BackgroundEmphysematous cholecystitis is a variant of acute cholecystitis which is generally caused by gas-forming organisms. Emphysematous cholecystitis may cause gas spreading within the subcutaneous tissue, peritoneal cavity and retroperitoneum.Case presentationWe present a case of emphysematous cholecystitis in a middle-aged diabetic patient who, postoperatively, presented edema in both flanks and left chest crepitation on palpation, associated with hemodynamic worsening. Computed tomography scan of the chest and abdomen revealed a large pneumomediastinum, pneumoretroperitoneum, gas in subcutaneous tissue and flank abscesses. In both blood and surgical wound exudate cultures, Escherichia coli was found.ConclusionEmphysematous cholecystitis should be considered as a possible cause of pneumomediastinum.

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In our experience, perforated cancers had higher survival rates and metastasis-free interval that non-perforated cancers, probably by a lower number of metastatic lymph nodes, smaller LNR and better TNM stage. Moreover the predictive value, in mortality rate, of metastatic lymph nodes and LNR was similar.

Colorectal tumor perforation is a life-threatening complication of this disease. However, little is known about the anatomopathological factors or pathophysiologic mechanisms involved.Pathological and immunohistochemical analysis of factors related with tumoral neo-angiogenesis, which could influence tumor perforation are assessed in this study. A retrospective study of patients with perforated colon tumors (Group P) and T4a nonperforated (controls) was conducted between 2001 and 2010. Histological variables (differentiation, vascular invasion, and location) and immunohistochemical (CD31, Growth Endothelial Vascular Factor (VEGF) and p53) related with tumor angiogenesis were analyzed.Of 2189 patients, 100 (4.56%) met the inclusion criteria. Of these, 49 patients had nonperforated (2.23%) and 51 had perforated tumors (2.32%). The P group had lower number of right-sided tumors (7/51, 13.7%) compared with controls (13/49, 36.7%) (P = .01). The high-grade tumors (undifferentiated) represented only 3.9% of the perforated tumors; the remaining 96.1% were well differentiated (P = .01). No differences between groups in the frequency of TP53 mutation or VEGF and CD31 expression were found. In the P group, only 2 (3.9%) had vascular invasion (P = .01). Of the 12 tumors with vascular invasion, only 2 were perforated (16.6%). The median number of metastatic lymph-nodes in P Group was 0 versus 3 in controls (Z = −4.2; P < .01).Pathological analysis of variables that indirectly measure the presence of tumor angiogenesis (differentiation, vascular invasion, and the number of metastatic lymph nodes) shows a relationship between this and the perforation, location, and tumor differentiation. We could not directly validate our hypothesis, by immunohistochemistry of TP53, VEGF, and CD31, that perforated tumors exhibit less angiogenesis.