buprenorphine hydrochloride The diagnosis of VPS induced bowel perforation is often difficult

The diagnosis of VPS-induced bowel perforation is often difficult and predominantly depends upon the clinical manifestations, abdominal X-ray, ultrasound, and CT results. Typically, bowel perforation is considered in shunted patients with unexplained fever or prominent abdominal symptoms. Additionally, gut buprenorphine hydrochloride meningitis, confirmed through CSF culture or pneumocephalus observed in the head CT, may be an indicator of intestinal perforation. However, many cases do not manifest shunt infection or peritonitis, and bowel perforation is recognized only during shunt revision for obstruction. By contrast, the diagnosis is easy if patients with prior VPS operation present with anal protrusion of the tube, as was the case in our patient. The plain abdominal roentgenogram revealed that the long peritoneal tube encircled the abdomen and progressed to the perineal region, and the CT scan revealed that the tube entered the ileum and progressed to the colon. Occasionally, a shuntogram can be used to demonstrate the mucosal pattern of the intestine, which was the case in the three patients with VPS-induced small-intestinal perforation reported in the literature.
The management of the VPS-induced small-intestinal perforation must be individualized according to the clinical conditions of the patients. Typically, removing the protruded shunt system and controling the infection, followed by CSF diversion, is the standard treatment protocol,; however, abdominal exploration for managing VPS-induced intestinal perforation is controversial. Several reports demonstrated that the peritoneal tube can be removed without abdominal exploration, because the opening into the bowel lumen is often small and self-sealing in the absence of peritonitis or abdominal abscess. Abdominal exploration for perforation repair might be required in cases accompanied by peritonitis, abdominal abscess, acute bowel perforation, failure of the closure of the fistulous tract following peritoneal tube removal, difficulty in removing the peritoneal tube, and knotting or twisting of the peritoneal tube. In a report reviewing 45 cases of VPS-induced intestinal perforation, the shunt tube was removed without abdominal exploration in 31 patients (68.9%), laparotomy for bowel repair was performed in eight patients (17.8%), and an unclear method of tube retrieval was used in six patients (13.3%). Concerning abdominal exploration, laparoscopic surgery can be performed as an alternative to laparotomy, however, only in one report was a patient with VPS-induced silent bowel perforation managed laparoscopically. Our patient had persistent intermittent abdominal pain and focal ileus; therefore, we performed laparoscopic surgery for diagnosis and definite repair. The resection of the involved ileum and anastomosis was performed extracorporeally through laparoscopy.
The prognosis for recovery in patients with VPS-induced bowel perforation is more accurate when bowel perforation is detected at the asymptomatic stage. However, if bowel perforation is undetected, patients are at a high risk of developing meningitis or ventriculitis, and the mortality rate may increase to 15%.

Ischemic bowel disease varies from full-thickness necrosis or gangrene to transient inflammation. The disease is caused by occlusion or stenosis either of the mesenteric artery or, less frequently, the vein. Some cases are idiopathic, whereas others may be due to decreased perfusion in the absence of a vascular lesion. Phlebosclerotic colitis is a rare chronic and gradually worsening ischemic colitis caused by phlebosclerosis of the mesenteric vein and its tributaries. Its symptoms are the gradual onset of right-side abdominal pain with or without diarrhea, and recurrent ileus. The most commonly affected site is the region from the terminal ileum to the sigmoid colon, particularly the cecum and ascending colon.
The characteristic radiologic findings of mesenteric phlebosclerosis are luminal narrowing, wall thickening of the affected colon (typically the proximal colon), and calcification of the mesenteric veins. Plain radiographs and computed tomography can easily detect the characteristic linear calcification of numerous branches of the mesenteric vein at the affected site.