Presentation delivered at a paediatric clinical meeting of the Federal Medical Center, Lokoja. Nigeria
This presentation doesn't serve as a substitute for texts and/or journals.
POSTERIOR URETHRAL VALVES- Pediatric Surgery
• Dear viewers,
• Greetings from “ Surgical Educator”
• Today I have uploaded one more video in Pediatric Surgery/Pediatric Urology- “ Posterior Urethral Valves”
• Posterior Urethral Valves is the congenital cause for Bladder Outlet Obstruction, resulting in abnormal development of the kidneys as well as the bladder.
• In this video, I talked about the learning outcomes, introduction, etiopathogenesis, clinical features, investigations, differential diagnosis, treatment, follow-up and prognosis of “ Posterior Urethral Valves”
• I hope you will enjoy the video for its educational value.
• You can watch all my teaching videos in the following links
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video.
Ureteropelvic junction obstruction by\ Eman Salman
It was used for student presentation in Urology course rotation
I Hope you find what is helpful for your knowledge ♥
POSTERIOR URETHRAL VALVES- Pediatric Surgery
• Dear viewers,
• Greetings from “ Surgical Educator”
• Today I have uploaded one more video in Pediatric Surgery/Pediatric Urology- “ Posterior Urethral Valves”
• Posterior Urethral Valves is the congenital cause for Bladder Outlet Obstruction, resulting in abnormal development of the kidneys as well as the bladder.
• In this video, I talked about the learning outcomes, introduction, etiopathogenesis, clinical features, investigations, differential diagnosis, treatment, follow-up and prognosis of “ Posterior Urethral Valves”
• I hope you will enjoy the video for its educational value.
• You can watch all my teaching videos in the following links
• surgicaleducator.blogspot.com youtube.com/c/surgicaleducator
• Thank you for watching the video.
Ureteropelvic junction obstruction by\ Eman Salman
It was used for student presentation in Urology course rotation
I Hope you find what is helpful for your knowledge ♥
this presentation covers anatomy of the testis, embryological development, causes, clinical features, complications, differences between various types, investigations, and management of undescended testis.
this presentation covers anatomy of the testis, embryological development, causes, clinical features, complications, differences between various types, investigations, and management of undescended testis.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Hot Selling Organic intermediates
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
3. Introduction 1/2
An abnormal congenital obstructing membrane that is located within the
posterior male urethra.
First described by Hugh Hampton Young in 1919
Crescentic duplication of urethral mucosa forms valves
The paper thin valves arise from the verumontanum and extend
downwards and laterally to the side-walls of the urethra at the
apex of the prostate.
4. Introduction 2/2
During early stages of embryogenesis, the most caudal end of the wolffian
duct is absorbed into the primitive cloaca at the site of the future
verumontanum in the posterior urethra
The homolog to the male verumontanum from which the valves originate
is the female hymen.
Histologic studies suggest that PUVs are formed at approximately 4 weeks’
gestation as the wolffian duct fuses with the developing cloaca
5. Classification
Type I - Valves representing folds extending inferiorly from the
verumontanum to the membranous urethra (~95% of PUVs)
Type II - Bicuspid valves as leaflets radiating from the verumontanum
proximally to the bladder neck
Type III - Valves as concentric diaphragms within the prostatic urethra,
either above or below the verumontanum (~5% of PUVs)
6. Epidemiology
In the United States, PUV is the most common cause of lower urinary tract
obstruction in male neonates; the reported incidence ranges from 1 per 8000
to 1 per 25,000 live births.
Uba et al in Jos reprted 3 – 8 cases per annum, Jaja et al in Port Harcourt
observed that it accounted for 1 in 2447 children seen in their hospital.
A study done by Talabi et al in Ile-Ife in 2015 showed an incidence of 3 cases
per annum with a median age of 5 months at presentation.
The mean age of presentation according to a study done by Orumuah in
UBTH, Benin City is approx. 4years with 56.8% presenting after the age of 1
year.
PUVs occur exclusively in males.
7. Etiology
A PUV is a congenital obstruction caused by a malformation of the
posterior urethra. The significance of this obstruction depends on the
secondary effects on the bladder, ureters, and kidneys.
A type I PUV is believed to result from abnormal insertion and absorption
of the most distal aspects of the wolffian ducts during bladder
development.
Type III PUVs are observed as a membrane in the posterior urethra
believed to originate from incomplete canalization between the anterior
and the posterior urethra.
8. Pathophysiology
Due to the urethral obstruction, there is
• Thickened bladder wall with reduced bladder compliance during filling
• Vesicoureteric reflux
• Hydronephrosis and/or hydroureter
• Progressive renal calyceal dilatation and renal damage
9. Clinical Presentation 1/3
HISTORY
Urinary tract infection (UTI)
Diurnal enuresis in boys older than 5 years
Secondary diurnal enuresis
Voiding pain or dysfunction
Abnormal urinary stream
PUVs are sometimes discovered during evaluation of abdominal mass or
renal failure.
10. Clinical Presentation 2/3
PHYSICAL EXAMS
Most patients with PUV have normal physical examination findings. When
present, abnormal physical findings are the result of severe renal
insufficiency.
Neonates may present with severe pulmonary distress caused by lung
underdevelopment lung due to oligohydramnios. Findings include:
• Poor fetal breathing movements
• Small chest cavity
• Potter facies
• Indentation of the knees and elbows due to compression within the uterus
11. Clinical Presentation 3/3
In older children, physical findings can include
• poor growth, hypertension, and lethargy.
• An intermittent or weak urinary stream is an unreliable sign.
• A large lower abdominal mass may represent a markedly distended urinary
bladder
13. Investigations 1/5
1. Abdominopelvic USS
Renal parenchyma, collecting system dilatation, bladder wall thickness, and
presence of ascites.
Because newborns commonly have relative hypovolemia during the first
few days of life, the recommendations are to perform ultrasonography
after the first week of life if findings from the first ultrasound examination
were normal in a child with previously diagnosed antenatal hydronephrosis
before making a final determination that the hydronephrosis has resolved
14.
15. Investigations 2/5
2. Voiding cystourethrography
VCUG under fluoroscopy, with imaging of the posterior urethra, especially
during the voiding phase.
The diagnosis of PUV is indicated by visualization of the valve leaflets.
Other clues to the diagnosis are a thickened trabeculated bladder, a
dilated or elongated posterior urethra, and a hypertrophied bladder neck.
Diverticula, cellules, vesicoureteral reflux, and reflux into the ejaculatory
ducts secondary to elevated bladder and urethral pressures may also be
present.
16.
17.
18.
19. Investigations 3/5
3. Renal scintigraphy
4. Urodynamic evaluation: information about bladder storage and emptying.
20.
21. Investigations 4/5
5. Cystoscopy
Diagnostic - confirmation with cystoscopy is required in every child in
whom PUV is suggested after VCUG. In some, the filling defect observed
on VCUG may represent only external sphincter contraction during
voiding; in others, the valve leaflets are confirmed.
Therapeutic - valves are disrupted under direct vision by cystoscopy using
an endoscopic loop, Bugbee electrocauterization, or laser fulguration. In
extremely small infants (<2 kg), a 2-French Fogarty catheter may be passed
either under fluoroscopic or direct vision for valve disruption.
23. Management 1/8
MEDICAL INTERVENTION
Short-term goals involve treatment of pulmonary distress, immediate relief
of urethral obstruction (placement of a 5-French feeding tube), and fluid
and electrolyte management.
In children who survive the pulmonary distress, the long-term issues
include treatment of bladder dysfunction and renal insufficiency.
24. Management 2/8
Anticholinergic medications used to improve bladder compliance:
Oxybutinin, Tolderol, Hyoscyamine sulfate
Antibiotics for UTI
Renal replacement therapy
• Peritoneal dialysis
• Renal transplant after the first year of life
25. Management 3/8
NEWBORN CARE
the first step in treatment is to relieve bladder outlet obstruction by
placing a urethral catheter.
Cystoscopic valve ablation or vesicostomy is performed when the child is
stable.
In rare cases, a urethral catheter cannot be placed, because of hypertrophy
of the bladder neck. These patients require cystoscopy under anesthesia
for catheter placement, suprapubic tube placement, or primary
vesicostomy.
26. Management 4/8
SURGICAL INTERVENTION
1. Postnatal primary valve ablation:
Ideal treatment involves transurethral incision of the PUV during the first
few days of life. Current infant resectoscopes are available in 8 French and
smaller sizes.
The valves can be incised at the 12-, 5-, and 7-o'clock positions, with either
a cold knife or an electrocautery.
Some surgeons prefer to leave a catheter in place for 2-3 days after the
procedure. The timing of the postoperative VCUG varies and ranges from
several days to several months.
27. Management 5/8
Comparison of the posterior urethral diameter with anterior urethral
diameter can provide an objective measure of valve ablation
In most patients, the posterior urethra is markedly dilated. Postincision
diameter should decrease if the incision is successful.
One third of patients require a second incision to achieve an appreciable
level of posterior urethral reduction.
28. Management 6/8
2. Vesicostomy:
When urethral size precludes safe valve ablation, a communicating channel
between the bladder and lower abdominal wall (ie, vesicostomy) can be
created to provide bladder drainage.
Vesicostomy use has decreased because most patients can be safely
drained and can undergo valve ablation.
29. Management 7/8
3. Cutaneous ureterostomies
• Loop
• End
• Y – ureterostomies
• Ring type
Complications are that of ureteral devascularization, inadequate drainage
and stomal stenosis
32. Prognosis 1/2
Over the past 30 years, the prognosis of children with PUV has steadily
improved.
In the past, most children were found to have PUV only after presenting
with urosepsis or progressive renal insufficiency.
Older series demonstrated mortality figures approaching 50% by late
adolescence.
Today, most individuals with PUV are discovered when antenatal
ultrasonography reveals hydronephrosis.
Prompt resolution of bladder obstruction, aggressive treatment of bladder
dysfunction, and improved surgical techniques have lowered the neonatal
mortality to less than 3%.
33. Prognosis 2/2
PUVs are the cause of renal insufficiency in approximately 10-15% of
children undergoing renal transplant, and approximately one third of
patients born with PUV progress to ESRD in their lifetimes. the child grows,
renal metabolic demand increases proportionately.
Failure of creatinine to nadir below 0.8 mg/dL in the first year of life is an
indication of limited renal reserve. These patients are at risk for
progression to ESRD
Improved dialysis and transplantation techniques have significantly
improved not only mortality but also quality of life for these children .
Additionally, medical and surgical management can achieve urinary
continence in nearly all patients.
34. Conclusion
Posterior urethral valve remains the commonest cause of bladder outlet
obstruction in male children.
Its management is multimodal and multidisciplinary
Ablation of the valve remains the commonest and more successful means
of surgical intervention.
Prognosis depends on the severity and timing of presentation.
35. References 1/3
Archampong E, et al. BAJA’s Principle and practice of surgery, 5th Edition.
2015
Orumah AJ, et al, African Journal of Paediatric Surgery. 2015 Jan-Mar;12(1):
18-22
Jaja T, et al. Posterior urethral valve in childhood in Port Harcourt, Nigeria.
Port Harcourt Med J. 2012;6:10-6
Uba AF, et al. Posterior urethral valves in childhood: Experience in a center
with scarce facilities. Afr J Urol. 2007;13:124-31
Talabi A, et al. Posterior urethral valves in children: pattern of presentation
and outcome of initial treatment in Ile-Ife, Nigeria. Nigeria Journal of
Surgery. 2015 Jul-Dec; 21(2): 151-156
36. References 2/3
Young HH, Fronz WA, Baldwin JC. Congenital obstruction of the posterior
urthera. J Urol. 1919. 3:289.
Dewan PA, Goh DG. Variable expression of the congenital obstructive
posterior urethral membrane. Urology. 1995 Mar. 45(3):507-9.
Heikkilä J, Holmberg C, Kyllönen L, Rintala R, Taskinen S. Long-term risk of
end stage renal disease in patients with posterior urethral valves. J Urol.
2011 Dec. 186(6):2392-6.
Horowitz M, Harel M, Combs A, Glassberg K. Surveillance cystoscopy in the
management of posterior urethral valves. J Urol. Apr 2009. 181:172.