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- Author or Editor: Christine Egger x
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Abstract
Objective—To determine and compare levels of sedation achieved by IM administration of diphenhydramine, saline (0.9% NaCl) solution, and acepromazine in dogs.
Design—Prospective randomized study.
Animals—56 dogs.
Procedure—Dogs were randomly assigned to receive diphenhydramine at 2, 4, or 8 mg/kg (0.9, 1.8, or 3.6 mg/lb, respectively) IM; acepromazine at 0.1 mg/kg (0.05 mg/lb) IM; or saline solution at 0.05 mL/kg (0.02 mL/lb) IM. Sedation was assessed by use of a 6-category descriptive system based on observation and interaction.
Results—Dogs in the acepromazine group had significantly higher sedation scores than did dogs in the saline solution or diphenhydramine groups at 30 minutes. Dogs in the diphenhydramine groups did not have significantly different sedation scores from dogs in the saline solution group at any time point.
Conclusions and Clinical Relevance—Diphenhydramine did not cause clinically appreciable sedation in healthy dogs. Diphenhydramine is not suitable as a sole sedative prior to general anesthesia in dogs. (J Am Vet Med Assoc 2005;226:1092–1094)
Abstract
Objective—To determine the association among signalment, health status, other clinical variables, and treatments and events during cardiopulmonary cerebral resuscitation (CPCR) with the return of spontaneous circulation (ROSC) for animals with cardiopulmonary arrest (CPA) in a veterinary teaching hospital.
Design—Cross-sectional study.
Animals—161 dogs and 43 cats with CPA.
Procedures—Data were gathered during a 60-month period on animals that had CPA and underwent CPCR. Logistic regression was used to evaluate effects of multiple predictors for ROSC.
Results—56 (35%) dogs and 19 (44%) cats had successful CPCR. Twelve (6%) animals (9 dogs and 3 cats) were discharged from the hospital. Successfully resuscitated dogs were significantly more likely to have been treated with mannitol, lidocaine, fluids, dopamine, corticosteroids, or vasopressin; had CPA while anesthetized; received chest compressions while positioned in lateral recumbency; and had a suspected cause of CPA other than hemorrhage or anemia, shock, hypoxemia, multiple organ dysfunction syndrome, cerebral trauma, malignant arrhythmia, or an anaphylactoid reaction and were less likely to have been treated with multiple doses of epinephrine, had a longer duration of CPA, or had multiple disease conditions, compared with findings in dogs that were not successfully resuscitated. Successfully resuscitated cats were significantly more likely to have had more people participate in CPCR and less likely to have had shock as the suspected cause of CPA, compared with findings in cats that were not successfully resuscitated.
Conclusions and Clinical Relevance—The prognosis was grave for animals with CPA, except for those that had CPA while anesthetized.
Abstract
Objective—To evaluate the effects of ketamine, magnesium sulfate, and their combination on the minimum alveolar concentration (MAC) of isoflurane (ISO-MAC) in goats.
Animals—8 adult goats.
Procedures—Anesthesia was induced with isoflurane delivered via face mask. Goats were intubated and ventilated to maintain normocapnia. After an appropriate equilibration period, baseline MAC (MACB) was determined and the following 4 treatments were administered IV: saline (0.9% NaCl) solution (loading dose [LD], 30 mL/20 min; constant rate infusion [CRI], 60 mL/h), magnesium sulfate (LD, 50 mg/kg; CRI, 10 mg/kg/h), ketamine (LD, 1 mg/kg; CRI, 25 μg/kg/min), and magnesium sulfate (LD, 50 mg/kg; CRI, 10 mg/kg/h) combined with ketamine (LD, 1 mg/kg; CRI, 25 μg/kg/min); then MAC was redetermined.
Results—Ketamine significantly decreased ISOMAC by 28.7 ± 3.7%, and ketamine combined with magnesium sulfate significantly decreased ISOMAC by 21.1 ± 4.1%. Saline solution or magnesium sulfate alone did not significantly change ISOMAC.
Conclusions and Clinical Relevance—Ketamine and ketamine combined with magnesium sulfate, at doses used in the study, decreased the end-tidal isoflurane concentration needed to maintain anesthesia, verifying the clinical impression that ketamine decreases the end-tidal isoflurane concentration needed to maintain surgical anesthesia. Magnesium, at doses used in the study, did not decrease ISOMAC or augment ketamine's effects on ISOMAC.
Abstract
Objective—To compare the effectiveness of preoperative PO and SC administration of buprenorphine and meloxicam for prevention of postoperative pain-associated behaviors in cats undergoing ovariohysterectomy.
Design—Randomized controlled study.
Animals—51 female cats (4 to 60 months old; weight range, 1.41 to 4.73 kg [3.1 to 10.4 lb]).
Procedure—Cats received 1 of 5 treatments at the time of anesthetic induction: buprenorphine PO (0.01 mg/kg [0.0045 mg/lb]; n = 10), buprenorphine SC (0.01 mg/kg; 10), meloxicam SC (0.3 mg/kg [0.14 mg/lb]; 10), meloxicam PO (0.3 mg/kg; 10), or 0.3 mL of sterile saline (0.9% NaCl) solution SC (control group; 11). Sedation scores and visual analog scale and interactive visual analog scale (IVAS) pain-associated behavior scores were assigned to each cat 2 hours before and at intervals until 20 hours after surgery.
Results—Cats receiving meloxicam PO or SC had significantly lower IVAS scores (2.91 and 2.02, respectively), compared with IVAS scores for cats receiving buprenorphine PO (7.55). Pain-associated behavior scores for cats administered buprenorphine or meloxicam PO or SC preoperatively did not differ significantly from control group scores. Rescue analgesia was not required by any of the cats receiving meloxicam, whereas 3 of 10 cats receiving buprenorphine PO, 2 of 10 cats receiving buprenorphine SC, and 1 of 11 cats receiving the control treatment required rescue analgesia.
Conclusions and Clinical Relevance—On the basis of pain-associated behavior scores, cats receiving meloxicam PO or SC before ovariohysterectomy appeared to have less pain after surgery than those receiving buprenorphine PO preoperatively. (J Am Vet Med Assoc 2005;227:1937–1944)
Abstract
OBJECTIVE To evaluate the effect of MgSO4, alone and in combination with propofol, on the minimum alveolar concentration preventing motor movement (MACNM) in sevoflurane-anesthetized dogs.
ANIMALS 6 healthy purpose-bred adult male Beagles (least squares mean ± SEM body weight, 12.0 ± 1.1 kg).
PROCEDURES Dogs were anesthetized 3 times at weekly intervals. The MACNM was measured 45 minutes after induction of anesthesia (baseline; MACNM-B) and was determined each time by use of a noxious electrical stimulus. Treatments were administered as a loading dose and constant rate infusion (CRI) as follows: treatment 1, MgSO4 loading dose of 45 mg/kg and CRI of 15 mg/kg/h; treatment 2, propofol loading dose of 4 mg/kg and CRI of 9 mg/kg/h; and treatment 3, MgSO4 and propofol combination (same doses used previously for each drug). A mixed-model ANOVA and Tukey-Kramer tests were used to determine effects of each treatment on the percentage decrease from MACNM-B. Data were reported as least squares mean ± SEM values.
RESULTS Decrease from MACNM-B was 3.4 ± 3.1%, 48.3 ± 3.1%, and 50.3 ± 3.1%, for treatments 1, 2, and 3, respectively. The decrease for treatments 2 and 3 was significantly different from that for treatment 1; however, no significant difference existed between results for treatments 2 and 3.
CONCLUSIONS AND CLINICAL RELEVANCE MgSO4 did not affect MACNM, nor did it potentiate the effects of propofol on MACNM. Administration of MgSO4 in this study appeared to provide no clinical advantage as an anesthetic adjuvant.
Abstract
Objective—To evaluate the effect of IV administration of tramadol hydrochloride on the minimum alveolar concentration of isoflurane (ISOMAC) that prevented purposeful movement of rabbits in response to a noxious stimulus.
Animals—Six 6- to 12-month-old female New Zealand White rabbits.
Procedures—Anesthesia was induced and maintained with isoflurane in oxygen. A baseline ISOMAC was determined by clamping a pedal digit with sponge forceps until gross purposeful movement was detected or a period of 60 seconds elapsed. Subsequently, tramadol (4.4 mg/kg) was administered IV and the posttreatment ISOMAC (ISOMACT) was measured.
Results—Mean ± SD ISOMAC and ISOMACT values were 2.33 ± 0.13% and 2.12 ± 0.17%, respectively. The ISOMAC value decreased by 9 ± 4% after tramadol was administered. Plasma tramadol and its major metabolite (M1) concentrations at the time of ISOMACT determination varied widely (ranges, 181 to 636 ng/mL and 32 to 61 ng/mL, respectively). Intervals to determination of ISOMACT and plasma tramadol and M1 concentrations were not correlated with percentage change in the ISOMAC. Heart rate decreased significantly immediately after tramadol administration but by 10 minutes afterward was not different from the pretreatment value. Systolic arterial blood pressure decreased to approximately 60 mm Hg for approximately 5 minutes in 3 rabbits after tramadol administration. No adverse effects were detected.
Conclusions and Clinical Relevance—As administered, tramadol had a significant but clinically unimportant effect on the ISOMAC in rabbits. Higher doses of tramadol may provide clinically important reductions but may result in a greater degree of cardiovascular depression.
Abstract
Objective—To investigate the effects of the concurrent administration of 70% N2O on the minimum alveolar concentration (MAC) for sevoflurane in dogs, the MAC derivative that blocks motor movement (MACNM), and the MAC derivative that blocks autonomic responses (MACBAR).
Animals—7 adult sexually intact male mixed-breed dogs.
Procedures—For each dog, anesthesia was induced with sevoflurane delivered via a face mask. Initially, the baseline MAC, MACNM, and MACBAR for sevoflurane were determined by use of a noxious stimulus (50 V, 50 Hz, and 10 milliseconds) applied subcutaneously over a midulnar region. Nitrous oxide (70%) was added to the breathing circuit, and MAC, MACNM, and MACBAR were determined again. Percentage changes from the respective baseline concentrations for MAC, MACNM’ and MACBAR were calculated after the administration of N2O.
Results—Baseline median values for the MAC, MACNM, and MACBAR for sevoflurane were 1.75%, 2.00%, and 2.50%, respectively. Addition of 70% N2O significantly decreased MAC, MACNM, and MACBAR by 24.4%, 25.0%, and 35.2%, respectively, and these values did not differ significantly from each other.
Conclusions and Clinical Relevance—Supplementation with 70% N2O caused a clinically important and significant decrease in the MAC, MACNM’ and MACBAR for sevoflurane in dogs.
Abstract
OBJECTIVE To determine the minimum infusion rate (MIR) of propofol required to prevent movement in response to a noxious stimulus in dogs anesthetized with propofol alone or propofol in combination with a constant rate infusion (CRI) of ketamine.
ANIMALS 6 male Beagles.
PROCEDURES Dogs were anesthetized on 3 occasions, at weekly intervals, with propofol alone (loading dose, 6 mg/kg; initial CRI, 0.45 mg/kg/min), propofol (loading dose, 5 mg/kg; initial CRI, 0.35 mg/kg/min) and a low dose of ketamine (loading dose, 2 mg/kg; CRI, 0.025 mg/kg/min), or propofol (loading dose, 4 mg/kg; initial CRI, 0.3 mg/kg/min) and a high dose of ketamine (loading dose, 3 mg/kg; CRI, 0.05 mg/kg/min). After 60 minutes, the propofol MIR required to prevent movement in response to a noxious electrical stimulus was determined in duplicate.
RESULTS Least squares mean ± SEM propofol MIRs required to prevent movement in response to the noxious stimulus were 0.76 ± 0.1 mg/kg/min, 0.60 ± 0.1 mg/kg/min, and 0.41 ± 0.1 mg/kg/min when dogs were anesthetized with propofol alone, propofol and low-dose ketamine, and propofol and high-dose ketamine, respectively. There were significant decreases in the propofol MIR required to prevent movement in response to the noxious stimulus when dogs were anesthetized with propofol and low-dose ketamine (27 ± 10%) or with propofol and high-dose ketamine (30 ± 10%).
CONCLUSIONS AND CLINICAL RELEVANCE Ketamine, at the doses studied, significantly decreased the propofol MIR required to prevent movement in response to a noxious stimulus in dogs.
