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.
Case Description—A 2-year-old spayed female Border Collie was treated with IV lipid emulsion (ILE) after ingesting 6 mg/kg (2.73 mg/lb) of an equine ivermectin anthelmintic paste 8 hours prior to examination.
Clinical Findings—On initial examination, the dog had stable cardiovascular signs but had diffuse muscle tremors and was hyperthermic. Neurologic evaluation revealed that the dog was ataxic and had mydriasis with bilaterally absent menace responses and pupillary light reflexes. The remaining physical examination findings were unremarkable. Results of CBC, serum biochemical analysis, venous blood gas analysis, and measurement of plasma lactate concentration were also within reference limits.
Treatment and Outcome—The dog was treated with ILE in addition to supportive care with IV fluid therapy and cardiovascular, respiratory, and neurologic monitoring. The use of ILE treatment was initiated in this patient on the basis of previous clinical and experimental evidence supporting its use for toxicosis resulting from lipid-soluble agents. An initial bolus of 1.5 mL/kg (0.68 mL/lb) of a 20% sterile lipid solution was administered IV over 10 minutes, followed by a constant rate infusion of 0.25 mL/kg/min (0.11 mL/lb/min) over 60 minutes that was administered twice to treat clinical signs of ivermectin toxicosis. The dog was discharged from the hospital 48 hours after admission and was clinically normal within 4 days after ivermectin ingestion. Further diagnostic evaluation subsequently revealed that this dog was unaffected by the multidrug resistance gene (MDR-1) deletion, known as the ATP-binding cassette polymorphism.
Clinical Relevance—Ivermectin toxicosis in veterinary patients can result in death without aggressive treatment, and severe toxicosis often requires mechanical ventilation and intensive supportive care. This is particularly true in dogs affected by the ATP-binding cassette polymorphism. Novel ILE treatment has been shown to be effective in human patients with lipid-soluble drug toxicoses, although the exact mechanism is unknown. In the patient in the present report, ILE was used successfully to treat ivermectin toxicosis, and results of serial measurement of serum ivermectin concentration supported the proposed lipid sink mechanism of action.
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.
OBJECTIVE To establish the minimum toxic dose of isoniazid in dogs, characterize the clinical signs and outcomes for dogs following isoniazid ingestion, and determine whether IV administration of pyridoxine to dogs with isoniazid toxicosis is protective against death.
DESIGN Retrospective case series.
ANIMALS 137 dogs with isoniazid toxicosis.
PROCEDURES The electronic database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center was reviewed from January 2004 through December 2014 to identify dogs with isoniazid toxicosis. For each dog identified, information extracted from the medical record included signalment, estimated dose of isoniazid ingested, clinical signs, treatment, and outcome. Follow-up communication with pet owners or primary care veterinarians was performed when necessary to obtain missing information.
RESULTS Clinical signs of isoniazid toxicosis were observed in 134 of 137 (98%) dogs and included seizures (n = 104), CNS signs without seizures (94), and gastrointestinal (41), cardiovascular (19), urogenital (4), and respiratory (1) abnormalities. Of the 87 dogs for which the outcome was available, 61 survived, 18 died, and 8 were euthanized. Probability of survival was positively associated with body weight and IV administration of pyridoxine and negatively associated with dose of isoniazid ingested and presence of seizures. Dogs that received pyridoxine IV were 29 times as likely to survive as dogs that did not receive pyridoxine IV.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated rapid diagnosis of isoniazid toxicosis and prompt treatment of affected dogs with pyridoxine and other supportive care were imperative for achieving a successful outcome.
Objective— To determine indications for and outcomes of positive-pressure ventilation (PPV) in cats, document ventilator management, and identify factors
associated with outcome.
Design— Retrospective study.
Animals— 53 cats that underwent PPV.
Procedure— Information on signalment, history, concurrent diseases, clinical findings, results of venous blood gas analyses and clinicopathologic testing, treatment, ventilator settings, and outcome was retrieved from the medical records. Data for cats that survived were compared with data for cats that died or were euthanatized while undergoing PPV.
Results—PPV was initiated for management of respiratory failure (36 cats [68%]), cardiac arrest (9 [17%]), neurologic impairment (6 [11%]), and nonresponsive hypotension (2 [4%]). Eight cats (15%) survived, 19 (36%) died, and 26 (49%) were euthanatized while undergoing PPV. Cats that survived had a longer duration of ventilation than did those that died or were euthanatized and had a significantly higher incidence of ventilator-associated pneumonia. Signalment and ventilator settings were not associated with outcome. Cats that had no clinical evidence of pulmonary disease but
required PPV because of primary neurologic disease had a higher survival rate (2/6) than did cats that
required PPV because of respiratory failure (5/36), cardiac arrest (1/9), or nonresponsive hypotension (0/2).
Conclusions and Clinical Relevance—Results suggest that the survival rate for cats requiring PPV may be lower than reported survival rates for dogs. Death was attributable to progressive respiratory failure, nonresponsive hypotension, kidney failure, or neurologic
impairment. (J Am Vet Med Assoc 2005;226:924–931)
Objective—To determine the effects of racing and
nontraining on plasma thyroxine (T4), free thyroxine
(fT4), thyroid-stimulating hormone (TSH), and thyroglobulin
autoantibody (TgAA) concentrations in sled
dogs and compare results with reference ranges
established for dogs of other breeds.
Animals—122 sled dogs.
Procedure—Plasma thyroid hormone concentrations
were measured before dogs began and after they finished
or were removed from the Iditarod Trail Sled
Dog Race in Alaska and approximately 3 months after
Results—Concentrations of T4 and fT4 before the race
were less than the reference range for nonsled dogs in
26% and 18% of sled dogs, respectively. Immediately
after racing, 92% of sled dogs had plasma T4 concentrations
less than the reference range. Three months after
the race, 25% of sled dogs had plasma T4 concentrations
less than the reference range. For T4, fT4, TSH, and
TgAA, significant differences were not detected in samples
collected before the race versus 3 months later.
Conclusions and Clinical Relevance—Plasma T4, fT4,
and TSH concentrations decreased in dogs that complete
a long distance sled dog race. Many clinically normal
sled dogs have plasma T4 and fT4 values that are
lower than the reference range for nonsled dogs. We
suggest that the reference ranges for sled dogs are 5.3
to 40.3 nmol/L and 3.0 to 24.0 pmol/L for plasma T4 and
fT4 concentrations, respectively, and 8.0 to 37.0 mU/L
for TSH. (J Am Vet Med Assoc 2004;224:226–231)
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.
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.