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.

There was good agreement between plasma pi meas and piA + G in blood samples obtained from hypoproteinemic horses immediately before infusion of HES. Use of a predictive nomogram did not, however, account for the oncotic effect of HES. Results of comparison of pi meas to piA + G after HES infusion suggest that a significant oncotic effect was maintained for 24 hours in the study horses.

Summary The formation of cranial thoracic masses (CTM) as a sequel to infectious pleuropneumonia is described. Using ultrasound, masses were diagnosed subjectively as abscesses or loculations. Eight of 99 cases with pleuropneumonia had CTM. Clinical signs associated with the presence of a CTM included increased heart rate, jugular distention, forelimb ‘pointing’ and caudal displacement of the heart. Techniques used for diagnostic ultrasonographic examination of the cranial thorax are described. Five of the eight horses with CTM responded to conservative medical management; the other three required percutaneous drainage of the mass to relieve worsening signs of cardiac decompensation. Improvements in cardiovascular parameters were evident within 12 h of drainage. The indications for and limitations of invasive drainage of cranial thoracic masses are discussed.

Summary Six horses had been admitted to the hospital because of illness other than renal failure; diarrhoea, myositis, abdominal pain and/or suspected bacterial sepsis. Hypotension and disseminated intravascular coagulopathy were frequent findings in the horses. Abnormally high serum creatinine concentration and urine specific gravity of less than 1.022 were found in the horses with acute renal failure. Hyponatremia and hypochloraemia were the most common abnormal electrolyte findings. Pronounced hyperkalaemia was not found. Variable degrees of tubular necrosis were seen in three of the four horses that had kidney sections submitted for microscopic examination. Renal cortical necrosis occurred in one horse. Intravenous fluid and electrolyte replacement was the most important therapy in those cases that were non‐oliguric. Furosemide, mannitol and dopamine were used in horses with oliguria. The prognosis was generally good if the predisposing cause could be corrected and the acute renal failure was not oliguric.

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.

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