Inguinal herniation of the transplant ureter is rare, and there is a paucity of reports in the literature. Herniation is usually secondary to implanting a long redundant ureter and may be precipitated by its course over the spermatic cord. Most often, there is loss of the allograft owing to delayed presentation and chronic ureteric obstruction. Here, we report a case of inguinal herniation of a transplant ureter with obstruction and graft dysfunction.A 72-year-old man presented 9 years after deceased-donor kidney transplant, with progressive graft dysfunction and a symptomatic right inguinal hernia. A nephrostogram and subsequent surgery confirmed herniation of a loop of transplant ureter into the inguinal canal with a proximal dilated ureter and hydronephrosis. A long and redundant ureter had been anastomosed "over" the spermatic cord to the bladder during the original operation. The ureter was shortened by excising the distal segment, and the proximal dilated ureter was anastomosed to the bladder passing it "underneath" the spermatic cord. We used a Vicryl (polyglactin 910) mesh to repair the hernia. The graft function improved to baseline levels after the nephrostomy and remained stable after the surgery.This case emphasizes the need to keep the ureter short, and the importance of passing it underneath the spermatic cord before anastomosing to the bladder. Transplant and general surgeons should be aware of such presentations of graft dysfunction with inguinal hernia to avoid delayed diagnosis and graft loss.

Aim To identify the reasons for referrals, foetal demise, termination of pregnancies in relation to foetal heart conditions, trend in yield rate and place of delivery. Methods Retrospective review of all the tertiary foetal cardiology referrals in South Wales, UK from 2002 to 2008. Results A total of 1744 mothers were referred for tertiary fetal cardiology assessment of which 1280 (73%) were normal. 442 (25%) of foetuses had confirmed cardiac anomalies. Reasons for referral Structural heart anomalies-37%, associated congenital anomalies-9%,family history of congenital heart disease-22%,foetal arrhythmias-10%, maternal congenital heart disease-6%, increased nuchal thickness-15.5%. Fetal demise Hypoplastic condition-31%, AVSD's-31%,tetrology of fallot-7%,outflow tract -left ventricular (3%),right ventricular(7%),ebsteins-7%, other conditions-14%. Termination of pregnancies Hypoplastic conditions- 36%,AVSD's-23%,transposition of great arteries-11%,truncus arteriosus-5%,tetrology of fallor-4%, right sided -7%;left sided5% obstructive lesions. Total yield rate (confirmed foetal cardiac anomaly) Increased from12%-2002,17%-2003,22%-2004,31%-2005,37%-2006,39%-2007 and 49%-2008. Place of delivery 68% were delivered in tertiary cardiac centres,20% were delivered in neonatal intensive care centres and 12% were delivered in district general hospitals with high dependency neonatal support only. Conclusions Structural heart anomalies and family history of congenital heart conditions were the main reasons for tertiary fetal cardiology assessment. Hypoplastic heart conditions and atrio ventricular septal defects were the main reasons for foetal demise and termination of pregnancies. Successful training of antenatal ultrasonographers in including outflow tract views in addition to the routine four chamber view led to increase in yield rate. Early identification of major congenital cardiac anomalies and counselling led to delivering in tertiary cardiac surgical centres.

Objective To assess the rate of antenatal detection of hypoplastic left heart syndrome (HLHS) and its outcome antenatally and postnatally. This review was undertaken to improve counselling and provide better surgical survival information for expecting parents in the future. Methods All cases of HLHS detected antenatally between January 2002 and December 2008 were included in the study. Fetal medicine and fetal cardiac databases at a tertiary fetal cardiology centre as well as CARIS central database in Wales were utilised to carry out the review. The notes were carefully scrutinised to rule out any confounding variables. Results There were 55 cases of HLHS in South Wales over this period, 50 of which were detected antenatally. 24 of these were terminated following counselling and two ended up in still birth. Hence, there were 24 live births with HLHS. Of these, one died without undergoing any surgery. The remaining 23 cases underwent surgery but five children died. Eighteen of them are alive and are under follow-up. HLHS is an isolated defect in majority of cases (38 out of 50). The rate of chromosomal abnormality is 10% (5 out of 50). Conclusion HLHS is one of the most high-risk lesions in children with congenital heart disease. Antenatal detection rate for HLHS has been satisfactory at 90% in Wales. Termination rate remains high despite substantial improvement in survival after surgery. Post surgical survival stands at 78% in our series with a maximum follow-up of 8 years. Counselling is essential for parents to make an informed decision.

Objective To assess the rate of chromosomal problems with complete atrio-ventricular septal defect. This study was undertaken to improve counselling and provide better information for expecting parents in the future. Methods All cases of complete atrio-ventricular septal defect detected antenatally between January 2002 and December 2008 were included in the study. Fetal medicine and fetal cardiac databases at a tertiary fetal cardiology centre as well as CARIS central database in Wales were utilised to carry out the review. The notes were carefully scrutinised to rule out any confounding variables. Results There were 47 cases of CAVSD in South Wales over this period, 32 of which were detected antenatally. Ten of these were terminated following counselling and three ended up in still birth with one fetal loss. Hence, there were 18 live births with HLHS. Of these, six died postnatally, five of these had chromosomal problems. 23 of the cases diagnosed antenatally had chromosomal problems. 8 of the 10 terminations were complicated with associated chromosomal problems. Two out of the three stillbirths and the fetal loss was also complicated by associated chromosomal anomaly. Out of the 18 live births, 12 had chromosomal problems. Trisomy 21 was the commonest karyotypic abnormality (18 out of 23) in CAVSD with Trisomy 18 comprising the remainder. Conclusion CAVSD is a common congenital heart defect. Antenatal detection rate for CAVSD stands at 68% in Wales. It is associated with a high rate of chromosomal problems (72%). Counselling is essential for parents to make an informed decision.

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