Summary Venous air embolism was suspected in 3 hospitalised horses on the basis of an inadvertently open jugular venous line. Subsequently the 3 horses developed clinical signs including cardiovascular collapse, cardiac dysrhythmia, pulmonary oedema, behavioural abnormalities and neurological signs consistent with central nervous system injury. Treatment included intranasal oxygen therapy, i.v. fluid administration and anti‐inflammatory therapy. Specific therapy aimed at treating air embolism in man is reviewed, with pertinent therapy potentially applicable to horses emphasised.

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Cholesterinic granulomas have been previously reported as an incidental post mortem in horses. Three adult horses with diencephalic dysfunction due to cholesterinic granulomas are described. All the horses exhibited profound depression, somnolence and reluctance to move. One horse experienced generalised seizures. Cerebrosinal fluid was xanthochromic with an elevated total protein in two of the cases evaluated. The large cholesterinic granulomas caused expansion of the lateral ventricle and secondary hydrocephalus due to the build up of cerebrospinal fluid behind the mass. Cholesterinic granulomas are believed to result from choroid plexus congestion and haemorrhage.

The medical approach to treatment of cholangiohepatitis and cholelithiasis in 9 horses is described. Seven horses were treated successfully and returned to normal use, with a minimum follow-up period of 12 months. Long-term antimicrobial therapy was believed to be critical in those cases that survived, with a median treatment duration of 51 days (range 17-124 days). Treatment failure was associated with severe periportal and bridging hepatic fibrosis from biopsy material obtained at admission in 2 horses, one of whom also presented with hyperammonaemic hepatic encephalopathy. Transabdominal ultrasound was used diagnostically in each case to obtain hepatic biopsy material for histopathology and bacterial culture, to evaluate hepatic size and echogenicity and to identify and monitor the dissolution of hepatoliths. Histologically, all horses had evidence of suppurative cholangiohepatitis with varying degrees of periportal and bridging fibrosis. Discrete hyperechoic calculi were identified in 4 cases, but all horses had ultrasonographic evidence of biliary obstruction with numerous dilated bile ducts. Aerobic and anaerobic cultures of liver biopsy material were negative from 7 horses, but 2 different species of Escherichia coli were obtained from one horse, and Bacteroides vulgatus and Escherichia coli were isolated from another. In all 7 horses that survived, clinical recovery was seen before normalisation of biochemical indices of hepatobiliary function including gammaglutamyl transaminopeptidase (GGT), alkaline phosphatase (AP), bile acids and serum bilirubin. Serum GGT levels were monitored extensively as a marker of hepatobiliary disease and actually increased during the initial period of clinical improvement in horses that recovered. Supportive medical therapy with i.v. fluids was also a critical part of the therapy of several cases in this report, both acutely and in the management of chronic cases that deteriorated clinically during treatment. Previous therapeutic failures may well be related to treatment periods of inadequate duration, and the authors recommend that antimicrobial therapy should be continued until GGT values are normal.

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Summary The characteristics of the ocular manifestations of equine motor neuron disease (EMND) are described. Forty‐two horses with histories, clinical signs and necropsies compatible with EMND were the subjects of this study. Ophthalmoscopic lesions that varied in severity were found in 40 of 42 horses and appeared as a distinct pigmented reticulated pattern at the tapetal‐nontapetal junction or throughout the fundus, depending upon severity. The pattern colours ranged from yellow brown to black. Areas of hyperreflectivity formed mosaic patterns in the tapetal fundus. ERG B‐wave amplitudes were usually at least 50% reduced and many animals showed extinguished amplitudes. None of the horses had apparent visual impairment. Histopathologically, all 42 horses had retinal pigment epithelial (RPE) congestion with ceroid‐lipofuscin. Retinal degeneration was variable even within the eyes. Thin layer chromatography (TLC) analysis of the RPE and neural retina identified both green and orange emitting fluorescent compounds not found in normal horses. All unsupplemented horses had plasma vitamin E levels <1.0 μg/ml. The potential significance of this report is the pathognomonic role the ocular manifestations exhibit in helping to diagnose equine motor neuron disease. In memory of John Cummings, we dedicate this manuscript.

Ponies given dried red maple (Acer rubrum L.) leaves at a dose of 3.0 gm/kg body weight became ill and died one to five days after administration of the leaves. Two clinical patterns of disease were seen. Ponies given dried leaves collected after September 15 died by 18 hours, while ponies given dried leaves collected before September 15 became ill with a hemolytic syndrome and died by three to five days. Freshly harvested leaves administered immediately after collection did not produce disease in ponies, but when dried, they became toxic and remained so for at least 30 days. Overnight freezing did not alter the toxicity of the leaves. Leaves were toxic when administered at doses of 1.5 gm/kg of body weight. The clinical signs of ponies with the hemolytic syndrome included polypnea, tachycardia, icterus, cyanosis, scleral petechiation, and brownish discoloration of the urine and blood. Blood changes of ponies with the hemolytic syndrome included anemia, hemoglobinemia, Heinz bodies, depletion of erythrocyte reduced glutathione, increased erythrocyte fragility, and increased serum levels of aspartate amino transferase, sorbitol dehydrogenase, plasma protein, and bilirubin. Lesions of ponies that died from the hemolytic syndrome included icterus, centrilobular hepatic degeneration, hemoglobinemic nephrosis, and erythrophagocytosis by splenic, adrenal, and hepatic phagocytes. Only brownish discoloration of the blood and mild centrilobular hepatic degeneration were observed in the four ponies that died peracutely.