Am?. N . Z . J . Surg. 1992. 62. 916-921

THE PRUNE BELLY SYNDROME S. CRANKSON" AND S . AHMED' "Department of Surgery, Social Insurunce Hospital and 'Depurtment of Surgery, King Fuisal Speciulist Hospitul & Research Centre, Riyadh, Kingdom oj.Saudi Arabia Introduction The prune belly syndrome get its name from the characteristic appearance of the abdominal wall which i s loose and wrinkled and shows variable degrees of muscle hypoplasia (Fig. I). In addition, there are usually major associated urinary tract abnormalities and undescended testes in male patients. The rare female cases of prune belly syndrome are associated with major genital tract abnormalities and also other system abnormalities.' The majority have either an incomplete or questionable form of the syndrome.3 Thus, the classic prune belly syndrome is essentially a male condition which also goes by the titles Eagle-Barrett syndrome, the triad syndrome and the urethral obstruction malformation complex.

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Incidence The incidence of prune belly syndrome has been reported to range from 1 in 29000 to I in 50000 live births. However a number of prenatally diagnosed cases not previously recognized are now being A high incidence has been reported in Saskatchewan, Canada and in Nigeria.'-'' Prune belly syndrome has been documented in siblings and there appears to be a strong association between twinning and the syndrome.'- I' Chromosomal aberrations, although rare, may also be encountered. '?-I5

Fig. 1. Prune belly soon after birth. There is severe wrinkling of the abdominal wall. The scrotum was empty and the thoracic cage is poorly developed.

Aetiology The aetiology of prune belly syndrome is unclear but considerable evidence has now accumulated to support the view that it is secondary to fetal lower urinary tract obstruction. Golbus et al. demonstrated the pathological sequence that produces prune belly syndrome by serial prenatal ultrasound examinations. These strongly support the concept that the syndrome is a result of fetal urethral obstruction." Combpondence: Dr Saeed Ahmed, Department of Surgery. MBC 40, King Faisal Specialist Hospital & Research Centre. PO Box 3354, Riyadh I 121 I , Kingdom of Saudi Arabia. Accepted for publication 19 March I992

Furthermore, Harrison et al. and Gonzalez er ul. have also produced the classical features of prune belly syndrome in the fetal lamb by causing urethral obstruction. I 7 , I x Prune belly syndrome is also a common finding in foetuses with urethral atresia. I' Manivel er ul. reviewed 29 cases of prune belly syndrome and reported urethral obstruction in 45% .*" Beasley et ul. also suggested that urethral obstruction plays an important role in the pathogenesis of prune belly syndrome.2' The mechanism of fetal urethral obstruction is not clear. Hoagland and Hutchins suggested that a kink in the prostatic urethra may be obstructive whereas Greskovich and Nyberg proposed that the obstruction may be secondary to a

PRUNE BELLY SYNDROME

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just below the lower pole of the kidney to the flap valve mechanism resulting from prostatic hypoplasia and sacculation of the posterior ~ r e t h r a . ~ ' . ~ ~ureterovesical junction and the testicular vessels are ~ h o r t .Histologically, ~,~~ prepubertal testes in prune The urethral obstruction may be transient but of belly syndrome are said to be identical to normal sufficient duration to produce the known abdominal immature testes." However Massad ef a / . have rewall and urinary tract features of the syndrome. The cently reported atypical germ cells with large nuclei distended bladder or possibly the mega-ureters hinand prominent nucleoli in the prune belly testis; findder the descent of the testes from the abdomen to ings similar to intratubular germ cell ne~plasia.~' the s c r o t ~ m . ~The "'~~ obstructive theory does not About 65-75% of cases of prune belly syndrome explain all the features of prune belly syndrome have abnormalities outside the urinary tract.38.3' and the alternative embryological theory contends Pulmonary abnormalities were reported in 30"h of that the abdominal wall and urinary tract changes neonatal autopsies.32These together with chest wall are secondary to abnormal mesenchymal developand musculoskeletal system abnormalities, includment.4,23,26327 It would appear that the obstructive ing rib cage narrowing, varus deformity of the feet, and embryological mechanisms are complementary congenital dislocation of the hip, atretidabsent foot or to each other and the additional features of the synleg are likely to be secondary to oligohydramnios.23 drome are secondary to oligohydramnios. Cardiac abnormalities are also reported in about 10% of patients with prune belly ~yndrome.~') GasAnatomic features trointestinal abnormalities that may be encountered include intestinal malrotation, Hirschsprung's disThe abdominal wall defect is variable and may be ease, anorectal abnormalities and ga stro~c hisis." ~" ' ~~~ patchy in distribution. Above the umbilicus, the oblique muscles and the rectus abdominus are usuMore recently, growth retardation and developmental delay without end-stage renal failure have been ally affected.*' Below the umbilicus, the transverreported. 3y sus abdominus and rectus abdominus muscles are affected and the lower abdominal wall may have little organized muscle tissue.2'~*s Clinical presentation Whereas urethral atresia is a recognized associaPrune belly syndrome is an important cause of fetal tion of prune belly syndrome, in general, the prostatic urethra is elongated and wide between the uropathy and about 20% of cases are stillborn or bladder neck and the urogenital diaphragm where die early in the neonatal period from severe renal there is an apparent narrowing.29 The bulbar and dysplasia or pulmonary hypoplasia. However, this penile urethra are normal. Histologically, smooth syndrome has a broad spectrum and those surviving muscle fibres of the prostate are reduced with an beyond the neonatal period may have the fully estabincrease in connective tissue content.30 lished clinical syndrome with bilateral renal involvement or mild and incomplete forms of the syndrome The bladder is usually large, smooth and thickwith minimal renal involvement and stable renal walled, identified by Workman and Kogan as the f~nction.~" The wrinkled appearance of the abdomiobstructive type when compared with the nonobstructive thin-walled bladder which may be seen nal wall is obvious at birth with visible intestinal oc~asionally.~' Histologically, the obstructive type peristalsis, palpable abdominal organs and absent testes. There may be other obvious external abnorof bladder shows increased muscle thickness and malities, such as chest deformity, limb and anorectal normal ratio of connective tissue whereas the nonabnormalities. There may be signs of pulmonary obstructive type shows increased connective tissue. The bladder neck is wide and ill defined and the insufficiency and superimposed urinary tract infection may complicate the clinical picture. trigone is large with large widely separated ureteric orifices allowing vesico-uretericreflux in the majority of cases.'* Management The ureters are usually elongated and tortuous, and show patchy or absent muscle fibres with inThe newborn with prune belly syndrome must be creased collagen tissue.33 The upper ureter usually evaluated urgently and appropriate treatment initiated. An urgent chest X-ray is necessary to exclude contains relatively more smooth muscle elements when compared with the lower ureter.'" pulmonary abnormalities including pneumothorax Renal involvement in prune belly syndrome varies and cardiac investigations may also be advisable.'s from case to case.32 There may be renal agenesis Detailed laboratory investigations including serum and over 50% of cases show features of renal dyscreatinine, urea, electrolytes, urinalysis and urine culture should be performed followed by urinary plasia including multicystic kidney^.'^ In others tract ultrasonography carefully evaluating the status there is marked hydronephrosis but the occasional of the kidneys, the ureters and the bladder.'" Renal case may have normal kidneys. nuclide investigations are usually necessary for The intra-abdominal testes vary in position from

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CRANKSON AND AHMED

anatomical and renal function studies. These include [99mTc]-gluconate, [99"Tc]-glucoheptonate (GHA) and [9'mTc]-Dimercaptosuccinic acid (DMSA) for renal morphology and differential renal function, [99"'Tc]-diethylenetriaminepentaacetic acid (DTPA) for glomerular filtration rate and ['231]orthoiodohippurate for effective renal plasma flow.46 A diuretic renogram with [""'Tc]-DTPA may be useful in differentiating between obstructive and non-obstructive ureterohydronephrosis. If the condition of the baby is stable with a good urinary output, micturating cysto-urethrogram may be delayed but is usually necessary to complete the e ~ a l u a t i o n . 'A~ significant number of cases will be shown to have large abnormal bladders together with vesico-ureteric reflux and dilated posterior urethras (Figs 2, 3). Advanced cases of prune belly syndrome with renal dysplasia and lung hypoplasia do not survive the neonatal period and the mild or incomplete forms of the syndrome require close and careful follow-up, but urinary tract surgery is not usually necessary. Cases with the fully established syndrome with bilateral ureterohydronephrosis with or Fig. 2. Cystogram showing abnormal bladder and massive bilateral refluxing mega-ureters but micturating films without vesico-ureteric reflux may be managed could not be obtained. non-operatively. but we favour early reconstructive surgery. Non-operative management should include antibiotic prophylaxis, monitoring of renal function and observation of bladder function. Yearly urinary tract ultrasonography is advisable and functional investigations such as renal nuclide scan and urodynamics performed as necessary. In the absence of proven obstruction, proven functional deterioration or complicating urinary tract infection, non-operative management is continued and it is remarkable how well some cases progress despite rather frightening radiDuckett reported 5 1 patients with prune belly syndrome: 14 were managed non-operatively but a multitude of operations were necessary in the others.48 The importance of lower urinary tract obstruction in prune belly syndrome needs to be emphasized as it is usually associated with a poor p r o g n ~ s i s . ' ~ . ~ ~ Reinberg et al. reviewed the causes of renal failure in prune belly syndrome stressing the importance of vesico-ureteric reflux and also of obstruction which must be properly managed.' Workman and Kogan categorized prune belly syndrome into obstructive and non-obstructive types from bladder histology, stressing the importance of careful evaluation and treatment of the former." Another argument in favour of operative management is that urinary stasis and urinary infection contribute significantly to the morbidity, loss of renal function and mortality in prune belly syndrome. 50 However before a decision Fig. 3. Expression cysto-urethrogram under general anaesin favour of surgical correction is made, precise thesia shows elongated and wide posterior urethra and abrupt narrowing distally, typical of prune belly syndrome. imaging assessment is recommended, including di-

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uretic renography , pressure perfusion studies and urodynamics, when The surgical management also has to be i n d i ~ i d u a l i z e d . ~ ~ The surgical options that need to be discussed specifically in relation to prune belly syndrome include total reconstruction, temporary diversion including vesicostomy, procedures to improve bladder emptying include reduction cystoplasty and external sphincterotomy, abdominal wall plication and management of the abdominal testes. It must be stressed that the poor abdominal wall and the pulmonarylchest abnormalities not only predispose prune belly syndrome patients to chest infections but also to problems with anaesthetic management and sedation. In patients with gross bilateral vesico-ureteric reflux, with or without a unilateral non-functioning kidney, we favour total urinary tract reconstruction.53 The ureters are shortened before anti-reflux ureteric reimplantation for which purpose the pullthrough technique is r e ~ o m m e n d e d Ureteric .~~ tailoring may also be necessary and may improve ureteric peri~talsis.”~’~ Nephrectomy may be necessary for a unilateral non-functioning or poorly functioning kidney. Temporary urinary diversion may be performed when primary reconstruction is not contemplated or is contraindicated. Percutaneous nephrostomy or cystostomy would appear to be the most suitable for this purpose, but we prefer vesicostomy particularly when there is a complicating urinary tract i n f e ~ t i o nHowever .~~ vesicostomy may not provide optimal renal drainage in patients with gross ureteric tortuosity and would have little effect on associated primary or secondary pelviureteric junction obstruction. Cutaneous pyelostomy or ureterostomy may therefore be necessary in some cases. The urinary bladder is very abnormal in patients with prune belly syndrome but the degree of bladder distension does not correlate with the degree of o b s t r ~ c t i o n .Whereas ~ some patients are able to empty their bladders completely, others have a significant post-micturition residual. Bladder function may deteriorate with age and careful surveillance is recommended. Urodynamically , some patients show normal bladder function while others show abnormal dynamics and a relative outflow obstruction ,34.55 Reduction cystoplasty which may be performed as an isolated procedure or combined with primary urinary tract reconstruction improves bladder function by making detrusor contractions more effective in achieving bladder emptying.s6 For proven urinary outflow obstruction we have found external sphincterotomy to be a very satisfactory procedure .36,56 The occasional patient with prune belly syndrome may have true posterior urethral valves which need to be eradicated.” The abdominal wall in patients with prune belly

syndrome may be reconstructed as an isolated procedure or at the time of urinary tract reconstruct i ~ n . ~ ’ ~ ’Although ’,~~ the abdominal wall defect causes cosmetic and functional problems such as abnormal posture, susceptibility to chest infections and constipation, the wrinkled appearance smoothens and the cosmetic appearance improves with growth.6o Routine abdominal wall reconstruction is therefore not recommended, although various abdominal binders may be used to advantage. Orchidopexy is justifiable in patients with prune belly syndrome although no cases of paternity have been recorded.38 Bilateral orchidopexy should be combined with elective urinary tract reconstruction as subsequent orchidopexy is more difficult after ureteric surgery.j4 In patients not requiring urinary tract reconstruction, orchidopexy should be performed in infancy using the Fowler-Stephens technique.24*“ Alternatively, testicular autotransplantation may be performed.6’ However long-term follow-up of the testes is also advisable because of the risk of germ cell turnours.”

Prognosis Prune belly syndrome patients require careful, lifelong follow-up with regular assessment of kidney and bladder function and also of the testes. The prognosis depends upon the degree of renal involvement, bladder function, pulmonary function and also on the impact of associated abnormalities. Despite appropriate treatment, about 30% of patients will eventually develop end-stage renal disease requiring renal dialysis and tran~plantation.~’.~’ Renal function deterioration may develop as a result of chronic pyelonephritis, obstructive or reflux nephropathy and hyperperfusion of the remaining nephrons at p ~ b e r t y . ” , ~ ’In. ~contrast ~ with posterior urethral valves, prune belly syndrome does not adversely affect the outcome of renal transplantation.65

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2. REINRERFY . , SHAPIRO E., MANIVEL J. C., MANLEY C. B., PETUNATOG. & GONLALEZ R. (1991) Prune belly syndrome in females: a triad of abdominal musculature deficiency and anomalies of the urinary and genital systems. J . Pediatr. 118, 395-8. 3. RABINOWITL R . & SCHILLINGER J. F. (1977) Prune belly syndrome in the female subject. J . Urol. 118, 454-6. 4. NUNNI . N . & S T ~ P HF. ~ ND.S (1961) The triad syn-

drome: a composite anomaly of the abdominal wall, urinary system and testes. J . Urol. 86, 782-94. 5 . PAGONR . A , , SMITHD. W. & SHEPARD T. H. (1979) Urethral obstruction malformation complex: a cause

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of abdominal muscle deficiency and the ‘prune belly’. J . Pediatr. 94, 900-6. 6. GARLINGER P. &OnJ . (1974) Prune belly syndrome. Possible genetic implications. Birth Defec.ts 10, 173-80. E. C. (1981) An epi7. BAIRDP. A. & MACDONALD demiologic study of congenital malformations of the anterior abdominal wall in more than half a million consecutive live births. Am. J . Hum. Genet, 33. 470-8. 1..R BAR-ZIVJ . & KATZM . (1985) Prenatal 8. M ~ I Z N E ultrasonic diagnosis of the extreme form of prune belly syndrome. JCU 13. 581-3. 9 . A D ~ Y O K WA N.UA. & FAMILUSI J. B. (1982) Prune belly syndrome in two siblings and a first cousin. Possible genetic implications. Am. J . Dis. Child. 136, 23-5. 10. Ivts E. J . (1974) The abdominal muscle deficiency triad syndrome-experience with ten cases. Birth Defects 10. 127-35. 1 I . GABOARDI F . , STtRPA A.. THI~BAIE. et a / . (1982) Prune-belly syndrome: report of three siblings. Helv. Pediutr. Acta 37, 283-8. 12. PErERSEN D. S . , Fist[ L. & KAsS A . S . (1972) Twins with congenital deficiency of abdominal musculature. J . Urol. 107, 670-2. M . , DOYLEK . & TRUNCA C . (1980) The 13. LLBINSKY association of ‘prune belly’ with Turner’s syndrome. Am. J . Dis. Child. 134, 1171-2. 14. FRYDMAN M., MACtNIS R. E., M O H A N D A S T. K. & KABACK M . M . (1983) Chromosome abnormalities in infants with prune belly syndrome: association with Trisomy 18. Am. J . Med. Gene/. IS, 145-8. 15. BtCKMANN H . , REHDtR H. & RALSKOLBR. (1984) Prune belly sequence associated with Trisomy 13. Am. J . Med. Genet. 19,603-4. 16. GOLHUS M. S . , HARRISON M . R., FILLY R. A.. CALLEN P. W. & K4rz M. (1982) In utero treatment of urinary tract obstruction. Am. J . Ohstet. Gvnecol. 142, 383-8. M. R., Ross N.. NOALLR. & D t LORIMIER 17. HARRISON A. A . (1983) Correction of congenital hydronephrosis in utero I . The model: Fetal urethral obstruction produced hydronephrosis and pulmonary hypoplasia in fetal lambs. J . Pediotr. Snrg. 18, 247-56. 18. GOYL,AI.EZ R . , REINBERG Y . , BLIRKE B., W ~ L LT. S & V t R x i E R R. L. (1990) Early bladder outlet obstruction in fetal lambs induces renal dysplasia and the Prunebelly syndrome. J . Pediutr. Surg. 25. 342-5. 19. S I ~ I N H A RGU. ,THVCAN W . . WOODE., W ~ B ETR. & LYPVCH R. ( 1990) Long-term survival in an infant with urethral atresia. J . U r d . 143. 336-7. ~ .c., ~ . PE1 rlNAI‘O G., R ~ I N H EYR. Y , GONLAl.tL 20. M A N I VJ. R., B U R KB.~ & D E H N ~LR . P. (1989) Prune belly syndrome: clinicopathologic study of 29 cases. Pediutr. Patho/. 9, 691-71 1 2 I . BEASI E Y S . W . , BHTANAY F. & HUTSON J. M. (1988) The anterior urethra provides clues to the etiology of prune belly syndrome. Pediutr. Surg. Itit. 3, 169-72. M. H. & HmCiuNS G . M. (1987) Obstruct22. HOAGLAND ive lesions of the lower urinary tract in the prune belly syndrome. Arch. Pcithol. Lah. Med. 111, 154-6. 23. GRESKOVICH F. J . & N Y B ~ RL. C M. JR (1988) The prune belly syndrome: a review of its etiology, defects. treatment and prognosis. J . Urol. 140, 707-12.

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24. WWDAROJ . R. & PARKOTT T. S . (1978) Orchiopexy in the prune belly syndrome. Br. J . Urol. 50, 348-51. 25. MONIEI . W. & MONIEB. J . (1979) Prune belly syndrome and fetal ascites. Terutolog)) 19, 1 I I - 17. J . (1981) Etiology and patho26. STRAUBE. & SPRANCER genesis of the prune belly syndrome. Kidney Int. 20, 695-9. 27. BURTON B. K . & DILLARD R. G . (1984) Brief clinical report: prune belly syndrome: observations supporting the hypothesis of abdominal overdistention. Am. 3. Med. Genet. 17, 669-72. D. T . , MONTOYA F., OKADA K . , GALIOTO 28. MININBERC F. & PRESUTTI R. (1973) Subcellular muscle studies in the prune belly syndrome. J . Urol. 109, 524-6. 29. KROOVAND R. L . , AL-ANSARI R. M. & P~RLMCTTER A . D. (1982) Urethral and genital malformations in prune belly syndrome. J . Urul. 127, 94-6. 30. DEKLERK D. P. & SCOTTW. (1978) Prostatic maldevelopment in the prune belly syndrome: a defect in prostatic stromal-epithelial interaction. J . Urol. 120, 341-4. 31. WICGERH. J. & BLANCW. A. (1977) The prune belly syndrome. In: Patholog! Annual, Part I (Ed. S . C. Sommers and P. P. Rosen), pp. 17-39. AppletonCentury-Crofts, New York. 32. WORKMAN S . J . & KWANB. A. (1990) Fetal bladder histology in posterior urethral valves and the prune belly syndrome. J . Urol. 144, 337-9. w. J. (1977) Ultrastructural 33. EHRLlCH R. M. & BROWN anatomic observations of the ureter in the prune belly syndrome. Birfh Defects 13, 101-3. 34. WOODARD I . R . & ZUCKER I . (1990) Current management of the dilated urinary tract in prune belly syndrome. Urol. Clin. North Am. 17, 407-18. 35. W ~ O D A RJ U . R. (1978) The prune belly syndrome. Urol. Clin. North Am. 5 , 73-93. 36. WOODHOUSE C . R . J . , RANSLEY P. G. & Wit.Li,ms D. I. (1982) Prune belly syndrome - report of 47 cases. Arch. Dis.Child. 57, 856-9. D. T.. ZADlNA s. P. & GILBERT E. (1984) 37. UHELINC Testicular histology in triad syndrome. Urology 23, 364-6. 38. MASSAUC. A., COHENM. B.. KOGAN B. A. & BECK^ S l E A D J . H. (1991) Morphology and histochemistry of infant testes in the prune belly syndrome. J . U r d . 146, 1598-600. 39. GARY D. F., MACLUSKY I. B.. CHURCHILL B . M. & MrLORlE G. ( 1 986) A broader spectrum of abnormalities in the prune belly syndrome. J . Urol. 135. 324-6. 40. ADEBONOJO F. 0. (1973) Dysplasia of the anterior abdominal musculature with multiple congenital anomalies, Prune belly or triad syndrome. J . Nut/ Med. Assoc,. 65, 327-33. 41. BURFIGE K. A , , Aiooio J . , BEREONW . E.. H E N S I E T. w., BLANCw. & LATrlMER J . K. (1987) Prune belly syndrome: 35 years of experience. J . (irol. 137, 86-90. D. 42. ChWTHtRN T. H . , BOY TEN^ C. A. D. & GRANT ( 1979) Prune belly syndrome associated with Hirschsprung’s disease. Am. J . Dis. Child. 133, 652-3. C. L. JR. GROSSMAN H. & NOVAK R. (1978) 43. MORGAN Imperforate anus and colon calcification in association with the prune belly syndrome. Pediutr. Rudiol. 7 . 19-21.

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55. SNYDER H. M., HARRISON N. W.. WHITFIELD H. N. & WILLIAMS D. I . (1976) Urodynamics in the prune belly syndrome. Br. J. Urul. 48, 663-70. A . D. (1976) Reduction cystoplasty in 56. PERLMUTT~R prune belly syndrome. J . Urol. 116, 356-62. I. A. (1983) Posterior urethral valve 57. AARONSON masquerading as the Prune belly syndrome. Br. J . Urol. 55, 508-12. 58. RANDOLPH J . G . , CAVEITC. & ENG G. (1981) Abdominal wall reconstruction in the prune belly syndrome. J . Pediafr. Surg. 16. 96c)-3. 59. EHRI-ICH R. M . , LESAVOY M. A. & FINER. N. (1986) Total abdominal wall reconstruction in the prune belly syndrome. J . Urol. 136, 282-5. 60. MCMULLIN N. D., HUTSONJ . M. & KELLYJ . H . (1988) Minimal surgery in the prune belly syndrome. Pediurr. Surg. Int. 3, 51-4. 61. GIBBONS M. D., CROMIE W. J . & DUCKETT J . W. JR (1979) Management of the abdominal undescended testicle. J . U r d . 122, 76-9. A. (1990) Management of the impalpable 62. BIANCHI testis. The role of microvascular orchidopexy. Pedinrr. Surg. Int. 5 , 48-53. , MANIVEL J . c., PErrlNATO G. & GON63. R E I N B ~YR. G Z A L ~ ZR. (1991) Development of renal failure in children with the prune belly syndrome. J . Urol. 145, 1017-19. 64. DUNNB. R.. ANDERSON S . & BRENNER B . M. (1986) The heniodynamic basis of progressive renal disease. Semin. Nephrol. 6, 122-38. 65. REINBERG Y . , MANIVEL J . C., FRYD D., NAJARIAN J . S. & GONZALKZ R. (1989) The outcome of renal transplantation in children with the prune belly syndrome. J . Urol. 142. 1541-2.

The prune belly syndrome.

Am?. N . Z . J . Surg. 1992. 62. 916-921 THE PRUNE BELLY SYNDROME S. CRANKSON" AND S . AHMED' "Department of Surgery, Social Insurunce Hospital and '...
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