A large number of plants can cause adverse effects when ingested by animals or people. Plant toxicity is due to a wide diversity of chemical toxins that include alkaloids, glycosides, proteins and amino acids. There are several notable toxic plants for which a specific chemical responsible for toxicity has not been determined. There are many examples of species differences in terms of their sensitivity to intoxication from plants. Pets, such as dogs and cats, and people, especially children, are frequently exposed to the same toxic plants due to their shared environments. On the other hand, livestock are exposed to toxic plants that are rarely involved in human intoxications due to the unique environments in which they are kept. Fortunately, adverse effects often do not occur or are generally mild following most toxic plant ingestions and no therapeutic intervention is necessary. However, some plants are extremely toxic and ingestion of small amounts can cause rapid death. The diagnosis of plant intoxication can be challenging, especially in veterinary medicine where a history of exposure to a toxic plant is often lacking. Analytical tests are available to detect some plant toxins, although their diagnostic utility is often limited by test availability and timeliness of results. With a few notable exceptions, antidotes for plant toxins are not available. However, general supportive and symptomatic care often is sufficient to successfully treat a symptomatic patient.

5-Hydroxytryptamine, or serotonin, is a biogenic amine most noted for its role as a neurotransmitter. Manipulation of serotonin in animal models was used as a tool for studying its role in humans. Through such research serotonin has been shown to modulate gastrointestinal motility, peripheral vascular tone, cerebral vascular tone, and platelet function and has been implicated in the pathophysiology of mood disorders, emesis, migraine, irritable bowel syndrome (IBS), and pulmonary and systemic hypertension. The knowledge gained is being directly applied back to animals in research on drugs that manipulate the serotonergic system in dogs and cats. Increasing use and availability of drugs that manipulate the serotonergic system has created a circumstance through which a novel toxicity was discovered in both humans and animals. Serotonin Syndrome describes the clinical picture seen in humans and animals with serotonin toxicity. This paper provides a review the physiology of serotonin and its involvement in the pathophysiologic mechanisms of various conditions, including the Serotonin Syndrome.

Serotonin syndrome, or serotonin toxicity, is a serious disorder attributable to exaggerated serotonergic function in the brain, most commonly after antidepressant overdose or after combining several psychotropic medications. Similar condition (serotonin syndrome-like behavior) can be evoked in animals experimentally, following administration of serotonergic drugs. In addition to pharmacological stimulation, some genetic and other factors may contribute to serotonin toxicity, prompting the need for new experimental genetic models relevant to this disorder. Here we discuss current problems and perspectives regarding genetic animal models of serotonin-related syndromes, and outline the potential utility of these models in experimental neurochemistry and clinical research.

This paper reviews the preclinical and clinical evidence regarding the use of the dietary supplement 5-hydroxytryptophan (5-HTP) for the treatment of depression. In the absence of supplementation with exogenous 5-HTP, the amount of endogenous 5-HTP available for serotonin synthesis depends on the availability of tryptophan and on the activity of various enzymes, especially tryptophan hydroxylase, indoleamine 2,3-dioxygenase, and tryptophan 2,3-dioxygenase (TDO). Factors affecting each of these are reviewed. The amount of 5-HTP reaching the central nervous system (CNS) is affected by the extent to which 5-HTP is converted to serotonin in the periphery. This conversion is controlled by the enzyme amino acid decarboxylase, which, in the periphery, can be blocked by peripheral decarboxylase inhibitors (PDIs) such as carbidopa. Preclinical and clinical evidence for the efficacy of 5-HTP for depression is reviewed, with emphasis on double-blind, placebo-controlled (DB-PC) trials. Safety issues with 5-HTP are also reviewed, with emphasis on eosinophilia myalgia syndrome (EMS) and serotonin syndrome.

Interferon-alpha (IFN) is widely used in the treatment of certain cancers and viral infections, including hepatitis C (HCV). Unfortunately, depression is a common side effect of IFN therapy, affecting approximately a third of HCV patients receiving IFN therapy. Studies have shown that selective serotonin reuptake inhibitors (SSRIs) can effectively treat IFN-induced depression in only 63-75% of cases. For the remaining percentage, depression often necessitates dose reduction of or discontinuation from IFN therapy. Emerging evidence indicates that IFN may cause depression by affecting brain serotonin. IFN has been shown to increase serotonin reuptake and to decrease serotonin synthesis. We hypothesize that SSRIs are not fully effective because they affect only serotonin reuptake, not serotonin synthesis, and that effective treatment must address both uptake and synthesis. 5-Hydroxytryptophan (5-HTP) effectively increases central nervous system synthesis of serotonin. It is the immediate precursor of serotonin and is widely available as a dietary supplement, which is well absorbed after an oral dose. Several double-blind studies have shown 5-HTP to be effective in the treatment of nondrug-induced depression. We hypothesize that patients who become depressed on IFN will respond to the synergistic combination of SSRIs plus 5-HTP.

OBJECTIVE To report the clinical characteristics of toad toxicity in domestic dogs in Brisbane. DESIGN A retrospective analysis of clinical cases. PROCEDURE All cases of toad poisoning which presented to a northern suburbs emergency clinic in Brisbane over a 30-month period beginning in April 1999 were reviewed. RESULTS A total of 90 canine cases of suspected toad poisoning were reviewed. Small breed dogs accounted for 76% of cases. Jack Russell, Silky, and Fox Terriers were the most represented breeds. Cases were reported year round, with fewest cases over the winter months. The most common clinical signs were increased salivation (78% of cases), and red oral mucous membranes (63% cases). Seizures occurred in 31% of cases. Generally the outcome was excellent with 96% survival.

Many medications are available today by prescription or in over-the-counter preparations. This article reviews the pharmacokinetics, mechanism of action, toxicity, clinical signs, and management procedures necessary for some oral medications. The medications reviewed include selective serotonin reuptake inhibitors, benzodiazepines, amphetamines or amphetamine like drugs, carprofen, cyclooxygenase-2 inhibitors, pseudoephedrine, calcium channel blockers, and baclofen.

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

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.

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.

The ALICE experiment has measured the inclusive J/ψ production in Pb-Pb collisions at sqrt[s_{NN}]=2.76  TeV down to zero transverse momentum in the rapidity range 2.5<y<4. A suppression of the inclusive J/ψ yield in Pb-Pb is observed with respect to the one measured in pp collisions scaled by the number of binary nucleon-nucleon collisions. The nuclear modification factor, integrated over the 0%-80% most central collisions, is 0.545±0.032(stat)±0.083(syst) and does not exhibit a significant dependence on the collision centrality. These features appear significantly different from measurements at lower collision energies. Models including J/ψ production from charm quarks in a deconfined partonic phase can describe our data.

The ALICE Collaboration has measured the inclusive production of muons from heavy-flavor decays at forward rapidity, 2.5<y<4, in pp and Pb-Pb collisions at sqrt[s_{NN}]=2.76  TeV. The p_{t}-differential inclusive cross section of muons from heavy-flavor decays in pp collisions is compared to perturbative QCD calculations. The nuclear modification factor is studied as a function of p_{t} and collision centrality. A weak suppression is measured in peripheral collisions. In the most central collisions, a suppression of a factor of about 3-4 is observed in 6<p_{t}<10  GeV/c. The suppression shows no significant p_{t} dependence.

INTRODUCTION For day-case laparoscopic surgery to be successful, patient selection is of the utmost importance. This study aimed to assess the feasibility of day-case laparoscopic Nissen fundoplication and to identify factors that may lead to readmission and overstay. METHODS A retrospective review of all patients who underwent day-case laparoscopic Nissen fundoplication over a 4-year period (2006 through 2010) was undertaken. Patient age, social circumstances, and other demographics were recorded as well as any comorbidities and ASA score. The primary endpoint measured was rate of readmission and overstay. RESULTS A total of 72 patients fulfilled the inclusion criteria for day-case surgery. Five patients (6.94%) required admission immediately following the procedure, ie, overstayed or were readmitted. The rates were 1.38%(P=.05, CI 95%) for readmission and 5.55%(P=.05, CI 95%) for overstay. Six (8.33%) patients were classified as ASA III, and 3 (50%) were readmitted or overstayed. CONCLUSION Day-case laparoscopic Nissen fundoplication is a feasible, safe option. The authors conclude that ASA score of III and increasing age correlate with an increasing incidence of overstay and readmission. Therefore, we would recommend the use of integrated pathways and advanced planning to reduce these rates.

Carcinoma of breast is the second most common cancer among women next to uterine cervical cancer in Bangladesh. It was well established that 5 years survival rates greatly vary among the different stages of carcinoma of breast disease. The study was carried out to see the stages of presentation of carcinoma of breast patient to a tertiary level hospital attended first time for medical help as well as to find out the factors responsible for the late (advanced) stage presentation. This descriptive type of cross sectional study was carried out in the department of surgery, Mymensingh Medical College and Hospital (MMCH) during the period of May 2010 to April 2011. A total of 110 cases admitted with carcinoma breast diagnosed by means of FNAC positive or suspicious findings were selected purposively during the study period. Patients were staged initially according to the TNM staging system by through clinical examination as well as final clinicopathological stages were done after histopathological examination of the resected specimen (breast with or without axillary lymphnode) in resectable cases. Among the advanced stage presentation, attempts were made to find out the factors responsible for advanced stage of the disease. The results showed that carcinoma of breast predominantly a disease of female and comparatively younger age group 40-49 years affected mostly in 40.9% cases with a mean age of 44.02±10.32 years. Premenopausal lady mostly affected in 63.6% cases. Majority of patients presented in advanced stage of the disease in 62.8% cases. Multiple factors were observed responsible for the advanced stage of the disease - among them delay in hospital presentation, poor socioeconomic condition and illiteracy have found to be associated which were statistically significant (p<0.001). It was needed for mass awareness program against the breast cancer in our society. Necessary steps should be taken for the initiation of breast self examination (BSE) to patients and clinical breast examination (CBE) to health care providers.

<sc>l</sc>-Arginine (ARG), an essential amino acid, is the endogenous source of the deleterious nitric oxide. Dietary ω-3 polyunsaturated fatty acid (PUFA)-enriched fish oil (FO) has been shown to reduce the severity of certain types of cancers, cardiovascular disease, and renal disease. Present study examined whether feeding of FO/flaxseed oil (FXO) would have protective effect against ARG-induced nephrotoxicity. ARG-induced nephrotoxicity was recorded by increased serum creatinine and blood urea nitrogen. ARG significantly altered the activities of metabolic and brush border membrane (BBM) enzymes. ARG caused significant imbalances in the antioxidant system. These alterations were associated with increased lipid peroxidation (LPO) and altered antioxidant enzyme activities. Feeding of FO and FXO with ARG ameliorated the changes in various parameters caused by ARG. Nephrotoxicity parameters lowered and enzyme activities of carbohydrate metabolism, BBM and inorganic phosphate (32Pi) transport were improved to near control values. ARG-induced LPO declined and antioxidant defense mechanism was strengthened by both FO and FXO alike. The results of the present study suggest that ω-3 PUFA-enriched FO and FXO from seafoods and plant sources, respectively, are similarly effective in reducing ARG-induced nephrotoxicity and oxidative damage. Thus, vegetarians who cannot consume FO can have similar health benefits from plant-derived ω-3 PUFA.

The aim of the present study was to investigate the safety and efficacy of local implantation of BMP-7 for the treatment of resistant non-unions in the upper and lower limb. Fifty-two patients (30 males, mean age 52.8years; range 20-81) were treated with local BMP-7 implantation in a bovine bone-derived collagen paste with or without revision of fixation. Thirty-six patients had closed injuries, ten had open injuries and six had infected non-unions. Patients had undergone a mean of 2 (1-5) operations prior to implantation of BMP-7. Clinical and radiological union was achieved in 94% at a mean time of 5.6months (3-19). Two patients with subtrochanteric femoral fractures failed to achieve union secondary to inadequate fracture stabilisation, persistent unfavourable biological environment and systemic co-morbidities. One patient developed synostosis attributed to the BMP-7 application. This study demonstrates BMP-7 implanted in a bovine-derived collagen paste is an effective adjunctive treatment for resistant non-unions in the upper and lower limb.

The yield of charged particles associated with high-p(t) trigger particles (8<p(t)<15 GeV/c) is measured with the ALICE detector in Pb-Pb collisions at √s(NN)=2.76 TeV relative to proton-proton collisions at the same energy. The conditional per-trigger yields are extracted from the narrow jetlike correlation peaks in azimuthal dihadron correlations. In the 5% most central collisions, we observe that the yield of associated charged particles with transverse momenta p(t)>3 GeV/c on the away side drops to about 60% of that observed in pp collisions, while on the near side a moderate enhancement of 20%-30% is found.

Objective-To determine the effectiveness and adverse effects of apomorphine and 3% hydrogen peroxide solution used for emesis in dogs. Design-Prospective observational study. Animals-147 dogs that received apomorphine (IV or placed in the conjunctival sac) or 3% hydrogen peroxide solution (PO) to induce emesis after exposure to toxic agents. Procedures-Data regarding signalment; agent information; type, dose, route, and number of emetic administrations; whether emesis was successful; number of times emesis occurred; percentage of ingested agent recovered; and adverse effects were collected via telephone during American Society for the Prevention of Cruelty to Animals Animal Poison Control Center operations and stored in a database for analysis. Mann-Whitney and Fisher exact tests were used to evaluate emetic success rates. Results-Apomorphine and 3% hydrogen peroxide solution successfully induced emesis in 59 of 63 (94%) and 76 of 84 (90%) of dogs, respectively. Mean time to onset of emesis after the first dose of emetic was 14.5 and 18.6 minutes when hydrogen peroxide (n = 37) and apomorphine (31) were used, respectively, with mean durations of 42 and 27 minutes, respectively. Mean estimates for recovery of ingested agents were 48% for hydrogen peroxide and 52% for apomorphine. Adverse effects were reported in 16 of 112 (14%) dogs for which information was available. Conclusions and Clinical Relevance-3% hydrogen peroxide solution and apomorphine effectively induced emesis in dogs when used as directed. Emesis occurred within minutes after administration and helped recover substantial amounts of ingested agents. Adverse effects of both emetics were considered mild and self-limiting.

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.

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.

A 1-year-old dog ingested a mixture of blood agar and Mycoplasma agar plates. The Mycoplasma agar plates contained thallium acetate, which resulted in an estimated minimum dose of 5 mg thallium acetate/kg bodyweight. Clinical signs over the course of 2-3 weeks included vomiting, diarrhea, weight loss, alopecia, dysphonia, ataxia, paresthesia, intension tremors, megaesophagus with subsequent aspiration pneumonia, and several seizure episodes. The dog was treated with intravenous fluids and placement of a gastric feeding tube. Thallium concentrations in hair were 8.2 µg/g in samples taken on day 19, 16.4 µg/g in samples taken 3 months after exposure, 13.4 µg/g in samples taken 5 months after exposure, and nondetectable in samples taken 7 months after exposure. The blood thallium concentration was 190 µg/l on day 19 and nondetec table 3 months after exposure. Megaesophagus and dysphonia continued for 10 months after exposure. This case of thallium poisoning following ingestion of mycoplasma agar plates demonstrates that unusual sources of thallium still exist and suggests that thallium toxicosis should be included in the list of differential diagnoses in dogs presented with megaesophagus, especially if alopecia and other unexplained peripheral neuropathies are present. Hair and blood samples are useful specimens to reach an accurate diagnosis even if taken several weeks post exposure. The postexposure blood and hair thallium concentrations reported in this case are useful data for diagnosticians investigating dogs with potential thallium poisoning.

CASE HISTORY A 5-year-old entire female Huntaway from a sheep and beef farm was one of four dogs that developed clinical signs including hypersalivation, depression, blindness and ataxia after the death of another dog. A 4-year-old female Huntaway farm dog from a second farm was observed to be sitting down more often than usual on the day after being fed part of a calf carcass that had been treated with an abamectin pour-on. CLINICAL FINDINGS The first dog was ataxic and depressed but did respond to sound. The second dog presented with an acute onset of blindness, mydriasis, absence of a menace response, hypersalivation, gait abnormalities (e.g. high stepping gait and ataxia), and depression. Other presenting signs included muscle tremors, dehydration and difficulty eating. No abnormalities were detected from routine haematology and biochemistry. Analysis of samples of plasma from both dogs revealed concentrations of abamectin of 0.149 mg/L and 0.260 mg/L for the first and second dogs, respectively. Buccal swabs taken from the first dog for DNA testing for the ABCB1 gene mutation, gave a negative result. DIAGNOSIS In addition to the presenting signs which suggested a toxicosis, both dogs had measurable concentrations of abamectin in plasma confirming exposure. CLINICAL RELEVANCE Farm dogs exposed to concentrated pour-on products containing abamectin have been poisoned and recover or die. The product labels do not carry any warnings as to the risk of poisoning to dogs. This paper discusses two incidents affecting six farm dogs, but the authors are aware of more toxicoses in farm dogs exposed to abamectin.

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.

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 A 0.65-kg (1.43-lb) 24-month-old sexually intact male albino pet rat was examined because of a 3-week history of hypodipsia, apparent blindness, and sudden change in behavior. CLINICAL FINDINGS The rat was able to move around its cage but appeared unaware of its surroundings, was visually unresponsive, and seemed unusually aggressive. The rat's hind limbs appeared mildly paretic, and it had sporadic difficulty placing its hind limbs on a flat surface. Given the rat's age, history, and physical examination findings, the primary differential diagnosis was a pituitary tumor. Magnetic resonance imaging (MRI) of the rat's brain was performed and revealed a large pituitary mass, which was indicative of a tumor. TREATMENT AND OUTCOME Cabergoline (0.6 mg/kg [0.27 mg/lb], PO, q 72 h) was administered. On follow-up MRI 2 months later, the pituitary mass had substantially decreased in size. For 6 months following the second MRI study, the rat continued to receive the same dosage of cabergoline and had no clinical signs of disease or unusual behavior. However, at 8.5 months after the start of the treatment, the rat was in poor condition and had clinical signs similar to those initially. A third MRI study was performed and revealed substantial regrowth of the mass. The rat was euthanized and a necropsy was performed; a histopathologic diagnosis of pituitary adenoma was made. CLINICAL RELEVANCE Pituitary adenomas have long been recognized as a common finding in geriatric rats (> 18 months old). Affected rats may respond favorably to oral administration of cabergoline.

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.