Memoire Online - Posterior urethral valves in children: a review of 28 cases in Yaounde, Cameroon

Thesis Submitted in Partial Fulfilment for the
Requirements of End of Course Diploma
(Specialist Diploma in Clinical Sciences, Option Paediatrics)

Patho-physiological changes induced by posterior
urethral valves on the urogenital tract .. ..38

I pray you continue to help and guide me in my daily and professional activities so that the future be brighter and life more worthwhile.

My wife - Ema, my sons - Edmond and Roland. Thanks for the perseverance and may we hope for brighter days in the nearest future.

To my mum - NDISI Tabitha, late Dad CHIABI David, Uncle NGONG Mathias and all my brothers and sisters. This work is entirely the fruit of your sacrifice

To all children with posterior urethral valves. I love you and I promise to take special care of you

Thanks for encouraging me to do this work despite all the difficulties I had. You have made me learn and understand a bit of Paediatric Urology. Thanks for everything.

Thanks for accepting to supervise this work. I highly appreciate the advice and encouragement you gave me. All through my residency you had been like a mother to me.

Thanks for accepting to supervise this work despite your tight schedule. Thanks very much indeed.

Prof TETANYE EKOE, Dr ABENA OBAMA, Dr DOUMBE Pierre, Dr KAGO Innocent, Dr MBONDA Elie, Dr TCHOKOTEU Pierre Fernand, Dr TIETCHE Felix, Dr MONEBENIMP Francisca, Dr ONDOA MEKONGO Martin, Dr YAP John, Dr NSANGOU Innoussa. I hope to apply all the technical skills you taught me in examining and treating my patients.

Special thanks to Dr TCHOKOTEU Pierre Fernand and Dr ENGOUDOU née Douala MOUTENG Valentine of the General Hospital. My first staggering steps in Paediatrics were with you when I was still premature. You encouraged me to go on.

Thanks to Dr KAMDEM Annie and husband Mr Jean Paul KAMDEM, Dr Amos KAMDEM. Thanks for all the material and moral support you gave me in the most difficult moments of my life. I pray our friendship blossom as the morning roses.

Thanks to my friends Mr EYÀA Jean Dominique, Mr KAMTO Victor, Mr KEUKAM Justin, Mr TCHOUGA Phillipe, Mr NANKAM Bernard, Mr KEMAJOU Augustin. You were close to me in very trying moments of my career. Accept my sincere thanks

Thanks to my long time friends Dr TAKOU Virgine, Dr BIBEE MAYI, Dr TSIAGADIGUI Jean Gustave, Dr MBANGTANG Celestine (University of Zimbabwe), Dr NYOM Elizabeth (FMBS). It has been very rough but worth the while.

Finally, sincere thanks to Miss Evelyn BANINLA and Mr MBUYONGHA Nico for sparing their time to type and arrange this work.


POSTERIOR URETHRAL VALVES IN CHILDREN: A review of 28 cases in Yaounde
b)	*MAITRES DE CONFERENCES*
1	ASONGANYI TAZOACHA	Biochimie / Immunologie
2	ATCHOU Guillaume	Physiologie Humaine
3	BEJANGA Beltus	Chirurgie Généra/e
4	BENGONO née CISSE TOURE Geneviève	O.R.L.
5	DJOUMESSI Sosthène	Biochimie
6	DOH Anderson SAMA	Gynécologie /Obstétrique
7	DONGMO Louis	Anatomie / Neurologie
8	GONSU FOTSIN Joseph	Radiologie/Imagerie Médicale
9	JATO Johnson GAMNGONG	Chimie Pharmaceutique
10	JUIMO Alain Georges	Radiologie /Imagerie Médicale
11	KAMDOM MOYO Joseph	Gynécologie /Obstétrique
12	KOUEKE Paul	Dermatologie / Vénérologie
13	LEKE Robert Ivo	Gynécologie /Obstétrique
14	MBAKOP André	Anatomie Pathologique
15	MUNA Walinjom	Médicine Interne / Cardiologie
16	NKAM Maurice	Pharmacologie /Thérapeutique
17	NDJITOYAP NDAM Elie - Claude	Médecine Interne /Gastro - entérologie
18	NDUMBE Peter	Microbiologie / Immunologie
19	NGOGANG Jeanne	Biochimie
20	NGUIMBOUS Jean François	Chirurgie Thoracique / Cardio vasculaire
21	NJIKAM KAYA Lawrence	Pharmacie Galénique
22	SAME - EBOKO Albert	Parasitologie
23	SOSSO Maurice	Chirurgie Générale
24	TETANYE EKOE	Pédiatrie
25	TSALA MBALA Pierre	Physiologie Humaine
26	YOUMBISSI TCHETAGNI Joseph	Médecine Interne / Néphrologie

1	ADIOGO Dieudonné	Microbiologie
2	AMANA Jean Paul	Radiologie/Imagerie Diagnostique
3	ANYANGWE née NWIGWE Stella	Santé Publique
4	BELLEY PRISO Eugène	Gynécologie-Obstétrique
5	BEFIDI MENGUE née NJEE N B, Rosa	Parasitologie
6	BIYIHA Dieudonné	Anesthésie-Réanimation
7	BOB' OYONO Jean Marie	Anatomie/Chirurgie Pédiatrique
8	DONG à ZOK	Biophysique /Médecine Nucléaire
9	EBANA	Ophtalmologie
10	ELOUNDOU	Neuro-chirurgie
11	ESSOMBA Arthur	Chirurgie Générale
12	ETOM EMPIME	Neuro-chirurgie
13	KASIA Jean-Marie	Gynécologie-Obstétrique
14	KINGUE Samuel	Médecine Interne / Cardiologie
5	LOLO Berthe	Psychiatrie
16	MBANYA née SHU Dora	Hématologie
17	MBU Robinson ENOW	Gynécologie-Obstétrique
18	MELAMAN SEGO Frédéric	Physiologie
19	MONEBENIMP Franscisca	Pédiatrie
20	MONNY LOBE Marcel	Hématologie
21	MOUELLE SONE	Radiothérapie
22	MOUSSALA	Ophtalmologie
23	NJEE BUGHA Théodore	Neuro-chirurgie
24	NOUEDOUI Christophe	Médecine Interne / Endocrinologie
25	NJOYA OUDOU	Médecine Interne / Gastro -entérologie
26	NSANGOU INNOUSSA	Pédiatrie
27	NTONE ENYIME Félicien	Psychiatrie
28	ONDOA MEKONGO Martin	Pédiatrie
29	ONDOBO ANDZE Gervais	Chirurgie Pédiatrique
30	SENDE Charlotte	Radiologie/Imagerie Médicale
31	SHASHA VIBAN Willibroad	Gynécologie-Obstétrique
32	TCHOUNWOU Paul Bernard	Environnement /Toxicologie
33	WANKAH Christian	Santé Publique

«Posterior urethral valves is a heterogeneous disorder with a sequelae ranging from voiding dysfunction without renal impairment to early onset of renal failure and death»

« the picture as usually described is but one end of a spectrum and there are

Nous avons étudié 28 cas d'enfants traités ou suivis pour valves de l'urètre postérieure du l^er Janvier 1985 au 31 Décembre 1996 au CHU, à l'Hôpital Central et à l'Hôpital Général de Yaoundé.'

Nos objectifs ont été d'étudier les aspects épidémiologiques des valves de l'urètre postérieure à Yaoundé, de décrire la présentation c1inique, les procédures diagnostiques et le devenir post-chirurgical en termes de fonction rénale, de croissance et d'anornalies urinaires chez ces enfants

L'étude a comporté 2 phases: une rétrospective transversale et l'autre prospective longitudinale descriptive, durant lesquelles nous avons étudié les données cliniques (anamnèse, procédures diagnostiques, traitement et suivi). Ce suivi comportait la surveillance clinique du jet urinaire, du poids, de la taille, des complications post-opératoires, de l'urée et la créatinine sanguine, ainsi que de l'uroculture.

L'âge des patients à la première consultation après le début des symptômes variait entre 1 jour et 8 ans (moyenne 1,6 ans). L'age des patients au moment du diagnostic variait entre 9 jours et 13 ans (moyenne 2.9 ans). L'intervalle moyen entre l'âge à la première consultation et l'âge au moment du diagnostic était de 9.7 mois.

Le diagnostic des valves a été fait par échographie chez 3 patients (sur la base de l'hydronéphrose bilatérale, vessie de lutte et dilatation de l'urètre postérieure). Chez les 25 patients restants le diagnostic a été fait à la fois par l'échographie et par la cystographie mictionnelle

Considérant l'âge des patients au moment du diagnostic, ceux-ci ont été' divisés en trois groupes :

Groupe I : (âge inférieur à 1 mois au moment du diagnostic): 5 patients. Groupe II (âge compris entre 1 mois et 12 mois): 9 patients.

Groupe III: (âge supérieur à 12 mois au moment du diagnostic): 14 patients. Dans les antécédents, on note le plus souvent des infections urinaires à répétition (50%), une hypertension artérielle chez 7% des patients (en insuffisance rénale terminale).

Les symptômes urinaires les plus fréquemment retrouvés sont la miction « goutte-à-goutte » (60.7%), dysurie (54%) et rétention urinaire (25%). Les symptômes

extra-urinaires les plus fréquents sont la fièvre (25%) et 'un retard de croissance (25%).

Les principaux signes physiques sont: hernies ombilicales (21%) et distensions vésicales (10.7%). Une ascite urinaire est retrouvée chez 2 patients.

Nous avons pu avoir les résultats d'uroculture chez 19 de nos patients: 12 étaient stériles; chez les 7 autres, les germes retrouvés étaient des bactéries Gram-négatif: E. coli (26%), Pseudomonas aeroginosa (11 %), Moraxella (11%), Klebsiella pneumoniae (11 %), Enterobacter aerogenes (5 %) et Proteus mirabilis (5%).

La fonction rénale au moment du diagnostic a été appréciée par le calcul de la filtration glomérulaire (F.G) (à partir de la formule de COCKCROFT) Elle était très altérée avec une F.G à 5ml/min/ 1.73m² dans le Groupe I, à 14ml/min/1.73m² dans le Groupe II et 19m1/min/l.73m² dans le Groupe III.

Cependant, 12 patients seulement ont été revus pour évaluation dans la phase prospective et parmi eux, 9 patients seulement ont fait les tests de fonction rénale.

Nous avons comparé la F.G au moment du diagnostic et a l'évaluation finale chez ces 9 patients.

On a noté une amélioration de la fonction rénale chez 6 patients (66,7%) avec une augmentation de la F.G. moyenne passant de 23.7m1/min/1 73m² à 58,8ml/min/1.73m². Chez 2 patients (22%), on a noté une détérioration de a fonction rénale avec une F.G moyenne passant de 53,5m1/min/1,73m² à 33ml/min/1.73m². Chez 2 patients, la F.G est restée stable à 15ml/min/1,73m²

Une analyse comparative du poids (au moment du diagnostic et de l'évaluation finale) a également été faite chez 9 patients. Ces poids ont été reportés sur les courbes de croissance de la NCHS (National Center for Health Statistics). Au moment du diagnostic, 8 de ces 9 patients avaient un retard de croissance inférieur au 50ème percentile. A l'évaluation finale nous avons noté une amélioration de La croissance chez 5 patients mais seulement 2 sont passés au dessus de 50ème percentile.

L'urographie intraveineuse (UIV) a été faite chez 6 patients et a montré une uretèro -hydronéphrose bilatérale chez 5 patients (83%), un retard de sécrétion chez 1 patient (17%) et un rein gauche muet chez 1 patient 17%.

La scintigraphie a été faite chez 2 patients et chez l'un d'eux, il y avait une forte suspicion de dysplasie rénale

L'exploration urodynamique de la vessie a été faite chez 2 patients et a montré une réduction de la compliance vésicale chez l'un des patients

En ce qui concerne le traitement, 26 patients ont subi une intervention chirurgicale les 2 patients restants ayant été perdus de vue après le diagnostic.

Vingt patients ont eu une ablation endoscopique des valves, 4 une vesicostomie de Blocksom, 3 une cystostomie et 2 une ablation par sonde.

Les interventions chirurgicale secondaires ont été: urétéroplastie (3), nephrostomie (4), circoncisions (4), urétérostomie (4), diverticulectomie (5) et urétérostomie pour sténose urétrale secondaire a une ablation par sonde (6).

Lors de l'évaluation finale, nous avons noté 6 décès (21%), 10 perdus de vue (36%) et 12 revus à la phase prospective de l'étude. Les causes de décès ont été : septicémie 3 cas (50%), syndrome de levée d'obstacle, 2 cas (33%) et insuffisance rénale chronique, 1 cas (17%).

A la fin de l'étude, nous arrivons à la conclusion que les valves de l'urètre postérieure sont diagnostiquées tardivement au Cameroun, quand l'insuffisance rénale et le retard de croissance sont déjà avancés. Le suivi des ces patients est insuffisant principalement parce que cette pathologie aussi bien que ses répercussions sur la fonction rénale et la croissance ne sont pas bien comprises.

Toute infection urinaire chez l'enfant soit correctement investiguée (surtout à l'échographie) car elle peut être la première manifestation des valves de l'urètre postérieur ou d'une autre uropathie obstructive.

Les complications des valves de l'urètre postérieur et leur prise en charge soient bien connues.

Un effort soit fait par les obstétriciens, les pédiatres et les radiologues afin qu'un diagnostic précoce, puisse être posé pour qu'une prise en charge adéquate soit instituée dans les plus brefs délais.

We reviewed the files of 28 children treated or followed up for posterior urethral valves (PUV) from 1st January 1985 to the 31st of December 1996 in the University Teaching Hospital, Central Hospital and the General Hospital in Yaoundé.

Our specific objectives were to review the epidemiological aspects of PUV in Yaoundé, assess the clinical presentation, diagnostic procedures and outcome following surgery in terms of renal function, patient growth and urinary abnormalities.

The study was a retrospective cross-sectional and a prospective longitudinal descriptive review of clinical data, during which the history diagnostic procedures, treatment and follow-up parameters were noted; (stream, weight, height, BUN, creatinine, urine cultures and post - operative complications).

The mean age of the patients at diagnosis was 2.9 years (range 9 days to 13 years) and the mean age at first consultation after onset of symptoms was 1.6 years (range 1 day to 8 years). The mean interval between age of first consultation and age at diagnosis was 9.7 months.

The diagnosis of PUV was made on ultrasound in 3 patients on the basis of bilateral uretero - hydronephrosis, thick - wall trabeculated bladder and a dilated posterior urethra. In the remaining 25, diagnosis was made on both ultrasound and voiding cystourethrograms. Considering the age of diagnosis, the patients were divided into three groups: Group I (age of diagnosis less than 1 month) 5 patients; Group II (1 month -12 months) 9 patients and Group III (age greater than 12 months) 14 patients.

The past history showed mostly recurrent urinary tract infection (UTI) in 50% of the patients and hypertension in 7% of the patients who had end-stage renal failure. The most frequent urinary symptoms were dribbling (60.7%), dysuria (54%) and urine retention (25%) whereas the most frequent non-urinary symptoms were fever (25%) and failure to thrive (25%). The main physical findings were umbilical hernias (21%) and bladder distension (10.7%), urinary ascitis was present in 2 patients (7%).

Results of urine cultures were available in 9 patients, 12 were sterile Pathogens cultured in 7 patients were gram negative bacteria: E. coli (26%) Pseudomonas aeroginosa (11%), Moraxella (11%), Kiebsiella pneumoniae (11%), Enterobacter aerogenes (5%), and Proteus mirabilis (5%).

Renal function at diagnosis , assessed from the Glomerular-Filtration Rate (GFR) (calculated from COCKCROFT'S FORMULA ) was markedly impaired with a GFR at 5 ml/min/1.73m² in Group I, 14m1/min/1.73m² in Group II and 19 ml/min/1.73m² in Group III. However, 12 patients turned up for evaluation in the prospective phase of the study and only 9 could do renal function tests. We compared the GFR at diagnosis and at final evaluation in these 9 patients. 6 (66.7%) had improved renal function with a mean GFR increasing from 23.7 ml/min/l.73m² to 58.8 ml/min/1.75m². 2 (22%) had deteriorated renal function with a mean GFR dropping from 53.5 ml/min to 33 rnl/min/l.73m² whereas in 2 the GFR remained stable, at 15m1/min/l.73m².

Comparative weight analysis (at diagnosis and at final follow-up) was also done in the same 9 patients. The weights were plotted onto NCHS (National Centre for Health Statistics) growth charts. At diagnosis 8 of the 9 patients (88.9%) had growth retardation with weights below the 50^th percentile. At final evaluation 5 patients had improved growth, but only 2 had gone above the 50^th percentile.

Intravenous pyelography (IVP) was done in 6 patients and it showed bilateral uretero-hydronephrosis in 5 (83%), late secretion in 1(17%) and a non-functioning left kidney in 1(17%). Scintigraphy was done in 2 patients and in 1 there was a strong suspicion of dysplastic kidneys. Bladder urodynamic studies were undertaken in 2 patients and reduced bladder compliance was noted in 1.

Concerning treatment 26 patients underwent surgery. 2 were lost to follow up after diagnosis. 20 patients underwent endoscopic valve ablations, 4 Blocksom vesicostomies, 3 cystostomies and 2 catheter ablations. Secondary procedures performed were: ureterosplasty (3), nephrostomy (4), circumcisions (4), ureterostomy (4), diverticulectomy (5) and urethrostomy [for meatal stenosis following catheter ablations] (6).

At final evaluation we noted 6 deaths (21%). 10 lost to follow-up (36%) and 12 reassessed. Causes of the deaths were septicemia: 3 cases (50%), post-obstructive diuresis: 2 cases (33 %) and chronic renal failure: 1 case (17%). 8 cases of incontinence were noted in the whole series.

still diagnosed very late with renal impairment and growth retardation already advanced. Follow-up of these patients is inadequate mainly because the pathology is not well understood as well as its repercussions on renal function and growth.

The urinary stream of children be clinically evaluated in routine consultations.

Any urinary tract infection in a child be adequately investigated (especially with ultrasound) as it might be the first manifestation of PUV or any other obstructive uropathy.

An effort be made by obstetricians, paediatricians and radiologists in making early diagnosis so that appropriate management be started as soon as possible.

Posterior Urethral Valves (PUV) are congenital membranous recesses in the posterior urethra in males (7). They are the most common cause of lower urinary tract obstruction in male infants (7,8,9,10,11,12, 13,14,15,16,19).

The incidence of PUV is reported to be 1 in 8000 live births according to CASALE A.J. cited in (10) and 1 in 25 000 live births according to ATWEL J.D. (4). The incidence in Oman is reported to be 1 in 2375 new-born males (16) which is considerably higher than any previously reported series. This was associated with an increased rate of consanguinity but there was no clear pattern of inheritance. In Yaoundé, they constitute the second cause of obstructive uropathies (1 3.3%) after uretero-pelvic junction obstruction (14.6%) according to NNOMZO'O (62) whereas it represents 15.22% of all uropathies in children in Côte d'Ivoire (18).

In infants especially neonates, the clinical presentation may be atypical in the form of diarrhoea, vomiting, fever, convulsions, abdominal masses (hydronephrotic kidneys, distended bladder, foetal or neonatal urinary ascitis with retroperitoneal urinomas), failure to thrive or even sepsis (11, 13, 19, 20, 22). Some new-borns who present an unexpected respiratory distress syndrome and/or an unexplained pneumothorax or pneumomediastinum, may be found to have obstructive uropathy - usually posterior urethral valves and pulmonary hypoplasia (8, 11). In older boys, the presenting symptoms are usually recurrent urinary tract infections and dribbling or straining to urinate (8, 11, 20, 21, 22). In small infants, the condition may be so advanced when first seen, that renal failure secondary to gross bilateral hydroureters and hydronephrosis dominates the clinical picture (22). Clinical suspicion may be missed especially in neonates because of the non-urological symptomatology.

The long-term consequences of such obstruction including impaired renal function and infection, remain serious problems for these patients despite newer methods of diagnosis and treatment (13). Because of the threat of premature death, early diagnosis and appropriate management are imperative. All infants or older children with urinary tract infections or abnormal voiding stream should benefit from

appropriate radiological investigations. Renal dysplasia and renal failure are the primary causes of death in neonates with PUV who survive initial pulmonary problems (23).

According to CHURCHILL B.M. (24) the treatment of PUV is now in its fourth major phase. The first phase was recognition of the entity. The second was treatment but in which the mortality rate, particularly in neonates in the first month was almost 50 percent in most major series. The third phase consisted of markedly improved survival rates, in which the mortality rate in most tertiary paediatric urology centres was less than 10 percent. In the fourth phase the challenge after having kept these children alive is to get optimal renal function, so that optimal growth and the late complications of dialysis and transplantation are avoided.

It is in this light that we reviewed the files of 28 patients with PUV followed up in the University Teaching Hospital, Central Hospital and the General Hospital in Yaoundé over an 11 year period (1st January 1985 to 31st December 1996) to assess the diagnostic methodology and outcome.

To the best of our knowledge, no study has been done with these objectives in Cameroon. We hope to come out with pertinent findings and recommendations which will help physicians make early diagnosis and institute appropriate management thus avoiding long-term renal compromise and death from this disorder.

of renal function, patient growth, urinary tract abnormalities, dialysis and transplantation).

Functionally, the urogenital system can be divided into two entirely different components (1) The urinary system and (2) the genital system.

Embryologically and anatomically however, they are intimately interwoven Both develop from a common mesodermal ridge along the posterior wall of the abdominal cavity, and the excretory ducts of both systems, initially enter a common cavity, the cloaca.

With further development, the overlapping of the two Systems is particularly evident in the male. The primitive excretory duct first functions as a urinary duct but later is transformed into the main genital duct Moreover , in the adult the urinary as well as the genital organs discharge urine and semen through a common duct, the penile urethra.

Three different, slightly overlapping kidneys are formed during intra -uterine life in man: the PRONEPHROS, the MESONEPHROS, and METANEPHROS or permanent kidney.

PRONEPHROS: In the human embryo the pronephros is represented by a 7 to 10 solid cell groups in the cervical region ( Fig. 3B) The first formed vestigial nephrotomes regress before the last ones are formed, and at the end of the fourth week all indications of the pronephric system have disappeared.

*MESONEPHROS: During regression of the pronephric system, the first excretory tubules of the mesonephros appear. They lengthen rapidly, form an «S» - shaped loop, and acquire a glomerulus at their medial extremity. Here the tubule forms the Bowman's capsule.

Fig. 1 Diagrammatic representation of the male genital system. The midline structures are shown in a sagittal section;

bilateral structures, such as testis, epididymis, vas deferens, and seminal vesicle, are depicted intact.

The capsule and glomerulus form together a mesonephric (renal) corpuscle - At the opposite end the tubule enters the longitudinal collecting duct known as the mesonephric or Wolfian duct (fig 3).

In the middle of the second month, the mesonephros forms a large ovoid organ on each side of the midline. Since the developing gonad is located on its medial side the ridge formed by both organs is known as the urogenital ridge. While the caudal tubules are still differentiating the cranial tubules and glomeruli show degenerative changes and by the end of the second month, the majority has disappeared. A few of the caudal tubules and the mesonephric duct however persist in the male but disappear in the female. Although great resemblances in ultra structure exist between the mesonephros and metanephros, functional activity of the mesonephros has not been demonstrated in the human embryo.

*METANEPHROS OR PERMANENT KIDNEY: The third urinary organ, the metanephros or permanent kidney appears in the fifth week. Its excretory units develop from the metanephric mesoderm (fig 4) in the same manner as in the mesonephric system.

The collecting ducts of the permanent kidneys develop from the ureteric bud, an outgrowth of mesonephric duct close to its entrance into the cloaca (fig 4). The bud penetrates the metanephric tissue, which, as a cap is moulded over its distal end (Fig. 4) Subsequently the bud dilates forming the primitive renal pelvis; simultaneously it splits into a caudal portion, the future major calyces. Each calyx, while penetrating into the metanephric tissue, forms two new buds. These buds continue to subdivide until 12 or more generations of the tubules have been formed. While at the periphery more tubules are formed until the end of the fifth month, the tubules of the second order enlarge and absorb those of the third and fourth generations, thus forming the minor calyces of the renal pelvis. During further development, the collecting tubules of the fifth and successive generations elongate considerably and converge on the minor calyx, thereby forming the renal pyramid. Hence , the ureteric bud gives rise to the ureter, renal pelvis, the major and minor calyces and approximately one to three million collecting tubules.

Each newly formed collecting tubule is covered at its distal end by a so-called metanephric tissue cap. Under the inductive influence of the tubule cells of the tissue cap form small vesicles, the renal vesicles which in turn give rise to small tubules. These tubules form the nephrons or excretory units. The proximal end of the nephron forms the Bowman's capsule of the renal glomerulus. The distal end forms an open connection with one of the collecting tubules, thus establishing a passageway from the glomerulus to the collecting unit. Continuous lengthening of the excretory tubule results in the formation of the proximal convoluted tubule, the loop of Henle, and the distal convoluted tubule.

Fig.3a Schematic transverse sections through embryos at various stages of development to show the formation of the nephric tubule. A, At 21 days; B, at 25 days. Note the formation Of the external and internal glomeruli, and the open connection between the coelomic cavity and the nephric tubule (modified after Heuser).

Fig. 3b A, Schematic diagram showing the relation of the intermediate mesoderm of the pronephric, mesonephric, and metanephric systems. In the cervical and upper thoracic regions the intermediate mesoderm is segmented; in the lower thoracic, lumbar, and sacral regions it forms a solid, unsegmented mass of tissue, the nephrogenic cord. Note the longitudinal collecting duct, initially formed by the pronephros but later taken over by the mesonephros. B, Schematic representation of the excretory tubules of the pronephric and mesonephric systems in a five-week-old embryo. Note the remnant of the pronephric excretory tubules and longitudinal collecting duct. 31

Fig 4 Schematic drawing to show the relationship of the hindgut and cloaca at the end of the fifth week. The

Fig. 5: Diagrams showing the division of the cloaca into the urogenital sinus and anorectal canal. Note that the mesonephric duct is gradually absorbed into the wall of the urogenital sinus and that the ureters enter separately. A, End of the fifth week; B, seven weeks; C, eight weeks.

Fig 6 A, Development of the urogenital sinus into the urinary bladder, the pelvic part of the urogenital sinus, and the definitive urogenital sinus. B, In the male the definitive urogenital sinus develops into the penile urethra. The prostate gland is formed by outbuddings of the urethra, while the seminal vesicles are formed by an outbudding of the ductus deferens.

Fig 7 Dorsal view of the bladder to show the relationship of the ureters and mesonephric ducts during development. Initially the ureter is formed by an outgrowth of the mesonephric duct, but with time it obtains a separate entrance into the urinary bladder. Note the trigone of the bladder formed by incorporation of the mesonephric ducts.

Hence the kidney develops from two different sources (1) the matanephric mesoderm which provides the excretory units and (2) the ureteric bud which gives rise to the collecting system.

During the fourth to seventh week of development, the uro-urectal septum divides the cloaca into the ano-rectal canal, and the primitive urogenital sinus (Fig.5). The cloacal membrane itself is then divided into the urogenital membrane, anteriorly, and the anal membrane, posteriorly (Fig.5C).

Three portions of the primitive urogenital sinus can be distinguished: (1) the upper and largest part is the urinary bladder (Fig. 6A). Initially the bladder is continuous with the allantois, but when the lumen of the allantois is obliterated, a thick fibrous cord, the urachus remains, connecting the apex of the bladder with the umbilicus. In the adult, the ligament is known as the median umbilical ligament; (2) A rather narrow canal, the pelvic part of the urogenital sinus; which in the male gives rise to the prostatic and membranous parts of the urethra; (3) the definitive urogenital sinus, also known as the phallic part of the urogenital sinus. It is considerably flattened from side to side and is separated from the outside by the urogenital membrane.

During division of the cloaca, the caudal portions of the mesonephric ducts are gradually absorbed into the wall of the urinary bladder (Fig.7). Consequently the ureters, initially outbuddings of the mesonephric ducts, enter the bladder separately (Fig.7B). As a result of the ascent of the kidneys, the orifices of the ureters move further cranial; those of the mesonephric ducts more close together to enter the prostatic urethra and in the male, become the ejaculatory ducts (Fig.7C, D). Since both the mesonephric ducts and the ureters are of mesodermal origin, the mucosa of the bladder formed by incorporation of the ducts, the trigone of the bladder is of mesodermal origin. The remaining part of the bladder is derived from the urogenital sinus and is endodermal in origin. With time, the mesodermal lining of the trigone is replaced by endodermal epithelium so that finally the inside of the bladder is completely lined with epithelium of endodermal origin. 34

The epithelium of the male and female urethra is of endodermal origin, while the surrounding connective and smooth muscle tissue are derived from the splanchnic mesoderm. At the end of the third month, the epithelium of the prostatic urethra begins to proliferate and forms a number of outbuddings which penetrate the surrounding mesenchyme. In the male, these buds form the prostatic gland (Fig.6 B). In the female, the cranial part of the urethra gives rise to the urethral and paraurethral glands.

Currently, the most accepted view is that type I valves arise from the urethrovaginal folds which become the plicae colliculi in the course of development. The origin of the urethrovaginal folds is a matter of dispute. Some authors believe that these folds represent the fibrous track left behind by the Wolfian ducts as they migrate posteriorly and medially around the wall of the urogenital sinus until they meet the paramesonephric duct at the müllerian tubercle in the middling, whereas others think they represent the anterior potion of the hymenal ring and thus would be müllerian derivatives.

However abnormal formation or regression of these plicae colliculi may be involved in the genesis of typical PUV which are exaggerations of the normal folds. Type III membranes may be variable in origin. Some may represent type I valves with marked anterior fusion, whereas others may represent incomplete disappearance of the urogenital membrane.

A genetic component has been postulated from occasional observations of PUV in twin and no-twin siblings (8, 11, 27, and 16). But the genetic factors in the pathogenesis of PUV are poorly understood. PUV have also been described to be associated with other chromosomal abnormalities ad Down's Syndrome (19, 26).

D. CLASSIFICATION OF POSTERIOR URETHRAL VALVES

LANGENBECK in 1802 is credited with the first description of PUV, but in 1919 YOUNG H.H, FRONTZ W.A and BALDWIN J.C. reported 36 cases, 12 from a personal series and a further 24 from the world literature (cited by DINNEEN and Duffy in 10). YOUNG et al described 3 types of valves -Fig.8 (cited in 28, 29, 30, 11, 12, 2, 13, and 31)

Type I: It is a bicuspid valve that originates just distal to the verumontanum on the floor of the posterior urethra and diverges distally in an antero-lateral orientation to fuse anteriorly in the midline at the twelve o'clock position at the anterior wall just proximal to the membranes urethra. The appearance endoscopically is that of two membranes, paired in a manner similar to the vocal cords, fused anteriorly. The fusion creates a valve which obstructs the outflow of urine while allowing the retrograde passage of catheters or irrigating fluid 95% of PUV are Type I, with variations in leaflet thickness and in the degree of coalescence at the twelve o'clock position. The resulting obstruction consists of filmy membranes which are easily disrupted, or at worst, a thickened tissue with a small inferior opening. This type corresponds to the "Spinnaker Sail" appearance.

Type II: They are a series of folds that run between the verumontanum and the bladder neck and probably are non-obstructive.

Type III: They are obstructing diaphragms with a central opening, located in the membranous urethra. They do not have a typical attachment to the inferior portion of the verumontanum and are of a different embryological origin. There are two subgroups: III_a. - below the verumontanum; and IIIb above the verumontanum.

The YOUNG's classification however, developed largely on the basis of autopsy dissection before the advent of endoscopy, has some inaccuracies and does not correspond well to modern ideas of the normal anatomy and embryology of this region (11). 37

The three types of valves described in YOUNG's series had undergone urethral manipulation before assessment and so this classification has been criticized (10).

This misconception appears to result from post-mortem dissections from the anterior approach, cutting through the fused anterior portion of a structure that modern endoscopic studies reveal is actually a diaphragm with a lumen, making it appear as if there were two leaflets instead of a membrane (11).

In a similar fashion, there are superficial fibroelastic bundles that pass upward and laterally towards the base of the bladder. These are the structures that YOUNG et al thought correspond to Type II valves. Although they are occasionally quite prominent, most authors agree that these structures are almost never obstructive (11). Current endoscopic evidence (29, 30, 11) dismiss the existence of Type II valves.

According to DEWAN (29), the acceptance of a single basic morphology for the posterior urethral pathology suggests that there is only one embryological process, which is probably a persistence of the normal attachment of the verumontanum to the posterior urethra. He has thus proposed a nomenclature for valves different from YOUNG's classification. The type III valve which is a more distal bulbar obstructing membrane with a central hole may well constitute a persistence of the urogenital diaphragm and referred to as COBB's COLLAR, whereas the term COPUM (Congenital Obstructive Posterior Urethral Membrane) may be appropriate for the posterior urethral valves (Type I).

E. PATHOPHYSIOLOGIC CHANGES INDUCED BY PUV ON THE URO- GENITAL TRACT(32, 10, 11, 33, 64, 17, 35, 36)

Proximal to the obstruction, the urethral dilates and balloons. A proximal diverticulum may develop and dilatation and gaping of the prostatic and ejaculation ducts may occur. PUV have been mentioned as a possible cause of urethro-ejaculatory

reflux of infected or sterile urine (with possibility of bilateral obstruction of the genital

tract) and presumed to be a possible cause of acute epididymitis and infertility. Under normal circumstances, the reflux of urine into the male genital tract is impossible. The anti-reflux mechanism is effected by the oblique passage of the ejaculatory duct through the thick prostatic tissue. This mechanism might be rendered incompetent by the extreme attenuation of the foetal prostatic tissue consequent upon excessive dilatation of the obstructed prostatic urethra. It should be noted that the foetal kidneys start producing urine during the third month of gestation would prevent the growth of the prostate; early urethral obstruction would prevent the growth of the prostrate and the development of a competent anti-reflux mechanism. Infertility could also result from retrograde ejaculations following surgery on the bladder neck.

Early, the detrusor and trigonal thickening and hypertrophy compensate for the outlet obstruction and lead to complete bladder emptying. This change leads to progressive development of the bladder trabeculation, cellules then diverticula. Beyond a certain phase, bladder decompensation occurs and is characterized by the above changes, pins variable amounts of residual urine. Trigonal hypertrophy leads to secondary ureteral obstruction due to increased resistance to flow through the intravesical ureter. With the detrusor decompensation and residual urine accumulation, there is stretching of the hypertrophied trigone, which increases ureteral obstruction. This is the mechanism of back pressure on the kidneys in the presence of vesical outlet obstruction, while the uretero-vesical junction maintains its competence. Catheter drainage of the bladder relieves trigonal stretch and improves drainage from the upper tract. A very late change with persistent obstruction (more frequently encountered with neurogenic dysfunction) is decompensation of the uretero-vesical junction, leading to reflux, which aggravates the back pressure in the upper tract by exposing it to abnormally high intravesical pressure, in addition to favouring (the onset or persistence ) of urinary tract infection. Should ureteral obstruction be unilateral a compensatory hypertrophy of the contralateral kidney will develop. Total renal function therefore remains normal.

Bladder diverticula and unilateral vesicoureteral reflux may serve as 'popoff' mechanisms to buffer high pressures in the urinary tract. Patients with PUV may also develop valve bladders, which are thick walled, poorly compliant and often with high resting pressures even at small urine volumes. It is this high bladder pressure that is so damaging to the urinary tract. Bladder dysfunction (unstable, poorly compliant and over distended bladders which are variations of the same basic urodynamic pattern) that changes with time towards decompensation is clearly a contributory factor to urinary incontinence.

The renal pelvis and calyces being subjected to progressively increasing volumes of retained urine progressively distend. The pelvis first shows evidence of hyperactivity and hypertrophy and then progressive dilatation and atony. The calyces show the same changes to a variable degree depending on whether the renal pelvis is intra or extra-renal. In the latter, the calyceal dilatation may be minimal in spite of marked pelvic dilatation. In the intra -renal pelvis, calyceal dilatation and renal parenchymal damage are maximum. The successive phases seen with obstruction are rounding of the fornices, followed by flattening of the papillae and finally clubbing of the minor calyces.

In neonates and infants there may be extravasation of urine at the level of the renal pelvis or the ureterovesical junction with formation of urinary ascitis and perirenal

and retroperitoneal urinomas resulting in abdominal distension v. Renal Parenchymal changes

Since urine formation begins between the ninth and twelfth weeks of gestation corresponding to the formation of the inner cortical nephrons in the centrifugally developing kidney , obstruction to urinary outflow could increase hydrostatic pressure and thus affect the environment of the foetal kidney during the very early phases of morphogenesis, resulting in hypoplastic or dysplastic renal development in addition to simple hydronephrosis whereas obstruction late in gestation may produce simple hydronephrosis It should be noted that nephron differentiation occurs up to the thirty-second week of gestation.

With progressive pelvicalyceal distension, there is parenchymal compression against the renal capsule. This, plus the more important factor of compression of the arcuate vessels as a result of the expanding distended calyces results in a marked drop in renal blood flow. This phenomenon leads to progressive parenchymal compression and ischemic atrophy. Lateral groups of nephrons are affected more than central ones, leading to patchy atrophy with variable degree of severity. The glomeruli and proximal convoluted tubules suffer most, of this ischemia. Associated with the increased intrapelvic pressure there is progressive dilatation of the collecting and distal tubules with compression and atrophy of tubular cells.

Whereas dilation of the calices and the thinness of the parenchyma my be explained on the bases of atrophy from back pressure of obstruction and reflux, the etiology of variants such as asymmetrical kidney morphologies, the occurrence of near normal renal parenchyma in some kidneys exhibiting all the ureteral and caliceal stigmas of severe obstruction and dysplasia, is not the same.

HENNEBERY and STEPHENS (37) have clearly demonstrated that these variants may be due to ectopic origins of the ureteral buds from the most caudal part of the Wolfian duct, which leads to induction of defective or sparse mesenchyme of the tail end of the nephrogenic cord with resultant dysplasia and hypoplasia, respectively. The key to the potential quality of the renal parenchyma is the ureteral orifice. This is the "bud theory" of the renal morphology 41

Consent was obtained from all the parents before admission into the study. Explanations as to the innocuity of the study were given as well as benefits incurred from regular follow-up after surgery to avoid short and long-term complications. 44

The data collected was analysed in a computer (type NCR) using the Epi-lnfo medical software.

		I (N=5)	II (N=9)	III (N =14)	TOTAL (%)
A)	URINARY SYMPTOMS
	Dribbling	2	5	10	17(60.7)
	Dysuria	1	7	7	15 (54)
	Urine retention	1	2	4	7 (25)
	Chronic renal failure	1	1	2	4 (14)
	Hematuria	-	1	3	4 (14)
	Pollakiuria	-	1	1	2 (7)
	Pyuria	-	1	1	2 (7)
	Oedemato-ascitic syndrome (urinary ascitis)	1	-	-	2 (7)
	Hypogastric pain	-	1	1	1 (3.6)
	Paraphimosis	-	-	-	1 (3.6)
	Incontinence	-	1	1	1 (3.6)

B)	NON-URINARY SYMPTOMS
	Fever	1	4	2	7 (25)
	Failure to thrive	1	4	2	7.(25)
	Vomiting	-	2	1	3 (10.7)
	Diarrhoea	-	3	-	3 (10.7)
	Dehydration	-	2	1	3 (10.7)
	Anorexia	1	2	-	3 (10.7)
	Respiratory distress	1	-	1	2 (7%)
	Abdominal distension	1	-	1	2 (7%)
	Polydypsia	-	-	1	1 (3.6)

	I (N = 5)	II (N = 9)	III (N = 14)	TOTAL (%)
Umblical hernia	3	1	2	6 (21)
Bladder distention	1	-	2	3 (10.7)
I V S D	2	-	-	2 (7)
Hepatomegally	1	-	1	2 (7)
Bilateral flank masses	-	1	1	2 (7)
Oedemato-ascitic syndrome	1	-	1	2 (7)
Hydrocoele	-	2	-	2 (7)
Trisomy 21	1	-	-	1 (3.6)
Bilateral inguinal hernia	1	-	-	1 (3.6)
Paraphimosis	-	1	-	1 (3.6)
Splenomegally	1	-	-	1 (3.6)
Neonatal jaundice	1	-	-	1 (3.6)

Urine cultures were available in 19 patients. In 12 they were positive of the above pathogens and sterile in 7. One patient had both a klebsiella pnuemoniae and Proteus

+ Bilateral renal parenchyma atrophy and megaureters in 1 (6%) + Megaureters with the left ectopic (6%)

VUR was bilateral in 4 patients and on the right in 1 patient. Large urine residual volumes were present in 2 patients. Hutch's diverticulum was noted in 2.

Voiding cystourethrogram of a 9 day old child showing a large trabeculated bladder, dilated

posterior urethra and a filling defect at the posterior urethra indicating a PUV.

Control cysto urethrogram in an 8 year old boy following resection of PUV at the age of 2 years showing a normal bladder wall and posterior urethra.

NB There was a strong suspicion of dysplasia in the patient with bilateral atrophy.

2 patients were lost to follow-up after diagnosis and didn't undergo and surgery. One patient with terminal renal failure underwent ureterostomy in France but was lost to follow-up.

5 Patients did not have endoscopic resection. 4 in the vesicostomy group (2 died and 2 pending by the end of the study) and 1 in the catheter ablation group.

Table 17: EVALUATION OF RENAL FUNCTION AND WEIGHTS AT DIAGNOSIS AND AT FINAL FOLLOW-UP PRE-OPERATIVELY:

	Age	Weight	BUN (mg%)	Creatinine (mg%)	GFR ml/min/1.73m²
A.N	23 months	12.5	1.8	1	24
D.Y	16 months	10	50	1.1	18
E.N	3.5 months	4.22	22	1.2	7
F.K	10 years	33.5	32	0.8	76
J.B	2 years	12	42	1.8	13
K.K.E	2.5 years	12.8	14	0.4	61
N.J	11 months	6.1	-	0.8	15
N.C	14 months	9.5	36	0.4	46
N.M	3 weeks	3.47	73	1.6	4

	Age	Weight	BUN (mg%)	Creatinine (mg%)	GFR ml/min/1.73m²
A.N	11 yrs 11months	32.5	-	1	58
D.Y	9 years	23	69	1.1	38
E.N	14 months	9.980	23	0.58	33
F.K	12.5 years	37.8	13	0.6	112
J.B	9 years	27	62	1.8	20
K.K.E	9 years	25.4	34	1.3	36
N.J	2 years	10.8	91	1.4	15
N.C	6 years	19.4	38	1.2	30
N.M	6 years	19.8	29	0.4	92

I. EPIDEMIOLOGIC FACTORS

The mean age at diagnosis of all the 28 patients was 2.9 years (range 9 days to 13 years ) which is significantly higher than that reported by COULIBALY, 2 years (18). In a series of 100 cases reported by SMITH et al (31), 42% of PUV were diagnosed before 1 month, and 56% before 1 year. In our series 50% of PUV were diagnosed after 12 months. The mean age at diagnosis in the series reported by WARSHAW et al (38) was 39 days.

The mean age of the first consultation after onset of symptoms was 1.6 years (range 1 day to 8 years). The mean interval between age of first consultation and age of diagnosis was 9.7 months which is still higher than 51 days, reported by COULIBALY et al in Côte d'Ivoire (18). The mean number of follow-ups was 3 (range 0 to 10)

We decided to divide our patients into 3 groups (see Table 1) because it is believed that chronological age at presentation is a relatively well -defined marker for delineating severity (14).

UTI was noted in 50% of our patients. LOTTMAN (52) noted it in 64 % of his cases, ATWEL (4) in 34% and COULIBALY (18) in 85% of their cases. Hypertension was noted in 2 patients (7%) who presented with end-stage renal failure. In 1 patient there was a family history of renal disease. The cousin had end -stage renal failure from PUV, underwent kidney transplant and is currently undergoing hemodialysis.

In our series an abnormal urinary stream with dribbling was most frequent in 60.7% of the patients, followed by dysuria. ANGWAFO et al (5) noted in 100% of their patients. ATWEL (4) noted in 17% and LOTTMAN (52) in (32%). Dysuria was the second most frequent complaint (54%) but was the most frequent (46%) in COULIBALY's series (18). Most mothers don't know the characteristics of a normal

urinary stream, so it should be well described when seeking to know about the presence or absence of dribbling. Two patients with end-stage chronic failure were observed in our series.

One had undergone kidney transplant in France. Of the non-urinary symptoms fever (25%) and failure to thrive (25%) were most frequent. COULIBALY et al (18) noted respectively 22% and 11%. 32% of the non-urinary symptoms were digestive (vomiting, diarrhoea and dehydration)

Umbilical hernias were most observed ( 21 %). This finding is very rare in literature but it was 68.2% in the series reported by ANGWAFO et al (5). It should be noted that our series was much larger than that of ANGWAFO et al. Bladder distention occurred in 69.8% in COULIBALY's series and was the most frequent physical finding. Bladder distention was the second most frequent finding in our patients. ISVD was noted in 2 patients and diagnosed in the neonatal period. We noted the presence of trisomy 21 associated an IVSD. The possible association of PUV and trisomy 21 has been reported by some authors (39). It has been suggested that infants with trisomy 21 should be screened with ultrasonography for renal and urological abnormalities early in life because they have increased risk of developing PUV and obstructive uropathy.

II. INVESTIGATIONS

Leucocytosis and microcytic anaemia were noted respectively in 63% and 79% of our cases. Uraemia was noted in 12 patients (57%) with BUN greater than 45 mg% and hyperkaliemia in 5 patients (56%).

Urine cultures were requested for in all patients but results were available in 19. 7 cultures were sterile and of the 12 in which pathogens were identified, E. coli was the

most frequent (26%) followed by Pseudomonas aeroginosa (11%). In COULIBALY's series (18) E. coli was also the most frequent pathogen followed by Pseudomonas aeroginosa, and no pathogens in 26%. No pathogens were identified in 37% of our patients. In the series reported by FALL et al (20) the most frequent pathogen was Pseudomonas (50%) followed by Klebsiella (38%).

In all our patients, the mothers had undergone at least one prenatal ultrasonographic examination, but no case was diagnosed antenatally. Diagnosis of PUV could be made as early as 16-18 weeks of gestation (19). The major benefit of antenatal ultrasonography is to allow early diagnosis of urinary tract malformations before post-natal infection worsens the prognosis3)

In the post-natal period transperineal voiding ultrasound is non-invasive and useful in diagnosing PUV. With a posterior urethral diameter of at least 6 mm during voiding as a criterion for transperineal ultrasound diagnosis of obstruction, sensitivity is 100%, specificity 89% and a positive predictive value of 89% (12).

In our series 18 patients had results of ultrasound examinations available. Bilateral ureterohydronephrosis was noted in 94%, trabeculated bladder wall (67%) and a dilated posterior urethra in 72% of the patients.

In 3 of our patients, diagnosed on ultrasound in the first month, no further radiological investigations were done because of severe sepsis and uraemia. They all underwent emergent vesicostomies.

Apart from the 3 patients mentioned above, all our patients had VCUG, but results at diagnosis were available only in 18, vesico-ureteral reflux was present in 5 patients (28%); bilateral in 4 (22%) and unilateral (on the right) in 1 case (6%). COULIBALY et al found 13.51 % (bilateral) and 24% (unilateral). It is reported (11) that reflux may present in up to 60% of the patients with PUV and that, when unilateral, it is most often

on the left and associated with a poorly functioning or non-functioning kidney and persists despite surgery. However if on the right it is associated with a functioning kidney and resolves in most patients (11). Direct evidence of valves was noted in 7 patients (39%) and present as filling defects in the posterior urethra. Hutch's diverticulum which is a paraureteral diverticulum was noted in 2 patients. One patient developed urosepsis after a retrograde urethrocystography and was treated.

This was done in 6 patients and showed bilateral uretero-hydronephrosis in 5 (83%), late secretion in 1 (17%), non-functional left kidney in 1 (17%). COULIBALY et al (18) found 80% of their cases with upper tract dilatation and 20% with non-functioning kidneys.

Radionuclide evaluation is superior to IVP in evaluating renal functions and gives reproducible information about total and differential renal function, but it does not provide a sensitive and accurate illustration of the anatomic changes in the kidney .(40). Two patients benefited from this examination (one in France and one in Britain). In one there was strong suspicion of bilateral renal dysplasia.

Bladder urodynamics are necessary in evaluating the bladder-sphincter complex and will help in the diagnosis of bladder dysfunction (41). The same two patients benefited from this examination.

III. TREATMENT (Tables 13 and 14)

Of our 28 patients, 2 were lost to follow-up immediately after diagnosis and so did not undergo surgery. 1 patient with end-stage renal failure had ureterostomy in France. So only 25 patients had at least one major surgical procedure mentioned in Table 13. A

BLOCKSOM vesicostomies were done in 6. 2 were closed by the end of the study after endoscopic ablation. Of the remaining 4, 2 were yet to be closed amongst which one, who had vesicostomy at the age of 3 weeks was lost to follow-up and was later seen at the age of 6 years in the prospective phase of the study ; and 2 had died at 2 days post -op. of septicaemia. BLOCKSOM vesicostomy is a tubeless bladder diversion. It was first performed by BLOCKSOM in 1956 in a 75 year old man with carcinoma of the urethra (42). The advantages are that it is tubeless, readily reversible, easy to perform and does not require any appliance. By decompressing the urinary tract it allows a very ill, often azotemic and septic child to recover from the long-term effects of obstruction or severe reflux (42). Definitive reconstructive surgery can be postponed until the patient's condition is optimal, renal function has improved or stabilized, infection is finished or until the patient's size is more appropriate for the particular procedure.

All the patients who underwent cystostomy later underwent endoscopic ablation. Two cases of catheter ablation were done before the advent of endoscopic surgery in Cameroon. 1 later underwent endoscopic resection and the other went into end-stage renal failure and died.

Secondary procedures were performed in only 11 patients. High diversions were performed in 6 cases - 3 ureterostomies and 3 nephrostomies for severe bilateral hydronephrosis. All the ureterostomies and nephrostomies were closed Primary ureteroplasties were done in 4 patients. One patient had urethrostomy for meatal stenosis following catheter ablation done elsewhere. Catheter ablation is abandoned in our institutions since the advent of endoscopic surgery.

Although controversy still exists as to the management of PUV, the current attitude is a primary valve ablation followed by observation and vesicostomy reserved for patients in whom valve ablation is not technically possible or in a child with severe renal failure .(43, 44,31,45). The long-term outcomes with primary diversion and primary valve ablation are the same, but performance and reversibility of diversion

IV. OUTCOME OF THE PATIENTS (Table 15)

The overall mortality was 21 %. COULIBALY et al (18) had 15%; FALL et al (20)14%, LOTTMAN (46) 4% and WARSHAW et al (38) 4.5%. 10 patients (36%) were lost to follow-up

Causes of deaths: 3 died of septicaemia, 2 post-obstructive diuresis and 1 of chronic renal failure

* Septicemia:1 patient (2 months old) died 2 days after an emergent vesicostomy for uraemia, from Pseudomonas septicaemia. l (3 months) died of klebsiella sepsis and cardiac decompensation and 1 (2 years old) died of klebsiella pneumonia and Enterobacter cloacae septicaemia one week after having undergone endoscopic resection and ureteroplasty for bilateral hydronephrosis.

* Chronic renal failure: The patient who died of chronic renal failure was 18 years old. He had undergone catheter ablation in the neonatal period, developed end-stage renal failure at 7 and had a kidney transplantation (the donor was the mother) in France. Before transplantation he had had a nephrostomy and several peritoneal dialysis. Back home in Cameroon, he was on immunosuppressors (Cyclosporine and Azathioprine) developed skin Kaposi sarcoma, severe lung infection graft rejection and died.

* Post -obstructive diuresis: One patient (9 days old) died 2 days after an emergency BLOCKSOM vesicostomy for uraemia. The other 4 months old died 2 months after endoscopic resection, in a hospital out of Yaounde. He had developed gastro-enteritis, and this added to the polyuria he has been having and inadequate dehydration caused severe dehydration and death.

Post-obstructive diuresis is persistent polyuria following valve ablation or relief of any obstruction of the urinary (47, 48). This can provoke a dramatic urinary loss of salt and water and hypotonic urine. Severe polyuria carries a risk of dehydration, particularly with diarrhoea and vomiting or high solute feeds (47). There are two major causes: (48)

1) Urea, through its osmotic effect and possibly natriuretic humoral substances 73

which inhibit the reabsorption of NaCl and water in the proximal and distal tubules.

2) Obstruction per se, possibly through increased pressure within the renal pelvis

inhibits the reabsorption of fluid and loss of urine concentration ability. Appropriate but cautious fluid replacement should be administered to patients with post-obstructive diuresis depending in large, on what is excreted.

V. RENAL FUNCTION (Tables 6 and 17)

Of the 12 patients we had in the prospective phase, renal function tests (BUN and creatinine) were done only by 9 (3 did not do because of financial constraints). BUN is not a good predictor of renal function because of its variability with factors as dietary proteins, fever, hydration and liver damage. GFR as calculated from timed urine collection and serum creatinine is often inaccurate in infants because of problems in collection of the urine (45). A nadir creatinine valve less than or equal to 0.8 mg /dl by 12 months of age has been described a good predictor of good renal function at the time of final evaluation (38). Serum creatinine is valid only as it relates to muscle mass, therefore a blanket endorsement of 0.8 mg/dl at 1 year of age doesn't take into account the variability in body size (45). So we calculated the GFR from COCKCROFT's FORMULA considering the weight, age and serum creatinine. No patient had GFR above 100 ml/min/1.73m² at diagnosis and only 2 had GFR above 50 ml/min/1.73m² at diagnosis. At the end of the follow-up 6 patients had improved GFR (one above 100 ml/min/1.73 m², two between 50 and 100 ml/min/1.73 m² and three below 50 ml/min/1.73m^2. Contrarily in 2 patients it dropped, from 46 to 30 in one, and from 61 to 36 ml/min/l.73m² in the other. In one patient it remained stable at 15 ml/min/1 .73m². An important observation is that despite these low GFR, these children manifested no signs of renal failure.

In man, the relationship between the duration of obstruction and the degree of recovery of renal function after release is not known (48). Return of function depends upon many factors other than the length of obstruction, such as absence of infection,

presence of an intrarenal or extrarenal pelvis in the obstructed kidney, and the degree of pyelolymphatic and pyelovenous blood flow (48). However the ultimate objective in the management of infants and children with obstructive uropathies is long-term preservation of renal function (36).

Chronic renal failure occurs in a significant number of children with a history of posterior urethral valves (32, 49). Causes include intrauterine renal dysplasia and hydronephrotic damage, vesico-ureteral reflux, continued bladder outlet obstruction and vesical dysfunction, (23, 49), postnatal UTI, hyperfiltration and glomeoulosclerosis. Abnormal bladder compared to these other factors for causing end-stage renal disease remains unknown (49). The valve bladder syndrome, involves a poorly compliant, small capacity bladder leading to upper tract dilatation and renal compromise that is amendable to improvement via bladder augmentation with intestine (32).

Although the choice of surgical treatment for patients with PUV often involves an attempt to stop the course of progressive renal failure, many are born with severe renal dysplasia that leads to inevitable progressive renal failure regardless of the primary method of treatment (32). HENNEBERRY and STEPHENS proposed that renal dysplasia associated with posterior urethral valves is not secondary to reflux or transmitted high pressures, but rather results from aberrant caudal budding of the ureter from the mesonephric duct with subsequent abnormal induction of mesenchyma (37). Renal dysplasia occurs before the 10^th week of gestation before ultrasound can diagnose (3). The experience of CLOSE C.E. et al (32) suggest that there is a window for healing in neonates that is limited to the first few months of life with primary valve ablation.

Ultrasonographic demonstration of corticomedullary junctions in infancy appears to be a useful, favourable prognostic index in boys with posterior urethral valves and possibly other obstructive uropathies (50). The single ultrasonographic parameter showing significant correlation with eventual renal function was the appearance of the corticomedullary junctions. Additional ultrasonographic findings, including hydroureteronephrosis, cortical echogenicity, cortical thickness, bladder wall thickness

VI. GROWTH (Table 17 and NCHS Growth Charts)

We had the weights of the 9 patients assessed for renal function. Most preoperative heights were not available so we considered only the pre-operative and post-operative weights. The weights were plotted onto NCHS ( NATIONAL CENTER FOR HEALTH STATISTICS ) Growth Charts.

Pre-operatively there was growth retardation in 8 patients and 1 had a weight at the 50th percentile.

> Between the 25th and 50th percentile : 2 patients > Between the 10th and 25th percentile : 3 patients > Below the 5th percentile : 3 patients

At the final evaluation, 5 patients had improvement in their growth curves and in 4 there was regression in growth.

> Between the 75th and 90th percentile: 1 patient > Between the 25th and 50th percentile: 1 patient > At the 25th percentile: 2 patients

> Between the 10th and 25th percentile: 1 patient > At the 10th percentile: 1 patient

> Between the 5th and 10th percentile: 1 patient > Below the 5th percentile: 1 patient

The mean age at diagnosis of the 5 patients who had an improved growth was 11.4 months and that of the 4 who had regression of their growth curve was 42.3 months. KRUEGER R.P et al (15) noted that the follow-up growth potential was less in those patients presenting at the youngest age and improved as the age of presentation 76

increased. KRUEGER's explanation of his findings was that if renal impairment occurs in infancy, the growth failure is more pronounced than is when renal disease occurs later in life. According to YURI REINBERG et al (51) renal function is the only predictor of body growth.

A possible explanation to our findings could be that patients in our series had less obstructing valves with onset of the renal impairment later in life see table 6. We compared the pre-operative GFR of those who had improved growth with those with regression in growth and it was 26.6 ml/min/l.73m² and 32.75 ml/min/l.73m². When we analysed the GFR in the two groups by the WILCOXON's Rank Sum Test, P was 0.46 so greater than the 5% level of probability (P > 0.05) indicating that the difference in GFR in the two groups is statistically non-significant. Our sample was probably too small to draw meaningful statistical conclusions from the association body growth and GFR at diagnosis.

According to KRUEGER et al (15) growth failure is more apparent with regard to linear growth but is also manifested as a failure to gain weight. It is reported that a GFR of 25 to 30 ml/min/1.73m² is the threshold under which growth begins to be stunted, but this figure must be considered a rough approximation, and some children continue to grow at their centiles with a lower GFR (52).

Growth retardation is one of the most striking effects of chronic renal failure in childhood (52). Among the factors that may interfere with growth in children with renal insufficiency are nephrosis with massive and permanent proteinuria entailing severe protein depletion, water and electrolyte disturbances, hypertension, anaemia, renal osteodystrophy, hormonal and metabolic disturbances and protein -energy malnutrition (52).

VII. INCONTINENCE

Incontinence is a frequent complaint of patients treated for posterior urethral valves. It was present in 8 cases (29%) in our series. It occurred in 19% of patients in

CONNOR and BURBIGE's study (53). According to COCHAT (19) it is present in 10-30% of cases of PUV and gradually disappears after puberty, following growth of the prostatic tissue. Formerly it was thought to be due to surgical trauma on the bladder neck and distention of urethral musculature bladder dysfunction (53, 9). The loss of urine concentrating ability leading to large volumes of dilute urine, has been reported in boys with PUV (54). The combination of polyuria with poor bladder dysfunction or compliance almost inevitably causes incontinence (10, 54). Therapy includes, clean intermittent catheterization and anticholinergic medications. Augmentation cystoplasty may be needed in case of high intravesical pressures despite anticholinergic therapy (19, 54).

Despite our efforts to request parents to bring their children for follow-up, we were very disappointed with the poor turn out. Of the 22 patients not known to have died at the beginning of the study only 12 came, but then only 9 were able to do simple renal function tests as BUN and creatinine not to talk of control ultrasounds and cystourethrograms. The other 3 went away promising to come back at least with results of BUN and creatinine but they are yet to return. One patient who had vesicostomy at the age of 3 weeks and was lost to follow-up turned up after receiving our message. Although he was doing fine and going to school with the renal function satisfactory (GFR 4 ml/min/1.73m² at 3 weeks of age to 92 ml/min/1..73m² at the age of 6 years) there was already stomal stenosis. The mother promised to bring him back for closure of the vesicostomy but is yet to come.

The mean number of follow - up visits was 3 (range 0-10) which is not adequate. It is undoubted that more than 28 patients with posterior urethral valves were managed in the three hospitals from 1985 to 1997 but poor keeping of patient records in the archives didn't permit us to have more. Simple information as address, weights, heights, laboratory and radiological investigations were lacking in most files.

> That the ammiotic fluid be carefully assessed as part of routine prenatal visits. In case of oligohydramnios, obstructive uropathy should be suspected and an ultrasound requested so that management should be started at least soon after birth. While in some series (31) more than 40% of PUV are diagnosed in the first month of life, 50% of our cases were diagnosed above 1 year with a mean age at diagnosis of 2.9 years

> That PUV should not be regarded as a rare entity in Cameroon. We are convinced that there are many more undiagnosed cases in our health institutions. As CAMPBELL stated (cited in 35) «Prostatic urethral valves are not rare, they are just rarely identified».

> that the complications of PUV be well understood and management known. Three patients died of septicaemia and two of post -obstructive diuresis . These deaths could have at least been reduced if appropriate measures were taken promptly.

> Any child with a urinary tract infection or suspected symptoms should benefit from urine cultures and radiological investigations (at least ultrasonography) because these could be first manifestations of obstructive uropathy.

> The urinary stream of children should be clinically evaluated during routine consultations and any abnormal stream should be investigated. We were unable to recruit a 32 year old man (because he was out of town) who had been undergoing hemodialysis for chronic renal failure and was diagnosed and treated for PUV at the age of 21 years. He has been having mild symptoms since infancy and these did not draw attention towards PUV.

This is an illustration of mild cases which evolve undiagnosed to end - stage renal failure and as HENDREN (37) rightly states: «the picture as usually described is but one end of a spectrum and that there are many less severe and dramatic cases which escape recognition».

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who had Urinary tract problems and was followed -up by Dr ANGWAFO, for a control check -up.

This control examination is free -of - charge and even urgent because these children might develop long - term complications.

You should contact Dr CHIABI Andreas (Paediatric resident) in the Paediatric service of the Yaounde General Hospital if you come before March 1997; if later contact me in the Pediatric service of the Yaounde Central Hospital Pavillon Jeanne Irene BIYA.

Weight: P50: Height:		P50:	BSA:
	No [ 1	Ext. Urogenital Malformations: Yes [ 1 Type :

		Abdominal Mass: Yes [ 1 Location:
	No [ 1l	Others:
		V. INVESTIGATIONS

CBC: WBC: PN:		PL:
RBC :
FIB: MCV:
Urine Culture: Positive: [ ] Negative: [	]
Germ :
WBC: RBC:
BUN: Creatinine:
Creatinine Clearance:
K+ Na+		CL

Ultra Sound: Antenatal: Yes [ ] No [ ]
Normal [ ] Abnormal [ ] Postnatal:	Precise:
	YES [ ] [ ] [ ] [ ]	NO [ ] [ ] [ ] [ ]
Amenorhoea: -Uretero Hydronephrosis: Trabeculated bladder: Dilated post. urethral: Renal cortex:
Renal size:
Others :
Voiding Cystourethrogram	YES [ ] [ ] [ ] [ ]	NO [ ] [ ] [ ] [ ]
VUR Trabeculated bladder Dilated post. urethra Presence of valve Others:

IVP --Normal Uretero Hydronephrosis Yes [ ] No [ ]
Stage:
Symetry: Yes [ ] No [ ]
Late secretion: Yes .[ ] No [ ] Others: