Management of rectal stump leak following emergency Hartmann's procedure / Gerenciamento do vazamento do coto retal após o procedimento de emergência de Hartmann

ABSTRACT We report on the management of three cases of rectal stump leak and sepsis following urgent Hartmann's procedure for perforated sigmoid diverticulitis or large bowel obstruction. Two patients had significant risk factors for poor tissue healing. All patients developed features of sepsis and computer tomography scans demonstrated rectal stump leak with adjacent collections. All patients required reoperation for drainage and washout of abscess. An intraperitoneal catheter system was introduced together with drains in order to continue on the ward until tract was formed. There was no mortality and minimal morbidity. The key to management of rectal stump leak is the early and aggressive drainage of the associated collection and continued irrigation of the stump.

RESUMO Relatamos o tratamento de três casos de vazamento de coto retal e sepse após o procedimento de urgente de Hartmann para diverticulite sigmoide perfurada ou obstrução do intestino grosso. Dois pacientes apresentaram fatores de risco significativos para uma má cicatrização tecidual. Todos os pacientes desenvolveram características de sepse e tomografia computadorizada demonstraram vazamento de coto retal com coleções adjacentes. Todos os pacientes necessitaram de reoperação para drenagem e lavagem do abscesso. Um sistema de cateter intraperitoneal foi introduzido junto com os drenos para continuar na enfermaria até a formação do trato. Não houve mortalidade e morbidade mínima. A chave para o gerenciamento do vazamento de coto retal é a drenagem precoce e agressiva da coleta associada e a irrigação contínua do coto.

Mouse Model of Mutated in Colorectal Cancer Gene Deletion Reveals Novel Pathways in Inflammation and Cancer.

BACKGROUND & AIMS: The early events by which inflammation promotes cancer are still not fully defined. The MCC gene is silenced by promoter methylation in colitis-associated and sporadic colon tumors, but its functional significance in precancerous lesions or polyps is not known. Here, we aimed to determine the impact of Mcc deletion on the cellular pathways and carcinogenesis associated with inflammation in the mouse proximal colon. METHODS: We generated knockout mice with deletion of Mcc in the colonic/intestinal epithelial cells (MccΔIEC) or in the whole body (MccΔ/Δ). Drug-induced lesions were analyzed by transcriptome profiling (at 10 weeks) and histopathology (at 20 weeks). Cell-cycle phases and DNA damage proteins were analyzed by flow cytometry and Western blot of hydrogen peroxide-treated mouse embryo fibroblasts. RESULTS: Transcriptome profiling of the lesions showed a strong response to colon barrier destruction, such as up-regulation of key inflammation and cancer-associated genes as well as 28 interferon γ-induced guanosine triphosphatase genes, including the homologs of Crohn's disease susceptibility gene IRGM. These features were shared by both Mcc-expressing and Mcc-deficient mice and many of the altered gene expression pathways were similar to the mesenchymal colorectal cancer subtype known as consensus molecular subtype 4 (CMS4). However, Mcc deletion was required for increased carcinogenesis in the lesions, with adenocarcinoma in 59% of MccΔIEC compared with 19% of Mcc-expressing mice (P = .002). This was not accompanied by hyperactivation of ß-catenin, but Mcc deletion caused down-regulation of DNA repair genes and a disruption of DNA damage signaling. CONCLUSIONS: Loss of Mcc may promote cancer through a failure to repair inflammation-induced DNA damage. We provide a comprehensive transcriptome data set of early colorectal lesions and evidence for the in vivo significance of MCC silencing in colorectal cancer.