ABSTRACT
Avian ocular disease may be primary or a manifestation of systemic disease. Various infectious and noninfectious diseases have been reported to cause ocular pathology. Thorough physical examination and diagnostic testing are necessary to determine a treatment plan.
Subject(s)
Bird Diseases/diagnosis , Blepharitis/veterinary , Conjunctivitis/veterinary , Corneal Diseases/veterinary , Keratitis/veterinary , Animals , Bird Diseases/etiology , Bird Diseases/therapy , Birds , Blepharitis/diagnosis , Blepharitis/etiology , Blepharitis/therapy , Conjunctivitis/diagnosis , Conjunctivitis/etiology , Conjunctivitis/therapy , Cornea/anatomy & histology , Corneal Diseases/diagnosis , Corneal Diseases/etiology , Corneal Diseases/therapy , Keratitis/diagnosis , Keratitis/etiology , Keratitis/therapy , OphthalmologyABSTRACT
OBJECTIVE: To determine if topical ophthalmic diclofenac sodium 0.1% solution alters renal parameters in the domestic chicken, and to determine if the drug is detectable in plasma after topical ophthalmic administration. ANIMALS: Thirty healthy domestic chickens. PROCEDURES: Over 7 days, six birds were treated unilaterally with one drop of artificial tear solution (group 1), 12 birds were treated unilaterally (group 2) and 12 bilaterally (group 3) with diclofenac sodium 0.1% ophthalmic solution. Treatments were provided every 12 h in all groups. Pre- and post-treatment plasma samples from all birds were evaluated for changes in albumin, total protein, and uric acid. Post-treatment samples of all birds, collected 15 min post-administration, were analyzed by high-performance liquid chromatography with mass spectrometry for diclofenac sodium detection. A randomly selected renal sample from each group was submitted for histopathologic review. RESULTS: Changes in pre- and post-treatment plasma albumin were significant (P < 0.05) in groups 2 and 3, but not for group 1. Pre- and post-treatment changes in total protein and uric acid were not significant for any group. Diclofenac sodium was not detectable (limit of detection = 0.10 ng/mL) in plasma samples from birds in group 1. Post-treatment concentration of diclofenac in group 3 was statistically greater than group 2 (P = 0.0008). Histopathologic changes did not identify diclofenac-induced acute renal tubular necrosis. CONCLUSIONS: Ophthalmic diclofenac sodium 0.1% administered topically every 12 h in one or both eyes for 7 days is detectable in systemic circulation in the domestic chicken, but does not cause overt significant changes in plasma uric acid or total protein.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/pharmacokinetics , Diclofenac/pharmacokinetics , Ophthalmic Solutions/pharmacokinetics , Administration, Ophthalmic , Animals , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Anti-Inflammatory Agents, Non-Steroidal/blood , Biological Availability , Chickens , Diclofenac/adverse effects , Diclofenac/blood , Female , Kidney/drug effects , Ophthalmic Solutions/adverse effects , Serum Albumin/metabolism , Uric Acid/metabolismABSTRACT
OBJECTIVE: To evaluate the effect of topical ophthalmic 0.005% latanoprost alone and in combination with 0.1% diclofenac on healthy horses. ANIMALS STUDIED: Twelve healthy adult horses. PROCEDURES: A randomized, masked crossover design was used with horses divided into three groups for once daily treatment in one randomly selected eye. For arm 1 of the study, Group D (n = 3) received 0.1% diclofenac, Group L (n = 3) received 0.005% latanoprost, and Group DL (n = 6) received 0.005% latanoprost and 0.2 ml of 0.1% diclofenac. For arm 2 of the study, horses from Group D and L were placed into Group DL and horses from Group DL were placed into either Group D or L. Evaluations of intraocular pressure (IOP), vertical pupil diameter, aqueous flare, conjunctival hyperemia, epiphora, blepharospasm, and blepharoedema were performed 4 times daily on days 1 and 2 (baseline), days 3 to 7 (arm 1 treatment), days 8 to 11 (washout), days 12 to 16 (arm 2 treatment), and days 17 and 18 (return to baseline). RESULTS: During the treatment period, significant reduction in IOP and vertical pupil diameter occurred in treated eyes of Groups L and DL, but not Group D. These variables did not differ significantly between Groups L and DL. Blepharospasm, blepharoedema, epiphora, and conjunctival hyperemia scores were significantly higher in Group L than in Groups D and DL. CONCLUSIONS: Latanoprost reduced IOP in healthy horses and signs of drug-induced discomfort were mitigated by concurrent use of diclofenac.
Subject(s)
Antihypertensive Agents/pharmacology , Diclofenac/pharmacology , Intraocular Pressure/drug effects , Ophthalmic Solutions/pharmacology , Prostaglandins F, Synthetic/pharmacology , Administration, Topical , Animals , Antihypertensive Agents/administration & dosage , Diclofenac/administration & dosage , Double-Blind Method , Drug Therapy, Combination/veterinary , Horses , Latanoprost , Ophthalmic Solutions/administration & dosage , Pilot Projects , Prostaglandins F, Synthetic/administration & dosage , Pupil/drug effectsABSTRACT
OBJECTIVE: To describe cases of suspected anticoagulant rodenticide toxicity manifesting with predominantly ocular signs. MATERIALS AND METHODS: Six canine cases that presented to veterinary referral hospitals for ocular abnormalities and were diagnosed with suspected or confirmed anticoagulant rodenticide ingestion were reviewed for commonalities in presentation and outcome. RESULTS: Five dogs had unilateral ocular signs and one dog had bilateral manifestations. Signs included subconjunctival hemorrhage, exophthalmos, and commonly orbital pain without other significant physical examination findings. Prothrombin time was measured in 5 of 6 dogs and was prolonged in all. Partial thromboplastin time was measured in 4 of 6 dogs and was prolonged in all. Complete blood cell count and serum chemistry profiles demonstrated mild, if any, abnormalities. Five dogs had known anticoagulant rodenticide exposure, and rodenticide ingestion was suspected in 1 additional case based on clinical signs, clinical pathologic abnormalities, and response to treatment. Five of 6 cases were hospitalized overnight for plasma transfusions along with oral or injectable vitamin K1 , and all dogs were treated with oral vitamin K1 for 30 days. All dogs experienced complete resolution of clinical signs within 6 weeks of initiating treatment. CONCLUSIONS: Anticoagulant rodenticide toxicity can present with predominantly ocular manifestations. Rodenticide ingestion should be considered in dogs with unilateral or bilateral subconjunctival hemorrhage, exophthalmos, and orbital pain.
Subject(s)
Anticoagulants/poisoning , Dog Diseases/chemically induced , Eye Diseases/veterinary , Rodenticides/poisoning , Animals , Dogs , Eye Diseases/chemically induced , Female , Male , Retrospective StudiesABSTRACT
OBJECTIVE: To compare the effect of commercially available solution and compounded ointment formulations of dorzolamide(2%)-timolol(0.5%) on intraocular pressure (IOP) of normal horses. ANIMALS: Eighteen clinically normal horses. PROCEDURES: A randomized, masked prospective design was used with horses divided into two equal groups. One eye of each horse was selected for topical ophthalmic treatment with either 0.2 mL of dorzolamide(2%)-timolol(0.5%) solution or 0.2 g of dorzolamide(2%)-timolol(0.5%) ointment every 12 h for 5 days. The contralateral eye of horses in both groups was untreated. Rebound tonometry was performed every 6 h starting 2 days prior to and ending 2 days after the treatment period. RESULTS: The mean IOP reduction in eyes treated with the solution or ointment formulations was 13%. Untreated eyes in both groups experienced a lesser but still statistically significant reduction in IOP. The IOP values did not return to baseline within 48 h of the last treatment. CONCLUSIONS AND CLINICAL RELEVANCE: The commercially available solution and compounded ointment formulations of ophthalmic dorzolamide(2%)-timolol(0.5%) had similar effects on IOP in normal horses. Persistent IOP reduction following cessation of treatment may indicate prolonged drug effect or acclimation of horses to tonometry.