The effects of ketamine hydrochloride and diazepam on the intraocular pressure and pupil diameter of the dog’s eye

Objective To determine the effects of 10% ketamine hydrochloride and 0.5% diazepam on intraocular pressure (IOP) and horizontal pupil diameter (HPD) in the canine eye. Procedures Ten healthy dogs for each treatment group were used in this study. In the first group, 20 mg/kg ketamine hydrochloride was injected intravenously; in the second, 0.5 mg/kg diazepam was similarly injected; and in the third, a control group, 0.9% saline was used. In all groups, IOP and HPD were measured every 5 min for 35 min in the first group, and 60 min in the second and third group. Results A maximum increase in IOP was obtained 5 min after ketamine injection, with IOP of 23.2 ± 5.8 mmHg (a 45.0% increase compared to baseline) in the right eye and 22.9 ± 5.9 mmHg (a 43.5% increase) in the left eye (both significant at P < 0.01). A significant IOP increase was observed throughout the research period of 35 min. Statistically significant increases in HPD (P < 0.05) were observed only at 5 and 25 min after ketamine injection. A significant increase in IOP was obtained 10 min after diazepam injection, showing a maximum IOP 20 ± 5.0 mmHg in the right eye (9.3% increase) and 19.9 ± 5.1 mmHg (8.7% increase) in the left eye (both significant at P < 0.05). HPD decreased during the study period, reaching the lowest level 30 min post‐treatment. Conclusions This study showed a substantial increase in IOP after ketamine injection and a less substantial, but still significant increase after diazepam injection. These findings should be taken into consideration when using these drugs in dogs with fragile corneas, or in dogs predisposed or affected by glaucoma.     

Pharmacokinetics of midazolam administered concurrently with ketamine after intravenous bolus or infusion in dogs

Brown, S.A., Jacobson, J.D., Hartsfield, S.M. Pharmacokinetics of midazolam administered concurrently with ketamine after intravenous bolus or infusion in dogs. J. vet. Pharmacol. Therap. 16 , 419–425. Midazolam, a water-soluble benzodiazepine tranquilizer, has been considered by some veterinary anaesthesiologists to be suitable as a combination anaesthetic agent when administered concurrently with ketamine because of its water solubility and miscibility with ketamine. However, the pharmacokinetics of midazolam have not been extensively described in the dog. Twelve clinically healthy mixed breed dogs (22.2–33.4 kg) were divided into two groups at random and were administered ketamine (10 mg/kg) and midazolam (0.5 mg/kg) either as an intravenous bolus over 30 s (group 1) or as an i.v. infusion in 0.9% NaCl (2 ml/kg) over 15 min. Blood samples were obtained immediately before the drugs were injected and periodically for 6 h afterwards. Serum concentrations were determined using gas chromatography with electron-capture detection. Serum concentrations were best described using a two-compartment open model and indicated a t_½α of 1.8 min and t_½β.p of 27.8 min after i.v. bolus, and t_½α f 1–35 min and t_½β of 31.6 min after i.v. infusion. The calculated pharmacokinetic coefficient B was significantly smaller after i.v. infusion (429 ± 244 ng/ml) than after i.v. bolus (888 ± 130 ng/ml, P = 0.004). Furthermore, AUC was significantly smaller after i.v. infusion (29 800 ±6120 ng/h/ml) than after i.v. bolus (42 500 ± 8460 ng/h/ml, P < 0.05), resulting in a larger Cl_B after i.v. infusion (17.4 ± 4.00 ml/min/kg than after i.v. bolus (12.1 ± 2.24 ml/min/kg, P < 0.05). No other pharmacokinetic value was significantly affected by rate of intravenous administration.     

Effects of Intravenous Detomidine on Intraocular Pressure Readings Obtained by Applanation Tonometry in Clinically Normal Horses

This study was conducted to determine effects of intravenous detomidine on intraocular pressure (IOP) readings obtained by applanation tonometry in clinically normal horses. Twenty horses were randomly divided into two groups of 10 each (treatment and control). All horses in the treatment group received intravenous detomidine alone (20 μg/kg). The horses in the control group received only intravenous saline (0.2 mL/100 kg). The IOP values were measured before the treatment (T₀) and then at 5 (T₅), 20 (T₂₀), 60 (T₆₀), and 120 (T₁₂₀) minutes after drug administration in both groups. A significant decrease in IOP values was observed in both right and left eyes of the horses in the treatment group at T₅, T₂₀, and T₆₀ in comparison with the baseline values (P < .001). The observed decrease was only statistically significant in the right eyes of the treatment group horses at T₁₂₀ (P = .044). Mean IOP was not significantly altered at any time point during the treatment period compared with the baseline evaluations in both eyes of the horses in the control group. This study demonstrates that the use of intravenous detomidine lowers IOP quickly.     

Effects of ketamine‐diazepam and ketamine‐acepromazine combinations on intraocular pressure in rabbits

ObjectiveTo determine the effects of ketamine-diazepam and ketamine-acepromazine combinations on intraocular pressure (IOP) in rabbits.Study designRandomized clinical trial.AnimalsSixteen adult New Zealand white rabbits approximately one year old, weighing 2.3 ± 0.2 kg were used in this study.MethodsThe animals were randomly divided into two groups of eight each (KA and KD). The pre-treatment IOPs were recorded in both groups (T0). All rabbits in group KA received intramuscular ketamine-acepromazine (ketamine 30 mg kg^?1+ acepromazine 0.5 mg kg^?1). Ketamine-diazepam (ketamine 30 mg kg^?1 + diazepam 1 mg kg^?1) was administered intramuscularly in members of group KD. The IOP values were measured at 5 (T₅), 15 (T₁₅), and 20 (T₂₀) minutes after drug administration in both treatment groups.ResultsSignificant increases in IOP values were observed in both treatment groups at T_5, T₁₅, and T₂₀ in comparison to the baseline values. In group KA the mean ± SD IOP at T_5, T₁₅, and T₂₀ were 37 ± 13 (p < 0.001), 35 ± 4 (p < 0.001) and 34 ± 4 mmHg (p < 0.001). The post-treatment mean ± sd values in group KD were 23 ± 8 (p = 0.002), 23 ± 5 (p < 0.001) and 23 ± 6 mmHg (p = 0.001) at 5, 15, and 20 minutes respectively.Conclusion and clinical relevanceBoth ketamine-diazepam and ketamine-acepromazine combinations increased IOP after intramuscular administration in rabbits.     

Effects of Intravenous Detomidine on Schirmer Tear Test Results in Clinically Normal Horses

This study was conducted to determine the effects of intravenous detomidine on Schirmer tear test (STT) results in clinically normal horses. Eighteen adult horses were randomly divided into two groups of nine horses each. The treatment group was sedated with intravenous detomidine alone (20 μg/kg), and the control group received only intravenous saline (0.2 mL/100 kg). Schirmer tear test was performed just before intravenous administration of detomidine or saline in treatment and control groups, respectively. Schirmer tear tests were repeated 5, 20, 60, and 120 minutes later. Horses enrolled in this study consisted of nine males and nine females. Breeds were Arabian and Hanoverian, ranging from 3 to 6 years in age. In the treatment group, the pretreatment and subsequent posttreatment mean ± standard deviation values were 17.0 ± 6.9 (0 minutes), 11.8 ± 2.9 (5 minutes), 12.1 ± 2.0 (20 minutes), 12.1 ± 3.1 (60 minutes), and 15.0 ± 2.8 (120 minutes) mm wetting/min. In this group of horses, a significant reduction was observed in STT values at 5, 20, and 60 minutes after treatment with detomidine hydrochloride in comparison to the pretreatment values (analysis of variance with post hoc testing; P₅ = 0.004, P₂₀ = 0.007, P₆₀ = 0.006). There was no significant difference between baseline values and posttreatment values in the control saline group (P ≥ .08). We conclude that intravenous detomidine causes a significant reduction in STT values in clinically normal horses. In horses, practitioners should measure STT values before intravenous administration of detomidine to accurately assess the results.     

The pharmacokinetics of midazolam after intravenous,intramuscular, and rectal administration in healthy dogs

Intravenous benzodiazepines are utilized as first‐line drugs to treat prolonged epileptic seizures in dogs and alternative routes of administration are required when venous access is limited. This study compared the pharmacokinetics of midazolam after intravenous (IV), intramuscular (IM), and rectal (PR) administration. Six healthy dogs were administered 0.2 mg/kg midazolam IV, IM, or PR in a randomized, 3‐way crossover design with a 3‐day washout between study periods. Blood samples were collected at baseline and at predetermined intervals until 480 min after administration. Plasma midazolam concentrations were measured by high‐pressure liquid chromatography with UV detection. Rectal administration resulted in erratic systemic availability with undetectable to low plasma concentrations. Arithmetic mean values ± SD for midazolam peak plasma concentrations were 0.86 ± 0.36 μg/mL (C₀) and 0.20 ± 0.06 μg/mL (C_max), following IV and IM administration, respectively. Time to peak concentration (T_max) after IM administration was 7.8 ± 2.4 min with a bioavailability of 50 ± 16%. Findings suggest that IM midazolam might be useful in treating seizures in dogs when venous access is unavailable, but higher doses may be needed to account for intermediate bioavailability. Rectal administration is likely of limited efficacy for treating seizures in dogs.     

Hemodynamic Effects of Epidural Ketamine in Isoflurane-Anesthetized Dogs

Objective —The purpose of this study was to determine the hemodynamic effects of epidural ketamine administered during isoflurane anesthesia in dogs. Study Design —Prospective, single-dose trial. Animals —Six healthy dogs (five males, one female) weighing 25.3 ± 3.88 kg. Methods —Once anesthesia was induced, dogs were maintained at 1.5 times the predetermined, individual minimum alveolar concentration (MAC) of isoflurane. Dogs were instrumented and allowed to stabilize for 30 minutes before baseline measurements were recorded. Injection of 2 mg/kg of ketamine in 1 mL saline/4.5 kg body weight was then performed at the lumbosacral epidural space. Hemodynamic data were recorded at 5, 10, 15, 20, 30, 45, 60, and 75 minutes after epidural ketamine injection. Statistical analysis included an analysis of variance (ANOVA) for repeated measures over time. All data were compared with baseline values. A P < .05 was considered significant. Results —Baseline values ±standard error of the mean (X ± SEM) for heart rate, mean arterial pressure, mean pulmonary artery pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, stroke index, systemic vascular resistance, pulmonary vascular resistance, and rate-pressure product were 108 ± 6 beats/min, 85 ± 10 mm Hg, 10 ± 2 mm Hg, 3 ± 1 mm Hg, 5 ± 2 mm Hg, 2.3 ± 0.3 L/min/m², 21.4 ± 1.9 mL/beat/m², 3386 ± 350 dynes/sec/cm⁵, 240 ± 37 dynes/sec/cm⁵, and 12376 ± 1988 beats/min±mm Hg. No significant differences were detected from baseline values at any time after ketamine injection. Conclusions —The epidural injection of 2 mg/kg of ketamine is associated with minimal hemodynamic effects during isoflurane anesthesia. Clinical Relevance —These results suggest that if epidural ketamine is used for analgesia in dogs, it will induce minimal changes in cardiovascular function.     

Comparison between S(+) ketamine–diazepam and S(+) ketamine–midazolam on anesthetic induction and recovery in dogs

S(+) ketamine, one of the two enantiomers of racemic ketamine, is a phencyclidine derivative that induces amnesia and analgesia. Its activity is related to blockade of NMDA receptors and some opioid action. We compared anesthetic induction and recovery quality with S(+) ketamine in combination with diazepam or midazolam in 10 dogs (ASA 1) admitted for elective surgery. After all clinical examinations, the dogs were separated into two groups (G I and G II). All animals received acepromazine (0.1 mg kg^?1) and fentanyl (5 µg kg^?1) IM, 20 minutes before induction with S(+) ketamine (6 mg kg^?1) and diazepam (0.5 mg kg^?1) IV (G I) or midazolam 0.2 mg kg^?1 (G II) IV. The doses of diazepam and midazolam were chosen according to the literature. All dogs were intubated and then maintained with halothane in oxygen at a vaporizer setting sufficient to maintain surgical anesthesia. Quality of induction, time needed for intubation, heart rate, respiratory rate, SpO₂, time to extubation, and quality of recovery were evaluated. The results were analyzed by Student's t‐test. Smooth induction and recovery were observed in all animals. The time to intubation was 45 ± 20 (GI) and 25 ± 6 seconds (GII), HR was 122 ± 12 (GI) and 125 ± 7 beats minute^?1 (GII), RR was 17 ± 2 (GI) and 21 ± 3 breaths minute^?1 (GII), SpO₂ was 96 ± 2 (GI) and 94 ± 1% (GII), time to extubation was 7 ± 3 (GI) and 4 ± 1 minutes (GII). No statistical differences were found in analyses, although time to intubation was less in GII. The results suggested that both combinations could be used safely for anesthetic induction in healthy dogs.     

Effect of anesthetic induction with propofol,alfaxalone or ketamine on intraocular pressure in cats: a randomized masked clinical investigation

ObjectiveTo compare the effect of propofol, alfaxalone and ketamine on intraocular pressure (IOP) in cats.Study designProspective, masked, randomized clinical trial.AnimalsA total of 43 ophthalmologically normal cats scheduled to undergo general anesthesia for various procedures.MethodsFollowing baseline IOP measurements using applanation tonometry, anesthesia was induced with propofol (n = 15), alfaxalone (n = 14) or ketamine (n = 14) administered intravenously to effect. Then, midazolam (0.3 mg kg^?1) was administered intravenously and endotracheal intubation was performed without application of topical anesthesia. The IOP was measured following each intervention. Data was analyzed using one-way anova and repeated-measures mixed design with post hoc analysis. A p-value <0.05 was considered significant.ResultsMean ± standard error IOP at baseline was not different among groups (propofol, 18 ± 0.6; alfaxalone, 18 ± 0.7; ketamine, 17 ± 0.5 mmHg). Following induction of anesthesia, IOP increased significantly compared with baseline in the propofol (20 ± 0.7 mmHg), but not in the alfaxalone (19 ± 0.8 mmHg) or ketamine (16 ± 0.7 mmHg) groups. Midazolam administration resulted in significant decrease from the previous measurement in the alfaxalone group (16 ± 0.7 mmHg), but not in the propofol group (19 ± 0.7 mmHg) or the ketamine (16 ± 0.8 mmHg) group. A further decrease was measured after intubation in the alfaxalone group (15 ± 0.9 mmHg).Conclusions and clinical relevancePropofol should be used with caution in cats predisposed to perforation or glaucoma, as any increase in IOP should be avoided.     

WHICH AIRWAY PRESSURE SHOULD BE APPLIED DURING BREATH‐HOLD IN DOGS UNDERGOING THORACIC COMPUTED TOMOGRAPHY?

This randomized controlled trial study aimed to identify the optimal positive pressure (PP) level that can clear atelectasis while avoiding pulmonary hyperinflation during the breath‐hold technique in dogs undergoing thoracic computed tomography (CT). Sixty dogs affected by mammary tumors undergoing thoracic CT for the screening of pulmonary metastases were randomly assigned to six groups with different levels of PP during the breath‐hold technique: 0 (control), 5 (PP5), 8 (PP8), 10 (PP10), 12 (PP12), and 15 (PP15) cmH₂O. The percentage of atelectatic lung region was lower in the PP10 (3.7 ± 1.1%; P = 0.002), PP12 (3.4 ± 1.3%; P = 0.0001), and PP15 (2.8 ± 0.9%; P = 0.006) groups than in the control group (5.0 ± 2.3%), and the percentage of poorly aerated lung region was lower in the PP8 (15.1 ± 2.6%; P = 0.0009), PP10 (13.0 ± 2.0 %; P = 0.002), PP12 (13.0 ± 2.2 %; P = 0.0002), and PP15 (11.1 ± 1.9%; P = 0.0002) groups than in the control group (19.8 ± 5.0). The percentage of normally aerated lung region, however, was higher in the PP10 (79.7 ± 4.1%; P = 0.005), PP12 (79.8 ± 5.1%; P = 0.0002), and PP15 (80.2 ± 4.9%; P = 0.002) groups than in the control group (73.4 ± 6.6%). A PP of 10–12 cmH₂O during the breath‐hold technique should be considered to improve lung aeration during a breath‐hold technique in dogs undergoing thoracic CT.     

Effects of topical administration of 1% brinzolamide on intraocular pressure in clinically normal horses

Reasons for performing study: Only few drugs with limited efficacy are available for topical treatment of equine glaucoma. Objective: To evaluate the effect of topical administration of 1% brinzolamide on intraocular pressure (IOP) in clinically normal horses. Methods: Healthy mature horses (n = 20) with normal ocular findings, were studied. The IOP was measured 5 times daily (07.00, 11.00, 15.00, 19.00 and 23.00 h) over 10 days. On Days 1 and 2, baseline values were established. On Days 3–5 one eye of each horse was treated with one drop of 1% brinzolamide every 24 h immediately following the 07.00 h measurement. On Days 6–8 the same eye was treated with 1% brinzolamide every 12 h (07.00 and 19.00 h). Measurements on Days 9 and 10 documented the return of IOP to baseline values. Statistical analysis of the data was performed. Results: In the treated eye a significant decrease in IOP compared to baseline values was noted during both the 24 and 12 h dosing periods (P<0.001). During the once‐daily treatment protocol an IOP reduction of 3.1 ±1.3 mmHg (14%) from baseline was recorded. During the twice‐daily protocol a total IOP reduction of 5.0 ± 1.5 mmHg (21%) was achieved. Conclusion: Intraocular pressure was significantly decreased by 1% brinzolamide in a once‐daily and a twice‐daily treatment protocol in normotensive eyes. These findings suggest that brinzolamide might also be effective in horses with an elevated IOP. Potential relevance: This drug may be useful for treatment of equine glaucoma.     

Lithium dilution cardiac output and oxygen delivery in conscious dogs with systemic inflammatory response syndrome

Objective: Compare cardiac index (CI) and oxygen delivery index (DO₂I) in conscious, critically ill dogs to control dogs; evaluate the association of CI and DO₂I with outcome. Design: Prospective non‐randomized clinical study. Setting: Veterinary teaching hospital. Animals: Eighteen client‐owned dogs with systemic inflammatory response syndrome (SIRS) and 8 healthy control dogs. Measurements and Main Results: CI of dogs with SIRS was measured using lithium dilution at times 0, 4, 8, 16, and 24 hours. Data collected included physical exam, arterial blood gas (ABG) and hemoximetry. CI of control dogs was measured 3 times with 1 measurement of ABG. Mean CI ± SE in SIRS patients was 3.32 ± 0.95 L/min/m²; lower than controls at 4.18 ± 0.22 L/min/m² (P<0.001). Mean DO₂I ± SE in SIRS patients was 412.91 ± 156.67 mL O₂/min/m²; lower than controls at 785.24 ± 45.99 mL O₂/min/m² (P<0.001). There was no difference in CI (P=0.49) or DO₂I (P=0.51) for dogs that survived to discharge versus those that did not. There was no difference in mean CI (P=0.97) or DO₂I (P=0.50) of survivors versus non‐survivors for 28‐day survival. Survivors had lower blood glucose (P=0.03) and serum lactate concentrations (P=0.04) than non‐survivors. Conclusions: CI and DO₂I in conscious dogs with SIRS were lower than control dogs, which differs from theories that dogs with SIRS are in a high cardiac output state. CI and DO₂I were not significantly different between survivors and non‐survivors. Similar to previous studies, lactate and glucose concentrations of survivors were lower than non‐survivors.     

Dexmedetomidine and midazolam interaction is synergistic with isoflurane and additive with halothane in terms of MAC reduction

Dexmedetomidine and midazolam have synergistic interaction for the sedative/hypnotic and analgesic effects. The purpose of this study was to assess the type of interaction between dexmedetomidine and midazolam for the immobilizing effect in terms of MAC reduction of either halothane (HAL) or isoflurane (ISO). Fifty‐six rats were randomly allocated into one of eight groups (n = 7): SAL + HAL group received saline solution and halothane, SAL + ISO group received saline solution and isoflurane, DEX + HAL group received an intravenous continuous infusion of dexmedetomidine (0.25 μg kg^–1minute^–1) and halothane, DEX + ISO group received an intravenous continuous infusion of dexmedetomidine (0.25 μg kg^–1 minute^–1) and isoflurane, MID + HAL group received an intravenous bolus of midazolam (1 mg kg^–1) and halothane, MID + ISO group received an intravenous bolus of midazolam (1 mg kg^–1) and isoflurane, DEX +MID + HAL group received dexmedetomidine (0.25 μg kg^–1 minute^–1), midazolam (1 mg kg^–1) and halothane and DEX + MID + ISO group received dexmedetomidine (0.25 μg kg^–1 minute^–1), midazolam (1 mg kg^–1) and isoflurane. The tail clamp method was used for MAC determination. Heart rate, invasive arterial blood pressure, respiratory rate and rectal temperature were continuously monitored. Arterial blood gases were analyzed at the end of each experiment. Data were analyzed using a one‐way anova and a Tukey‐Kramer test for multiple comparisons. A p < 0.01 value was considered statistically significant. MAC values were adjusted to the barometric pressure at sea level. Control MAC_bar values expressed as mean ± SD were 1.31 ± 0.11% for HAL and 1.46 ± 0.05% for ISO. Percentages of MAC reduction were 72 ± 17% for HAL and 43 ± 14% for ISO in DEX groups, 26 ± 11% for HAL and 20 ± 9% for ISO in MID groups, and 90 ± 5% for HAL and 78 ± 5% for ISO in DEX + MID groups. The interaction between dexmedetomidine and midazolam in terms of MAC reduction can be described as additive with halothane and synergistic with isoflurane.     

Effect of medetomidine-butorphanol and dexmedetomidine-butorphanol combinations on intraocular pressure in healthy dogs

ObjectiveTo assess the effects of intravenous (IV) medetomidine-butorphanol and IV dexmedetomidine-butorphanol on intraocular pressure (IOP).Study designProspective, randomized, blinded clinical study.AnimalsForty healthy dogs. Mean ± SD body mass 37.6 ± 6.6 kg and age 1.9 ± 1.3 years.MethodsDogs were allocated randomly to receive an IV combination of dexmedetomidine, 0.3 mg m^?2, combined with butorphanol, 6 mg m^?2, (group DEX) or medetomidine 0.3 mg m^?2, combined with butorphanol 6 mg m^?2, (group MED). IOP and pulse (PR) and respiratory (f_R) rates were measured prior to (baseline) and at 10 (T10), 20 (T20), 30 (T30) and 40 (T40) minutes after drug administration. Oxygen saturation of hemoglobin (SpO₂) was monitored following sedation. Data were analyzed by anova followed by Dunnett's tests for multiple comparisons. Changes were considered significant when p < 0.05.ResultsFollowing drug administration, PR and f_R were decreased significantly at all time points but did not differ significantly between groups. Baseline IOP in mmHg was 14 ± 2 for DEX and 13 ± 2 for MED. With both treatments, at T10, IOP increased significantly (p < 0.001), reaching 20 ± 3 and 17 ± 2 for DEX and MED respectively. This value for DEX was significantly higher than for MED. There were no significant differences in IOP values between groups at any other time points. At T30 and T40, IOP in both groups was below baseline (DEX, 12 ± 2 and 11 ± 2: MED 12 ± 2 and 11 ± 2) and this was statistically significant, for DEX.Conclusions and clinical relevanceAt the documented doses, both sedative combinations induced a transient increase and subsequent decrease of IOP relative to baseline, which must be taken into consideration when planning sedation of animals in which marked changes in IOP would be undesirable.     

Effect of central corneal thickness on intraocular pressure with the rebound tonometer and the applanation tonometer in normal dogs

Objective To evaluate the effect of central corneal thickness (CCT) on the measurement of intraocular pressure (IOP) with the rebound (TonoVet^®) and applanation (TonoPen XL^®) tonometers in beagle dogs. Animal studied Both eyes of 60 clinically normal dogs were used. Procedures The IOP was measured by the TonoVet^®, followed by the TonoPen XL^® in half of the dogs, while the other half was measured in the reverse order. All CCT measurements were performed 10 min after the use of the second tonometer. Results The mean IOP value measured by the TonoVet^® (16.9 ± 3.7 mmHg) was significantly higher than the TonoPen XL^® (11.6 ± 2.7 mmHg; P < 0.001). The IOP values obtained by both tonometers were correlated in the regression analysis (γ² = 0.4393, P < 0.001). Bland–Altman analysis showed that the lower and upper limits of agreement between the two devices were ?0.1 and +10.8 mmHg, respectively. The mean CCT was 549.7 ± 51.0 μm. There was a correlation between the IOP values obtained by the two tonometers and CCT readings in the regression analysis (TonoVet^® : P = 0.002, TonoPen XL^® : P = 0.035). The regression equation demonstrated that for every 100 μm increase in CCT, there was an elevation of 1 and 2 mmHg in IOP measured by the TonoPen XL^® and TonoVet^®, respectively. Conclusions The IOP obtained by the TonoVet^® and TonoPen XL^® would be affected by variations in the CCT. Therefore, the CCT should be considered when interpreting IOP values measured by tonometers in dogs.     

Comparison of the effect of hypertonic hydroxyethyl starch and mannitol on the intraocular pressure in healthy normotensive dogs and the effect of hypertonic hydroxyethyl starch on the intraocular pressure in dogs with primary glaucoma

PURPOSE: The purpose of this study was to determine if intravenous hypertonic hydroxyethyl starch (7.5%/6%) (HES) could decrease the intraocular pressure (IOP) in healthy normotensive dogs, and compare its effect with that of mannitol (20%) (experimental study). In addition, the potential IOP-lowering effect of hypertonic HES was evaluated in six dogs with primary glaucoma (clinical study). MATERIAL AND METHODS: Experimental study: eight male ophthalmoscopically and clinically healthy Beagles were included in this study. The IOP of each dog was measured by applanation tonometry in both eyes to obtain control values at 10:00, 10:15, 10:30, 10:45, 11:00 a.m., and then every hour until 6:00 p.m. prior to the first treatment (control period). Each dog received, with at least 2-week intervals and in a random order, an intravenous (IV) infusion of 4 mL/kg hypertonic HES (1.2 g/kg NaCl; 0.96 g/kg HES) and 4 mL/kg mannitol 20% (1 g/kg) over a period of 15 min starting at 10:00 a.m. IOP was measured oculus uterque (OU) at the same time intervals as in the control study. The differences in IOP between the treatment groups and the baseline IOP (before the start of infusion), between oculus sinister (OS) and oculus dexter (OD) and between the same time points of all groups were determined with a Student's t-test for paired samples (P = 0.05). Clinical study: six dogs with primary glaucoma (representing seven eyes) received an IV infusion of 4 mL/kg hypertonic HES over a period of 15 min. IOP was measured before and 15 and 30 min after starting the infusion. RESULTS: Experimental study: no significant difference between IOP of both eyes was found. A significant decrease in IOP from baseline value was recorded at 15, 30, 45, and 60 min after the start of mannitol infusion (mean amplitude in IOP decrease 3.21 mmHg; P < 0.05) and at 15 and 30 min in dogs treated with HES (mean amplitude in IOP decrease 2.43 mmHg; P < 0.05). At 120 and 180 min there was a significantly higher IOP (P < 0.05) in HES treatment group compared to the values of the control group. Clinical study: in 5/7 eyes diagnosed with primary glaucoma a maximum decrease in IOP of an average of 24% from the baseline value (IOP before start of the infusion) was observed (range of decrease 2-21 mmHg). In three of these five cases the maximum decrease was reached at 15 min and in two cases at 30 min. In one case an increase in IOP of 35% (+ 18 mmHg) was seen after 15 min and 26% (+ 13 mmHg) after 30 min. Case 4 showed an increase in IOP of 5% (+ 3 mmHg) after 15 min and a decrease of 6% (- 4 mmHg) after 30 min. CONCLUSIONS: Intravenous hypertonic HES is comparable to intravenous mannitol 20% in lowering the intraocular pressure in healthy normotensive dogs. But this effect lasted half an hour longer after mannitol. In 6/7 eyes with primary glaucoma, hypertonic HES decreased IOP.     

Schirmer tear tests and intraocular pressures in conscious and anesthetized koalas (Phascolarctus cinereus)

Objective To estimate mean Schirmer tear test (STT) and intraocular pressure (IOP) values in healthy koalas both conscious and anesthetized. Methods Data were gathered from koalas in Victoria, Australia. Conscious examinations were performed on captive koalas. Free‐ranging (wild) koalas were examined under anesthesia. Anesthesia was induced using alfaxalone, and animals were maintained on oxygen and isoflurane if required. All animals were healthy and had no surface ocular pathology detectable during slit lamp biomicroscopy. STT I tests were performed using commercial STT test strips placed in the lower fornix for 1 min. IOP was measured using an applanation tonometer after topical anesthesia. The higher value of the two eyes for both STT and IOP was analyzed. STT was measured in 53 koalas (34 conscious, 19 anesthetized) and IOP was measured in 43 koalas (30 conscious, 13 anesthetized). A two‐sample t‐test was used to compare means. A P‐value <0.05 was regarded as significant. Mean ± SD is presented. Results The mean higher STT in conscious koalas was 10.3 ± 3.6 mm wetting/min and in anesthetized koalas it decreased to 3.8 ± 4.0 mm wetting/min (P < 0.0001). The mean higher IOP in conscious koalas was 15.3 ± 5.1 mmHg, and in anesthetized koalas it was 13.8 ± 3.4 mmHg (P = 0.32). There was no effect of sex on either STT or IOP. Conclusions The mean and SD of STT and IOP values for koalas both conscious and anesthetized were reported. The mean STT was significantly reduced by alfaxalone anesthesia.     

Effects of ketamine, diazepam, and their combination on intraocular pressures in clinically normal dogs

OBJECTIVE: To evaluate the effects of ketamine, diazepam, and the combination of ketamine and diazepam on intraocular pressures (IOPs) in clinically normal dogs in which premedication was not administered. ANIMALS: 50 dogs. PROCEDURES: Dogs were randomly allocated to 1 of 5 groups. Dogs received ketamine alone (5 mg/kg [KET5] or 10 mg/kg [KET10], IV), ketamine (10 mg/kg) with diazepam (0.5 mg/kg, IV; KETVAL), diazepam alone (0.5 mg/kg, IV; VAL), or saline (0.9% NaCl) solution (0.1 mL/kg, IV; SAL). Intraocular pressures were measured immediately before and after injection and at 5, 10, 15, and 20 minutes after injection. RESULTS: IOP was increased over baseline values immediately after injection and at 5 and 10 minutes in the KET5 group and immediately after injection in the KETVAL group. Compared with the SAL group, the mean change in IOP was greater immediately after injection and at 5 and 10 minutes in the KET5 group. The mean IOP increased to 5.7, 3.2, 3.1, 0.8, and 0.8 mm Hg over mean baseline values in the KET5, KET10, KETVAL, SAL, and VAL groups, respectively. All dogs in the KET5 and most dogs in the KETVAL and KET10 groups had an overall increase in IOP over baseline values. CONCLUSIONS AND CLINICAL RELEVANCE: Compared with baseline values and values obtained from dogs in the SAL group, ketamine administered at a dose of 5 mg/kg, IV, caused a significant and clinically important increase in IOP in dogs in which premedication was not administered. Ketamine should not be used in dogs with corneal trauma or glaucoma or in those undergoing intraocular surgery.     

The effect of a single dose of topical 0.005% latanoprost and 2% dorzolamide/0.5% timolol combination on the blood-aqueous barrier in dogs: a pilot study

Objective To determine the effects of 0.005% latanoprost and 2% dorzolamide/0.5% timolol on the blood‐aqueous barrier (BAB) in normal dogs. Animals studied Eight mixed‐breed and pure‐breed dogs. Procedures Baseline anterior chamber fluorophotometry was performed on eight normal dogs. Sodium fluorescein was injected and the dogs were scanned 60–90 min post‐injection. Seventy‐two hours following the baseline scan, one eye received one drop of latanoprost. Fluorophotometry was repeated 4 h after drug administration. Following a washout period, the identical procedure was performed 4 h after the administration of dorzolamide/timolol. The degree of BAB breakdown was determined by comparing the concentrations of fluorescein within the anterior chamber before and after drug administration. BAB breakdown was expressed as a percentage increase in the post‐treatment fluorescein concentration over the baseline concentration: %INC [Fl] = {([Fl]_post – [Fl]_baseline)/[Fl]_baseline} × 100. The percentage increase in fluorescein concentration in the treated eye was compared to that in the nontreated eye using a paired t‐test with significance set at P ≤ 0.05. Results Following administration of latanoprost, the fluorescein in the treated eyes increased 49% (± 58%) from baseline compared to 10% (± 31%) in the untreated eyes (P = 0.016). Following administration of dorzolamide/timolol, the fluorescein concentration increased 38% (± 54%) compared to baseline vs. 24% (± 38%) in the untreated eyes (P = 0.22). Conclusions The results of this study show that topical latanoprost may cause BAB disruption in normal dogs while topical dorzolamide/timolol may have no effect on the BAB in normal dogs.     

Continuous infusion of ketamine in hypovolemic dogs anesthetized with desflurane

Objective: To evaluate the cardiorespiratory effects of continuous infusion of ketamine in hypovolemic dogs anesthetized with desflurane. Design: A prospective experimental study. Animals: Twelve mixed breed dogs allocated into 2 groups: saline (n=6) and ketamine (n=6). Interventions: After obtaining baseline measurements (time [T] 0) in awake dogs, hypovolemia was induced by the removal of 40 mL of blood/kg over 30 minutes. Anesthesia was induced and maintained with desflurane (1.5 minimal alveolar concentration) and 30 minutes later (T75) a continuous intravenous (IV) infusion of saline or ketamine (100 μg/kg/min) was initiated. Cardiorespiratory evaluations were obtained 15 minutes after hemorrhage (T45), 30 minutes after desflurane anesthesia, and immediately before initiating the infusion (T75), and 5 (T80), 15 (T90), 30 (T105) and 45 (T120) minutes after beginning the infusion. Measurements and main results: Hypovolemia (T45) reduced the arterial blood pressures (systolic arterial pressure, diastolic arterial pressure [DAP] and mean arterial pressure [MAP]), cardiac (CI) and systolic (SI) indexes, and mean pulmonary arterial pressure (PAP) in both groups. After 30 minutes of desflurane anesthesia (T75), an additional decrease of MAP in both groups was observed, heart rate was higher than T0 at T75, T80, T90 and T105 in saline‐treated dogs only, and the CI was higher in the ketamine group than in the saline group at T75. Five minutes after starting the infusion (T80), respiratory rate (RR) was lower and the end‐tidal CO₂ (ETCO₂) was higher compared with values at T45 in ketamine‐treated dogs. Mean values of ETCO₂ were higher in ketamine than in saline dogs between T75 and T120. The systemic vascular resistance index (SVRI) was decreased between T80 and T120 in ketamine when compared with T45. Conclusions: Continuous IV infusion of ketamine in hypovolemic dogs anesthetized with desflurane induced an increase in ETCO₂, but other cardiorespiratory alterations did not differ from those observed when the same concentration of desflurane was used as the sole anesthetic agent. However, this study did not evaluate the effectiveness of ketamine infusion in reducing desflurane dose requirements in hypovolemic dogs or the cardiorespiratory effects of ketamine–desflurane balanced anesthesia.