Faik Yaylak

The clinical features of Fournier’s gangrene and the predictivity of the Fournier’s Gangrene Severity Index on the outcomes

Fournier’s gangrene (FG) is a rare, rapidly progressive, fulminant form of necrotizing fasciitis of the genital, perianal and perineal regions. Several factors have been reported to contribute to the clinical outcomes. The primary aims of this study were to examine the clinical features of patients with FG and evaluate the predictivity of the Fournier’s Gangrene Severity Index (FGSI) score on the outcomes. We carried out a collective retrospective chart review of patients diagnosed and treated for FG in three reference centers between January 1995 and July 2007. Seventy-two patients with FG with were included to the study. Data were collected on medical history, symptoms, physical examination findings, admission and final laboratory tests, timing and extent of surgical debridement and antibiotic therapy. Perianal and perirectal abscess, scrotal abscess and urethral stenosis were the leading etiological factors. Diabetes mellitus was the predominant risk factor. Etiological factors and risk factors did not significantly contribute to survival or mortality, and duration of the symptoms was significantly longer in the non-survivors group (Pxa0<xa00.05). The FGSI scores were higher in the non-survivors group. Regression analysis showed a FGSIS score of 10.5 as the cut-off to the outcome. Based on these results, we conclude that a patient’s metabolic status and the extent of disease at presentation are the most important factors determining the prognosis of FG. The FGSI score may be considered as an objective and simple tool to predict the outcome in the patient with FG and should be used in further studies of FG patient series for comparison purposes.

Silymarin attenuates the renal ischemia/reperfusion injury-induced morphological changes in the rat kidney

ObjectivesRenal ischemia/reperfusion (I/R) injury is associated with increased mortality and morbidity rates due to acute renal failure (ARF). Oxidative stress induced with renal I/R injury directly affects glomerular and tubular epithelium through reactive oxygen species. Several studies have been directed to the treatment of renal I/R injury. The aim of this study was to test the attenuation with silymarin (SM) treatment of renal I/R injury-induced morphological changes in the rat kidney.MethodsA total of 32 adult male Sprague-Dawley rats were evaluated in four groups. Group I (sham), Group II (renal I/R), Group III (renal I/R injury + SM 50xa0mg per kg) and Group IV (renal I/R injury + SM 100xa0mg per kg) were designed to evaluate the dose-dependent effects of SM on the morphological changes of renal I/R injury. Renal I/R injury were induced with left renal pedicle occlusion for 45xa0min followed with reperfusion for 6xa0h under anesthesia. After induction of I/R injury, left nephrectomies were performed for histopathological examinations.ResultsAfter renal I/R injury, significant tubular dilatation, tubular vacuolization, pelvic inflammation, interstitial inflammation, perirenal adipose infiltration, tubular necrosis and glomerular necrosis (cortical necrosis) were observed. However, even with low dose SM in Group III (50xa0mg per kg SM), histopathological changes due to I/R injury were prevented.ConclusionsThe results of this study have demonstrated that SM significantly prevents renal I/R injury-induced renal tubular changes in the rat. SM in 50xa0mg/kg was observed to be sufficient to significantly prevent renal tubular necrosis. Further, to our literature knowledge, this is the first specific study to demonstrate the preventive effect of SM on renal I/R injury.

Liver tissue inducible nitric oxide synthase (iNOS) expression and lipid peroxidation in experimental hepatic ischemia reperfusion injury stimulated with lipopolysaccharide: the role of aminoguanidine.

BACKGROUNDnHepatic ischemia-reperfusion (HIR) is a severe condition that is seen after hepatic arterial injury and in hepatic grafts in living donor transplantation. HIR not only causes liver injury by lipid peroxidation, but also stimulates systemic and portal endotoxemia. Also, lipopolysaccharide (LPS) induces hepatic injury mediated by inducible nitric oxide synthase (iNOS). There is little knowledge on the role of specific iNOS inhibitors in prevention of HIR injury followed by LPS administration. The aim of this study on a LPS induced HIR model was to investigate the effect of aminoguanidine (AG) administration on hepatic tissue iNOS expression and lipid peroxidation when given before or after LPS.nnnMETHODSnSix groups were designed; A: Sham, B: HIR, C: HIR + AG, D: HIR + LPS, E: HIR + LPS + AG, F: HIR + AG + LPS. No substance was given to the rats in Group A and B. HIR injury was induced with vascular occlusion for 45 min and reperfusion for 45 min. Drugs were given intraperitoneally 10 min before reperfusion. Serum and tissue analysis for myeloperoxidase (MPO), and malondialdehyde (MDA), and tissue NA+/K+ adenosine 5triphosphatases (ATPase) and tissue iNOS staining were performed. Permission for this study was obtained from the local Ethics Committee.nnnRESULTSnThe level of MPO, MDA, and iNOS staining scores in Group B were significantly higher than Group A and ATPase was lower in Group B (P < 0.05). Contrary to results in Group C, results of MPO, MDA, and iNOS staining scores of Group D was higher than Group B (P < 0.05); however, although iNOS in Group C was lower than Group B, the difference was not significant (P > 0.05). MPO and MDA levels of Groups E and F were significantly lower than Group D. Level of ATPase in Group F was significantly different from Groups D and E. iNOS scoring was low in Group F compared with Group D (P < 0.05). MDA, MPO, and iNOS levels of Group F was lower than Group E, and ATPase of Group F was higher than Group E (P < 0.05).nnnCONCLUSIONSnThe results of this study in a LPS induced HIR model showed that LPS after HIR aggravated HIR injury by increasing neutrophil activation and lipid peroxidation both in serum and liver tissue and iNOS in liver, and depleting energy in liver. AG, a selective iNOS inhibitor, ameliorated the negative effects of endotoxemia induced by LPS after HIR; however, energy depletion and iNOS expression in liver tissue were attenuated only when AG was administered prior to LPS. The findings of this study supported the hypothesis that LPS after HIR would aggravate HIR injury and AG would ameliorate this aggravated injury.

The Effect of Aminoguanidine on Blood and Tissue Lipid Peroxidation in Jaundiced Rats With Endotoxemia Induced With LPS

Obstructive jaundice (OJ) is a severe condition that leads to several complications. One of the important problems in OJ is the increased incidence of endotoxemia, which is the result of bacterial translocation (BT) and defective host immune response. Lipid peroxidation (LP) is an important problem in OJ and sepsis in which nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity are increased and antioxidative activity is decreased. Formation of peroxynitrite (ONOO−) anion leads to cellular damage and apoptosis. In this experimental study, we explore the effect of specific iNOS inhibitor aminoguanidine (AG) on blood and tissue (liver and renal) LP and iNOS levels in jaundiced rats with endotoxemia induced with lipopolysaccharide (LPS). Rats were randomized into six groups; group A, sham; group B, obstructive jaundice (OJ); group C, OJ + LPS; group D, OJ + AG; group E, OJ + LPS + AG; group F, OJ + AG + LPS. Serum malondialdehyde (MDA) and serum myeloperoxidase (MPO) activity and liver and renal tissue MDA, MPO, and Na+/K+-ATPase activity levels were detected in biochemical methods. Liver and renal tissue iNOS levels were examined immunohistopathologically. Serum and tissue MDA and MPO levels and tissue iNOS expression were increased significantly in groups B, C, and E, while tissue ATPase levels were decreased significantly in the same groups. In the group treated with AG (group D), serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. In group F, if AG was administrated before LPS, we observed that serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. Thus, our study showed that AG had a protective effect when it was administrated before LPS, but it failed to prevent tissue iNOS expression and LP if there was established endotoxemia in OJ.

The Effect of Preoperative Intravenous Use of Tenoxicam: A Prospective, Double-Blind, Placebo-Controlled Study

In this study, we aimed to investigate the postoperative pain relief effect of preoperative tenoxicam usage in patients who undergo elective laparoscopic cholecystectomy or groin hernia repair. Eighty patients undergoing laparoscopic cholecystectomy or groin hernia repair procedures were randomized to receive either physiologic serum at 100 mL (group I, n = 40) or 20 mg iv tenoxicam (group II, n = 40) immediately before induction. Postoperative analgesic requirement, peroperative side effects and complications of drugs, operating time, postoperative mobilization time and pain score, hospitalization time, and patient pleasure were recorded. Postoperative pain was assessed by the visual analogue scale (VAS) on the recovery unit (RU), at 4, 8, and 24 h and every day at the same times in the morning. The RU median VAS score was also not different when Group 1 was compared with Group 2 (p =. 97). However, the postoperative 4-h and 8-h median VAS score was significantly less (p =. 01 and p =. 03, respectively); first postoperative mobilization time was earlier in group 2 (p =. 32). The median pain score and intramuscular analgesic requirement of patients were also reduced in Group 2 in postoperative day 1 (p =. 015). The median duration of intramuscular analgesic requirement and total amount of intramuscular analgesic used in patients were also significantly less in Group 2 (p =. 0001 and p =. 0001, respectively). Thus, this study showed that preoperative use of iv tenoxicam is safe, simple, and effective for postoperative pain relief after laparoscopic cholecystectomy or inguinal hernia repair.

Protective effects of simvastatin administered in the experimental hepatic ischemia-reperfusion injury rat model

BACKGROUNDnHepatic ischemia-reperfusion (I/R) injury is a major complication in clinical practice. Previous studies suggest that statins have pleiotropic effects in addition to cholesterol-lowering effects. In this study, we aimed to investigate the hepatoprotective role of two different doses of simvastatin (SV) pretreatment in rats with experimental hepatic I/R injury.nnnMETHODSnAdult male Sprague-Dawley rats were divided into four groups (n = 7 in each group) :control, I/R, I/R with 2.5-mg/kg SV, and I/R with 5.0-mg/kg SV. Before hepatic I/R was induced, SV was injected intraperitoneally at doses of 2.5 and 5.0 mg/kg. After 45-min ischemia and a 60-min reperfusion period, the animals were euthanized, and liver tissues were excised. Tissue levels of malondialdehyde and nitric oxide, and activities of superoxide dismutase, glutathione peroxidase, and catalase were measured. Liver tissues were also evaluated histopathologically and immunohistochemically.nnnRESULTSnHistopathologic evaluation showed that 5.0-mg/kg SV reduced hepatic damage and apoptosis. Pretreatment with 5.0-mg/kg SV reduced malondialdehyde and nitric oxide levels (P < 0.01) and increased superoxide dismutase, glutathione peroxidase, and catalase activities significantly (P < 0.001, P < 0.01) in I/R with 2.5-mg/kg SV compared with I/R group. In addition, SV decreased Kupffer cell activation, and hypoxia-inducible factor-1α and vascular endothelial growth factor protein levels.nnnCONCLUSIONSnThe results of this study suggest that 5.0-mg/kg SV pretreatment may be protective against hepatic I/R injury. This effect can be achieved by antioxidant and antiapoptotic activities.

Antiadhesive and anti-inflammatory effects of pirfenidone in postoperative intra-abdominal adhesion in an experimental rat model

BACKGROUNDnPirfenidone (PF) is a potent antifibrotic and anti-inflammatory agent. We investigated the protective effect of PF against postoperative intra-abdominal adhesions.nnnMATERIAL AND METHODSnThirty male Sprague-Dawley rats were divided into three groups (n = 10 in each group). In group 1 (control), adhesion induction was performed by cecal abrasion, and no treatment was administered. In group 2 (vehicle), for 2 wk after adhesion induction, 0.4%-carboxymethylcellulose was administered by gavage. In group 3 (PF treatment), for 2 wk after adhesion induction, 500-mg/kg/d PF was administered by gavage. On the 15th postoperative day, the animals were killed, and cecal and peritoneal tissues were excised. The adhesions were graded macroscopically. The protein concentrations and mRNA expression levels of the following genes were measured in the tissues: matrix metallopeptidase-9 (MMP-9); tissue inhibitor of metalloproteinase-1 (TIMP-1); tumor necrosis factor-alpha (TNF-α); and transforming growth factor-beta 1 (TGF-β1). The tissue samples were also evaluated histopathologically.nnnRESULTSnMacroscopic and histopathologic evaluation showed that PF-reduced adhesion and inflammation (P < 0.001, P = 0.004, respectively). Pretreatment with PF-reduced TIMP-1, TNF-α, and TGF-β1 protein concentrations (P < 0.001, P < 0.001, and P < 0.001, respectively) and mRNA expression levels (P = 0.030, P = 0.005, and P = 0.016, respectively) and increased MMP-9 protein concentrations (P < 0.001) and mRNA expression (P = 0.021).nnnCONCLUSIONSnThe findings of this study suggest that PF can be used as a protective agent to prevent the development of peritoneal adhesions and inflammation during the postoperative period.

Management of fistula of ileal conduit in open abdomen by intra-condoit negative pressure system

INTRODUCTION We aimed to present the management of a patient with fistula of ileal conduit in open abdomen by intra-condoid negative pressure in conjunction with VAC Therapy and dynamic wound closure system (ABRA). PRESENTATION OF CASE 65-Year old man with bladder cancer underwent radical cystectomy and ileal conduit operation. Fistula from uretero-ileostomy anastomosis and ileus occurred. The APACHE II score was 23, Mannheim peritoneal index score was 38 and Björck score was 3. The patient was referred to our clinic with ileus, open abdomen and fistula of ileal conduit. Patient was treated with intra-conduid negative pressure, abdominal VAC therapy and ABRA. DISCUSSION Management of urine fistula like EAF in the OA may be extremely challenging. Especially three different treatment modalities of EAF are established in recent literature. They are isolation of the enteric effluent from OA, sealing of EAF with fibrin glue or skin flep and resection of intestine including EAF and re-anastomosis. None of these systems were convenient to our case, since urinary fistula was deeply situated in this patient with generalized peritonitis and ileus. CONCLUSION Application of intra-conduid negative pressure in conjunction with VAC therapy and ABRA is life saving strategies to manage open abdomen with fistula of ileal conduit.

Atresia of the appendix vermiformis: A rare case of developmental abnormality

Acute appendicitis, which requires immediate surgical intervention, is an important diagnosis in patients with acute abdomen. However, developmental abnormalities may interfere with the preoperative diagnosis and surgical treatment in some cases. Agenesis and atresia of the cecal vermiform appendix is an extremely rare clinical diagnosis. In addition, preoperative diagnosis may be difficult in some cases. Thus, diagnosis of the congenital absence of the vermiform appendix requires a thorough exploration of the retrocecal and ileocecal regions. A 59-year-old male was admitted from the emergency services with right lower abdominal pain. A celiotomy was performed with the suspicion of acute appendicitis. However, an atresia of the vermiform appendix was observed. The patients appendix was thus removed. Pathological examination confirmed suppurative appendicitis. This case underlines the importance of the clinical entity for surgeons who may deal with a similar case.

The role of erythropoietin in hemorrhagic shock-induced liver and renal injury in rats.

IntroductionThe aim of the present study was to evaluate the role of erythropoietin (EPO) in liver and renal injury following hemorrhagic shock (HS) after inhibition of tyrosine kinase activity in rats..MethodsForty-eight Sprague-Dawley rats were assigned to six groups: (I) HS alone; (II) HS followed by retransfusion; (III) EPO and genistein followed by HS; (IV) EPO and genistein followed by HS, followed by retransfusion; (V) HS followed by EPO and genistein; and (VI) HS followed by EPO and genistein, followed by retransfusion. HS was induced for 60 minutes after withdrawal of 30% of the calculated total blood volume of each rat from the left femoral artery. Blood and tissue samples (from the kidney and liver) were obtained 60 minutes after HS in Group I, III, and V; blood and tissue samples were obtained 60 minutes after retransfusion in Group II, IV, and VI. In Group III and IV, EPO was given 60 minutes before HS, and genistein 30 minutes before HS. In Group V and VI, EPO and genistein were given 30 minutes after HS.ResultsLiver and renal injury were significantly attenuated with EPO and genistein administration.ConclusionThese results suggest that EPO is effective in attenuating liver and renal injury in HS, even with inhibition of tyrosine kinase activity with genistein.