In-hospital and 6-month mortality rates after open elective vs open emergent colectomy in patients older than 80 years.

BACKGROUND: There are few reports of long-term outcomes in elderly patients after open colectomy. OBJECTIVE: This study aimed to determine the in-hospital and 6-month outcomes and identify the variables associated with mortality after colectomy in patients ≥ 80 years of age. DESIGN: The charts of patients ≥ 80 years of age, who underwent open colectomy, were analyzed. Data included indications for operation, underlying diagnoses, preoperative functional status, type of procedure, length of procedure, length of stay, ASA grade, complications, and in-hospital and 6-month mortality rates. Univariate and multivariate logistic regression analyses were conducted to ascertain risk factors for mortality. P values of < .05 were considered significant. MAIN OUTCOME MEASURES: The main outcome measures were in-hospital and 6-month mortality. RESULTS: One hundred sixty-two patients ≥ 80 years of age underwent colectomy: 99 patients emergently; 63, electively. Postoperative acute renal failure (3% vs 19%, P = .0032) and in-hospital deaths were significantly higher (4.7% vs 28%, P = .0002) among the patients undergoing emergent colectomies. The mortality rate among emergent cases rose from 28% in-hospital to 52% at 6 months. Mortality among the elective cases increased similarly from 4.7% to 28.5%. Admission from a nursing facility was associated with higher in-hospital mortality (47.6% vs 14.9%, P = .0005). Discharge to a skilled nursing facility was associated with a higher 6-month mortality rate compared with discharge to home (40% vs 17%). Length of procedure, postoperative complications, perioperative blood transfusion, and emergent indications for operation independently predicted in-hospital mortality. Postoperative complications and emergent diagnosis independently predicted 6-month mortality. The 6-month mortality rate varied according to the underlying diagnosis as follows: fulminant Clostridium difficile colitis (86%); ischemic colitis (60%); gastrointestinal bleeding (37%), and volvulus (40%). LIMITATIONS: This study was limited by its retrospective nature. CONCLUSIONS: Emergent open colectomy in elderly patients is associated with a high morbidity and mortality rate. The mortality rate rises by >20% in both elective and emergent cases at discharge to 6 months. Length of procedure, postoperative complications, and colectomy for emergent indications predicted mortality.

VILIP-1 expression in vivo results in decreased mouse skin keratinocyte proliferation and tumor development.

VILIP-1, a member of the neuronal Ca(2+) sensor protein family, is able to act as a tumor suppressor in carcinoma cells by inhibiting cell proliferation and migration. In order to study the role of VILIP-1 in skin carcinogenesis we generated transgenic mice overexpressing VILIP-1 in epidermis under the control of the bovine keratin K5 promoter (K5-VILIP-1). We studied the susceptibility of FVB wild type and VILIP-1 transgenic mice to chemically mediated carcinogenesis. After 30 weeks of treatment with a two-stage carcinogenesis protocol, all animals showed numerous skin tumors. Nevertheless, K5-VILIP-1 mice showed decreased squamous cell carcinoma (SCC) multiplicity of approximately 49% (p<0.02) with respect to the corresponding SCC multiplicity observed in wild type (WT) mice. In addition, the relative percentage of low-grade cutaneous SCCs grade I (defined by the differentiation pattern according to the Broders grading scale) increased approximately 50% in the K5-VILIP1 mice when compared with SCCs in WT mice. Similar tendency was observed using a complete carcinogenesis protocol for skin carcinogenesis using benzo(a)pyrene (B(a)P). Further studies of tumors and primary epidermal keratinocyte cultures showed that matrix metalloproteinase 9 (MMP-9) levels and cell proliferation decreased in K5-VILIP-1 mice when compared with their wild counterparts. In addition tissue inhibitor of metalloproteinase 1 (TIMP-1) expression was higher in K5-VILIP-1 keratinocytes. These results show that VILIP-1 overexpression decreases the susceptibility to skin carcinogenesis in experimental mouse cancer models, thus supporting its role as a tumor suppressor gene.