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Abstract: An intestinal fistula is a communication between the gut and another epithelial surface. Primary disease of the gut (Crohn’s disease, diverticular disease, colorectal cancer, radiation enteritis) can all lead to fistula formation which then requires resection of the diseased bowel to close the fistula. Injury (usually iatrogenic) produces a fistula through normal gut and if circumstances are favourable such an injury can close spontaneously. Some postoperative fistulae will not close spontaneously and they require a systematic approach that eliminates sepsis (S), restores nutrition (N), determines anatomy (A) and leads to a closure procedure (P) - SNAP. Sound abdominal closure is an essential feature of surgery to close an intestinal fistula. [Copyright &y& Elsevier]

Abstract: Intestinal fistulas are abnormal communications between the gut and an adjoining viscus or skin. They may be classified into those arising from diseased bowel (type I), where spontaneous closure is unlikely or injury to otherwise normal bowel (type II), where closure is more likely. They present a complex management problem, often involving a multidisciplinary team (surgeons, gastroenterologists, intensivists, dieticians, stoma therapists, pharmacists, experienced nursing staff, clinical psychologists). The management of type-I fistulas requires attention to the primary disease, and treatment is often surgical. Type-II fistulas, which arise postoperatively from damage to normal gut, should be managed initially by resuscitation because these patients can be severely septic. The next step, restitution, requires attention to ‘SNAP’ (sepsis, nutrition, anatomy and plan). Surgical reconstruction can then be planned, followed by rehabilitation. [Copyright &y& Elsevier]

The mechanism by which cigarette smoking promotes atherosclerosis remains unclear but may involve the endothelium and leukocytes. We postulated a direct acute effect of cigarette smoking on the endothelium and granulocytes by measuring granulocyte expression of L-selectin (flow cytometry) and serum L- and E-selectin (ELISA) before and after smoking in 12 smokers with peripheral vascular disease (claudicants) and 12 otherwise healthy controls.Mean (S.D.) granulocyte L-selectin, expressed as mean fluorescence intensity (MFI), increased in a dose-dependent fashion from 3.58±0.67 and 3.27±0.67 in controls and claudicants, respectively, to 3.77±0.75 and 3.49±0.79 10 min after smoking two cigarettes (p<0.002), and to 4.11±0.95 and 3.67±0.88 30 min after four cigarettes (p<0.001). Serum L-selectin was lower in claudicants at all time points throughout the study period compared with controls (p<0.005) but neither serum E- nor L-selectin levels changed following smoking.Smoking led to an increase in granulocyte expression of L-selectin, which may be important in granulocyte/endothelial adhesion and thus related to atherosclerosis. The lower serum L-selectin levels in claudicants, and the absence of a rise in serum adhesion molecules on smoking, suggests consumption by activated endothelial receptors that may be part of a negative feedback mechanism. [Copyright &y& Elsevier]