Equine inflammatory response to abdominal surgery in the absence of gastrointestinal disease.

OBJECTIVE: To investigate the, equine inflammatory response to ventral midline celiotomy in the absence of gastrointestinal disease in horses of varying body condition scores primarily using serial measurements of serum amyloid A (SAA). DESIGN: Experimental clinical study. SETTING: University teaching hospital. ANIMALS: Ten adult light breed horses free of any clinical disease, 5 with body condition score (BCS) 3-4/9 and 5 with BCS 7-8/9. INTERVENTIONS: Horses had a ventral midline celiotomy performed under general anesthesia, including manual decompression of the small intestine. SAA, semiquantitative fibrinogen, plasma lactate, and WBC count were measured in the blood preoperatively and at 12, 24, 48, 72, 120, and 168 hours postoperatively. Complete serum biochemistry was performed preoperatively and 24 and 72 hours postoperatively. Serial abdominocentesis was also performed with peritoneal fluid analysis of SAA, total protein, lactate, WBC count, and cytology. MEASUREMENTS AND MAIN RESULTS: Significant (P < 0.05) increases in serum SAA were noted at 12, 24, and 48 hours postoperatively (124.6 ± 68.6, 390.8 ± 209.0, 568.6 ± 197.7 µg/mL), and most horses had values approaching normal at 168 hours postoperatively (174.4 ± 307.7 µg/mL). Other values such as fibrinogen also increased in response to surgery but did not return to normal within the measured time points. Horses with high BCS did not have significantly different serum SAA compared to horses with low BCS. Peritoneal fluid SAA did not increase significantly at 12 hours postoperatively. CONCLUSIONS: The information from this study can be used to help determine the effect of anesthesia and surgical intestinal manipulation resulting in increased SAA when a comparison to clinical or experimental cases is needed.

Double outlet right ventricle with subpulmonary ventricular septal defect (Taussig-Bing anomaly) and other complex congenital cardiac malformations in an American Quarter Horse foal.

A 4-week-old American Quarter Horse colt presented with a recent history of diarrhea and decreased activity level. On initial physical examination, the animal was bright and alert and major findings were limited to a loud systolic heart murmur radiating widely over both sides of the thorax. While in the hospital, the clinical condition of the foal warranted further imaging to determine the cause and extent of cardiac disease. A variety of congenital cardiac malformations were identified during echocardiographic examination and autopsy, including a double outlet right ventricle and a subpulmonary interventricular septal defect (Taussig-Bing anomaly), ventricular inversion with atrioventricular discordance, tricuspid valve atresia, a septum primum interatrial septal defect, mitral valve dysplasia with a cleft in the septal mitral valve cusp, aortic, and subaortic stenosis, tubular hypoplasia of the ascending aorta and the aortic arch, a patent ductus arteriosus, an aberrant circumflex coronary artery, and aberrant left and right subclavian arteries. Echocardiographic and postmortem findings of the cardiac defects in this foal are presented and discussed.

The effect of hypothermia on influx of leukocytes in the digital lamellae of horses with oligofructose-induced laminitis.

Sepsis-related laminitis (SRL) is a common complication in the septic/endotoxemic critically-ill equine patient, in which lamellar injury and failure commonly lead to crippling distal displacement of the distal phalanx. Similar to organ injury in human sepsis, lamellar injury in SRL has been associated with inflammatory events, including the influx of leukocytes into the lamellar tissue and markedly increased expression of a wide array of inflammatory mediators at the onset of Obel grade 1 (OG1) laminitis. The only treatment reported both clinically and experimentally to protect the lamellae in SRL, local hypothermia ("cryotherapy"), has been demonstrated to effectively inhibit lamellar expression of multiple inflammatory mediators when initiated at the time of administration of a carbohydrate overload in experimental models of SRL. However, the effect of hypothermia on leukocyte influx into affected tissue has not been assessed. We hypothesized that cryotherapy inhibits leukocyte emigration into the digital lamellae in SRL. Immunohistochemical staining using leukocyte markers MAC387 (marker of neutrophils, activated monocytes) and CD163 (monocyte/macrophage-specific marker) was performed on archived lamellar tissue samples from an experimental model of SRL in which one forelimb was maintained at ambient temperature (AMB) and one forelimb was immersed in ice water (ICE) immediately following enteral oligofructose administration (10g/kg, n=14 horses). Lamellae were harvested at 24h post-oligofructose administration (DEV, n=7) or at the onset of OG1 laminitis (OG1, n=7). Both MAC387-positive and CD163-positive cells were counted by a single blinded investigator on images [n=10 (40× fields/digit for MAC387 and 20x fields/digit for CD163)] obtained using Aperio microscopy imaging analysis software. Data were assessed for normality and analyzed with a paired t-test and one-way ANOVA with significance set at p<0.05. MAC387-positive cells were present in low numbers in the lamellar tissue and were decreased in the hypothermic limbs (vs. AMB limbs, p<0.05) in the OG1 group; no change in CD163-positive cell numbers was noted across the conditions of the model. This study demonstrated that hypothermia of the distal limbs instituted early in the disease process in the horse at risk of SRL significantly attenuates the increase of MAC387-positive leukocytes in the digital lamellae, but has minimal effect on increases in lamellar concentrations of the major leukocyte cell type present in that tissue, CD163-positive mononuclear cells.