential advances, the management of most toxicoses still relies on the application of sound veterinary medical principles.