Search Results
You are looking at 1 - 8 of 8 items for
- Author or Editor: Douglass K. Macintire x
- Refine by Access: All Content x
Summary:
In a prospective clinical trial, low-dose, continuous, iv infusion of insulin (dosage, 2.2 U/kg of body weight, q 24 h) was used to treat 21 dogs with diabetic ketoacidosis. Mean (± sd) blood glucose concentration at the onset of treatment was 550 ± 150 mg/dl and after 6 hours, was 350 ± 106 mg/dl, with a mean decline of 34 ± 16 mg/dl/h. By 12 hours, mean blood glucose was 246 ± 85 mg/dl, with a mean decline of 28 ± 14 mg/dl/h during the second 6 hours of treatment. Mean duration of treatment required to reach a blood glucose concentration ≤ 250 mg/dl was 10 ± 4 hours, with a range of 4 to 24 hours. Ketonuria was observed for 26 ± 14 hours (range, 6 to 12 hours). Hypoglycemia developed in 3 of 21 dogs during treatment, but responded to iv administration of a glucose solution and to a reduction in rate of insulin delivery. Potassium supplementation was required in 15 of 21 dogs. Mean bicarbonate concentration was 11.6 ± 3.4 mEq/L before treatment and was 18.2 ± 0.7 mEq/L after 24 hours. Fifteen of 21 dogs (71%) survived to be discharged. Mean duration of treatment with the insulin infusion was 50 ± 30 hours (range, 7 to 124 hours). In this series of dogs, continuous, low-dose, iv infusion of insulin provided a gradual and consistent reduction in blood glucose concentration while ketoacidosis, electrolyte balance, and dehydration were corrected. Although hypoglycemia, hypokalemia, hypophosphatemia, and cerebral edema remain potential complications of any treatment for diabetic ketoacidosis, this protocol appears to provide a safe and effective treatment method.
Objective—
To determine the typical history of and physical and clinicopathologic findings in dogs with heat-induced illness, and to correlate these findings with outcome.
Design—
Retrospective study.
Animals—
42 dogs with heat-induced illness.
Procedure—
Dogs were included in the study if other medical problems had not been previously diagnosed and if clinical signs of illness developed after exposure to a warm environment. Information obtained from each record included time of year heat-induced illness developed, signalment, history, clinical signs, physical examination findings, results of clinicopathologic tests, treatment, clinical course, outcome, and necropsy results.
Results—
Overall, 27 dogs survived and 15 died or were euthanatized. Time of year was recorded for 40 dogs. Thirty-one of the 40 were examined before July. Hypothermia and coma at the time of initial examination were associated with a poor outcome. Serum cholesterol, albumin, and total protein concentrations were significantly lower, serum total bilirubin and creatinine concentrations were significantly higher, and ventricular arrhythmias were detected significantly more frequently in dogs that did not survive than in dogs that did. (J Am Vet Med Assoc 1996;209:1894–1899)
Abstract
Objective—To identify subclinical Babesia gibsoni infection in American Pit Bull Terriers from the southeastern United States and to determine the genetic sequence of parasite DNA isolated from these dogs.
Design—Case series.
Animals—33 American Pit Bull Terriers and 87 dogs of various other breeds.
Procedure—Blood smears were examined for microscopic evidence of the parasite, and DNA was extracted from blood samples and used in a polymerase chain reaction (PCR) assay designed to amplify the small subunit ribosomal RNA gene sequence of B gibsoni. Amplification products of the expected size were sequenced, and sequences were compared with published sequences for B gibsoni isolates. Hematocrit, platelet count, mean platelet volume, WBC count, and eosinophil count were compared between dogs with positive PCR assay results and dogs with negative results.
Results—Results of the PCR assay were positive for 18 of the 33 (55%) American Pit Bull Terriers, including all 10 dogs with microscopic evidence of parasitemia. Only 1 of these dogs was clinically ill at the time blood samples were collected. Results of microscopic evaluation of blood smears and of the PCR assay were negative for the 87 other dogs. Hematocrit and platelet count were significantly lower in dogs with positive PCR assay results than in dogs with negative results.
Conclusions and Clinical Relevance—Results suggest that American Pit Bull Terriers in the southeastern United States may be subclinically infected with B gibsoni. However, subclinical infection was not identified in dogs of other breeds from the same geographic area. (J Am Vet Med Assoc 2002;220: 325–329)
Abstract
Objective—To characterize rib, intrathoracic, and concurrent orthopedic injuries, and prognosis associated with traumatic rib fracture in cats.
Design—Retrospective study.
Animals—75 cats.
Procedure—Medical records from January 1980 to August 1998 were examined for cats with traumatic rib fracture. Signalment, cause of trauma, interval from trauma to evaluation at a veterinary teaching hospital, referral status and date, method of diagnosis, duration of hospitalization, number and location of rib fractures, presence of flail chest, costal cartilage involvement, intrathoracic and concurrent orthopedic injury, and clinical outcome were reviewed.
Results—Median age was 3 years. Twenty-five (58%) cats with reported cause of trauma were injured by interaction with another animal. Fortyseven (78%) cats that were treated survived. Cats that died had a median duration of hospitalization of < 1 day. Ten (13%) cats had flail chest. Sixty-five (87%) cats had intrathoracic injury (median, 2 injuries). Nine (100%) cats without detected intrathoracic injury that were treated survived. Thirty-five (47%) cats had concurrent orthopedic injury. Cats with flail chest, pleural effusion, or diaphragmatic hernia were significantly more likely to die than cats without each injury.
Conclusions and Clinical Relevance—Traumatic rib fracture in cats is associated with intrathoracic and concurrent orthopedic injury. Aggressive treatment of cats with traumatic rib fracture is warranted, because the prognosis is generally favorable. Diagnosis and treatment of intrathoracic injury associated with traumatic rib fracture in cats should precede management of concurrent orthopedic injury. ( J Am Vet Med Assoc 2000;216:51–54)
Objective—
To document hepatozoonosis in dogs from Alabama and Georgia and to report associated clinical signs, method of diagnosis, response to treatment, and course of disease.
Design—
Retrospective case series.
Animals—
22 dogs in which Hepatozoon canis was identified by microscopic examination of skeletal muscle.
Procedure—
We reviewed medical records of all dogs with a definitive diagnosis of hepatozoonosis that were referred to the Auburn University Small Animal Clinic between 1989 and 1994.
Results—
Diagnoses were confirmed by microscopic identification of H canis schizont or merozoite stages in skeletal muscle. The gametocyte stage was not detected in smears of blood obtained from a peripheral vein, buffy-coat smears, or bone marrow evaluation. Common clinical signs included fever, cachexia, ocular discharge, pain, stiffness, and paresis. Laboratory abnormalities included marked leukocytosis, hypoglycemia, hypoalbuminemia, mild anemia, hyperphosphatemia, and high alkaline phosphatase activity. Periosteal bone proliferation was evident radiographically in 18 of 22 dogs. Renal lesions included amyloidosis (1 dog), interstitial nephritis (3), and mesangioproliferative glomerulonephritis (4). Treatment with the anticoccidial drug toltrazuril, despite an initial favorable response, failed to prevent relapse in all but 3 of 21 treated dogs. Mean survival time was 12.6 ± 2.2 months, with a mean time of remission before recurrence of clinical signs of 6 months.
Clinical Implications—
H canis infection in dogs can be associated with a distinct clinical syndrome that involves chronic myositis, debilitation, and death. The dogs of this report represent the first substantial number of domestic dogs naturally infected with H canis in the United States outside of the Texas Gulf Coast. Hepatozoon canis appears to be a serious pathogen in the United States that is becoming more widespread geographically. (J Am Vet Med Assoc 1997;210:916–922)
Abstract
Objective
To assess the accuracy of current antemortem and postmortem techniques for determining tracheal luminal stenosis.
Animals
15 dogs.
Procedure
Percentage of tracheal luminal stenosis (PTLS) was determined by 6 methods, using measurements obtained by radiography, tracheoscopy, and necropsy after selected tracheostomy techniques were performed. To calculate PTLS, dorsoventral tracheal diameter was measured from preoperative and postoperative lateral cervical radiographic views. Preoperative or normal tracheal segments adjacent to the stenotic area were used to obtain normal tracheal diameter measurements. Planimetrically determined cross-sectional area (CSA), obtained from pre- and postoperative tracheoscopic photographs, was used to calculate PTLS. The CSA of tracheal specimens obtained at necropsy was determined, using the formula for an ellipse. Percentage of luminal stenosis was calculated, using CSA of the stenotic site and of segments craniad and caudad to the site obtained at necropsy or at surgery. All methods were compared with the control method of planimetrically determined CSA of sections obtained at necropsy of the tracheostomy and segments craniad and caudad to the site.
Results
Correlation was poor for radiographic and tracheoscopic techniques (r = 0.146 to 0.458, P > 0.05) The formula for an ellipse accurately predicted PTLS when measurements obtained at surgery (r = 0.516, P = 0.049) or segments craniad and caudad (r = 0.853, P < 0.001) to the site were used.
Conclusion
Antemortem methods of assessing PTLS did not correlate with control planimetric methods. Methods using CSA determined by tracheal diameter were weakly correlated to control planimetric techniques.
Clinical Relevance
Accurate measurement of the degree of tracheal stenosis cannot be made in clinical patients using current techniques. (Am J Vet Res 1997;58:1051–1054)
Abstract
Objective—To determine clinical and pathologic findings before and after short-term (group 1) and longterm (group 2) treatment in dogs with Hepatozoon americanuminfection.
Design—Retrospective study.
Animals—53 dogs with H americanuminfection.
Procedure—Medical records of dogs that were treated for hepatozoonosis diagnosed on the basis of meront or merozoite stages in skeletal muscle were reviewed.
Results—Circulating gametocytes of H americanum were identified in 12 of 53 dogs. Dogs were treated with various drugs, including toltrazuril, trimethoprimsulfadiazine, clindamycin, pyrimethamine, and decoquinate. Mean WBC counts prior to treatment were 85,700 and 75,200 cells/µl in groups 1 and 2, respectively, and 1 month after initiation of treatment were 12,600 and 14,600 cells/µl, respectively. Initial response to treatment was excellent in all dogs. Twenty-three of 26 dogs in group 1 relapsed at least once and died within 2 years; mean (± SD) survival time was 12.6 ± 2.2 months. Twenty-two of 27 group-2 dogs survived; 11 dogs had no clinical signs and were still receiving decoquinate (mean duration of treatment, 21 months), 11 dogs had no clinical signs after treatment for 14 months (range, 3 to 33 months; mean survival time, 39 months [range, 26 to 53 months]), 2 dogs were lost to follow-up, and 3 dogs were euthanatized because of severe disease.
Conclusions and Clinical Relevance—Although no treatment effectively eliminated the tissue stages of H americanum, treatment with trimethoprim-sulfadiazine, clindamycin, and pyrimethamine followed by long-term administration of decoquinate resulted in extended survival times and excellent quality of life. ( J Am Vet Med Assoc 2001;218:77–82)
