Refining Bacteriuria as a Risk Factor for Complications After Urethroplasty: Identifying the Culprit.

OBJECTIVE: To determine which bacteria are associated with an increased risk of 90-day complications after urethroplasty. Preoperative bacteriuria is associated with an increased risk of complications after urethroplasty. However, it remains unclear which specific micro-organisms are the primary drivers of this morbidity. METHODS: A single-institution, 2-surgeon retrospective review was performed on patients undergoing urethroplasty from 08/2003 to 06/2021. Preoperative bacteriuria was considered significant when the patient had a mixed culture with ≥108 CFU/L or an identifiable micro-organism with ≥106 CFU/L. Descriptive statistics were used to summarize the results and chi-square was used to determine the association between 90-day complications (Clavien ≥2) and clinical characteristics/bacteria. RESULTS: Out of 1611 patients, 23.2% (373) had significant preoperative bacteriuria. The most common pathogens included coagulase-negative staphylococcus 18.5% (69), mixed growth 15.8% (59), Escherichia coli 10.7% (40), and Enterococcus 14.2% (53). 7.9% (128/1611) experienced a significant 90-day complication (Clavien-Dindo ≥2). Gram-negative bacilli including E coli, Pseudomonas sp, Klebsiella sp, Serratia sp, Citrobacter sp, Achromobacter sp, Stenotrophomonas sp, and Morganella sp were associated with higher rates of postoperative complications (14.2%; P = .01) as well as Enterococcus sp (15.1%; P = .03). However, gram-positive cocci (7.9%; P = .97), gram-positive bacilli (11.8%; P = .47), mixed growth (5.1%; P = .54) and Candida (16.7%; P = .27) were not. Neither escalating concentrations of bacteria (P = .44) or number of strains (P = .08) were associated with increased risk of complications. CONCLUSION: The main driver of bacteriuria-related complications after urethroplasty are gram-negative bacilli and Enterococcus sp. Patients with bacteriuria related to other micro-organisms can likely proceed with urethroplasty without increased risk of postoperative complications.

Routine Imaging After Bulbar Urethral Reconstruction Does Not Impact Surgical Outcomes and May Not Be Necessary.

OBJECTIVE: To assess whether omitting routine post-operative imaging adversely impacts clinical outcomes after bulbar urethroplasty. Contrast imaging is commonly performed prior to catheter removal after urethroplasty but the clinical need for this is unclear. METHODS: This was a matched, case-control analysis comparing patients undergoing routine voiding cystourethrogram (VCUG) prior to catheter removal after bulbar urethroplasty to patients without imaging. Patients were matched with respect to age, stricture etiology, length, and urethroplasty technique. Follow-up consisted of clinical assessment 3 weeks post-operatively for VCUG/catheter removal, cystoscopy at 3-4 months with clinical assessment annually. Outcome measures were 90-day complications (Clavien ≥2) and stricture recurrence (failure to pass a 16-Fr flexible cystoscope on follow-up). Chi-square and Kaplan-Meier analysis were conducted where appropriate. RESULTS: Hundred patients undergoing bulbar urethroplasty with VCUG prior to catheter removal were compared to 100 matched case controls without imaging. Groups did not differ with respect to failed endoscopic treatment (P = .82), prior urethroplasty (P = .09), comorbidities (P = .54), smoking (P = .42), or pre-operative bacteriuria (P = 1.00). The incidence of extravasation in the VCUG group was 2%. Overall 90-day complications were 9.5% and 15 patients developed recurrence with a median follow-up of 174 months. On chi-square analysis, 90-day complications did not differ between patients undergoing VCUG and those without (12% vs 7.0%; P = .34). On log-rank analysis, stricture recurrence did not differ between groups (P = .44). CONCLUSION: Routine imaging with VCUG after bulbar urethroplasty does not influence the risk of post-operative complications or stricture recurrence. Surgeons should consider avoiding this potentially unnecessary examination in routine clinical practice.

Prospective assessment of the incidence and associations of postvoid dribbling after urethroplasty Impact of surgical technique.

INTRODUCTION: The incidence and associations of postvoid dribbling (PVD) after urethroplasty remains unclear. The purpose of this study was to examine the impact of urethroplasty on PVD and factors associated with de novo PVD. METHODS: From 2011-2018, patients were offered enrollment in a prospective study assessing PVD after urethroplasty. PVD was assessed preoperatively and six months post-surgery with the question, "After urinating, do you have post-urination dribbling or leakage of urine?" Choices included, "Never" (1), "Occasionally" (2), "Sometimes" (3), "Most of the time" (4), or "All of the time" (5). A response of 3-5 was considered clinically significant. Wilcoxon signed-rank test was used to compare pre- and postoperative PVD, while logistic regression was used to determine the association between new-onset PVD and clinical variables. RESULTS: A total of 384 patients completed the study, with 46.9% (180) reporting PVD preoperatively compared to 39.8% (153) postoperatively (p=0.01); 18.0% (67) of patients experienced de novo PVD, 57.0% (219) no change, and 25.0% (96) reported improvement. On multivariable logistic regression, patients undergoing anastomotic urethroplasty were less likely to report de novo PVD (odds ratio [OR] 0.33, 95% confidence interval [CI] 0.13-0.83, p=0.02). No other factor was associated with de novo PVD, including age (p=0.59), stricture length (p=0.71), location (p=0.50), etiology (p=0.59), failed endoscopic treatment (p=0.18), previous urethroplasty (p=0.55), or recurrence (p=0.78). De novo PVD was not associated with patient dissatisfaction (10.1% vs. 7.6%, p=0.49). CONCLUSIONS: PVD is common in patients with urethral stricture. While there is an overall improvement after urethroplasty, 18.0% of patients will experience de novo PVD, with a reduced incidence in those undergoing anastomotic urethroplasty.

[Crigler-Najjar syndrome. Report of one case with a long term follow up]. / Evolución prolongada en síndrome de Crigler-Najjar tipo I.

Crigler-Najjar Syndrome is an uncommon genetic disorder characterized by the elevation of unconjugated plasmatic bilirubin secondary to deficiency of the enzyme uridine diphosphate glucuronyltransferase (UDP-GT). We report a 19-years-old woman with the syndrome diagnosed during the neonatal period, when she developed a severe jaundice in the first 10 days of life, reaching unconjugated bilirubin levels of 29 mg/dl, with normal liver function tests. After transient response to phototherapy, the patient was referred to a tertiary medical center in which an extensive work up ruled out other etiologies and the diagnosis of type I Crigler-Najjar syndrome was established. Currently, the patient has a mild mental retardation. She is receiving homemade phototherapy 18 h per day with acceptable control of bilirubin levels. Many mutations have been associated with UDP-GT dysfunction resulting in a broad spectrum of the disease. When bilirubin rises above physiological limits, it permeates the hematoencephalic barrier, inducing bilirubin impregnation of basal ganglia with secondary neuronal damage and necrosis. The worst outcome, kernicterus, is characterized by mental retardation, central deafness, ophthalmoplegia, ataxia, athetosis, spasticity, seizures and death. First line therapy includes phototherapy, but definitive therapy is liver transplantation before the occurrence of neurological damage.

Evolución prolongada en síndrome de Crigler-Najjar tipo I / Crigler-Najjar syndrome. Report of one case with a long term follow up

Crigler-Najjar Syndrome is an uncommon genetic disorder characterized by the elevation of unconjugated plasmatic bilirubin secondary to deficiency of the enzyme uridine diphosphate glucuronyltransferase (UDP-GT). We report a 19-years-old woman with the syndrome diagnosed during the neonatal period, when she developed a severe jaundice in the first 10 days of life, reaching unconjugated bilirubin levels of 29 mg/dl, with normal liver function tests. After transient response to phototherapy, the patient was referred to a tertiary medical center in which an extensive work up ruled out other etiologies and the diagnosis of type I Crigler-Najjar syndrome was established. Currently, the patient has a mild mental retardation. She is receiving homemade phototherapy 18 h per day with acceptable control of bilirubin levels. Many mutations have been associated with UDP-GT dysfunction resulting in a broad spectrum of the disease. When bilirubin rises above physiological limits, it permeates the hematoencephalic barrier, inducing bilirubin impregnation of basal ganglia with secondary neuronal damage and necrosis. The worst outcome, kernicterus, is characterized by mental retardation, central deafness, ophthalmoplegia, ataxia, athetosis, spasticity, seizures and death. First line therapy includes phototherapy, but definitive therapy is liver transplantation before the occurrence of neurological damage.