This factor along with peristaltic hypofunction

This factor, along with peristaltic hypofunction associated with diabetic autonomic neuropathy, may lead to raised intraluminal pressure, allowing the gas-producing bacteria to invade the colonic mucosa through mucosal breaks, forming pneumocysts. Histologically, the cysts of pneumatosis cystoides intestinalis are pseudocysts because they lack an epithelial lining. However, they may become surrounded by a rim of histiocytes, multinuclear giant cells, lymphocytes, neutrophils, eosinophils, granulomas, and fibrosis, especially after they collapse. An endoscopic examination could exhibit “polypoid” intraluminal masses corresponding to pneumocysts, which should not be misdiagnosed for a diffuse polyposis. Pneumatosis cystoides intestinalis remains a challenging diagnostic problem on biopsy material, except when a deep biopsy allows differential diagnosis with colonic polyposis. Because the cysts may rapidly deflate after the biopsy, this presentation provides an important clue for diagnosis. Contrast studies of the gastrointestinal tract can demonstrate filling defects within the intestinal lumen corresponding to protrusion of submucosal gas-filled cysts. Characteristic findings of pneumatosis cystoides intestinalis by computer tomography include circumferential collections of air adjacent to the lumen of the bowel that run in parallel with the wall of the bowel. However, those findings also mimic transmural infarction of the bowel in patients with intestinal ischemia. Patients with life-threatening bowel ischemia or perforation may present with metabolic acidosis, systemic ambroxol hydrochloride syndrome, and hepatic portal vein gas. Consideration of both image findings and clinical presentation could help in the differential diagnosis. Because the illness is usually a self-limited condition, and intramural gas cysts may disappear spontaneously over time, no specific therapy is, in most cases, needed, other than treatment of the underlying disease of pneumatosis cystoides intestinalis for patients who are asymptomatic or minimally symptomatic. Symptomatic pneumatosis cystoides intestinalis often responds to a conservative management, for example, oxygen therapy, administration of an elemental diet, antibiotic therapy, or discontinuation of the alpha-glucosidase inhibitor. Hyperbaric oxygen could be used to reduce the duration of oxygen administration and the potential risk of oxygen toxicity to the lung. When needed, hyperbaric oxygen therapy is the treatment of choice if there is no contraindication. Failure in recognition and treatment of the underlying disease of pneumatosis cystoides intestinalis will result in a high recurrence rate (50–78%).
Introduction Tumors in the cervical portion of the esophagus account for 7–10% of all esophageal cancers. Tracheoesophageal (TE) fistula occurs in approximately 5–15% of patients with esophageal cancer. Esophageal stents in this area have traditionally been considered to be contraindicated. An increased risk of perforation, pulmonary aspiration [by compromising upper esophageal sphincter (UES) function], migration of the prosthesis into the hypopharynx, and an intolerable foreign body sensation, are general concerns. Although a cervical esophageal lesion can be successfully managed by placement of a Polyflex stent across the UES temporarily without major complications, avoidance of a permanent esophageal stent across the UES is generally agreed upon. We report a patient with TE fistula recurrence after stenting. He was treated successfully with a modified self-expanding metal stent (SEMS) in addition to a previous SEMS.
Case report One month later, severe cough recurred. A plain chest film X-ray showed pneumonia. In view of the patient’s previous history, chest CT, esophagography and bronchoscopy (Fig. 1A) were performed to confirm TE fistula recurrence. The images revealed a TE fistula proximal to the previous SEMS. The new TE fistula was located at 20 cm from the incisor, which was rather close to the upper esophageal sphincter (UES). Considering that retraction of the first SEMS might cause further extension of the TE fistula, we did not remove the stent. Instead, we deployed another modified SEMS with a smaller funnel-shape proximal end (Fig. 2). The proximal end of the new SEMS was placed at 17 cm from the incisor.