The endoscopic appearance of chronic hypertrophic pyloric gastropathy (CHPG) in five dogs is described. Several patterns of enlarged mucosal folds that surrounded and obstructed the pyloric canal were observed. Initially, endoscopically obtained biopsy samples of mucosa were judged to be histologically normal. Diagnosis of CHPG was confirmed and relief of pyloric obstruction accomplished at exploratory laparotomy (in four dogs). Retrospective evaluation of pyloric tissue samples, obtained during endoscopy, identified subtle histological characteristics of CHPG. Gastric and duodenal neoplasia or antral polyps can mimic the endoscopic appearance of CHPG but can be differentiated based on their endoscopic and histological appearance. These cases show that endoscopic examination is a valuable procedure for the diagnosis of CHPG in dogs that chronically vomit.

The purposes of this study were to evaluate the efficacy of metoclopramide to aid passage of a flexible endoscope into the duodenum of dogs, and to determine whether the effect of metoclopramide is dependent on dose. In a randomized, blinded, complete-block design, 6 healthy dogs were anesthetized, then each was given saline solution or 1 of 4 doses of metoclopramide on different days. The ease of passage of a flexible, fiberoptic gastroscope through the pylorus was assessed independently by 3 endoscopists. Administration of metoclopramide hydrochloride at a dosage of 0.4 mg/kg of body weight, iv, made passage of a flexible endoscope into the duodenum significantly (P = 0.009) more difficult than when saline solution was administered; however, dosages of 0.1, 0.2 and 0.8 mg of metoclopramide/kg did not (P = 0.489, 0.842, and 0.092 respectively). It was concluded that metoclopramide did not facilitate, and at one dosage hindered, successful passage of a flexible endoscope into the duodenum of healthy dogs under the conditions of the study. Metoclopramide, therefore, cannot be recommended as an aid for passage of a flexible endoscope into the duodenum of dogs.

Cholecalciferol (vitamin D3) rodenticides, introduced in 1985, have caused significant toxicity in dogs at a fraction of the manufacturers' reported LD50 for dogs (88 mg pure cholecalciferol/kg). Toxicity is manifested by hypercalcemia, hyperphosphatemia, and occasionally azotemia. Clinical signs most commonly associated with the resultant hypercalcemia are polyuria, polydisia, depression, anorexia, weakness, and vomiting. This report describes a dog estimated to have consumed 1.5 to 3.0 mg/kg body weight of pure cholecalciferol. The most prominent signs were anorexia and weakness. The definitive diagnosis of chole-calciferol toxicity required a history of exposure and diagnostic tests to rule out other causes of hypercalcemia. Fluid diuresis, furosemide, prednisone, and calcitonin were used to lower serum calcium.

Modification of gastroduodenal motility has been proposed to aid endoscopic examination of the duodenum in dogs. The objective of this study was to evaluate the use of the following pharmacologic agents for facilitation of endoscopic intubation of the duodenum in 6 clinically normal dogs: metoclopramide HCl (0.2 mg/kg of body weight), atropine sulfate (0.045 mg/kg), glucagon (0.06 mg/kg), and isotonic saline solution. In a randomized, blinded, crossover design, the ease of endoscopic duodenal intubation was qualitatively scored by 3 endoscopists (in random order), using the following scale: 1 - immediate entry; 2 - rapid entry--moderate manipulation; 3 - difficult entry--multiple attempts; and 4 - no entry after 2 minutes [corrected]. Anesthesia was induced with thiopental and maintained with halothane. The 4 agents were diluted to a fixed volume and randomly administered. Duodenal intubation was attempted 2 minutes after IV injection of 1 of the agents. Four endoscopic procedures (1 for each agent) were performed on each dog with a minimum of 5 days between each procedure. In this study, no agent facilitated endoscopic duodenal intubation at the dose used. Instead, atropine and metoclopramide made duodenal intubation significantly more difficult, compared with use of saline solution. Difference between intubation after administration of glucagon and saline solution was not seen. On the basis of our findings, the use of these agents for facilitating endoscopic duodenal intubation is not recommended. In addition, in this study, we found that experience in endoscopic intubation is an important factor in determining the ease of duodenal intubation.

Peripheral hypomyelinization was found in 2 Golden Retriever littermates that had pelvic limb ataxia, depressed postural reactions, and depressed segmental reflexes. Diagnostic findings included infrequent denervation potentials, reduced or absent evoked potentials, and markedly diminished motor nerve conduction velocities. Light and electron microscopy of peripheral nerves revealed fewer than normal myelinated axons, myelinated sheaths inappropriately thin for the caliber of the fiber, poor myelin compaction, greater than normal numbers of Schwann cell nuclei, many Schwann cells with voluminous cytoplasm, and greater than normal amount of perineural collagen. Findings were compatible with a peripheral hypomyelinization process; a defect in Schwann cell function was suspected.