Dysphagia as a Missing Link Between Post-surgical- and Opioid-Related Pneumonia.

PURPOSE: Postoperative pneumonia remains a common complication of surgery, despite increased attention. The purpose of our study was to determine the effects of routine surgery and post-surgical opioid administration on airway protection risk. METHODS: Eight healthy adult cats were evaluated to determine changes in airway protection status and for evidence of dysphagia in two experiments. (1) In four female cats, airway protection status was tracked following routine abdominal surgery (spay surgery) plus low-dose opioid administration (buprenorphine 0.015 mg/kg, IM, q8-12 h; n = 5). (2) Using a cross-over design, four naive cats (2 male, 2 female) were treated with moderate-dose (0.02 mg/kg) or high-dose (0.04 mg/kg) buprenorphine (IM, q8-12 h; n = 5). RESULTS: Airway protection was significantly affected in both experiments, but the most severe deficits occurred post-surgically as 75% of the animals exhibited silent aspiration. CONCLUSION: Oropharyngeal swallow is impaired by the partial mu-opioid receptor agonist buprenorphine, most remarkably in the postoperative setting. These findings have implications for the prevention and management of aspiration pneumonia in vulnerable populations.

Application of eprinomectin-containing parasiticides at label doses causes neurological toxicosis in cats homozygous for ABCB11930_1931del TC.

The feline MDR1 mutation (ABCB11930_1931delTC) has been associated with neurological toxicosis after topical application of eprinomectin products labeled for feline use. Information was collected from veterinarians who submitted samples for ABCB11930_1931delTC genotyping. In most cases, the submission form indicated an adverse event involving eprinomectin, in other cases submitting veterinarians were contacted to determine whether the patient had experienced an adverse drug event involving eprinomectin. If so, additional information was obtained to determine whether the case met inclusion criteria. 14 cases were highly consistent with eprinomectin toxicosis. Eight cats were homozygous for ABCB11930_1931del TC (3 died; 5 recovered). Six cats were homozygous wildtype (2 died; 4 recovered). The observed ABCB11930_1931delTC frequency (57%) was higher than the expected frequency (≤1%) in the feline population (Fisher Exact test, p < 0.01). Among wildtype cats, four were concurrently treated with potential competitive inhibitors of P-glycoprotein. Results indicate that topical eprinomectin products, should be avoided in cats homozygous for ABCB11930_1931delTC. This is a serious, preventable adverse event occurring in an identifiable subpopulation treated with FDA-approved products in accordance with label directions. Acquired P-glycoprotein deficiency resulting from drug interactions may enhance susceptibility to eprinomectin-induced neurological toxicosis in any cat, regardless of ABCB1 genotype.

Filgrastim Use in the Treatment of Azathioprine-Induced Myelosuppression Toxicity After Prescription Error in the Feline.

Only one report on the successful use of filgrastim (granulocyte colony-stimulating factor) in cats for severe neutropenia following azathioprine toxicity exists. Here, we report on a case in which a cat was prescribed methimazole but the medication was filled incorrectly with azathioprine tablets and the prescription label indicated a methimazole dosing regimen that was administered for three days before recognition of the error. On presentation, the cat's physical examinations were consistent with previous examinations before ingestion of azathioprine. A complete blood cell count revealed neutropenia and leukopenia. The cat later developed hyporexia, dehydration, and vomiting. Treatment included antinausea and appetite stimulant medications, filgrastim, and antibiotics. Filgrastim given as subcutaneous injections over the course of treatment increased neutrophil cell counts after suppression. The cat made a full recovery after responding to the treatment protocol. Based on the perceived response to filgrastim in this single feline case report, its use can be considered for the treatment of azathioprine-induced neutropenia in cats.

The pharmacokinetics of single oral dose extended-release topiramate and adverse effects after multi-dose administration in healthy cats.

Current treatment options for feline epilepsy are limited to medications that require administration of multiple doses per day or administration of a capsule or large tablet. Expanding the current treatment options could improve patient and owner compliance and optimize seizure control. Topiramate has been used sparingly in veterinary medicine, and limited pharmacokinetic studies have focused on immediate release formulations in dogs. If effective and safe, topiramate extended-release (XR) could broaden the current treatment options for feline epilepsy. The aims of this two-phase study were to establish single-dose pharmacokinetics for topiramate XR in cats, identify a dosing regimen that maintains steady-state plasma drug concentrations within a reference range extrapolated from human medicine (5-20 µg/mL), and evaluate the safety of topiramate XR in cats following multidose administration. Topiramate XR administered orally at 10 mg/kg once daily for 30 days was sufficient to achieve the desired concentrations in all cats. While no clinically apparent adverse effects were observed, four out of eight cats developed subclinical anemia, calling into question the safety of topiramate XR with chronic administration. Further studies are necessary to better understand the potential adverse effects and overall efficacy of topiramate XR for the treatment of feline epilepsy.

Eyes Instead of Ears: Eye Injuries Following Ocular Exposure to Otic Medications.

To determine the epidemiology of ocular exposures and toxicoses in dogs and cats from otic products, 79 dog and cat cases with an ocular exposure to a topical otic medication were retrieved from the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center database. Prescription products were involved in 75/79 (95%) of cases, and over-the-counter products in 4 (5%). Clinical signs included conjunctivitis, blepharospasm, epiphora, ocular discharge, and corneal ulceration. Medication error, specifically involving mistaken identification (i.e., an otic product confused with an ophthalmic product), occurred in 68/79 (86%) of cases. In 4 of these 68 cases, an otic instead of an ophthalmic medication was mistakenly dispensed to the pet owner. Unintentional delivery (i.e., accidental ocular exposure in the course of an otic application) occurred in 9/79 (11%) of cases, and 2 (3%) cases involved intentional delivery of otic products to the eyes. Because mistaken identification was the most common cause of ocular toxicoses from otic products, separate storage and/or distinctive packaging for ophthalmic versus otic products could reduce medication errors. Animal poison control center epidemiological data can be used as a source of information regarding veterinary medication errors.

Incidences of steroid-induced diabetes mellitus and congestive heart failure in cats given non-immunosuppressive doses of methylprednisolone acetate: 1042 cats.

Objective: Corticosteroids are indicated to treat many feline diseases. However, side effects are a limiting factor in their use. The most concerning side effects are steroid-induced diabetes mellitus (SI-DM) and steroid-induced congestive heart failure (SI-CHF). This study aims to determine the incidences of these diseases in a large population of domestic cats seen at a privately-owned, feline-only practice. Animals: Cats in the study were client-owned patients of Alamo Feline Health Center in San Antonio, Texas. Control cats (controls) were examined as part of their routine health care. Procedures: The records of 732 cats that received methylprednisolone acetate (MPA) for various clinical indications were reviewed to determine how many developed SI-DM and SI-CHF. A similar record review of 310 controls was made to determine the incidence of spontaneous diabetes mellitus (Sp-DM) and spontaneous congestive heart failure (Sp-CHF). Control cats never received any oral or injectable corticosteroids. Results: Of the cats that received MPA, 28 developed SI-DM (3.83%) and 6 developed SI-CHF (0.82%). Of the controls, 22 developed Sp-DM (7.10%) and 6 developed Sp-CHF (1.90%). Conclusion: The incidences of developing SI-DM and SI-CHF were 3.83% and 0.82%, respectively; and the risk was not increased even when repeated doses of MPA were given. Clinical relevance: The authors consider the risk-benefit ratio sufficient to justify the use of MPA when it is indicated, especially if another drug cannot be substituted with the same therapeutic results.

Incidences du diabète sucré et de l'insuffisance cardiaque congestive induits par les stéroïdes chez des chats ayant reçu des doses non immunosuppressives d'acétate de méthylprednisolone : 1042 chats. Objectif: Les corticoïdes sont indiqués pour traiter de nombreuses maladies félines. Cependant, les effets secondaires constituent un facteur limitant leur utilisation. Les effets secondaires les plus préoccupants sont le diabète sucré induit par les stéroïdes (SI-DM) et l'insuffisance cardiaque congestive induite par les stéroïdes (SI-CHF). Cette étude vise à déterminer l'incidence de ces maladies dans une large population de chats domestiques vus dans une pratique privée exclusivement féline. Animaux: Les chats de l'étude étaient des patients appartenant à des clients du Alamo Feline Health Center à San Antonio, au Texas. Les chats témoins (témoins) ont été examinés dans le cadre de leurs soins de santé de routine. Procédures: Les dossiers de 732 chats ayant reçu de l'acétate de méthylprednisolone (MPA) pour diverses indications cliniques ont été examinés afin de déterminer combien d'entre eux ont développé du SI-DM et du SI-CHF. Un examen similaire des dossiers de 310 témoins a été réalisé pour déterminer l'incidence du diabète sucré spontané (Sp-DM) et de l'insuffisance cardiaque congestive spontanée (Sp-CHF). Les chats témoins n'ont jamais reçu de corticostéroïdes oraux ou injectables. Résultats: Parmi les chats ayant reçu du MPA, 28 ont développé du SI-DM (3,83 %) et 6 ont développé du SI-CHF (0,82 %). Parmi les témoins, 22 ont développé du Sp-DM (7,10 %) et 6 ont développé du Sp-CHF (1,90 %). Conclusion: Les incidences de développement de SI-DM et de SI-CHF étaient respectivement de 3,83 % et 0,82 %; et le risque n'a pas augmenté même lorsque des doses répétées de MPA ont été administrées. Pertinence clinique: Les auteurs considèrent le rapport bénéfice/risque suffisant pour justifier l'utilisation du MPA lorsqu'il est indiqué, notamment si un autre médicament ne peut lui être substitué avec les mêmes résultats thérapeutiques.(Traduit par Dr Serge Messier).

Iatrogenic adrenal atrophy following oral corticotherapy is not reliably identified ultrasonographically in cats.

Background: In dogs, corticosteroid administration is known to decrease adrenal gland height when measured ultrasonographically. However, comparable information is lacking in cats. Objectives: i) Validate that the adrenal height of our control population without corticosteroid administration was similar to previous data, ii) determine effects of dose and duration of oral corticosteroid therapy on adrenal height, and iii) determine an adrenal size threshold to differentiate cats receiving corticosteroids or not. Animals and procedures: Adult cats (N = 308) that received abdominal ultrasonographic examination(s) were retrospectively recruited and allocated into 2 groups: those with and without oral corticosteroid use. Cats receiving corticosteroids were subdivided into 6 subgroups by dose (supraphysiologic, anti-inflammatory, or immunosuppressive) and duration of therapy (≤ 1 mo or > 1 mo). Results: Adrenal height in cats without corticosteroid therapy was comparable to previous studies. An anti-inflammatory corticosteroid dose for > 1 mo caused a 21.4% decrease in adrenal height (mean difference of 0.8 mm; P = 0.009). However, no difference in adrenal height was noted in the other subgroups (P > 0.21), and no useful adrenal height threshold was established. Conclusion and clinical relevance: Feline iatrogenic adrenal atrophy may be difficult to establish with ultrasonography, as only cats receiving anti-inflammatory corticosteroid doses for > 1 mo had a modest (< 1 mm) decrease in adrenal height.

L'atrophie iatrogène des surrénales consécutive à une corticothérapie orale n'est pas identifiée de manière fiable par échographie chez le chat. Contexte: Chez le chien, l'administration de corticostéroïdes est connue pour diminuer la taille des glandes surrénales lorsqu'elle est mesurée par échographie. Cependant, des informations comparables manquent chez les chats. Objectifs: i) Valider que la taille des surrénales de notre population témoin sans administration de corticostéroïdes était similaire aux données précédentes, ii) déterminer les effets de la dose et de la durée de la corticothérapie orale sur la taille des surrénales, et iii) déterminer un seuil de taille des surrénales pour différencier les chats recevant des corticostéroïdes ou pas. Animaux et procédures: Des chats adultes (N = 308) qui ont subi un ou plusieurs examens échographiques abdominaux ont été recrutés rétrospectivement et répartis en 2 groupes : ceux avec et sans corticothérapie orale. Les chats recevant des corticostéroïdes ont été subdivisés en 6 sous-groupes selon la dose (supraphysiologique, anti-inflammatoire ou immunosuppresseur) et la durée du traitement (≤ 1 mois ou > 1 mois). Résultats: La taille des surrénales chez les chats sans corticothérapie était comparable à celle des études précédentes. Une dose de corticoïdes anti-inflammatoires pendant > 1 mois a entraîné une diminution de 21,4 % de la taille des surrénales (différence moyenne de 0,8 mm; P = 0,009). Cependant, aucune différence de taille surrénalienne n'a été notée dans les autres sous-groupes (P > 0,21) et aucun seuil de taille surrénalienne utile n'a été établi. Conclusion et pertinence clinique: L'atrophie surrénalienne iatrogène féline peut être difficile à établir par échographie, car seuls les chats recevant des doses de corticostéroïdes anti-inflammatoires pendant > 1 mois ont présenté une diminution modeste (< 1 mm) de la taille des surrénales.(Traduit par Dr Serge Messier).

Pharmacology, safety, efficacy and clinical uses of the COX-2 inhibitor robenacoxib.

Robenacoxib is a veterinary-approved non-steroidal anti-inflammatory drug (NSAID) of the coxib group. It possesses anti-hyperalgesic, anti-inflammatory and anti-pyretic properties. Robenacoxib inhibits the cyclooxygenase (COX)-2 isoform of COX selectively (in vitro IC50 ratios COX-1:COX-2, 129:1 in dogs, 32:1 in cats). At registered dosages (2 mg/kg subcutaneously in dogs and cats, 1-4 mg/kg orally in dogs and 1-2.4 mg/kg orally in cats), robenacoxib produces significant inhibition of COX-2 whilst sparing COX-1. The pharmacokinetic (PK) profile of robenacoxib is characterized by a high degree of binding to plasma proteins (>98%) and moderate volume of distribution (at steady state, 240 ml/kg in dogs and 190 ml/kg in cats). In consequence, the terminal half-life in blood (<2 h) is short, despite moderate body clearance (0.81 L/kg/h) in dogs and low clearance (0.44 L/kg/h) in cats. Excretion is principally in the bile (65% in dogs and 72% in cats). Robenacoxib concentrates in inflamed tissues, and clinical efficacy is achieved with once-daily dosing, despite the short blood terminal half-life. In dogs, no relevant breed differences in robenacoxib PK have been detected. Robenacoxib has a wide safety margin; in healthy laboratory animals daily oral doses 20-fold (dog, 1 month), eight-fold (cat, 6 weeks) and five-fold (dog, 6 months) higher than recommended clinical doses were well tolerated. Clinical efficacy and safety have been demonstrated in orthopaedic and soft tissue surgery, and in musculoskeletal disorders in dogs and cats.

The history and pharmacology of buprenorphine: New advances in cats.

Opiates have a long history of medical use as effective analgesics associated with well-described side effects, including euphoria, respiratory depression, constipation, bradycardia, and histamine release, among others. The search for opiate analogs that retain effective analgesic qualities without detrimental side effects has yielded numerous compounds, including buprenorphine. Early studies of buprenorphine demonstrated analgesic effectiveness with a favorable safety profile, leading to the approval of formulations for use in humans. Since then, advances in receptor theory and molecular cloning of opioid receptors have led to a deeper understanding of buprenorphine pharmacology. More recent studies of receptor affinity and intrinsic activity have shown that buprenorphine is a µ- and κ-opioid receptor agonist, a nociceptin orphanin peptide agonist, and a δ-opioid receptor antagonist. Buprenorphine appears to have a primary spinal analgesic mechanism with complex supraspinal actions. It is considered a full agonist for pain but a partial agonist for other clinical endpoints such as respiratory depression. In feline medicine, buprenorphine is approved as low- and high-concentration injectable solutions, in addition to the most recently introduced long-acting transdermal formulation. Several investigational and compounded formulations have also been evaluated. There are contrasting differentiable features that include pharmacokinetics, onsets- and durations-of-action, routes of administration, and formulation constituents. Available buprenorphine formulations allow clinicians to select a formulation based on the anticipated duration of pain associated with various surgical procedures, and to provide interventions as needed. In light of the newly approved transdermal buprenorphine solution in cats and progress in buprenorphine pharmacology, the objective of this review is to examine the history and pharmacology of buprenorphine relative to full opioid agonists, where appropriate, integrating these insights into advances within feline medicine.

Topical Minoxidil Exposures and Toxicoses in Dogs and Cats: 211 Cases (2001-2019).

Topical minoxidil is a medication for hair loss, initially available in the United States by prescription only and available since 1996 as an over-the-counter product. To determine the epidemiology of minoxidil exposures and toxicoses in dogs and cats, 211 dog and cat cases with topical minoxidil exposure were identified from the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center database. In 87 cases with clinical signs of toxicosis (62 cats, 25 dogs), case narratives were reviewed and coded for exposure-related circumstances. Unintentional delivery, especially while pet owners applied minoxidil for his/her own hair loss (e.g., pet licked owner's skin or pillowcase, pet was splashed during a medication spill), was the most common cat exposure circumstance. Exploratory behavior (e.g., searching through trash) was the most common dog exposure circumstance. Clinical signs occurred in dogs and cats even with low exposure amounts, such as drops or licks. In patients that developed clinical signs, most developed moderate or major illness (56.0% dogs, 59.7% cats). Death occurred in 8/62 (12.9%) cats that developed clinical signs after the pet owner's minoxidil use. Pet owners should be educated on the risk of dog and cat toxicosis from accidental minoxidil exposure.

Myoclonus and hypersensitivity of the hind limbs and tail with urinary retention following neuraxial administration of morphine in a cat.

An adult female domestic shorthair cat developed myoclonus, muscle rigidity, and hypersensitivity of the hind limbs and tail with urinary retention following neuraxial administration of morphine. Myoclonic contractions resolved following treatment with midazolam and a urinary catheter was placed until normal micturition returned. The cat was clinically normal 36 hours after neuraxial morphine injection. The cat underwent a second surgery without neuraxial morphine and control of postoperative pain required more intervention. Key clinical message: Neuraxial morphine may cause myoclonus and urinary retention. The response to pharmacological treatment of myoclonus is varied, but a benzodiazepine drug may be effective.

Myoclonie et hypersensibilité des membres postérieurs et de la queue avec rétention urinaire après administration neuraxiale de morphine chez un chat. Une chatte domestique à poils courts adulte a développé une myoclonie, une rigidité musculaire et une hypersensibilité des membres postérieurs et de la queue avec rétention urinaire après l'administration neuraxiale de morphine. Les contractions myocloniques se sont résolues après un traitement avec du midazolam et un cathéter urinaire a été placé jusqu'à ce que les mictions normales reviennent. Le chat était cliniquement normal 36 heures après l'injection neuraxiale de morphine. Le chat a subi une deuxième intervention chirurgicale sans morphine neuraxiale et le contrôle de la douleur postopératoire a nécessité plus d'intervention.Message clinique clé:La morphine neuraxiale peut provoquer une myoclonie et une rétention urinaire. La réponse au traitement pharmacologique de la myoclonie est variée, mais un médicament à base de benzodiazépine peut être efficace.(Traduit par Dr Serge Messier).

Understanding the effect of repeated administration of meloxicam on feline renal cortex and medulla: A lipidomics and metabolomics approach.

Repeated administration of meloxicam can cause kidney damage in cats by mechanisms that remain unclear. Metabolomics and lipidomics are powerful, noninvasive approaches used to investigate tissue response to drug exposure. Thus, the objective of this study was to assess the effects of meloxicam on the feline kidney using untargeted metabolomics and lipidomics approaches. Female young-adult purpose-breed cats were allocated into the control (n = 4) and meloxicam (n = 4) groups. Cats in the control and meloxicam groups were treated daily with saline and meloxicam at 0.3 mg/kg subcutaneously for 17 days, respectively. Renal cortices and medullas were collected at the end of the treatment period. Random forest and metabolic pathway analyses were used to identify metabolites that discriminate meloxicam-treated from saline-treated cats and to identify disturbed metabolic pathways in renal tissue. Our results revealed that the repeated administration of meloxicam to cats altered the kidney metabolome and lipidome and suggest that at least 40 metabolic pathways were altered in the renal cortex and medulla. These metabolic pathways included lipid, amino acid, carbohydrate, nucleotide and energy metabolisms, and metabolism of cofactors and vitamins. This is the first study using a pharmacometabonomics approach for studying the molecular effects of meloxicam on feline kidneys.

Correlation of MRI with the Neuropathologic Changes in Two Cats with Bromethalin Intoxication.

Two cats were presented with multifocal neurological signs. One cat's signs progressed over 2 wk; the other cat progressed over 5 days. Examinations were consistent with a process involving the prosencephalon, vestibular system, and general proprioceptive/upper motor neuron systems. MRI of the brain and cervical spinal cord reveal widespread T2 hyperintensity of the white matter. Affected areas included the cerebrum, cerebral peduncles, corticospinal tracts of the pons and medulla, and the cerebellum. T2 hyperintensity was present in all funiculi of the spinal cord. Diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) maps were consistent with cytotoxic or intramyelinic edema. Differential diagnosis included toxic or metabolic/degenerative leukoencephalopathies. Necropsies revealed widespread spongy degeneration of the central nervous system white matter. Toxicologic assays of liver specimens revealed desmethylbromethalin, a metabolite of bromethalin. Bromethalin is a rodenticide that causes uncoupling of oxidative phosphorylation. Antemortem diagnosis is challenging. DWI and ADC maps were instrumental in narrowing the differential diagnosis and raised the index of suspicion for bromethalin. Bromethalin intoxication should be considered in all animals with a progressive course of multifocal neurologic deficits. MRI, specifically, DWI and ADC maps, may serve as a biomarker of cytotoxic or intramyelinic edema associated with spongiform leukoencephalomyelopathy.

An analytical strategy for the identification of carbamates, toxic alkaloids, phenobarbital and warfarin in stomach contents from suspected poisoned animals by thin-layer chromatography/ultraviolet detection.

In this study, an analytical strategy to identify brucine, strychnine, methomyl, carbofuran (alkaline compounds), phenobarbital, and warfarin (acid compounds) using thin-layer chromatography (TLC) screening with ultraviolet (UV) detection at 254 nm in stomach content is shown. The optimum mobile phase was found to be a chloroform: ethyl acetate: diethylamine (0.5:8.5:1) mixture for alkaline substances while a mixture of chloroform: acetone (9:1) has given better results for acidic substances. As for extraction, an equal proportion between distillated water and crude material (1:1) is required. For alkaline compounds, a filtration system was created in order to avoid any interferences from the biological matrix while for acidic compounds only centrifugation (4000 rpm/10 minutes) was required to obtain an appropriate sample. After the respective pretreatments, a one-step liquid-liquid extraction (LLE) has been employed for alkaline substances using a 3 mL of chloroform: ethyl ether (2:1) mixture for 2 min while acidic analytes used 3 mL of chloroform only during 5 min. For both methodologies described, the respective organic layers were dried down and re-suspended with 50 µL of methanol for further TLC plate application. The methodologies have been developed, successfully validated and applied to gastric contents from real case samples of suspected animal poisoning. Positive results from TLC/UV screening were confronted with HPLC-UV and confirmed by GC-MS.

Effects of p.o. administered xylitol in cats.

Xylitol is commonly used as sugar substitute in households. While it has numerous beneficial effects on human health, it is highly toxic to dogs. The goal of this study was to examine whether xylitol has similar deleterious effects, such as hypoglycaemia and acute hepatic failure, on cats. Our research included six healthy middle-aged cats. Xylitol was dissolved in deionized water and administered p.o. at three doses (100, 500 and 1,000 mg/kg body weight). These dosages have been considered toxic and can cause liver failure or even death in dogs. After every xylitol administration, the basic health status and the blood glucose of cats were observed regularly. Additionally, prior to and 6, 24 and 72 hr after xylitol administration, blood samples were taken to check complete blood count, clinical biochemical parameters and enzymes such as ALT, ALKP, GGT, GLDH, bile acids, BUN, creatinine, phosphate, total protein, albumin, sodium and potassium. There were no significant changes (p > .05) in any of the haematological or biochemical parameters. Blood glucose concentrations did not show any significant alterations, except at 1,000 mg/kg dose, where a mild but significant increase was observed, but it was in physiological range. Based on our results, xylitol did not induce toxic effects on cats.

Evaluation of the safety of daily administration of capromorelin in cats.

Capromorelin is a ghrelin receptor agonist that is FDA approved for appetite stimulation in dogs. The objective of this study was to evaluate the safety of daily oral administration of capromorelin to cats over a range of doses and for an extended period. Two randomized, controlled studies were conducted: in Study 1, cats (n = 6 per group) received placebo or capromorelin at a dose of 9, 15, 30 or 60 mg/kg once daily for 14 days; and in Study 2, cats received capromorelin at 6 mg/kg (n = 8) or placebo (n = 4) once daily for 91 days. Cats were evaluated using clinical observations and clinical pathology test results for both studies, with the addition of postmortem examination in Study 1 and measurements of growth hormone and insulin-like growth factor 1 in Study 2. Abnormal clinical observations were limited to emesis, hypersalivation, lethargy/depression, head shaking and lip smacking, which occurred more frequently in the capromorelin-treated groups than in the placebo group. There were no clinically relevant differences in clinical pathology test results between the capromorelin and placebo groups in either study.

Critical incident technique analysis applied to perianesthetic cardiac arrests at a university teaching hospital.

OBJECTIVE: To apply the critical incident technique (CIT) methodology to a series of perianesthetic cardiac arrest events at a university teaching hospital to describe the factors that contributed to cardiac arrest. STUDY DESIGN: CIT qualitative analysis of a case series. ANIMALS: A group of 16 dogs and cats that suffered a perioperative cardiac arrest between November 2013 and November 2016. METHODS: If an arrest occurred, the event was discussed among the anesthesiologists. The discussion included a description of the case, a description of the sequence of events leading up to the arrest and a discussion of what could have been done to affect the outcome. A written description of the case and the event including animal signalment and a timeline of events was provided by the supervising anesthesiologist following discussion among the anesthesiologists. Only dogs or cats were included. After the data collection period, information from the medical record was collected. A qualitative document analysis was performed on the summaries provided about each case by the supervising anesthesiologist, the medical record and any supporting documents. Each case was then classified into one or more of the following: animal, human, equipment, drug and procedural factors for cardiac arrest. RESULTS: The most common factor was animal (n=14), followed by human (n=12), procedural (n=4), drugs (n=1) and equipment (n=1). The majority (n=11) of animals had multiple factors identified. CONCLUSIONS AND CLINICAL RELEVANCE: Cardiac arrests during anesthesia at a referral teaching hospital were primarily a result of animal and human factors. Arrests because of procedural, drug and equipment factors were uncommon. Most animals experienced more than one factor and two animals arrested after a change in recumbency. Future work should focus on root cause analysis and interventions designed to minimize all factors, particularly human ones.

Hypertriglyceridemia and transient corneal lipidosis in a cat following intravenous lipid therapy for permethrin toxicosis.

An 8-year-old male neutered domestic shorthair cat developed corneal lipidosis and marked hypertriglyceridemia approximately 36 hours after intravenous lipid therapy (IVLT) for the treatment of permethrin toxicosis. The cat's ocular changes resolved approximately 72 hours after IVLT without treatment. This study reports a rare complication of IVLT.

Hypertriglycéridémie et lipidose cornéenne transitoire chez un chat après une lipidothérapie intraveineuse pour une toxicose à la perméthrine. Un chat commun mâle stérilisé âgé de 8 ans a développé une lipidose cornéenne et une hypertriglycéridémie marquée environ 36 heures après une lipidothérapie intraveineuse (LTI) pour le traitement de la toxicose à la perméthrine. Les changements oculaires du chat se sont résorbés sans traitement environ 72 heures près la LTI. Cette étude signale une complication rare de la LTI.(Traduit par Isabelle Vallières).

Association of Polybrominated Diphenyl Ethers (PBDEs) and Polychlorinated Biphenyls (PCBs) with Hyperthyroidism in Domestic Felines, Sentinels for Thyroid Hormone Disruption.

BACKGROUND: Hyperthyroidism is the most common endocrine disorder observed in domestic felines; however, its etiology is largely unknown. Two classes of persistent organic pollutants, polybrominated diphenyl ethers (PBDEs) and polychlorinated biphenyls (PCBs) are known to interfere with thyroid hormone (TH) signaling and regulation; thus, it is postulated that they contribute to the etiopathogenesis of feline hyperthyroidism and pose a risk to humans and other species. In this case-control study, the concentrations of 13 PBDE and 11 PCB congeners were measured by gas chromatography mass spectrometry in serum or plasma samples from 20 hyperthyroid and 31 control cats in order to investigate the association between concentration of PBDE and PCB congeners and feline hyperthyroidism. Logistic regression analysis was used to determine whether elevated concentrations of individual congeners were associated with a higher risk of feline hyperthyroidism. RESULTS: Hyperthyroid cats had higher concentrations of four PBDE congeners (BDE17, BDE100, BDE47, and BDE49) and five PCB congeners (PCB131, PCB153, PCB174, PCB180, and PCB196), compared to control cats. In addition, the sum of both PBDE and PCB congener concentrations were elevated in the hyperthyroid group compared to control cats; however, only the increased PCB concentrations were statistically significant. The sum total PBDE concentrations in our feline samples were approximately 50 times greater than concentrations previously reported in human populations from a geographically similar area, whereas sum total PCB concentrations were comparable to those previously reported in humans. CONCLUSIONS: These observational findings support the hypothesis that PBDEs and PCBs may contribute to the etiopathogenesis of hyperthyroidism in felines. As domestic house cats are often exposed to higher concentrations of PBDEs than humans, they may serve as sentinels for the risk of TH disruption that these pollutants pose to humans and other species.