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- Author or Editor: Karol A. Mathews x
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Abstract
Objective—To determine whether administration of the nonsteroidal anti-inflammatory drugs meloxicam or carprofen to healthy dogs that were subsequently anesthetized and subjected to painful electrical stimulation has adverse effects on renal function as measured by glomerular filtration rate (GFR) and evaluation of serum concentrations of urea and creatinine.
Animals—6 male and 6 female healthy young-adult Beagles.
Procedure—A study was conducted in accordance with a randomized crossover Latin-square design. One of 3 treatments (saline [0.9% NaCl] solution, 0.2 mg of meloxicam/kg, or 4.0 mg of carprofen/kg) was administered IV 1 hour before anesthesia was induced by use of drugs in accordance with a standard anesthetic protocol (butorphanol tartrate and acepromazine maleate as preanesthetic medications, ketamine hydrochloride and diazepam for induction, and maintenance with isoflurane). Anesthetized dogs were subjected to intermittent electrical stimulation for 30 minutes. Direct, mean arterial blood pressure; heart rate; and respiratory rate were monitored. End-tidal isoflurane concentration was maintained at 1.5 times the minimum alveolar concentration. The GFR, as measured by plasma clearance of 99mTc-diethylenetriaminepentaacetic acid, and serum concentrations of serum and creatinine were determined 24 hours after induction of anesthesia.
Results—Neither meloxicam nor carprofen significantly affected GFR or serum concentrations of urea and creatinine, compared with values for the saline treatment.
Conclusions and Clinical Relevance—When administered 1 hour before onset of anesthesia and painful electrical stimulation, meloxicam or carprofen did not cause clinically important alterations of renal function in young healthy dogs. (Am J Vet Res 2004;65:1384–1390)
Abstract
Objective—To identify the normal gastric acid secretion profile in dogs and determine the degree of gastric acid suppression associated with 4 gastric acid suppressants.
Animals—12 healthy Beagles.
Procedure—Intragastric pH was measured continuously for 24-hour periods with a digital recording system placed via a gastrostomy tube. Baseline measurements were obtained when food was withheld and when dogs were fed a standard diet. Dogs were then treated with ranitidine (2 mg/kg, IV, q 12 h), famotidine (0.5 mg/kg, IV, q 12 h), pantoprazole (1 mg/kg, IV, q 24 h), omeprazole (1 mg/kg, PO, q 24 h), or saline solution for 7 days; intragastric pH was recorded on days 0, 2, and 6. Subsequently, the effects of administering famotidine (0.5 mg/kg, IV, q 8 h; 6 dogs) and omeprazole as a suspension (1 mg/kg, PO, q 12 h; 6 dogs) were evaluated. Median 24-hour intragastric pH, percentage of time pH was ≥ 3, and percentage of time pH was ≥ 4 were determined.
Results—Median pH, percentage of time pH was ≥ 3, and percentage of time pH was ≥ 4 were all significantly higher when food was withheld than when dogs were fed. Famotidine, pantoprazole, and omeprazole significantly suppressed gastric acid secretion, compared with saline solution, as determined on the basis of median 24-hour pH and percentages of time pH was ≥ 3 or ≥ 4. However, ranitidine did not. Omeprazole suspension suppressed gastric acid secretion.
Conclusions and Clinical Relevance—Results suggest that in healthy dogs, famotidine, pantoprazole, and omeprazole significantly suppress gastric acid secretion. Twice daily administration of a suspension of omeprazole, was the only regimen tested that approached the potential therapeutic efficacy for acidrelated disease when assessed by criteria used for human patients. (Am J Vet Res 2005;66:425–431)
Abstract
Objective—To assess accuracy and reliability of open-flow indirect calorimetry in dogs.
Animals—13 clinically normal dogs.
Procedure—In phase 1, oxygen consumption per kilogram of body weight (VO2kg) was determined in 6 anesthetized dogs by use of open-flow indirect calorimetry before and after determination of VO2/kg by use of closed-circuit spirometry. In phase 2, four serial measurements of VO2 and carbon dioxide production (VCO2) were obtained in 7 awake dogs by use of indirect calorimetry on 2 consecutive days. Resting energy expenditure (REE) was calculated.
Results—Level of clinical agreement was acceptable between results of indirect calorimetry and spirometry. Mean VO2/kg determined by use of calorimetry before spirometry was significantly greater than that obtained after spirometry. In phase 2, intraclass correlation coefficients (ICC) for REE and VO2 were 0.779 and 0.786, respectively, when data from all 4 series were combined. When the first series was discounted, ICC increased to 0.904 and 0.894 for REE and VO2, respectively. The most reliable and least variable measures of REE and VO2 were obtained when the first 2 series were discounted.
Conclusions and Clinical Relevance—Open-flow indirect calorimetry may be used clinically to obtain a measure of VO2 and an estimate of REE in dogs. Serial measurements of REE and VO2 in clinically normal dogs are reliable, but a 10-minute adaption period should be allowed, the first series of observations should be discounted, multiple serial measurements should be obtained, and REE. (Am J Vet Res 2001;62:1761–1767).
Abstract
Objective—To compare induction with hydromorphone and diazepam (HydroD) or oxymorphone and diazepam (OxyD) followed by maintenance with isoflurane in dogs with induced hypovolemia.
Animals—6 healthy mixed-breed dogs.
Procedure—The study used a crossover design. Measurements were obtained in normovolemic dogs during isoflurane. Hypovolemia was induced (blood loss of 30 mL/kg) and measurements repeated following recovery from anesthesia, after HydroD (hydromorphone, 0.1 mg/kg; diazepam, 0.2 mg/kg; IV) or OxyD (oxymorphone, 0.05 mg/kg; diazepam, 0.2 mg/kg; IV), after another dose of the same opioid, during administration of isoflurane (end-tidal concentration, 0.9%), and after glycopyrrolate (0.01 mg/kg, IV). Significant changes were identified.
Results—Induction effect was evident within 1 minute. All dogs were intubated after the second dose of opioid. No significant differences were found between inductions. The HydroD decreased heart rate (mean ± SEM, –41 ± 9.8 beats/min), whereas both inductions increased stroke index (0.4 ± 0.09 mL/kg/beat) and caused moderate respiratory depression. Cardiac index was decreased (±30.2 ± 6.04 mL/kg/min) and there was minor metabolic acidosis during isoflurane following HydroD, compared with values for anesthetized normovolemic dogs. Glycopyrrolate increased heart rate (50 ± 8.6 beats/min) and decreased systolic blood pressure (–23.2 ± 4.87 mm Hg) in dogs induced with HydroD and decreased stroke index (–0.3 ± 0.08 mL/kg/beat) for both inductions.
Conclusions and Clinical Relevance—Similar effects were detected after administration of HydroD or OxyD in hypovolemic dogs. Either combination should be safe for use in hypovolemic dogs. Administration of glycopyrrolate was not beneficial. (Am J Vet Res 2005;66:1227–1237)
Abstract
Objective—To determine the effectiveness and safety of 2 sedative-analgesic protocols to facilitate assisted ventilation in healthy dogs.
Animals—12 healthy dogs.
Procedures—Dogs were randomly assigned to 2 groups. Mean dosages for protocol 1 were diazepam (0.5 mg/kg/h [n = 3 dogs]) or midazolam (0.5 mg/kg/h [3]), morphine (0.6 mg/kg/h [6]), and medetomidine (1.0 μg/kg/h [6]). Mean dosages for protocol 2 were diazepam (0.5 mg/kg/h [n = 3]) or midazolam (0.5 mg/kg/h [3]), fentanyl (18 μg/kg/h [6]), and propofol (2.5 mg/kg/h [6]). Each dog received the drugs for 24 consecutive hours. All dogs were mechanically ventilated with adjustments in minute volume to maintain normocapnia and normoxemia. Cardiorespiratory variables were recorded. A numeric comfort score was assigned hourly to assess efficacy. Mouth care, position change, and physiotherapy were performed every 6 hours. Urine output was measured every 4 hours.
Results—Use of both protocols maintained dogs within optimal comfort ranges > 85% of the time. The first dog in each group was excluded from the study. Significant decreases in heart rate, oxygen consumption, and oxygen extraction ratio were evident for protocol 1. Cardiac index values in ventilated dogs were lower than values reported for healthy unsedated dogs. Oxygen delivery, lactate concentration, and arterial base excess remained within reference ranges for both protocols.
Conclusions and Clinical Relevance—Use of both protocols was effective for facilitating mechanical ventilation. A reduction in cardiac index was detected for both protocols as a result of bradycardia. However, oxygen delivery and global tissue perfusion were not negatively affected.
Abstract
Objective—To compare the safety and efficacy of preoperative administration of meloxicam with that of ketoprofen and butorphanol in dogs undergoing abdominal surgery.
Animals—36 dogs undergoing laparotomy, splenectomy, or cystotomy.
Procedure—Dogs were randomly assigned to 1 of 3 groups. In the first part of the study, dogs were given a single dose of meloxicam, ketoprofen, or a placebo, and buccal mucosal bleeding times were measured. In the second part of the study, dogs were given meloxicam, ketoprofen, or butorphanol prior to surgery. Dogs in the butorphanol group received a second dose immediately after surgery. Pain scores (1 to 10) were assigned hourly for 20 hours after surgery and used to determine an overall efficacy score for each dog. Dogs with a pain score ≥ 3 were given oxymorphone for pain. Dogs were euthanatized 8 days after surgery, and gross and histologic examinations of the liver, kidneys, and gastrointestinal tract were conducted.
Results—Overall efficacy was rated as good or excellent in 9 of the 12 dogs that received meloxicam, compared with 9 of the 12 dogs that received ketoprofen and only 1 of the 12 dogs that received butorphanol. No clinically important hematologic, biochemical, or pathologic abnormalities were detected.
Conclusions and Clinical Relevance—Results suggest that preoperative administration of meloxicam is a safe and effective method of controlling postoperative pain for 20 hours in dogs undergoing abdominal surgery; the analgesic effects of meloxicam were comparable to those of ketoprofen and superior to those of butorphanol. (Am J Vet Res 2001;62:882–888)
Abstract
Case Description—Methicillin-resistant Staphylococcus aureus (MRSA) was isolated from the tracheostomy tube of an 18-month-old castrated male Golden Retriever in the intensive care unit (ICU) of the Ontario Veterinary College. This prompted an investigation of MRSA colonization in other animals in the ICU.
Clinical Findings—On day 1 of the investigation, MRSA was isolated from nasal swabs obtained from 2 of 10 animals (2/7 dogs and 0/3 cats), including the index case. Subsequently, MRSA was isolated from 3 of 12 animals on day 9; 3 of 9 animals on day 13; and none of 14, 5, and 6 animals on day 20, 27, and 78, respectively. Overall, MRSA was isolated from 6 of 26 (23%) animals during the outbreak period (4/22 dogs and 2/4 cats). The apparent incidence of MRSA acquisition in the ICU from days 1 through 13 was 20% (5/25 animals). No clinical signs of MRSA infections developed. All isolates were indistinguishable from one another.
Treatment and Outcome—Infection-control measures including active surveillance of all animals in the ICU, barrier precautions, and hand hygiene were used to control the apparent outbreak.
Clinical Relevance—Methicillin-resistant S aureus is an emerging problem in veterinary medicine. Intensive care units may be at particular risk for periodic outbreaks of colonization and disease. The outbreak of this report highlights the potential for clinically inapparent transmission of MRSA within a facility; infection-control measures that might facilitate MRSA eradication should be considered in ICU settings.
Abstract
Objective—To determine the level of clinical agreement between 2 methods for the measurement of resting energy expenditure (REE).
Design—Prospective case series.
Animals—77 dogs.
Procedure—Oxygen consumption (O2) and CO2 production (CO2) were measured with an open-flow indirect calorimeter in healthy (n = 10) and ill (67) dogs. Measurements were collected at 3 time periods on 2 days. The O2 and the CO2 measurements were then used to calculate the REE values.
Results—Mean values of measured (MREE) and predicted (PREE) REEs in healthy dogs and a dog with medical illnesses or trauma were not significantly different. There was a significant difference on day 2 between the MREE and PREE in the group of dogs recovering from major surgery. More importantly, there was significant variation between the PREE and MREE on an individual-dog basis. The PREE only agreed to within ± 20% of the MREE in 51% to 57% of the dogs.
Conclusions and Clinical Relevance—The level of agreement between these two methods for determining the 24-hour REE was poor in individual dogs. The level of disagreement between the 2 methods indicates that these methods may not be used interchangeably in a clinical setting. Measurement of REE by use of indirect calorimetry may be the only reliable method of determining REE in an individual ill or healthy dog. (J Am Vet Med Assoc 2004;225:58–64)
Abstract
Objective—To determine whether duration of hospitalization in the intensive care unit (ICU) of a veterinary teaching hospital was associated with prevalence of antimicrobial resistance among rectal Escherichia coli isolates from dogs, whether antimicrobial treatment was associated with prevalence of antimicrobial resistance, and whether there were associations among antimicrobial drugs to which isolates were resistant.
Design—Prospective observational study.
Animals—116 dogs hospitalized in an ICU for ≥ 3 days.
Procedures—Rectal swab specimens were obtained every 3 days and submitted for bacterial culture for E coli. Isolates were tested for susceptibility to 12 antimicrobial agents by means of disk diffusion.
Results—For each additional day that a dog was hospitalized in the ICU, the odds of being colonized with an E coli isolate resistant to 1 or more of the 12 antimicrobials tested increased by a factor of 1.5, independent of antimicrobial treatment. Dogs that were treated with enrofloxacin were 25.6 times as likely to be colonized by a quinolone-resistant E coli strain as were dogs that did not receive any antimicrobials. Significant correlations were found for resistance to agents in the extended-spectrum cephalosporin group and the quinolone group.
Conclusions and Clinical Relevance—Results suggested that the proportion of rectal E coli isolates obtained from dogs housed for ≥ 3 days in a veterinary teaching hospital ICU that were resistant to antimicrobial agents increased as the duration of hospitalization in the ICU increased. Thus, ICU hospitalization time should be as short as possible to prevent development of antimicrobial resistance among rectal E coli isolates.
Objective
To describe and evaluate hemostatic function in critically ill dogs with clinical signs of diseases that predispose to disseminated intravascular coagulation (DIC).
Design
Prospective case series.
Animals
59 critically ill dogs (affected dogs) with clinical signs of diseases known to predispose to DIC and 52 clinically normal dogs (control dogs).
Procedure
Activated partial thromboplastin time (aPTT), prothrombin time (PT), thrombin clotting time (TCT), plasma fibrinogen concentration, serum concentration of fibrin and fibrinogen-related antigens (FRA), and plasma antithrombin III (AT III) activity were determined for all dogs. Results from affected dogs were compared with those of control dogs. In some affected dogs, postmortem tissue specimens were examined for evidence of microvascular thrombosis. A diagnosis of DIC was made by fulfilling at least 3 of the following criteria: 1) abnormal aPTT, PT, or TCT value, 2) low plasma fibrinogen concentration, 3) low plasma AT III activity, 4) high serum FRA concentration, or 5) low platelet count. To evaluate the severity of hemostatic dysfunction, 3 arbitrary categories (mild, moderate, and severe) were proposed.
Results
A diagnostic strategy based on moderate hemostatic dysfunction identified DIC in 16 of 59 (27.1%) affected dogs. The AT III activity was < 70% in 15 of 16 dogs with DIC. Microvascular thrombosis was observed in tissue specimens from 7 of 8 affected dogs. Serum FRA and plasma fibrinogen concena did not contribute in establishing a diagnosis of DIC.
Conclusions and Clinical Relevance
A diagnosis of DIC can be made when hemostatic dysfunction is moderate in dogs with clinical signs of diseases associated with DIC. (J Am Vet Med Assoc 1999;215:798–804).