Prevention of ischaemia-induced small intestinal adhesions in foals

Treatments addressing variously theorised pathophysiological mechanisms of small intestinal adhesions have been reported. This study applied those classes of treatments to the most clinically relevant aetiology of post operative adhesions.

Treatments addressing the pathophysiology of ischaemia-reperfusion induced adhesions would accordingly reduce the incidence of adhesions from this model.

Four classes of treatments were administered for 72 h to 16 foals subjected to complete ischaemia followed by reperfusion to create peritoneal adhesions. These groups were: 1) FPG group--flunixin meglumine (1.1 mg/kg bwt i.v., divided q.i.d.), potassium penicillin G (22,000 iu/kg bwt i.v., q.i.d.) and gentamicin (2.2 mg/kg bwt i.v., t.i.d.); 2) HEP group--heparin (80 iu/kg bwt subcut., b.i.d.); 3) DMSO group--dimethylsulphoxide (DMSO) (20 mg/kg bwt [diluted in 500 ml normal saline] i.v., b.i.d.); and 4) SCMC group--sodium carboxymethylcellulose (500 ml 3% sterile solution intraperitoneally, administered only at the beginning of surgery).

Post operative intestinal obstruction did not occur in any foal. After 10 days, necropsy revealed bowel-to-bowel adhesions in none of the FPG or DMSO groups, in 2/4 of the SCMC group, in 3/4 of the HEP group and 5/6 foals subjected to the procedure without treatment (UIR group).

Inhibition of the inflammation associated with ischaemia and reperfusion in foals treated with FPG or DMSO decreased small intestinal adhesions in foals.

Although anti-inflammatory therapy was shown to eliminate bowel-bowel adhesions in this controlled study, it must be remembered that clinical cases are without control. These therapies are advised to improve the result but are unlikely to eliminate the problem.