Suspected intermediate syndrome in a dog after organophosphate poisoning.

OBJECTIVE: To discuss the clinical presentation and successful treatment of a suspected case of intermediate syndrome due to organophosphate (OP) poisoning in a dog. CASE SUMMARY: Two dogs presented with acute cholinergic signs after ingesting an OP insecticide containing 50% acephate. Clinical signs consistent with acute cholinergic crisis resolved in both dogs within 24 hours postingestion. One dog developed an onset of neurological signs consistent with intermediate syndrome approximately 24 hours postingestion. This patient's clinical signs resolved with the use of pralidoxime chloride. NEW OR UNIQUE INFORMATION PROVIDED: OP poisoning most commonly presents as an acute cholinergic crisis, with rare instances of animals developing intermediate syndrome. Few reports of successful treatment and recovery from intermediate syndrome exist in the veterinary literature, particularly with instances in which 2 dogs within the same exposure setting were treated for acute cholinergic signs and only 1 progressed to an intermediate syndrome. This report also highlights the importance of early intervention with pralidoxime chloride prior to the onset of aging.

Clinical signs of cardiovascular effects secondary to suspected pimobendan toxicosis in five dogs.

The purpose of this study was to review the medical records of dogs that were either suspected or known to have ingested large doses of pimobendan and to describe the clinical signs associated with pimobendan toxicosis. The database of Pet Poison Helpline, an animal poison control center located in Minneapolis, MN, was searched for cases involving pimobendan toxicosis from Nov 2004 to Apr 2010. In total, 98 cases were identified. Of those, seven dogs that ingested between 2.6 mg/kg and 21.3 mg/kg were selected for further evaluation. Clinical signs consisted of cardiovascular abnormalities, including severe tachycardia (4/7), hypotension (2/7), and hypertension (2/7). In two dogs, no clinical signs were seen. Despite a wide safety profile, large overdoses of pimobendan may present risks for individual pets. Prompt decontamination, including emesis induction and the administration of activated charcoal, is advised in the asymptomatic patient. Symptomatic and supportive care should include the use of IV fluid therapy to treat hypotension and address hydration requirements and blood pressure and electrocardiogram monitoring with high-dose toxicosis. Practitioners should be aware of the clinical signs associated with high-dose pimobendan toxicosis. Of the dogs reported herein, all were hospitalized, responded to supportive care, and survived to discharge within 24 hr of exposure.

Alpha lipoic acid toxicosis in cats (2008-2016): Four cases.

OBJECTIVE: To review clinical signs, treatments, and outcome of 4 cases in cats after ingestion of alpha lipoic acid. CASE SERIES SUMMARY: Four cases with known alpha lipoic acid ingestions developed clinical signs. A consistent clinical sign in all cases was vomiting, while 2 of the 4 cases resulted in death. NEW OR UNIQUE INFORMATION PROVIDED: This is the first reported case series of alpha lipoic acid ingestions in cats.

Tobacco and cigarette butt consumption in humans and animals.

Discarded cigarette butts may present health risks to human infants and animals because of indiscriminate eating behaviours. Nicotine found in cigarette butts may cause vomiting and neurological toxicity; leachates of cigarette butts in aquatic environments may cause exposure to additional toxic chemicals including heavy metals, ethyl phenol and pesticide residues. This report reviews published and grey literature regarding cigarette butt waste consumption by children, pets and wildlife. Although reports of human and animal exposures number in the tens of thousands, severe toxic outcomes due to butt consumption are rare. Nonetheless, the ubiquity of cigarette butt waste and its potential for adverse effects on human and animal health warrants additional research and policy interventions to reduce the stream of these pollutants in the environment.

Adverse effects associated with inadvertent intravenous penicillin G procaine-penicillin G benzathine administration in two dogs and a cat.

CASE DESCRIPTION: 2 dogs and a cat were inadvertently given penicillin G procaine-penicillin G benzathine IV instead of propofol during induction of anesthesia for routine dental prophylaxis. One dog and the cat required hospitalization because of severe neurologic impairment and cardiopulmonary arrest (cat); the remaining dog did not develop any clinical signs. CLINICAL FINDINGS: In the 2 animals that developed signs consistent with an immediate adverse reaction, clinical signs included muscle tremors, seizures, blindness, vocalization, agitation, and transient loss of vision. Hypothermia, pruritus, hypotension, and cardiac arrest were also documented. TREATMENT AND OUTCOME: The 2 affected patients responded to treatment with anticonvulsant medications, centrally acting muscle relaxants, sedation, and intensive supportive care including IV fluid administration and oxygen supplementation as needed. Cardiopulmonary cerebral resuscitation was performed successfully in the cat. The dog that did not develop any clinical signs was not treated. The 2 affected patients recovered fully and were discharged from the hospital after 3 to 4 days with no apparent sequelae. CLINICAL RELEVANCE: Penicillin G procaine-penicillin G benzathine and propofol are common drugs in veterinary practice and may both be administered to patients undergoing elective procedures. Because of their similar milky white appearance, veterinarians should label syringes and take care to avoid this medication error. There is no specific antidote for penicillin orprocaine toxicosis. Aggressive and immediate treatment is required in patients that develop an adverse reaction to ensure a successful outcome.

Mirabegron Toxicosis in Dogs: a Retrospective Study.

Mirabegron is a selective beta (B)3 adrenoreceptor agonist marketed for human treatment of an overactive bladder (OAB). It has a wide margin of safety in humans, but in dogs, severe adverse effects have occurred. We sought to determine the effects and outcome of mirabegron toxicosis in dogs. A retrospective review of all calls within the Pet Poison Helpline (PPH), an international animal poison control center, database was performed for mirabegron exposures between 2013 and 2015. Potential ingested doses ranging from 1.31 to 8.3 mg/kg. Many dogs remained asymptomatic and no fatalities occurred in any dogs. The most commonly reported signs were tachycardia and erythema. While mirabegron was found to have a very narrow margin of safety and high toxicity risk to dogs during preclinical trials, effects appear to differ greatly in the nonclinical field environment and further study is needed.

Acute Hepatic Failure in a Dog after Xylitol Ingestion.

Xylitol is a five-carbon sugar alcohol produced from natural resources frequently used as a sugar substitute for humans. We report the development and successful treatment of acute hepatic failure and coagulopathy in a dog after xylitol ingestion. A 9-year-old 4.95 kg (10.9 lb) neutered male Chihuahua was evaluated at a veterinary clinic for vomiting after ingesting 224 g (45 g/kg, 20.5 g/lb) of granulated xylitol. Hypoglycemia developed within 1-2 h, elevated liver values, suggesting the development of acute hepatic failure, within 12 h and coagulopathy less than 24 h after ingestion. Treatment included maropitant, intravenous dextrose, phytonadione, metronidazole, and fresh frozen plasma. N-acetylcysteine (NAC) and S-adensoyl-L-methionine (SAMe) provided hepatic detoxification and support. The dog survived and liver values returned to normal within 1 month post ingestion. No adverse effects to hepatic function have been identified 2 years after acute xylitol toxicity. This paper is one of the few reports of successful management of a dog with hypoglycemia, hepatic failure, and coagulopathy caused by xylitol toxicity. To date, this is the highest published xylitol dose survived by a dog, as well as the only reported case that documents laboratory changes throughout the course of toxicity and includes normal hepatic indices for 7 months following xylitol toxicity. The rapidly expanding use of xylitol in a variety of products intended for human consumption has led to a rise in xylitol toxicity cases reported in dogs, and clinicians should be aware that more dogs may potentially be exposed and develop similar manifestations.

Toxicology of newer pesticides for use in dogs and cats.

The past 10 years have witnessed the development of several new insecticides that have been specifically designed to exploit physiologic differences between insects and mammals. This has resulted in products that seem to have a wide margin of safety when used in dogs and cats. Compared with the more acutely toxic organophosphorous, carbamate, and heavy metal insecticides as well as with the environmental problems of bioaccumulation associated with some of the organochlorine insecticides, these newer insecticides such as fipronil, imidacloprid, selamectin, lufenuron, and nitenpyram seem to alleviate these known problems while still providing satisfactory insecticidal activity.

Selective serotonin reuptake inhibitor (SSRI) toxicosis in cats: 33 cases (2004-2010).

OBJECTIVE: To evaluate a population of cats with selective-serotonin reuptake inhibitor (SSRI) toxicosis and characterize the population affected, list products ingested, the clinical signs observed, treatments performed, length of hospitalization, patient outcome, and overall prognosis. DESIGN: Retrospective study from 2004 to 2010. SETTING: Referral veterinary center. ANIMALS: Thirty-three witnessed cat SSRI ingestions. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The medical records of cats with a witnessed SSRI ingestion identified by review of an animal poison control center electronic database were evaluated. The most common SSRIs ingested were venlafaxine (Effexor; 12/33; 36%), fluoxetine (Prozac; 12/33; 36%), citalopram (Celexa; 6/33; 18%), and escitalopram (Lexapro; 3/33; 9%). Overall, 24% of cats (8/33) became symptomatic, while 76% (25/33) remained asymptomatic. Of the symptomatic cats, sedation was the most common clinical sign (6/8; 75%), followed by gastrointestinal signs (4/8; 50%), central nervous system stimulation (1/8; 13%), cardiovascular signs (1/8; 13%), and hyperthermia (1/8; 13%). Veterinary care was sought in 20 cats (20/33; 61%). Sixteen cats (16/20; 80%) were hospitalized, while 4 cats (4/20; 20%) were treated as outpatients. Treatment for hospitalized patients included administration of IV fluid therapy (14/16; 88%), activated charcoal (12/16; 75%), anti-arrhythmic agents (7/16; 44%), methocarbamol (6/16; 38%), cyproheptadine (6/16; 38%), anti-emetics (5/16; 31%), and sedation (5/16; 31%). Diagnostics included blood work (7/16; 44%), blood pressure measurement (3/16; 19%), and electrocardiogram monitoring (2/16; 13%). Mean hospitalization time for all cases of SSRI ingestion was 14.6 ± 7.8 hours (n = 16). All symptomatic cats in this study (8/8; 100%) had resolution of clinical signs and survived to discharge. CONCLUSIONS: The prognosis for SSRI ingestion in this population of cats was excellent. Decontamination and supportive care for at least 12-24 hours can be considered in cats with SSRI ingestion, particularly venlafaxine to monitor resolution of clinical signs.

Retrospective evaluation of toxicosis from selective serotonin reuptake inhibitor antidepressants: 313 dogs (2005-2010).

OBJECTIVE: To evaluate a clinical population of dogs exposed to selective serotonin reuptake inhibitor (SSRI) antidepressant medications and describe the clinical findings, epidemiological characteristics, outcome, and prognosis. DESIGN: Retrospective study (February 1, 2005-August 31, 2010). SETTING: Animal poison control helpline. ANIMALS: Three hundred thirteen dogs with presumed SSRI toxicosis. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Dogs with presumptive SSRI medication toxicosis identified by a review of the electronic database of Pet Poison Helpline, an animal poison control center, were evaluated. No clinical signs were reported in 76.3% (239/313) of cases. The remaining 23.6% (74/313) of cases demonstrated the following clinical signs: neurological 79.7% (59/74), gastrointestinal 25.6% (19/74), cardiovascular 9.5% (7/74), respiratory 8.2% (6/74), and thermoregulatory 6.7% (5/74). Of the dogs exhibiting neurological signs, 62.7% (37/59) showed depression, 37.2% (22/59) showed hyperactivity, 10.1% (6/59) exhibited ataxia, and 1.7% (1/59) showed other miscellaneous signs (eg, hyperesthesia). There was a significant difference between the dose ingested by symptomatic and asymptomatic dogs for fluoxetine (P = 0.0039), but not with any other SSRI. Ninety-four patients were confirmed to have received veterinary care. In cases where duration of veterinary care was determined (55/313), 67.2% (37/55) of dogs were hospitalized and 32.7% (18/55) treated as outpatients. The average duration of hospitalization was 18.5 hours, excluding outpatient visits. Of those patients that had complete follow-up information available (136/313), overall survival was 100%. CONCLUSIONS: The overall prognosis for animals with SSRI toxicosis is excellent with veterinary attention. Central nervous system depression was the most common clinical sign associated with SSRI toxicosis.

Baclofen toxicosis in dogs and cats: 145 cases (2004-2010).

OBJECTIVE: To identify dogs and cats with baclofen toxicosis and characterize the patient population, clinical signs, and outcome. DESIGN: Retrospective case series. ANIMALS: 140 dogs and 5 cats with baclofen toxicosis. PROCEDURES: An animal poison control center electronic database was reviewed from November 2004 through April 2010 to identify dogs and cats with baclofen toxicosis. Information on signalment, clinical signs, and amount of baclofen ingested was obtained. Clinical signs were categorized as CNS, gastrointestinal, general malaise, cardiovascular, respiratory, or urogenital. Follow-up communications were performed to determine overall outcome. RESULTS: Dogs had a median age of 0.67 years (range, 0.1 to 15 years) and cats of 1 year (range, 0.7 to 16 years). Of 145 patients, 133 (92%) developed clinical signs of baclofen toxicosis. A total of 259 signs fell within defined categories: CNS (121/259 [46.7%]), gastrointestinal (69/259 [26.6%]), general malaise (27/259 [10.4%]), cardiovascular (23/259 [8.9%]), respiratory (14/259 [5.4%]), and urogenital (5/259 [1.9%]). For 68 dogs with known survival status, survival rate was 83.8% (57/68); of these dogs, the amount of baclofen ingested was known for 53 (46 survivors and 7 nonsurvivors). Amount of baclofen ingested was significantly lower in survivor dogs (median, 4.2 mg/kg [1.91 mg/lb]; range, 0.61 to 61 mg/kg [0.28 to 27.7 mg/lb]), compared with nonsurvivor dogs (median, 14 mg/kg [6.4 mg/lb]; range, 2.3 to 52.3 mg/kg [1.04 to 23.77 mg/lb]. Of 5 cats, 2 survived, 1 died, and 2 had unknown outcomes. CONCLUSIONS AND CLINICAL RELEVANCE: Clinical signs of baclofen toxicosis occurred in most patients, with the CNS being the system most commonly affected.

Phenylpropanolamine toxicosis in dogs: 170 cases (2004?2009).

OBJECTIVE: To evaluate signalment, clinical signs, dose ingested, treatment requirements, duration of hospitalization, and outcome of dogs exposed to phenylpropanolamine. DESIGN: Retrospective case series. ANIMALS: 170 dogs with potential PPA toxicosis evaluated between 2004 and 2009. PROCEDURES: Dogs with potential PPA toxicosis were identified by reviewing the electronic database of an animal poison control center. RESULTS: 66 of the 170 (39%) dogs reportedly did not develop any clinical signs. Clinical signs reported in the remaining 104 (61%) dogs included agitation (n = 40), vomiting (27), mydriasis (19), lethargy (17), tremor or twitching (16), panting (15), bradycardia (13), tachycardia (12), hypertension (11), and erythema (8). Median dose ingested for all dogs was 29 mg/kg (13.2 mg/lb). Dogs developing clinical signs had a significantly higher median dose ingested (373 mg/kg [170 mg/lb]) than did dogs that did not develop clinical signs (18 mg/kg [8.2 mg/lb]). Likewise, median dose ingested for the 123 dogs treated as inpatients (36.9 mg/kg [16.8 mg/lb]) was significantly higher than the median dose for the 14 dogs treated as outpatients (20.5 mg/kg [9.3 mg/lb]). Median duration of hospitalization was 18 hours (range, 4 to 72 hours), and hospitalization time increased as the dose ingested increased. Survival rate was 99.4% (169/170); the dog that died had ingested a dose of 145 mg/kg (65.9 mg/lb). CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that with supportive care, the prognosis for dogs that had ingested an overdose of phenylpropanolamine was excellent.

Corneal ulceration in a dog following exposure to the defensive spray of a walkingstick insect (Anisomorpha spp.).

OBJECTIVE: To describe a case of corneal ulceration in a dog resulting from ocular exposure to the defensive spray of a walkingstick insect (Anisomorpha spp.). CASE SUMMARY: A 4-year-old, male Chihuahua in southeastern Louisiana presented to an emergency veterinary hospital approximately 20 hours after it was witnessed to have come in close proximity to a walkingstick insect. Within seconds of approaching the insect, the dog yelped, jumped backwards and developed lacrimation, blepharospasm, and periocular swelling of the left eye. Upon presentation, the dog was found to have blepharospasms and miosis of the left eye. Fluorescein stain was applied to the affected eye and diffuse corneal uptake of stain was noted. A diffuse superficial corneal ulceration was diagnosed and treated supportively with ocular flushing, topical antibiotics, ocular lubrication, and a 1% solution of ocular atropine, as well as systemic nonsteroidal anti-inflammatory agents. Clinical signs resolved 10 days after injury. NEW OR UNIQUE INFORMATION PROVIDED: While most species of walkingstick insects are considered harmless, certain species in the southeastern United States have the ability to spray defensive venom at their predators. Upon ocular exposure to the venom, the victim may experience intense pain followed by blurred vision, conjunctivitis, keratitis, and corneal ulceration. To date, there is only 1 previous reported case of ocular exposure to walkingstick venom in a dog although both children and animals may be at higher risk for ocular exposure due to their curious nature and proximity in size to the insect. Superficial corneal and conjunctival damage can occur following direct exposure to the defensive chemical spray of the Northern and Southern Twostriped walkingstick insects found in the southeastern United States and may be considered a differential diagnosis in cases involving diffuse corneal ulceration.

Potential zinc phosphide rodenticide toxicosis in dogs: 362 cases (2004-2009).

OBJECTIVE: To evaluate records of dogs exposed to zinc phosphide rodenticides and characterize the patient population, including breed, sex, age, body weight, time since exposure, development of clinical signs, clinical signs observed, treatments performed, veterinary care received, outcome, and overall prognosis. DESIGN: Retrospective case series. ANIMALS: 362 dogs with presumed zinc phosphide exposure. PROCEDURES: An electronic computer database from an animal poison control center was searched to identify dogs that ingested zinc phosphide between November 2004 and July 2009. RESULTS: Accurate information regarding development of clinical signs was available in 94.5% (342/362) of cases. Over half the dogs (58.8% [201/342]) did not develop clinical signs, and specific clinical signs were reported for the remaining 41.2% (141/342) of dogs. There were 180 total clinical signs recorded for these 141 dogs, with some dogs having developed > 1 category of clinical signs. Clinical signs involving the gastrointestinal tract were the most commonly reported type of clinical sign (66.7% [n = 120/180 reported signs]), followed by generalized malaise (17.8% [32/180]), CNS signs (8.9% [16/180]), respiratory signs (3.3% [6/180]), and cardiovascular signs (1.7% [3/180]). Approximately 65% (234/362) of patients received veterinary care (including decontamination via induction of emesis, gastric lavage, or activated charcoal administration), and of these dogs, 51.3% (120/234) were hospitalized. For the 296 dogs for which survival data were available, the survival rate was 98.3% (291/296). CONCLUSIONS AND CLINICAL RELEVANCE: Overall, the prognosis for zinc phosphide toxicosis was good. Zinc phosphide rodenticide toxicosis is a potential public health concern, and veterinary staff should be aware of this commonly used rodenticide.

Sleep aid toxicosis in dogs: 317 cases (2004-2010).

OBJECTIVE: To summarize the signalment, clinical signs observed, time to onset of clinical signs, duration of clinical signs, and the outcome in a large case series of nonbenzodiazepine sleep aid ingestions in dogs, including 2 sleep aids that have not been previously described in the veterinary literature. DESIGN: Retrospective study conducted between 2004 and 2010. SETTING: An animal poison control center based out of Bloomington, MN. ANIMALS: During this time frame, 453 cases were identified involving 467 dogs. Of these cases, 150 cases were excluded due to incomplete medical records, multipet households, or the inability to calculate a dose exposure. A total of 317 dogs with presumed sleep aid medication toxicosis were included. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Records of dogs with sleep aid medication toxicosis identified by a review of an animal poison control center electronic database were evaluated. The most common sleep aid medications ingested were zolpidem (240/317 [75.7%]), eszopiclone (62/317 [19.5%]), and zaleplon (15/317 [4.7%]). Overall, clinical signs developed in 36% of patients (115/317), while 64% (202/317) remained asymptomatic. The most common organ systems affected and clinical signs seen involved the central nervous system (eg, agitation, sedation) and gastrointestinal tract (eg, anorexia, hypersalivation, vomiting). CONCLUSIONS: Overall, the prognosis for dogs with sleep aid medication toxicosis was excellent, and no fatalities were reported in this clinical population. As significant clinical signs can still be seen with ingestion, appropriate decontamination is warranted in asymptomatic patients via emesis or gastric lavage, followed by activated charcoal administration. Symptomatic patients should be hospitalized for monitoring and supportive care for a minimum of 12 hours or until clinical signs resolve.