Serum Amyloid A concentrations in horses following anaesthesia with and without surgery

Introduction In horses, the serum concentration of the major acute phase protein Serum Amyloid A (SAA) increases following surgery, trauma or infection. The increase in SAA concentration following surgery under anaesthesia is thought to be due to surgically induced tissue trauma. The effect of anaesthesia itself on SAA is poorly documented. In this study, the SAA response was analysed in horses that were anaesthetised twice, once with and once without specific surgery, to examine whether the increased SAA concentration after surgery results partially from the anaesthetic procedure per se. Material and Methods Seven horses were anaesthetized once (treatment A) and then a second time - after six months - with an identical anaesthetic protocol except that they were subjected to surgical translocation of the carotid artery under anaesthesia (treatment B). Venous blood samples for analysis of SAA concentration and creatine kinase (OK) activity were taken before (one hour) and one, six, twelve, 24, 48 and 72 hours after the end of anaesthesia. The SAA concentration was quantified with an ELISA test kit and OK activity was determined by photometry. Data were displayed by descriptive statistics and the Wilcoxon T-test was used to assess the significance of differences. Results Both treatments were followed by an increase in SAA concentration. In treatment A, the SAA peak occurred 24 hours after the end of anaesthesia whereas it occurred 48 hours after treatment B. The increase in SAA was higher when surgery was performed (treatment B). After 72 hours there was a significant difference between the treatments. The median peak values for group A were 520.7 mg/l (quartile 25/75: 94.8/601.7 mg/l) and for group B 3,716.4 mg/l (quartile 25/75: 292.4/7,554.8 mg/l). CK activity increased following both treatments. Conclusion The rise of serum SAA concentration after-surgical procedures under general anaesthesia is partly due to the anaesthesia. A likely contributor is muscle damage following reduced muscle perfusion and local hypoxia due to the high intracompartmental muscle pressure that develops during anaesthesia and recumbency in the horse. Another cause may be the stress response, with increased levels of glucocorticoids due to the inhalation anaesthetic isoflurane.