External spermatic vein ligation improves the outcome of varicocele surgery: fact or fiction

Internal spermatic vein is the major route of testicular venous drainage However, Surgical failure after varicocelectomy is mostly due to persistent incompetent collaterals distal to the site of ligation of internal spermatic vein and the most important collaterals is the external spermatic vein. The aim of this study was to estimate the incidence of external spermatic vein in infertile patients and to evaluate the results of inguinal varicocelectomy with combined ligation of both internal and external spermatic veins. Eighty inguinal varicocelectomies were performed on 45 infertile patients with varicocele ranging in age from 20-40 years. There were 15 fertile control patients undergoing inguinal herniorrhaphy. There were 35 patients with bilateral varicocele and 10 patients with isolated left sided varicocele [Thirty-Seven patients with primary infertility and 8 patients with secondary infertility]. Grade 2 varicocele was the commonest one [52.5%]. External spermatic veins were detected in 57 varicocelectomies [71.25%]. Improvement in semen parameters was detected postoperatively. Pregnancy occurred in 14 cases [31%] on follow up period of one year after surgery. Subclinical recurrence of varicocele occurred in 3 patients [6.6%]. Vaginal hydrocele occurred in 2 patients [4.4%]. Among control group external spermatic vein was detected only in 2 patients [13.3%]. External spermatic vein is commonly found in patients with varicocele and its ligation during inguinal varicocelectomy improves the results of surgery. So, careful searching for this vein and its ligation is advised

Helicobacter pylori: does it play a role in pathogenesis of acute appendicitis

The exact aetiology of acute appendicitis remains uncertain but an infective origin has been proposed. It was postulated that helicobacter pylori infection could cause mucosa associated lymphoid tissue hypertrophy in the appendix to the extent that under certain conditions luminal obstruction and acute appendicitis might occur. This study was done to confirm whether helicobacter pylori forms part of the microenvironment of the appendix and whether it play a role in the pathogenesis of acute appendicitis. This study was performed on 62 patients with acute appendicitis ranging in age from 8 to 42 years. There were 39 females and 23 males. All patients subjected to open appendicectomy, fresh specimens from the appendix was taken and cultured on blood agar and subjected to urease test. Other specimens was subjected to histopathological examination. Pathological grading of the appendicitis was performed according to the depth of inflammatory infiltrate. 10 ml of blood was drawn from all patients for serological assessment of helicobacter pylori. Fifty patients had a pathological appendix [80.6%] with different grades of inflammation. The appendix was histologically normal in 12 patients [19.3%]. Forty-two cases [67.7%] were sero negative in whom the appendix was inflamed in 33 cases [78.6%]. Twenty cases [32.3%] were seropositive in whom the appendix was inflamed in 1 7 cases [85%]. Multiple organisms were grown on all plates and 7 biopsies were positive for urease activity. There was no evidence of helicobacter pylori in any sample on histological examination. We have concluded that helicobater pylori does not colonize the appendix and is unlikely to be a pathogenic stimulus for appendicitis. However, downstream effect of gastroduodenal infestation might induce immunological effect