Treatment of delayed jejunal perforation after irreducible femoral hernia repair with open abdomen management and delayed abdominal closure with skin flap approximation

Introduction: We show the management of a delayed jejunal perforation, after irreducible femoral hernia operation with the help of negative pressure therapy (NPT) and delayed abdominal closure (DAC) with skin flap approximation in an elderly woman for the first time in the literature. Presentation of case: A 76 year-old woman was admitted to the emergency department with irreducible femoral hernia and ileus. After examining the femoral hernia sac and noting the presence of viable intestine within the hernia sac, a femoral hernia repair with mesh was performed. At postoperative day 1 she started to defecate and oral intake was started. The patient was discharged on postoperative day 3. On postoperative day 8, she was re-admitted to the emergency department with septic shock. The patient underwent reoperation. Septic abdomen and delayed perforation from strangulated part of the jejunum were seen. A jejunostomy was opened and patient was treated with open abdomen management and delayed abdominal closure with skin flap. The ostomy was closed 4 months later. Discussion: The exact mechanism of delayed presentation of small bowel perforation remains controversial. Delayed intestinal perforation has rarely been reported after blunt abdominal trauma (BAT), conductive burn injuries of the bowel with cautery, or necrosis of strangulated bowel in a hernia sac. Open abdomen (OA) management is a life-saving and challenging strategy in severe generalized peritonitis. Conclusion: Delayed bowel perforation may develop after irreducible femoral hernia surgery. OA management with NPT and DAC with skin flap approximation are optimal treatment modalities for the hemodynamically instable patient

Prophylactic Ozone Administration Reduces Intestinal Mucosa Injury Induced by Intestinal Ischemia-Reperfusion in the Rat

Objectives. Intestinal ischemia-reperfusion injury is associated with mucosal damage and has a high rate of mortality. Various beneficial effects of ozone have been shown. The aim of the present study was to show the effects of ozone in ischemia reperfusion model in intestine. Material and Method. Twenty eight Wistar rats were randomized into four groups with seven rats in each group. Control group was administered serum physiologic (SF) intraperitoneally (ip) for five days. Ozone group was administered 1 mg/kg ozone ip for five days. Ischemia Reperfusion (IR) group underwent superior mesenteric artery occlusion for one hour and then reperfusion for two hours. Ozone + IR group was administered 1 mg/kg ozone ip for five days and at sixth day IR model was applied. Rats were anesthetized with ketamine∖xyzlazine and their intracardiac blood was drawn completely and they were sacrificed. Intestinal tissue samples were examined under light microscope. Levels of superoxide dismutase (SOD), catalase (CAT), glutathioneperoxidase (GSH-Px), malondyaldehide (MDA), and protein carbonyl (PCO) were analyzed in tissue samples. Total oxidant status (TOS), and total antioxidant capacity (TAC) were analyzed in blood samples. Data were evaluated statistically by Kruskal Wallis test. Results. In the ozone administered group, degree of intestinal injury was not different from the control group. IR caused an increase in intestinal injury score. The intestinal epithelium maintained its integrity and decrease in intestinal injury score was detected in Ozone + IR group. SOD, GSH-Px, and CAT values were high in ozone group and low in IR. TOS parameter was highest in the IR group and the TAC parameter was highest in the ozone group and lowest in the IR group. Conclusion. In the present study, IR model caused an increase in intestinal injury.In the present study, ozone administration had an effect improving IR associated tissue injury. In the present study, ozone therapy prevented intestine from ischemia reperfusion injury. It is thought that the therapeutic effect of ozone is associated with increase in antioxidant enzymes and protection of cells from oxidation and inflammation.PubMedWoSScopu

33 Questions about Triglycerides and Cardiovascular Effects: Expert Answers

WOS: 000396440800002PubMed ID: 2844673