Ann R Coll Surg Engl 2005; 87: 427-431 427The annual incidence of stoma formation in England is 20,800, 1 although recent literature would suggest that this figure is unnecessarily high. The management of obstructing left-sided colorectal cancer has changed in recent times, with increased use of on -table lavage with primary resection and anastomosis 2,3 and colorectal stenting 4 to avoid stoma formation. Sphincter preserving surgery for rectal cancer should also reduce permanent stoma rates. 5Persistently high morbidity and mortality rates associated with stoma creation and reversal are behind attempts to reduce their formation. Long-term complication rates of 58% in colostomies 6 and up to 76% in ileostomies 7 have been reported. It is also recognised that around 15% of temporary stomas created at the time of anterior resection become permanent. 8There has been much recent work examining risk factors for mortality in colorectal cancer surgery, 9 such as ASA grade and age, but whether the presence of a stoma affects mortality has not been previously examined. Studies have addressed the mortality following stoma reversal (0-4%), 10 but the literature is scant when stoma creation is concerned.We have examined whether the incidence of stoma formation is declining in the practice of a typical district general hospital, and investigated the prevalent morbidity and mortality associated with stoma creation, together with their risk factors. Patients and MethodsAll patients undergoing colostomy or ileostomy formation (elective and emergency) from January 1992 to December 2000 were identified. Data were collected from patient records maintained prospectively by the stomatherapy department, supported by information from operation notes and patient case records. Complications recorded were necrosis, prolapse, peristomal infection or abscess, retraction, stenosis, parastomal hernia, fistula and malignant change at the stoma site.Complications not included were skin excoriation and laparotomy wound problems.Operations were performed by one of seven consultant general surgeons or their registrars, three of whom had a declared interest in coloproctology. Patients undergoing bowel resection without stoma formation were not studied. Statistical analysisResults are expressed as the mean (SD) Stoma Care, Royal Glamorgan Hospital, Ynysmaerdy, Llantrisant, Mid-Glamorgan, UK ABSTRACT INTRODUCTION As stoma formation is thought to be declining, we performed a study to evaluate the rate of stoma formation and the impact on stoma complication rates, together with risk factors for complications.

Interleukin-6 signaling via its soluble receptor (sIL-6R) differentially regulates inflammatory chemokine expression and leukocyte apoptosis to coordinate transition from neutrophil to mononuclear cell infiltration. sIL-6R activities may, however, be influenced in vivo by the occurrence of two sIL-6R isoforms that are released as a consequence of differential mRNA splicing (DS) or proteolytic cleavage (PC) of the cognate IL-6R (termed DS- and PC-sIL-6R). Using human peritoneal mesothelial cells and a murine model of peritoneal inflammation, studies described in this work have compared the ability of both isoforms to regulate neutrophil recruitment. In this respect, DS- and PC-sIL-6R were comparable in their activities; however, these studies emphasized that IL-6 trans signaling differentially controls neutrophil-activating CXC chemokine expression. In vitro, stimulation of mesothelial cells with IL-6 in combination with either DS-sIL-6R or PC-sIL-6R showed no induction of CXC chemokine ligand (CXCL)1 (GROα) and CXCL8 (IL-8), whereas both isoforms enhanced CXCL5 (ENA-78) and CXCL6 (granulocyte chemotactic protein-2) expression. Moreover, when complexed with IL-6, both isoforms specifically inhibited the IL-1β-induced secretion of CXCL8. These findings were paralleled in vivo, in which induction of peritoneal inflammation in IL-6-deficient (IL-6−/−) mice resulted in enhanced keratinocyte-derived chemokine and macrophage-inflammatory protein-2 (the murine equivalent of CXCL1 and CXCL8) levels, but reduced LPS-induced CXC chemokine (the murine equivalent of CXCL5) expression. Reconstitution of IL-6 signaling in IL-6−/− mice with IL-6 and its soluble receptor isoforms corrected this chemokine imbalance and suppressed overall neutrophil infiltration. These data confirm that sIL-6R-mediated signaling primarily limits neutrophil influx; however, induction of CXCL5 and CXCL6 may regulate other neutrophil responses.

An aggressive surgical strategy with complete resection is predictive of long-term survival in selected patients with T4a rectal carcinoma. With optimal treatment local recurrence is a sign of systemic disease.

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