Summary Gastroduodenal ulceration is becoming recognised as an important disease ***in ***foals during the first few months of life. Aetiopathogenesis is presumed to be similar to peptic disease in humans associated with back diffusion of hydrogen ions into the mucosa. Many factors have been incriminated as predisposing foals to ulceration but few have been proven. To date, use of non‐steroidal anti‐inflammatory agents has been the only documented cause of gastroduodenal ulceration in foals. The clustering of affected foals on certain farms suggests an infectious aetiology but attempts to identify a causative organism have been unsuccessful. Four clinical syndromes defined for foals with gastroduodenal ulceration include: (1) silent ulcers, which occur most often in the non‐glandular stomach along the margo plicatus and are identified as incidental findings at necropsy; (2) active ulcers which are often manifested by abdominal pain, excessive salivation and bruxism; (3) perforating ulcers which usually result in a severe, diffuse peritonitis; and (4) pyloric or duodenal obstruction from a healing ulcer. General approaches to therapy of a foal with active ulceration consist of reduction of gastric acidity and enhancement of mucosal protection. Antacids and type 2 histamine receptor antagonists are used most often to neutralise or decrease acid secretion, respectively. Sucralfate, a locally active sulphated sucrose preparation, is commonly used as a cytoprotective agent. The efficacy and safety of many products used have not been evaluated adequately in foals. Perforating ulcers are usually associated with death or humane destruction of the foal because of fulminating peritonitis. Surgical intervention and bypass procedures are indicated in foals that develop pyloric or duodenal obstructions from healing ulcers.

The historical, clinical, diagnostic, and therapeutic aspects of pleuropneumonia are reviewed with emphasis placed on aggressive treatment and ultrasound diagnosis. The common sequelae are described, and appropriate treatment recommendations are included. A favorable prognosis may be expected for horses receiving long-term treatment.

Postoperative ileus is characterized by decreased gastrointestinal myoelectric activity and motility. Metoclopramide was used to treat experimentally induced postoperative ileus in six dogs. Contractile activity was monitored by extraluminal strain gages on the pyloric antrum and proximal segment of the duodenum, and myoelectric activity was measured by recording bipolar electromyograms (EMGs) at the pyloric antrum, pyloric canal, proximal segment of the duodenum, proximal and distal parts of the jejunum, and ileum. Measurements were obtained from animals without ileus (baseline) and those with ileus that were either untreated or treated with metoclopramide. Adynamic ileus was induced by rubbing a 50 cm segment of jejunum with a dry sponge for 5 minutes and exposing the bowel to the air for 30 minutes. Treated dogs received metoclopramide (0.4 mg/kg 4 times daily [QID] intravenously [IV]), whereas untreated dogs received a saline placebo, starting 1 hour after celiotomy closure. Recordings were made for 26 hours after induction of ileus. The phases of the migrating myoelectric complex (MMC) were identified and motility index values were determined. During ileus, the MMC phase II duration was increased at the duodenum and phase III duration was decreased at the antrum, pylorus, duodenum, and proximal segment of the jejunum (p less than 0.05). Motility index values were decreased at the antrum and duodenum during ileus (p less than 0.05). Treatment with metoclopramide reversed the MMC phase III inhibition at the antrum and pylorus, and partially reversed the inhibition at the duodenum and jejunum (p less than 0.05). Motility index values were restored to preoperative baseline values with metoclopramide treatment (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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