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Summary

Medical records of 23 dogs and 3 cats treated for noncardiogenic pulmonary edema (npe) resulting from airway obstruction (n = 8), cranial trauma (7), electric shock (7), or seizures (4) between 1987 and 1993 were reviewed. There were 18 purebred dogs, 5 mixed-breed dogs, 2 domestic shorthair cats, and 1 Siamese. Sixteen animals were male, and 10 were female. All but 7 were less than 1 year old. Time between the inciting incident and onset of respiratory tract signs ranged from minutes to several hours. Respiratory distress was the primary clinical sign for all animals with npe resulting from airway obstruction, cranial trauma, or seizures, and for 2 of the 7 animals with npe resulting from electric shock. The only consistent clinicopathologic abnormality was hyperglycemia, which was detected in 12 animals. Arterial blood gas partial pressures were measured in 11 animals; 10 were hypoxemic. On thoracic radiographs, the predominant pattern of pulmonary infiltration was alveolar. Symmetry of involvement, which was assessed by examining dorsoventral or ventrodorsal radiographic projections, could be determined for 23 animals. In 18, involvement was asymmetric, and in 13 of those 18, the right side was predominantly involved. On lateral radiographic projections, the caudodorsal quadrant of the lung field was involved primarily or as part of a diffuse distribution in all but 1 animal. Generally, animals with npe resulting from airway obstruction had the greatest degree of radiographic involvement, followed in decreasing order, by animals with npe resulting from cranial trauma, animals with npe resulting from seizures, and animals with npe resulting from electric shock. Overall, 9 animals died. Four of the 8 animals with npe resulting from airway obstruction and 2 of the 7 animals with npe resulting from cranial trauma died or were euthanatized because of the severity of the pulmonary compromise. One animal with npe resulting from electric shock developed seizures and died. Two of the 4 animals with npe resulting from seizures were euthanatized because of the underlying cause of the seizures. Overall, 20 of the 26 animals were discharged, died, or were euthanatized within 48 hours of admission to the hospital.

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in Journal of the American Veterinary Medical Association
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Summary

Medical records of 21 dogs and 2 cats treated for septic peritonitis were reviewed. Animals were between 1 and 12 years old, (mean, 6.5 years) and weighed between 6 and 51.4 kg (mean, 22.7 kg). Overall, 13 animals survived and were discharged from the hospital. Immediately after surgical correction of the underlying cause of peritonitis, most animals were tachycardic (mean heart rate, 148 beats/min; range, 80 to 204 beats/min), and many were hypotensive (mean arterial pressure, 84.4 mm of Hg; range, 44 to 156 mm of Hg). Hypotension was attributed to sepsis and hypovolemia secondary to extensive loss of fluid into the peritoneal cavity. Survivors did not differ from nonsurvivors with regard to mean arterial pressure immediately after surgery, and in most animals, hypotension could be corrected by iv administration of fluids. Three animals died after failing to respond to fluid treatment, despite concurrent administration of inotropic or pressor agents. Mean rate for crystalloid fluid administration was 12.8 ml/kg of body weight/h (range, 5 to 23.5 ml/kg/h) during the first 24 hours after surgery. Six of 23 animals had low urine output for a short time after surgery, but urine output increased when fluids were administered. Hypoalbuminemia developed in all animals (mean serum albumin concentration, 1.17 g/dl; range, 0.6 to 2.3 g/dl), and peripheral edema developed in 13. Neither lowest mean serum albumin concentration nor fluid administration rate was significantly different between animals that developed peripheral edema and those that did not. Fluid administration rates were significantly higher in nonsurvivors (15 ml/kg/h; range, 5.5 to 23.5 ml/kg/h) than in survivors (11 ml/kg/h; range, 5 to 17.5 ml/kg/h). Thirteen animals had evidence of pulmonary alveolar consolidation, and 9 had pleural effusions; however, fluid administration rates were not significantly different between animals that did and those that did not develop clinical respiratory disease. Eleven animals had pancreatitis at the time of surgery, or developed pancreatitis subsequently. Four animals developed disseminated intravascular coagulation, and only 1 survived. Indicators of a poor prognosis included refractory hypotension, cardiovascular collapse, and development of respiratory disease or disseminated intravascular coagulation. Development of pancreatitis, high serum concentrations of hepatic enzymes, high or low wbc count, hypo- or hyperglycemia, signs of abdominal pain, and abdominal effusion were not associated with outcome.

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in Journal of the American Veterinary Medical Association

Summary

An orally administered sulfonylurea drug, glipizide, was evaluated for treatment of diabetes mellitus. Confirmation of diabetes was based on evidence of appropriate clinical signs, persistent hyperglycemia, and glucosuria. Glipizide (5 mg, PO, q 12 h) was administered to each cat. Sixteen cats were fed a commercial high-fiber diet and 4 cats were fed a commercial low-fiber diet. Insulin was not administered to any cat during the study. Each cat was evaluated 2, 4, 8, and 12 weeks after initiation of treatment.

Three clinical responses to glipizide treatment were identified. Mean preprandial blood glucose concentration and mean blood glucose concentration during an 8-hour postprandial period decreased to < 200 mg/dl in 5 of 20 (25%) cats. In these 5 cats, glucosuria was no longer detected and clinical signs resolved by the 4-week reevaluation. Euglycemia was maintained after discontinuing glipizide treatment in 2 of these 5 cats. Glycemic control has been maintained in 2 of 5 of the responding cats for 5 and 7 months of glipizide treatment. One of 5 of the responding cats developed insulin-requiring diabetes mellitus after 6 months of glipizide treatment. Seven of 20 (35%) cats failed to respond to treatment. Mean preprandial blood glucose concentration and mean blood glucose concentration during an 8-hour postprandial period did not change from pretreatment values after 2 ± 1 months; glucosuria persisted and clinical signs progressively worsened. Insulin treatment was required to establish glycemic control in these 7 cats. Eight of 20 (40%) cats partially responded to glipizide treatment. Clinical signs and abnormalities identified on physical examination improved, and mean preprandial blood glucose concentration and mean blood glucose concentration during an 8-hour postprandial period decreased by 146 ± 105 and 110 ± 50 mg/dl, respectively, at the 12 week reevaluation, compared with pretreatment values, but blood glucose concentrations remained > 200 mg/dl and glucosuria persisted. These cats were treated with glipizide for a mean of 12 months (range, 7 to 21 months).

Adverse reactions to treatment included vomiting shortly after administration of glipizide (3 cats), hypoglycemia (3 cats), and increased serum hepatic enzyme activities (3 cats). Retrospective analysis of information obtained from the 20 cats at the time of entry into the study failed to identify any consistent factor that could be used to predict the cats’ response to glipizide treatment. Results of the study indicated that glipizide may be a viable alternative to insulin for treatment of diabetes mellitus in some cats.

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in Journal of the American Veterinary Medical Association

and lethargy. Clinical and Gross Findings On physical examination, the bearded dragon had a palpable cranial coelomic mass. Abnormal clinicopathologic values included hyperglycemia (1,348 mg/dL; reference range, 1 210 to 255 mg/dL) and mild

Open access
in Journal of the American Veterinary Medical Association

lethargic and inappetent after exiting brumation. Blood work performed by the referring veterinarian revealed severe leukocytosis (32.3 X 10 3 WBCs/μL; reference range, 1 1.45 X 10 3 to 19.0 X 10 3 WBCs/µL) and severe hyperglycemia (1,339 mg

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in Journal of the American Veterinary Medical Association

insulin secretion or sensitivity, compared with domestic ruminants. These high blood glucose concentrations are thought to be normal in camelids, although a number of hyperglycemic disorders have been described, including stress hyperglycemia, 2

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in American Journal of Veterinary Research

homeostasis Insulin Hyperglycemia Hypoglycemia ↑ Glycogenesis Amino acids Somatostatin ↑ Glycolysis Glucocorticoids a Ghrelin ↑ Fatty acid synthesis GH Glucocorticoids ↑ Protein synthesis Cholinergic

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in Journal of the American Veterinary Medical Association

resistance is linked to cardiovascular disease in humans through its effects on the vascular endothelium, 6 and this mechanism is also being examined in horses. 7 Resting hyperglycemia is not a common component of EMS in horses, 4 but abnormal glucose

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in American Journal of Veterinary Research

Hypoglycemia was defined as BG concentration < 75 mg/dL, and hyperglycemia was defined as BG concentration > 150 mg/dL. 21 Zone A of the error grids included sample results for which results of both the test and reference method similarly indicated hyper- or

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in American Journal of Veterinary Research

, pathological stage, postoperative pancreatitis, postoperative hyperglycemia, or hypoglycemia. 12 Not all studies agree on the significance of these factors. 7 , 12 Importantly, persistent hypoglycemia following surgical exploration has been reported in 20% to

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in Journal of the American Veterinary Medical Association