Animal Poison Control Center Research Articles

Methylphenidate toxicosis in dogs: 128 cases (2001–2008)

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. Retrospective case series. 128 dogs with MPH toxicosis or exposure. 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. 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. Ingestion of even small amounts of MPH can cause severe clinical signs in dogs. Monitoring and supportive care are recommended regardless of dose.

Presumptive hepatotoxicity and rhabdomyolysis secondary to phenazopyridine toxicity in a dog

To describe a rare, but potential clinical manifestation of phenazopyridine (PAP) toxicity in a dog. A 6-year-old spayed female Chihuahua was evaluated for ataxia and dysphagia after ingestion of 200 mg (66 mg/kg) of PAP hydrochloride. The dog was presented to the hospital with shifting leg lameness involving all 4 limbs, which progressed to reluctance to walk and severe diffuse muscle hyperesthesia. Clinical laboratory abnormalities included marked increases in serum alanine aminotransferase, aspartate aminotransferase, creatine kinase, mild increases in alkaline phosphatase, and increased c-Tnl-troponin concentration. Treatment included administration of intravenous fluids, muscle relaxants, pain medications, and hepatoprotectants for 5 days in the hospital, and medical management at home for an additional 5 days. Follow-up examinations performed 1 and 6 months after initial presentation revealed the dog to be clinically healthy with serum biochemical profiles within reference intervals. The purpose of this report is to describe an unusual manifestation of PAP toxicosis in a dog, which has not been previously reported in the literature. A review of the ASPCA Animal Poison Control Center database revealed 347 cases of PAP exposure in dogs during 2000-2009 underscoring the importance of being aware of this toxicity in the dog.

An overview of potentially life‐threatening poisonous plants in dogs and cats

AbstractObjectives:This article discusses the toxicity of the most common poisonous plants known to cause life‐threatening systemic effects or death in dogs and cats as reported to the ASPCA Animal Poison Control Center (APCC).Data sources:The article presents an overview of geographic distribution, toxic principle, clinical signs, clinical chemistry alterations, and treatment of intoxication as reported in the literature and based upon data retrieved from the APCC between January 2001 and December 2003.Summary:Most plant exposures in dogs or cats result in mild to moderate signs of vomiting and diarrhea while liver, kidney, central nervous system, or cardiovascular effects are rare. Some garden or household plants can cause serious systemic effects or death when a small amount of plant material has been ingested. Based on APCC records, the most frequently reported poisonous plants causing serious systemic effects include Lily (LiliumandHemerocallisspp.), Azalea (Rhododendronspp.), Oleander (Nerium oleander), Sago palm (Cycasspp.), Castor bean (Ricinus communis), Kalanchoe (Kalanchoespp.), and Autumn Crocus (Colchicum autumnale).Conclusion:Despite the variety of toxins present in the plants listed above, early clinical signs of toxicosis in dogs and cats can be nonspecific and can include vomiting, lethargy, anorexia, salivation, or diarrhea. Cardiac arrhythmias may be present with oleander, azalea, or kalanchoe ingestion. Evidence of liver or kidney damage (Cycas, Lilium, Hemerocallisspp.,Ricinus communis) may occur 1–2 days after the exposure. Treatment consists of early decontamination and supportive care and may vary according to the type of plant involved and clinical signs present.

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 × phosphorus product (Ca × 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 × P, and peak Ca × 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.

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.

Suspected toxicosis after topical administration of minoxidil in 2 cats

AbstractObjective: To discuss the clinical presentation and necropsy findings of 2 cats after topical administration of a minoxidil solution. Additionally, a potential management plan is offered for future cases.Case summary: Two cats with dermal exposure to topical minoxidil solution were identified from the ASPCA Animal Poison Control Center (APCC) files. Both cats were presented with lethargy and dyspnea within 36 hours of exposure. The cats were hypothermic, and had pulmonary edema and pleural effusion present on thoracic radiography. Both cats died despite supportive care. Necropsy of both cats confirmed pleural effusion and pulmonary edema and indicated cardiac compromise.New or unique information provided: Topical administration of minoxidil solution may cause life‐threatening pulmonary edema, pleural effusion, and cardiac dysfunction in the cat.

Veterinary toxicovigilance: objectives, means and organisation in France.

The CNITV (Centre National d’Informations Toxicologiques Veterinaires) at the National Veterinary School of Lyon has been operating as an Animal Poison Control Center since 1976 under the responsibility of the teachers from the Unit of Pharmacy Toxicology. It is organised as a non profit organization with the support of the fees from veterinary practitioners (about 650 adherents) and an executive board which defines the orientation and means of the center. It works in conjunction with the Center of Veterinary Pharmacovigilance and the Laboratory of Toxicological Analyses in the frame of the Unit of Pharmacy-Toxicology of the Veterinary School of Lyon. Since year 2000, the questions related to veterinary drugs (ADRs Adverse Drug Reactions) are dealt with by the Center of Veterinary Pharmacovigilance in the frame of the national system coordinated by the French Agency of Food Sanitary Security (AFSSA). So the CNITV deals with all questions related to veterinary toxicology except for veterinary drugs but including drugs for humans. The Laboratory of Toxicological Analyses performs various types of analyses on samples sent by veterinarians from the French territory, often after a contact with the Center. There are strong relations with the other disciplines of the Veterinary School, allowing for a rapid and quite efficient multidisciplinary approach of the cases and with the research activities in ecotoxicology of the department (bio-indicators, relation between biochemical toxicology and genetics).

Bread dough toxicosis in dogs

AbstractObjective: To provide information on the ingestion, and subsequent toxicity, of raw bread dough in dogs.Case summary: A report from the ASPCA animal poison control center (APCC) files of 3 cases of ingestion of raw bread dough by dogs. Clinical signs included vomiting, ataxia, blindness, hypothermia, and recumbency. All dogs were successfully treated for ethanol toxicosis.New information: Ingestion of bread dough can cause gastric obstruction, bloat, or ethanol toxicosis. The treatment of ethanol toxicosis, including decontamination, IV fluids, management of metabolic acidosis, and hypoglycemia is discussed. Yohimbine can be used in cases where the dog is comatose or has developed severe respiratory depression.

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.

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.

Ibuprofen Ingestion in Ferrets: 43 Cases January 1995–March 2000)

AbstractObjective: To summarize typical clinical signs, characterize the anticipated course of action, and give treatment recommendations for ibuprofen ingestion in ferrets.Design: Retrospective studyPatients: Records of 43 cases of ibuprofen ingestion in ferrets that were reported between January 1996‐March 2000, to the ASPCA Animal Poison Control Center (APCC).Measurements and Main Results: Twenty‐seven (93.1%) ferrets that had ingested ibuprofen developed neurologic signs, such as depression, coma, ataxia, recumbency, tremors, and weakness. In addition, 16 cases (55.2%) had one or more GI effects including anorexia, vomiting, retching or gagging, diarrhea, and melena. Polydipsia, polyuria, dysuria, renal failure, weight loss, shallow breathing, metabolic acidosis, dehydration, and hypothermia were also reported. Death was reported in 4 cases. The lowest dose associated with death was 220 mg/kg.Conclusion: Data in this study indicate that clinical signs of ibuprofen toxicosis in ferrets are more severe than those expected at similar dosages in dogs. The reason for this difference is poorly understood since the pathophysiology of ibuprofen is relatively unknown in ferrets. The onset of clinical signs appeared to occurr soon after ingestion and the toxic effects in ferrets typically involve the CNS, GI and renal systems. Treatment for ibuprofen toxicosis in the ferret includes stabilization, gastrointestinal decontamination, fluid diuresis, GI protection, and supportive care.(J Vet Emerg Crit Care 2001; 11(1):53–59)

Suspected caffeine and ephedrine toxicosis resulting from ingestion of an herbal supplement containing guarana and ma huang in dogs: 47 cases (1997-1999).

To describe the clinical signs following ingestion of an herbal supplement containing guarana and ma huang in dogs, estimate minimum dose at which clinical signs of toxicosis and death were reported, and evaluate treatment options. Retrospective study. 47 dogs with evidence of ingestion of an herbal supplement containing primarily guarana and ma huang. Records of dogs that had ingested an herbal supplement containing ma huang and guarana between July 1997 and October 1999 were retrieved from the National Animal Poison Control Center database. Data were retrieved and reviewed regarding signalment, dose ingested, clinical signs, laboratory test results, treatment, and final outcome. Cases were assessed by staff veterinarians as toxicosis or suspected toxicosis on the basis of strength of evidence supporting a diagnosis. Most dogs (80%) developed clinical signs of toxicosis within 8 hours of ingestion, and clinical signs persisted for up to 48 hours. Hyperactivity, tremors, seizures, and behavior changes were reported in 83% of dogs; other signs included vomiting (47%), tachycardia (30%), and hyperthermia (28%). Seventeen percent of the dogs died or were euthanatized. Estimated doses of guarana and ma huang ranged from 4.4 to 296.2 mg/kg (1.98 to 133.2 mg/lb) and 1.3 to 88.9 mg/kg (0.58 to 40.0 mg/lb) of body weight, respectively; minimum dose at which death was reported was 19.1 mg of guarana/kg (8.7 mg/lb) and 5.8 mg of ma huang/kg (2.6 mg/lb). Accidental ingestion of herbal supplements containing primarily guarana and ma huang in dogs can lead to a potentially lethal condition that may require prompt detoxification and supportive treatment for several days. Most dogs recovered with supportive treatment.

Management of Acetaminophen and Ibuprofen Toxicoses in Dogs and Cats

SummaryAcetaminophen and ibuprofen are commonly used in humans for their analgesic, anti‐pyretic, and anti‐inflammatory (ibuprofen) effects. Between January 1998 and March 2000, veterinarians at the ASPCA Animal Poison Control Center (APCC) consulted on more than 1,050 cases of accidental exposures to acetaminophen and 1,100 cases of ibuprofen ingestion in dogs and cats. Exposures to these medications can have serious effects on the animal's health. Fortunately, with prompt, aggressive treatment and good supportive care, most animals will recover completely.

Permethrin Spot‐On Toxicoses in Cats

SummarySpot‐on insecticides are becoming a popular type of flea control for pets. Spot‐on products available include those containing fipronil, imidicloprid, methoprene, and permethrin. Currently, over 15 brands of permethrin spot‐on products are labeled for “use in dogs only.” These products contain high concentrations (45–65%) of permethrin insecticide and are becoming a very popular choice for flea and tick control for dogs. Cats are highly sensitive to permethrin and inappropriate or accidental application of these products would be fatal. Though they have a wise margin of safety when used appropriately on dogs, even small amount of permethrin spot‐on products can cause severe clinical signs in cats. Indications of this species sensitivity have been documented by the National Animal Poison Control Center (NAPCC). In most cases, the owner applied the concentrated permethrin‐containing poduct to cats accidentally or intentionally. In some situations, the exposure seems to have resulted when the product was used on the dog and cats were playing with dog. (ASPCA, NAPCC, Unpublished data, 1995–1997).

5-Hydroxytryptophan toxicosis in dogs: 21 cases (1989-1999).

To determine epidemiologic characteristics, clinical findings, and treatment outcome of 5-hydroxytryptophan (5-HTP) toxicosis in dogs. Retrospective study. 21 dogs with evidence of accidental 5-HTP ingestion. Information was retrieved from the National Animal Poison Control Center database. Records of dogs ingesting 5-HTP between January 1989 and February 1999 were reviewed for information on signalment, dose ingested, clinical signs (onset, severity, duration), treatments administered, and outcome. Clinical signs of toxicosis developed in 19 of 21 (90%) dogs. Neurologic signs included seizures (9 dogs), depression (6), tremors (5), hyperesthesia (5), and ataxia (4). Gastrointestinal tract signs included vomiting or diarrhea (12 dogs), signs of abdominal pain (3), and hypersalivation (2). Other clinical signs were hyperthermia (7 dogs) and transient blindness (3). Three dogs died. No important clinical laboratory or necropsy findings were reported. The doses of 5-HTP ingested ranged from 2.5 to 573 mg/kg (1.1 to 260 mg/lb) of body weight; the minimum toxic dose reported in our study was 23.6 mg/kg (10.7 mg/lb), and the minimum lethal dose was 128 mg/kg (58.1 mg/lb). Onset of signs ranged from 10 minutes to 4 hours after ingestion, and signs lasted up to 36 hours. Of 17 dogs with clinical signs of toxicosis that received treatment, 16 recovered; treatment consisted of decontamination, seizure control, thermoregulation, fluid therapy, and supportive care. Ingestion of 5-HTP in dogs can result in a potentially life-threatening syndrome resembling serotonin syndrome in humans, which requires prompt and aggressive care.

Evaluation of castor bean toxicosis in dogs: 98 cases.

Castor beans (Ricinus communis) contain ricin. Ricin is a glycoprotein reported to cause hypotension, gastroenteritis, depression, and death. However, few deaths are reported following castor bean ingestion in animals. From January 1987 to December 1998, the American Society for the Prevention of Cruelty to Animals-National Animal Poison Control Center received 98 incidents of castor bean ingestion in dogs. The most commonly reported clinical signs were vomiting, depression, and diarrhea. Death or euthanasia occurred in 9% of the cases. The severity of clinical signs following castor bean ingestion may depend on whether the beans were chewed or swallowed whole.

A Retrospective Study of Pemoline Toxicosis in Dogs: 101 Cases (1987–1997)

SummaryPemoline is a central nervous system stimulant commonly used for Attension Deficit Disorder in humans. This study describes the clinical syndrome associated with pemoline ingestion as well as its treatment. Ten years worth (1987–1997) of records from the ASPCa National Animal Poison Control Center involving pemoline ingestion in dogs were reviewed. The data suggests that most dogs ingesting pemoline show signs of central nervous system and cardiovascular stimulation including hyperactivity, tremors, ataxia, seizure, tachycardia, hyperthermia, and mydriasis. Blood chemistry alterations included electrolyte imbalances in some dogs. The minimum dose reported to cause clinical signs was 2.8 mg/kg and the minimum dose reported to have caused death was 10 mg/kg. Dogs generally showed clinical signs within 30 minutes to 24 hours of ingestion. The duration of clinical signs ranged from 15 hours to four days. Ninety‐four percent of the dogs recovered with supportive treatment. (Vet. Emerg. & Crit. Care, 9:203–207, 1999)

Using the American Society for the Prevention of Cruelty to Animals-National Animal Poison Control Center as a toxicology resource

Veterinarians are frequently faced with cases involving potential toxicants, many of which are unfamiliar. The American Society for the Prevention of Cruelty to Animals-National Animal Poison Control Center (ASPCA-NAPCC) maintains a database listing thousands of pesticides, plants, household items, cleaning agents, human medications, and other products. This service is available 24 hours daily to provide information regarding the toxicity of product ingredients, dose calculation, and treatment recommendations in all species of animals, including birds and exotic pets.

Cycad palm toxicosis in dogs: 60 cases (1987-1997)

Objective To report clinical and epidemiologic information, summarize characteristic clinical signs and laboratory results, and describe the expected course of cycad toxicosis in dogs. Design Retrospective study. Animals 60 dogs with evidence of cycad ingestion. Procedure The National Animal Poison Control Center's case record database was searched for records of dogs ingesting cycad plants from January 1987 to November 1997. Data were retrieved on clinical signs, laboratory test results, exposure history, and physical examination findings. Cases were assessed as toxicosis, suspected toxicosis, or possible toxicosis. Results Records from 60 dogs were retrieved; 89.7% of the dogs were from the southern United States, 38.7% ingested seeds, 95% developed liver and gastrointestinal tract problems, and 53.3% had abnormal neurologic signs. High serum bilirubin concentration and alkaline phosphatase and alanine aminotransferase activities were the most common serum biochemical abnormalities. Although clinical signs were observed within 1 day, laboratory values did not change for 24 to 48 hours after cycad ingestion. Mortality rate was reportedly 32.1 %. Clinical Implications 68% of dogs responded well to treatment and supportive care. Dogs ingesting seeds are likely to develop more serious problems. Clinical signs can develop within 1 to 3 days and can last for several days. A tentative diagnosis should be made on the basis of history of ingestion, clinical signs, and duration of signs. Because of the nature of these toxins, cycad ingestion is serious and should be treated aggressively. (J Am Vet Med Assoc 1998;213:99-101)

A case–control study of acute ibuprofen toxicity in dogs

A case–control study used data in the National Animal Poison Control Center database to characterize risk factors for gastrointestinal ulceration and acute renal failure subsequent to the acute ingestion of ibuprofen in the dog. For gastrointestinal ulceration (GIU) subsequent to ibuprofen ingestion, four factors differentiated the 116 cases from the 93 controls. Risk of GIU was lower for dogs where the time from ingestion to intervention was known as opposed to missing (adjusted odds ratio (aOR)=0.12, p=0.0001). Risk of GIU was also lower for the Labrador breed (aOR=0.22, p=0.004). Risk of GIU was higher for each unit of the logarithm of time to intervention (aOR=2.63, p=0.0002) and for the German Shepherd breed (aOR=5.67, p=0.14). For acute renal failure (ARF) subsequent to ibuprofen ingestion, two factors differentiated the 80 cases from the 64 controls. Risk of ARF was lower for dogs where the time from ingestion to intervention was known as opposed to missing (aOR=0.15, p=0.0001). Risk of ARF was higher for each unit of the logarithm of time to intervention (aOR=2.16, p=0.01). Although this study failed to describe a dose–response relationship, it appears that there are significant breed differences in susceptibility to GIU subsequent to ibuprofen exposure. Time to intervention was critical for both GIU and ARF outcomes. Dogs, particularly German Shepherds, ingesting even small amounts of ibuprofen, may need to be managed aggressively.