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.