Fluid Therapy for Pediatric Patients.

Pediatric dogs and cats within their first 12 weeks of life have important electrolyte requirements and physiologic considerations that may impact fluid therapy. Fluid requirements are higher in pediatrics, while fluid losses are greater due to underdeveloped physiologic responses. Hydration and volume status are difficult to assess in young animals, and their small size makes intravenous (IV) access difficult to obtain. Young patients can quickly deteriorate from dehydration, poor husbandry, and infection and become critically ill, requiring prompt recognition, treatment, intensive care, and monitoring. Clinicians should be aware of all available routes of fluid administration including oral, subcutaneous (SC), intraperitoneal (IP), IV, and intraosseous (IO), and the limitations associated with each route.

Suspected hepatotoxicity secondary to trazodone therapy in a dog.

OBJECTIVE: To describe a case of suspected hepatotoxicity in a dog secondary to administration of trazodone. CASE SUMMARY: A 6-year-old, neutered, mixed breed dog was evaluated for a progressive increased liver enzyme activity over a 6-week period. The patient originally presented for raisin toxicosis, and hence, was having serial blood work monitoring performed. Trazodone was initially started at that time due to severe separation anxiety while hospitalized (consistently 5 out of 7 days of the week, for a 6-week duration). Due to continued increased liver enzyme activity, extensive workup was performed which included abdominal ultrasound, leptospirosis titers, bile acids, and liver biopsies. Histopathologic findings were consistent with acute hepatotoxicity. In the absence of other toxicants and the close proximity to drug administration, a drug-induced hepatopathy secondary to trazodone was presumed. Following discontinuation of trazodone therapy, the hepatopathy completely resolved and the patient fully recovered. NEW OR UNIQUE INFORMATION PROVIDED: While acute hepatotoxicity has been reported in human medicine secondary to the administration of trazodone, this is the first reported case of suspected hepatotoxicity in a dog secondary to trazodone therapy. Veterinary professionals should be aware of the rare potential adverse effect that may be seen in canine patients secondary to trazodone therapy. Appropriate clinicopathologic monitoring should occur in patients on chronic trazodone therapy.

Systemic lime sulfur toxicosis secondary to dermal exposure in two cats.

OBJECTIVE: To describe a case series of systemic lime sulfur toxicosis secondary to topical administration in 2 cats. CASE SUMMARY: Two cats from the same household that were being previously treated for Microsporum canis were presented following topical administration of an incorrectly diluted lime sulfur dip. A 30% solution was used rather than the recommended 3% solution, resulting in a 10-fold concentration overdose. The cats presented to the emergency service 1 hour after dermal application of the lime sulfur product at home. The first cat, a 2-year-old female, intact Cornish Rex, had severe hypotension, bradycardia, and hypothermia. Chemical burns were also present on the ventrum and paws. Clinicopathological data revealed profound acid-base disturbances, hypercalcemia, hyperphosphatemia, and azotemia. After aggressive fluid resuscitation, electrolyte supplementation, and treatment, the patient was stabilized and discharged after 5 days of hospitalization; full recovery was later reported. The second littermate, also a 2-year-old female, intact Cornish Rex, presented the following day with similar clinical signs, physical examination findings, and clinicopathological findings. After supportive care and 2 days of hospitalization, the patient was also discharged and reported to fully recover. NEW OR UNIQUE INFORMATION PROVIDED: This case series is the first to report systemic toxicosis secondary to dermal exposure of lime sulfur. As lime sulfur is commonly used in veterinary medicine for the treatment of ectoparasites, veterinary professionals should be aware of the significant signs of poisoning that can be seen as a result of iatrogenic dosing errors by pet owners or veterinary professionals.

Isoniazid toxicosis in dogs: 137 cases (2004-2014).

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.

Necroulcerative hemorrhagic gastritis in a cat secondary to the administration of 3% hydrogen peroxide as an emetic agent.

OBJECTIVE: To describe a case of necroulcerative gastritis in a cat secondary to administration of 3% hydrogen peroxide as an emetic agent. CASE SUMMARY: A 10-year-old neutered male domestic shorthair was evaluated for hematemesis less than 24 hours following ingestion of a piece of foam. The pet owner had administered 2 doses of 0.5-1.0 tablespoons (7.5-15 mL) of 3% hydrogen peroxide in an attempt to induce emesis at home; emesis was achieved and produced the foam foreign body. Due to the presence of protracted vomiting and hematemesis, the patient was then presented to an emergency facility for further diagnostics and treatment. Initial blood work was normal on presentation, and advanced imaging of the abdomen was performed. An exploratory laparotomy revealed no foreign material in the gastrointestinal tract; however, severe ulceration of approximately 60% of the gastric mucosa was observed around the cardia and extended from the fundus down through the body of the stomach to the lesser curvature. Due to the severity of ulceration and presumed poor prognosis, the patient was euthanized intraoperatively. Histopathology of the stomach wall was consistent with severe confluent necroulcerative and hemorrhagic pleocellular gastritis, presumed to be secondary to administration of 3% hydrogen peroxide, which was used as the primary emetic agent in this case. NEW OR UNIQUE INFORMATION PROVIDED: The oral administration of 3% hydrogen peroxide solution in cats can result in necroulcerative gastritis as a possible sequel. While hydrogen peroxide is considered a safe emetic agent in dogs, its use in cats is not recommended. As a result, the use of emetic agents in cats should be limited to veterinary administration, using alternative, safer emetic agents such as alpha-adrenergic agonists.

Fluid Therapy for Pediatric Patients.

Young puppies and kittens have unique physiologic needs in regards to fluid therapy, which must address hydration, vascular fluid volume, electrolyte disturbances, or hypoglycemia. Pediatric patients have a higher fluid requirement compared with adults and can rapidly progress from mild dehydration to hypovolemia. Simultaneously, their small size makes overhydration a real possibility. Patient size complicates fluid administration because catheters used in larger pets may be difficult to place. Routes of fluid administration used in the neonate or pediatric patient include oral, subcutaneous, intraperitoneal, intraosseous, and intravenous. Clinicians should be aware of the pros and cons of each route.

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.

Emergency management and treatment of the poisoned small animal patient.

This article reviews management of the acutely poisoned veterinary patient, including initial telephone triage, appropriate communication and history gathering from the pet owner, decontamination methods (including the use of appropriate emetic agents and dosing of activated charcoal), and general treatment of the poisoned patient. Symptomatic and supportive care of the poisoned patient includes the use of fluid therapy, gastrointestinal support (eg, antacids), central nervous system support (eg, muscle relaxants, anticonvulsants), sedatives/reversal agents (eg, phenothiazines, naloxone, flumazenil), hepatoprotectants, and miscellaneous antidotal therapy.

The use of high-dose insulin therapy and intravenous lipid emulsion to treat severe, refractory diltiazem toxicosis in a dog.

OBJECTIVE: To describe the novel use of high-dose insulin (HDI) therapy and intravenous lipid emulsion (ILE) to treat refractory, severe diltiazem toxicosis in a dog. CASE SUMMARY: A 4-year-old Pomeranian was presented for treatment 2.5 hours following ingestion of a diltiazem extended-release capsule. Toxic ingestion was calculated at a maximum exposure of 79 mg/kg, with a reported canine LD50 of 50 mg/kg. Clinical signs of progressive hypotension and severe bradycardia with atrial standstill were observed, which persisted despite treatment with atropine, calcium, glucagon, and dopamine. The novel use of HDI and ILE as part of therapy for diltiazem toxicosis resulted in clinical resolution of life-threatening signs. Within 1 hour of initiating HDI therapy, the clinical signs improved, and with continued treatment, the patient remained normotensive and survived to discharge. NEW OR UNIQUE INFORMATION PROVIDED: To the authors' knowledge, this is the first reported clinical case describing the use of both HDI and ILE therapy in the treatment of severe refractory diltiazem toxicosis in veterinary medicine. No significant adverse effects were observed from the treatment. In veterinary patients with severe refractory calcium channel blocker toxicosis, the use of HDI and ILE should be considered for life-threatening 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.

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.

Use of intravenous lipid emulsion to treat ivermectin toxicosis in a Border Collie.

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.

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.

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.

The use of intravenous lipid emulsion as an antidote in veterinary toxicology.

OBJECTIVE: To review the use of IV lipid emulsion (ILE) for the treatment of toxicities related to fat-soluble agents; evaluate current human and veterinary literature; and to provide proposed guidelines for the use of this emerging therapy in veterinary medicine and toxicology. DATA SOURCES: Human and veterinary medical literature. HUMAN DATA SYNTHESIS: Human data are composed mostly of case reports describing the response to treatment with ILE as variant from mild improvement to complete resolution of clinical signs, which is suspected to be due to the variability of lipid solubility of the drugs. The use of ILE therapy has been advocated as an antidote in cases of local anesthetic and other lipophilic drug toxicoses, particularly in the face of cardiopulmonary arrest and unsuccessful cardiopulmonary cerebral resuscitation. VETERINARY DATA SYNTHESIS: The use of ILE therapy in veterinary medicine has recently been advocated by animal poison control centers for toxicoses associated with fat-soluble agents, but there are only few clinical reports documenting successful use of this therapy. Evidence for the use of ILE in both human and veterinary medicine is composed primarily from experimental animal data. CONCLUSIONS: The use of ILE appears to be a safe therapy for the poisoned animal patient, but is warranted only with certain toxicoses. Adverse events associated with ILE in veterinary medicine are rare and anecdotal. Standard resuscitation protocols should be exhausted before considering this therapy and the potential side effects should be evaluated before administration of ILE as a potential antidote in cases of lipophilic drug toxicoses. Further research is waranted.

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.

The effect of noncardiac disease on plasma brain natriuretic peptide concentration in dogs.

OBJECTIVE: To evaluate the effects of noncardiac disease on c-terminal brain natriuretic peptide (cBNP) concentrations in dogs. DESIGN: Prospective observational study. SETTING: Urban university veterinary hospital. ANIMALS: Thirty-eight apparently healthy dogs, 28 dogs with cardiac disease (14 CHF, 14 non-CHF), and 81 dogs with primary noncardiac diseases. INTERVENTIONS: none. MATERIALS AND METHODS: Plasma was collected from each dog and analyzed for active (cBNP) B-type natriuretic peptide using an assay that is being investigated for commercial use (Biosite). MEASUREMENTS AND MAIN RESULTS: Dogs with CHF had significantly higher plasma cBNP concentrations than dogs with subclinical cardiac disease, apparently healthy dogs, or dogs with primary noncardiac disease. However, 21% (28/133) of dogs without CHF (including healthy dogs, dogs with primary noncardiac disease, and dogs with subclinical cardiac disease) had cBNP concentrations above previously identified diagnostic thresholds for CHF, reiterating the importance of reestablishing new diagnostic cutoffs when considering comorbidities affecting B-type natriuretic peptide levels. CONCLUSIONS: A clinically relevant proportion of nondyspneic dogs with primary noncardiac diseases have increased cBNP concentrations that exceed previously identified diagnostic thresholds, potentially limiting the ability of this test to identify CHF when noncardiac comorbidities exist. Interpretation of increased cBNP concentrations in such cases must be appropriately interpreted with further diagnostic investigation.

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.