OVC Pet Trust

OBJECTIVE: To prospectively assess whether multiple-site disk fenestration decreases the incidence of recurrent thoracolumbar intervertebral disk herniation (IVDH), compared with single-site disk fenestration, in small-breed dogs treated for IVDH. DESIGN: Randomized controlled clinical trial. ANIMALS: 207 client-owned dogs. PROCEDURES: Dogs undergoing decompressive surgery of the spinal cord because of thoracolumbar IVDH between 2001 and 2004 were randomly assigned to receive single-site disk fenestration at the level of surgical decompression (n = 103) or multiple-site disk fenestration of all disks from T11 through L4 (104). Follow-up consisted of complete reevaluation of patients, telephone surveys, and further surgery if signs indicative of recurrence occurred. RESULTS: 189 dogs were available for long-term follow-up: 95 dogs in the single-site disk fenestration group and 94 in the multiple-site disk fenestration group. Twenty-four dogs developed 28 confirmed episodes of recurrent thoracolumbar IVDH. The rate for first-time recurrence was 12.7% (24/189). First-time recurrence rates for single-and multiple-site disk fenestration groups were 17.89% (17/95) and 7.45% (7/94), respectively. Dogs undergoing single-site disk fenestration were significantly more likely to have recurrent thoracolumbar IVDH than were dogs undergoing multiple-site disk fenestration. Disk mineralization at the time of first surgery was associated with recurrence, and 87.5% (21/24) of recurrences occurred at a disk space adjacent to or 1 disk away from the initial lesion. Regardless of disk fenestration group, 22 of 24 (91.7%) recurrences occurred at a nonfenestrated disk space. CONCLUSIONS AND CLINICAL RELEVANCE: Multiple-site disk fenestration decreased the rate of recurrent IVDH in small-breed dogs, compared with the use of single-site disk fenestration.

OBJECTIVE: To determine effects of therapeutic dosages of aspirin, carprofen, deracoxib, and meloxicam on platelet function and systemic prostaglandin concentrations in healthy dogs. ANIMALS: 10 hound-crossbred dogs. PROCEDURES: Aspirin (10 mg/kg, PO, q 12 h), carprofen (4.4 mg/kg, PO, q 24 h), deracoxib (2 mg/kg, PO, q 24 h), meloxicam (0.1 mg/kg, PO, q 24 h), and a placebo were administered for 7 days in a random order to each of 10 healthy dogs; there was a 21-day washout period between subsequent treatments. One-stage prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen concentration, and plasma concentrations of thromboxane (TX)B(2) and 6-keto prostaglandin (PG)F(1alpha) were measured before and after treatment administration. Platelet function was assessed by use of a platelet-function analyzer and aggregation. RESULTS: Aspirin, carprofen, and meloxicam did not significantly affect platelet function. Deracoxib caused a mild decrease in platelet aggregation induced by 50microM ADP. Platelet number, Hct, PT, aPTT, and plasma TXB(2) and 6-keto PGF(1alpha) concentrations were unchanged after NSAID administration. Meloxicam administration resulted in a significant decrease in fibrinogen concentration, but results remained within the laboratory reference interval. CONCLUSIONS AND CLINICAL RELEVANCE: Oral administration of commonly used NSAIDs at therapeutic dosages in healthy dogs did not alter plasma TXB(2) and 6-keto PGF(1alpha) concentrations. Deracoxib administration resulted in a minor abnormality in platelet aggregation. Anti-inflammatory doses of aspirin did not affect platelet function as measured by use of optical aggregometry and a platelet-function analyzer. Further evaluation of the effects of aspirin and cyclooxygenase-2-selective inhibitors on hemostasis should be performed.

OBJECTIVE: To describe the effects of prednisone and acetylsalicylic acid (ASA) on results of thromboelastography in healthy dogs. ANIMALS: 16 male mixed-breed dogs. PROCEDURES: Dogs were randomly assigned to 3 treatment groups (4 dogs/group) that received prednisone (median dose, 2.07 mg/kg), ASA (median dose, 0.51 mg/kg), or both drugs, PO, every 24 hours from days 0 through 6. Another group received no treatment (control dogs; n = 4). Thromboelastography variables (reaction time, clotting time, α-angle, maximum amplitude [MA], global clot strength, coagulation index, and percentage of clot lysis at 60 minutes [CL(60)]) were evaluated in blood samples collected (prior to drug administration in treated dogs) on days 0 (baseline), 2, 4, and 6. RESULTS: Administration of ASA alone did not alter TEG variables. For treatment effect, mean global clot strength was increased in the prednisone and drug combination groups, compared with values for control dogs; MA was also increased in the prednisone and drug combination groups, compared with that of controls. For treatment-by-time effect, median CL(60) was increased in the prednisone group on day 6, compared with baseline value in the same dogs and with median CL(60) of the control group on day 6. Median CL(60) was also increased in the drug combination group on day 6, compared with the baseline value and with that of the control group on day 6. CONCLUSIONS AND CLINICAL RELEVANCE: Prednisone administered at approximately 2 mg/kg/d, PO, for 7 days with or without concurrently administered ASA increased clot strength and decreased clot lysis in healthy dogs.

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 microg/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 microg/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.

OBJECTIVE: To identify a causative mutation for dilated cardiomyopathy (DCM) in Doberman Pinschers by sequencing the coding regions of 10 cardiac genes known to be associated with familial DCM in humans. ANIMALS: 5 Doberman Pinschers with DCM and congestive heart failure and 5 control mixed-breed dogs that were euthanized or died. PROCEDURES: RNA was extracted from frozen ventricular myocardial samples from each dog, and first-strand cDNA was synthesized via reverse transcription, followed by PCR amplification with gene-specific primers. Ten cardiac genes were analyzed: cardiac actin, α-actinin, α-tropomyosin, β-myosin heavy chain, metavinculin, muscle LIM protein, myosinbinding protein C, tafazzin, titin-cap (telethonin), and troponin T. Sequences for DCM-affected and control dogs and the published canine genome were compared. RESULTS: None of the coding sequences yielded a common causative mutation among all Doberman Pinscher samples. However, 3 variants were identified in the α-actinin gene in the DCM-affected Doberman Pinschers. One of these variants, identified in 2 of the 5 Doberman Pinschers, resulted in an amino acid change in the rod-forming triple coiled-coil domain. CONCLUSIONS AND CLINICAL RELEVANCE: Mutations in the coding regions of several genes associated with DCM in humans did not appear to consistently account for DCM in Doberman Pinschers. However, an α-actinin variant was detected in some Doberman Pinschers that may contribute to the development of DCM given its potential effect on the structure of this protein. Investigation of additional candidate gene coding and noncoding regions and further evaluation of the role of α-actinin in development of DCM in Doberman Pinschers are warranted.

OBJECTIVE: To determine the effects of enteral administration of doxycycline, amoxicillin, cephalexin, and enrofloxacin at therapeutic dosages for a typical duration on hemostatic variables in healthy dogs. ANIMALS: 14 Beagles. PROCEDURE: Doxycycline (10 mg/kg, PO, q 12 h), amoxicillin (30 mg/kg, PO, q 12 h), cephalexin (30 mg/kg, PO, q 12 h), and enrofloxacin (20 mg/kg, PO, q 24 h) were administered in random order to 10 healthy dogs at standard therapeutic dosages for 7 days, with a 7-day washout period between subsequent antimicrobials. In addition, 4 Beagles served as control dogs. Variables were evaluated before and after antimicrobial administration; they included platelet count, Hct, 1-stage prothrombin time (PT), activated partial thromboplastin time (PTT), fibrinogen concentration, and platelet function. Platelet function was assessed via buccal mucosal bleeding time, aggregation, and a platelet-function analyzer. RESULTS: Administration of all antimicrobials caused a slight prolongation of 1-stage PT and activated PTT and slight decrease in fibrinogen concentration. Cephalexin caused a significant increase in 1-stage PT and activated PTT, amoxicillin caused a significant increase in activated PTT, and enrofloxacin caused a significant decrease in fibrinogen concentration. Platelet count or function did not differ significantly after administration of any antimicrobial. CONCLUSIONS AND CLINICAL RELEVANCE: Oral administration of commonly used antimicrobials in healthy dogs resulted in minor secondary hemostatic abnormalities, with no change in platelet count or function. Although these changes were clinically irrelevant in healthy dogs, additional studies of the effects of antimicrobial administration on hemostasis in animals with underlying disease processes are warranted.

OBJECTIVE: To describe the effects of lithium carbonate on thrombopoiesis in clinically normal dogs and in dogs treated with carboplatin. ANIMALS: 18 young adult sexually intact female Beagles. PROCEDURES: Dogs were assigned to each of 3 treatment groups (6 dogs/group). Group 1 received 150 mg of lithium carbonate (14 to 16 mg/kg), PO, every 12 hours on days 1 through 21. Group 2 received carboplatin (300 mg/m(2), IV) on day 0 and cephalexin (30 mg/kg, PO, q 12 h) on days 14 through 21. Group 3 received lithium, carboplatin, and cephalexin at the aforementioned doses and schedules. Plasma lithium and blood platelet concentrations were measured on days 0, 2, 4, 7, 9, 11, 14, 16, 18, and 21. Number of megakaryocytes in bone marrow specimens and the percentage of large unstained cells and CD34+ mononuclear cells in bone marrow aspirates were determined on days 0, 7, 14, and 21 by manual enumeration, automated hematologic analysis, and flow cytometric immunophenotyping, respectively. RESULTS: Plasma lithium concentrations ranged from 0.12 to 2.41 mmol/L. All dogs given lithium achieved a concentration within the target interval of 0.5 to 1.5 mmol/L by days 4 to 7. Thrombopoiesis was increased in dogs receiving lithium alone. All dogs given carboplatin developed mild thrombocytopenia. There were no differences between group 2 and group 3 throughout the study. CONCLUSIONS AND CLINICAL RELEVANCE: Lithium stimulated thrombopoiesis in clinically normal dogs. Lithium administration at the doses and schedules used, with concurrent administration of cephalexin, did not prevent thrombocytopenia induced by carboplatin.