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Summary Thirty mixed‐bred foals aged 2.5–6.5 months (mean 4.6 ± 1.0 months) with no clinical or radiographic signs of dyschondroplasia (DCP) were fed one of four diets for 16–18 weeks. Twelve foals were fed a Control diet which comprised ˜100% of the NRC recommendations for dietary energy (DE) and crude protein (CP). Six were fed a diet with ˜126% of NRC levels for CP and 12 foals were fed a diet with 129% of NRC levels for DE. The diets comprised 3 different formulations of rice‐based pellets with added maize oil for the High DE diet, and oaten chaff. Average daily gain, humeral length and wither height were slighly, but not significantly, different in the foals on the High DE diet than in those fed the Control or High CP diet. Clinical and radiographic signs of DCP were seen in 6 out of 12 foals fed the High DE diet. Not one of the foals fed High CP or Control diets showed any clinical and radiographical signs of DCP. The number and severity of DCP lesions found at post‐mortem examination were much greater in the High DE foals than in the Control and High CP foals. Multiple lesions of DCP were detected in 11 foals fed the High DE diet, in 1 foal fed the High CP diet and in 1 foal fed the Control diet. Histological lesions of DCP were confirmed in 18 foals; in all 12 of the High DE foals, 4 of the 6 High CP foals and 2 of the 12 Control foals. The number of histological lesions of DCP were significantly greater in the High DE foals than in the Control group (P < 0.0001). The incidence of lesions of DCP in the foals fed High CP was not significantly different from that in the Control foals (P = 0.11).

cTnI is elevated in horses with myocardial disease and elevated to a lesser degree in some horses with structural heart disease or lone arrhythmias. The association between cTnI concentration and survival was not clear.

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A single criterion was not determined to be pathognomonic for uremic encephalopathy in horses. Uremic encephalopathy should be considered as a differential diagnosis in horses with evidence of chronic renal failure and encephalopathic neurologic sign not attributable to other causes. Astrocyte swelling, which was common to all 4 horses examined at necropsy, may serve as a microscopic indicator of uremic encephalopathy in horses.

An 18‐week feeding trial was performed to investigate the effects of an omega‐3 (n‐3) fatty acid‐enriched ration on plasma fatty acid concentrations and platelet aggregation in healthy horses. Flaxseed oil served as the source of the n‐3 fatty acid alpha‐linolenic acid (ALA). Twelve horses were fed dietary maintenance requirements using a complete pelleted ration (80%) and timothy grass hay (20%) for a 2‐week acclimation period before being randomly assigned either to a treatment (group 1) or control (group 2) group. Group 2 horses (n = 6) were fed the diet described in the acclimation period, whereas group 1 horses (n = 6) were fed a 10% flaxseed oil‐enriched complete pellet (80%) and grass hay (20%). Biological samples and physical measurements were collected at one point during the acclimation period (week 0) and every 4 weeks thereafter (weeks 4, 8, 12, and 16). Body weight, CBC (including platelet count), plasma fibrinogen, electrolyte (Na, K, and Cl) concentrations, and biochemical profile enzyme activities (aspartate aminotransferase, alkaline phosphatase, gamma‐glutamyltransferase, and creatine kinase) did not change markedly with diet. Platelet aggregation was not altered by the supplementation of flaxseed oil in these healthy horses, although increases in plasma cis‐polyunsaturated 18‐carbon fatty acids C18:3; n‐3 (ALA) and C18:2; n‐6 (linoleic acid), biologically active C20:5; n‐3 (eicosapentaenoic acid [EPA]), and malondialdehyde (MDA) were evident. There were no marked decreases in C20:4; n‐6 (arachidonic acid [AA]) or increases in C22:6; n‐3 (docosahexaenoic acid [DHA]), signifying that flaxseed oil may have had a high percentage of omega‐6 (n‐6) fatty acids as well as n‐3 fatty acids, and this relatively high n‐6: n‐3 fatty acid ratio may have affected the biochemical effect of n‐3 fatty acids. In healthy horses supplemented with flaxseed oil, platelet aggregation was not altered, which may have been due to the limited biologic effect in healthy subjects or the inability of flaxseed oil to induce the necessary biochemical effect of replacing n‐6 fatty acids with n‐3 types.

The application of 99mTc-HMPAO labeled white blood cells to support the diagnosis of right dorsal ulcerative colitis was studied in two horses with a history and clinical signs consistent with phenylbutazone toxicity. These images were compared to a reference horse unaffected by right dorsal ulcerative colitis. Blood was collected aseptically in heparinized syringes from the patients for in vitro white blood cell (WBC) radiolabeling. The buffy coat was separated out and radiolabeled with 99mTc-HMPAO. The radiolabeled blood was re-injected i.v. and four images of the right and left side of the patient's abdomen were acquired at 4 hours and 20 hours post-injection. Results of the nuclear study revealed no abnormal findings in the abdomen at the four-hour post-injection images in any horse. Images obtained 20 hours post-injection revealed a linear uptake of radiolabeled WBCs in the right cranioventral abdomen in the region of the right dorsal colon in both horses with right dorsal ulcerative colitis. The reference horse had no radiopharmaceutical uptake in this region. This nuclear imaging study was a rapid, non-invasive method to identify right dorsal colon inflammation. These findings not only supported the diagnosis of right dorsal ulcerative colitis, but also facilitated appropriate medical management of each horse.