ASCITES IN THE NEWBORN*

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1 14 September 19E8 S.A. TYDSKRF VR GE 'EESKU DE 919 ASCTES N THE NEWBORN* J. M. Wy NE,t F.R.C.S., S. CYWES, M.MED. (SURG.), P. J. M. RETEF, CH.M. A D J. H. Louw, CH.M., F.R.C.S., Department of Paediatric Surgery, University of Cape Town and Red Cross War Memorial Children's Hospital, Cape Town Ascites may develop in the foetus and present at birth. when it frequently causes dystocia, or it may develop later during the early weeks of life, when it is referred to as 'neonatal ascites' in contradistinction to 'foetal ascites'. The earliest description of foetal ascites was given by Mauriceau 31 in n 1894 Fordyce" reviewed 63 cases from the literature, of which 46 came to autopsy, but, like other writers of this period, he included cases with peritonitis. He stressed the frequency of underlying abnormalities of the bowel, liver and urinary tract, and noticed an enlarged bladder in 16 cases. He failed to appreciate the true significance of this finding and attributed it to chronic peritonitis. Evidence of syphilis was found in only 9 of the 63 cases, but in spite of this, most 19th century writers '.,"," attributed the ascites to syphilis, even when other abnormalities were present. n 1919 Dorland D reviewed 80 cases of foetal ascites but did not record associated distension of the urinary tract. Most of the cases reported before 1952 were stillborn foetuses. Gross abdominal distension and difficulty experienced in delivery were the features emphasized. n 1952 James and Davis" f>ublished the first case of paediatric interest, recording the association of ascites with congenital urethral obstruction in a neonate aged 3 weeks. The urethral valves were treated and at 8 months the baby was alive and in good condition. n 1953 Lord,'" reporting 2 cases of ascites in the newborn, drew attention to the common association of foetal and neonatal ascites with lower urinary tract obstruction. She reviewed 28 adequately documented cases and found some underlying pathology in 22. Eighteen of these 22 had obstructive urinary tract lesions, and in 11 cases the obstruction was in the urethra, the majority being due to posterior urethral valves. Ascites may occasionally be associated with conditions other than urethral obstruction. The purpose of this paper is to outline the causes of ascites in the newborn and to illustrate some of these conditions with cases encountered at the Red Cross War Memorial Children's Hospital, Cape Town. ASCTES DUE TO UR ARY TRACT OBSTRUCTON Urinary tract obstruction is by far the commonest cause of ascites in the newborn.' n addition to the case reported by James and Davis" in 1952 we have found a further 16 cases of urinary ascites in the literature and by including 2 of our own we are now able to review a total of 19 cases. This series does not include the 22 cases reviewed by Lord.'" Posterior urethral valves were the commonest cause of the obstruction, accounting for 13 (probably 14) of the 19 cases with urinary ascites.',),,,,,","',30,.., n the remaining cases the obstruction was caused by a variety of lesions, viz. ureterocele,33 ureteric stenosis" and urethral atresia." n one case a ruptured bladder was found without any 'Date received: 4 December tpresently practi,ing in POri Elizabeth. obvious evidence of obstruction.'" Although posterior urethral valves are the commonest cause of urinary obstruction, ascites remains an uncommon complication of urinary tract obstruction. n 104 cases of urethral valves, Williams and Eckstein 46 encountered only one case with urinary ascites. The exact site of the leak from the urinary tract is not always apparent. n only 2 of the 19 cases a definite rupture of the bladder was found. n the cases where no obvious leak could be found, the supposition was that the urine perfused across a thinned-out area in the bladder wall. However, a definite leak from the renal pelvis has now been demonstrated in 5 recent cases, and in 3 others the finding of perirenal oedema has been very suggestive of a leak at this site. Swain et al." have shown that urine leaks from the renal pelvis into the subcapsular space in the first instance before it finally ruptures through into the peritoneal cavity. Dockroy' described a radiological 'halo sign' which is produced by the contrast medium in the extravasated urine around the kidney. Nearly half of the cases with urinary ascites present at birth. Although labour is usually premature, the birthweight is normal. The abdomen of the baby is distended, which may cause difficulty with delivery. Respiratory embarrassment due to the abdominal distension is not uncommon. The mortality in this group, i.e. where the ascites is present at birth, is extremely high, because there is very little functioning renal tissue present. There has only been 1 survivor in this group. n the cases where the urinary ascites presents laterusually between O days and 6 weeks-the history is of short duration. They present with vomiting, diarrhoea, progressive abdominal distension and deterioration in the infant's general condition. n this group, the results of treatment are vastly superior and, of the O patients who were treated surgically, 7 survived. Renal function in this group of cases is quite good. The ascites develops before irreversible renal damage has occurred, and the blood urea is only slightly raised. The following 2 case reports illustrate the features mentioned above. Case A 3-week-old male infant, J.T., was admitted to the neonatal surgical unit at the Red Cross War Memorial Children's Hospital, Cape Town, in August 1966 with a 2 day history of diarrhoea followed by vomiting, and rapid abdominal distension. Examination showed a moderately ill, slightly dehydrated 6 lb. 4 oz. baby. The pulse rate was 132 and there was some respiratory embarrassment. The abdomen was markedly distended, with prominent, dilated veins visible on the abdominal wall. ntraperitoneal free fluid was clinically detectable and there were no masses or tenderness. Bowel sounds were normal. A left inguinal fluid hernia was noted. 6

2 920 S.A. MEDCAL JOURNAL 14 September 1968 Fig. 1. Case 1. Supine and lateral erect X-rays of the abdomen showing the free fluid. nvestigations. Haemoglobin 12 5 G /00 ml. Serum sodium 122 meq./litre. Potassium 5 1 meq./litre. CWoride 90 meq./litre. Acid-base studies showed a ph of 7,148, peo, 73, base excess - 11,5, standard bicarbonate 15,5, blood urea 49 mg./100 ml. Supine and erect X-rays of the abdomen (Fig. ) showed gross abdominal distension with free fluid and dilated loops of small bowel. After correction of the electrolyte deficit and metabolic acidosis, laparotomy was performed. The peritoneal cavity contained 300 ml. of clear straw-coloured fluid. Both kidneys were large, the right more so than the left, and the bladder was distended. No other abnormality was found. Microscopy of the ascitic fluid showed proteinaceous debris with many polymorphs, and there was no growth on culture. A voiding cysto-urethrogram (Figs. 2 and 3) showed evidence of posterior urethral valves, a secondarily narrowed bladder neck and a grossly trabeculated bladder. There was free reflux up the right ureter which was dilated and tortuous. The right kidney was hydronephrotic, but no leakage of fluid could be demonstrated radiologically. Each kidney was exposed via a loin incision and found to be bulky and firm with an adequate amount of renal tissue. Both ureters were tortuous, but the right was more dilated than the left. The retroperitoneal tissues were oedematous and there were marked thickening and reaction of the left perirenal tissues. Although no definite perforation was seen, it was felt that these changes were suggestive of a leak from this kidney. Bilateral cuaneous ureterostomies were performed and the retroperitoneal area was drained. On discharge, at the age of 3t months, an intravenous pyelogram showed satisfactory renal function, the right kidney functioning more promptly than the left. Fig. 2. Case 1. Voiding cysto-urethrogram showing urethral obstruction due to posterior urethral valves.

3 14 September 1968 S.A. TYDSKRF VR GENEESKUNDE 921 Although bilateral hydronephrotic changes were the blood urea was only 37 mg./100 ml. pre~ent, nvestigations. Haemoglobin 13 5 G /100 ml. Sodium 134 meq./litre. Potassium 6 3 meq./litre. Blood urea 92 mg./ 100 ml. Astrup: ph peo, 36. base excess -11, standard bicarbonate Supine and erect X-ray of the abdomen confirmed the presence of free fluid. Paracentesi was performed and 450 m!. of straw-coloured fluid removed. Culture of the fluid was sterile. ntravenous pyelography (Fig. 4) showed marked hydronephrosis and hydro-ureter on the left side, with no ex- Fig. 3. Case 1. Cysto-urethrogram showing the trabeculated bladder, right ureteric reflux, hydronephrosis and a grossly dilated and tortuous ureter. The patient was readmitted at the age of 5 months. A cystoscopic examination through a perineal urethrostomy was performed and the bladder was seen to be trabeculated. Fleshy valves in the posterior urethra were resected with diathermy. At 8 months of age he was readmitted with a recurrence of urinary infection and slight stenosis of the cutaneous ureterostomies. The ureters at this stage were only slightly tortuous but functioned normally. The ureterostomies were refashioned and the urethra dilated. He was not brought to hospital for further follow-up and died at home at 1 year of age, most probably as a result of recurrent urinary infection. Case 2 A 2-week-old male infant, R.K., was admitted to the neonatal surgical unit at the Red Cross War Memorial Children's Hospital, Cape Town, in April 1967 with a history of vomiting for 5 days before admission. The right scrotum had been swollen for 4 days and the abdomen distended for 3 days. The father had noticed that the baby had a poor urinary stream with dribbling micturition. Pregnancy had been complicated by oligohydramnios. Examination showed an ill, drowsy, 6 lb. 11 oz. infant with definite respiratory embarrassment. The abdomen was grossly distended due to intraperitoneal free fluid, with many dilated veins coursing over the abdominal wall. Fig. 4. Case 2. ntravenous pyelogram showing left hydronephrosis and hydro-ureter. There is no function on (he right side. cretion of the contrast medium on the right. The bladder was distended and hypertrophied. The voiding cysto-urethrogram showed right ureteric reflux with only slight dilatation of the right ureter and renal pelvis. Contrast medium leaked freely from the right kidney into the retroperitoneal tissues (Fig. 5). The bladder was hypertrophied and the posterior urethra dilated with an obstruction in the bulbous urethra (Fig. 6). This was interpreted as an obstruction by posterior urethral valves which had ballooned downwards into the bulbous urethra. At laparotomy it was found that the right kidney was atretic and had ruptured, whereas the left kidney looked normal but the ureter was dilated. Bilateral nephrostomie were performed by inserting a loop of polythene tubing which traversed the entire renal pelvis, entering a superior calyx and coming out through an inferior calyx, with adequate holes in the catheter to drain the whole pyelon. The virtue of this type of nephrostomy drainage is that it can be replaced readily. At 3 months of age the urethral valves were destroyed by cautery through a perineal urethrostomy. Urine excretion from the right kidney was persistently very poor and intravenous pyelography showed no recovery of function on that side. At 4 months of age, a right nephro-ureterectomy was performed. The kidney

4 922 S.A. MEDCAL JOURNAL 14 September 1968 measured 3 cm. between poles. Section showed marked dilatation of the pelvis and loss of renal parenchyma. Fig. 5. Case 2. Simultaneous intravenous pyelogram and voiding cysto-urethrogram which shows a trabeculated bladder, right ureteric reflux and extravasation of contrast medium in the perirenal tissues. The dilated left ureter and renal pelvis are outlined by the intravenous pyelogram. Fig. 6. Case 2. Cysto-urethrogram showing the trabeculated bladder and dilated posterior urethra due to the obstruction of stretched and bulging urethral valves. Histology showed evidence of chronic pyelonephritis in the remaining renal tissue. At present his general condition is good and the kidney is excreting urine well. CHYLOUS ASCTES Chylous ascites is a rare condition. n 1951 Gribetz and Kanof'" could find only 25 recorded cases in children, 8 of whom had ascites present at birth and 2 of whom developed ascites during the neonatal period. Since then we have traced a further 16 cases where the ascites developed before the age of 2 months "..."".,..." and add a further case of our own. Males are affected twice as commonly as females. n adults chylous ascites is usually due to lymphomatous or some other intra-abdominal malignancy causing lymphatic obstruction, but in the newborn it is usually due to a congenital abnormality or obstruction of the lymphatic system. n some cases a stenosis of the thoracic duct has been found." At laparotomy dilated lacteas are usually noticed, sometimes associated with reactive lymph nodes in the root of the mesentery. t has been suggested that there is failure of communication between peripheral and major ymphatics," but in several cases division of obstructing intra-abdominal adhesions or congenital bands,""... " or closure of a defect in the mesentery" has cured the ascites. Less commonly a lymphangioma has been found in the root of the mesentery.' Clinically the onset is insidious and the course is often protracted. Where the ascites is present at birth it is seldom severe enough to interfere with delivery. Abdominal distension may produce respiratory embarrassment and is commonly associated with pneumonia. About 40% of cases present with a fluid hernia with or without clinically detectable free intraperitoneal fluid, and in many of the cases the diagnosis was only made after chylous ascitic fluid had been found in a patent inguinal hernial sac. Occasionally chylothorax or lymphoedema of one of the limbs may be associated with chylous ascites. The majority recover spontaneously on conservative therapy alone, and about 20% come to surgery because of associated intestinal obstruction or an inguinal fluid hernia. n about 10% of cases the chylous ascites persists and these cases may develop hypoproteinaemia and anaemia and have an increased susceptibility to infection. The following case report illustrates some of the features mentioned above. Case 3 A 3-day-old, 6 lb. 15 oz. male baby, H.H., was admitted to the neonatal surgical unit of the Red Cross War Memorial Children's Hospital in February 1963, suffering from anorectal agenesis with rectovesical fistula, which was confirmed radiologically. The abdomen was distended due to the low intestinal obstruction. A right transverse colostomy was performed and at this stage it was noted that the abdomen contained a small amount of yellowish clear fluid. Six-and-a-half weeks later the child developed a tense left inguinoscrotal swelling which did not transilluminate. At exploration a hernial sac was found which contained milky fluid. Laparotomy was performed and 400 rn. of

5 14 September 19(;8 S.A. TYDSKRF VR GENEESKUNDE 923 chylous ascitic fluid were found in the peritoneal cavity. Dilated lymphatics were seen on the bowel wall and in the mesentery, with enlarged glands in the root of the mesentery. Many adhesions were found between loops of bowel, but there was no obvious obstruction to the bowel. These adhesions may have played some part in precipitating the ascites. The postoperative course was uncomplicated and the ascites did not reaccumulate. The child subsequently underwent a sacro-abdominoperineal pull-through operation, and the colostomy was closed 3 months later. There was no ascitic fluid present at either of these operations. The child is now 4 years old and remains well, and there has been no recurrence of the ascites. n a congested part of the right lobe a well-defined gumma was present. The kidneys and bladder were norma.. SYPDLS n 1894 Fordyce' could find only 9 cases of ascites with convincing evidence of underlying syphilis. According to Lord,"" the last convincing report was by Apert in 1895,' and we have not found any further reports in the recent literature. Syphilis must, therefore, be an exceedingly rare cause of foetal ascites. The following case report serves to illustrate this condition. Case 4 A 4 lb. 9 oz., 4-hour-old male infant, H.B., was admitted to the neonatal surgical unit at the Red Cross War Memorial Children's Hospital in May 1966 in a collapsed state, with haematemesis, melaena and abdominal distension. Examination showed a limp, premature infant with extensive skin bruising and bleeding from the mouth. The abdomen was distended, with clinically detectable free intraperitoneal fluid, and a mass was felt extending down from the right lobe of the liver. Respiratory distress due to the abdominal distension necessitated intermittent positive-pressure ventilation. The haemoglobin was 8 GjlOO rnl. and the prothrombin index less than loo~ on admission. Supine and erect X-rays of the abdomen showed free intra-abdominal fluid with a mass extending down from the right lobe of the liver (Fig. 7). The clinical and radiological findings suggested a diagnosis of haemoperitoneum from a subcapsular haematoma of the right lobe of the liver in a baby with overt haemorrhagic disease of the newborn." Treatment was commenced with vitamin K" fresh blood, fresh frozen plasma and sodium bicarbonate. When the prothrombin index had risen to 65%, 7 hours after admission, laparotomy was performed. At operation an intrinsic mass of the right lobe of the liver was found, as well as 200 ml. of clear ascitic fluid. Both the mother and baby had positive Wassermann reactions. The baby succumbed and, at necropsy, haemorrhages were noted in the skin, oesophagus, mediastinum, both lungs and subarachnoid and intraventricular spaces. The pericardium and abdomen contained clear straw-coloured fluid. The foramen ovale and ductus arteriosus were patent. The spleen was large and reactive. The liver (Fig. 8) was large (154 G) with numerous small subcapsular haemorrhages, and on section there was a well-defined geographical infarct involving the right lobe of the liver. Fig. 7. Case 4. Supine X-ray of the abdomen showing tree intraperitoneal fluid. There appears to be a mass extending down from the right lobe of the liver. Histology of the liver showed an extensive syphilitic type of cirrhosis associated with a considerable degree of extramedullary haemopoiesis. Some sections showed, in addition, many focal areas of haemorrhage. There was a considerable infiltrate of polymorphs, eosino- Fig. 8. Case 4. Cut section of the liver showing the dark infarcted wedge in the right lobe with a small pale gumma just below it.

6 924 S.A. MEDCAL JOUR AL 14 September 1968 phils and plasma cells, and several micro-gummata were noted. The pancreas showed some peri-acinar fibrosis in keeping with congenital syphilis. The lungs howed intraalveolar haemorrhages, and in addition there was much pulmonary hyaline membrane. BLE ASCTES Bile peritodltls is another uncommon condition which occurs in the neonatal period. 'Bile a cites' is a better term, as the clinical picture is unlike that of peritonitis in the newborn' and unlike the infected biliary peritonitis een in adult.'. The clinical presentation may be either acute or chronic. n the acute form the history is of short duration, usually of 1-3 day, and the infant is acutely il!. n 5 cases of acute biliary ascites reviewed by Lees and Mitchell,' 3 occurred in neonates and 2 in children over a year. The presenting symptoms are vomiting, anorexia and abdominal distension. The infants have pyrexia and leucocytosis, and some abdominal tenderness and guarding may be evident. The diagnosis is made at laparotomy which is performed for the acute abdominal emergency. Sixteen cases of chronic biliary ascites have been reported.""'" The clinical picture is fairly constant. Fluctuating jaundice, acholic stools, and gradual painless abdominal distension with vomiting develop during the first 6 weeks of life. Similar to other cases of neonatal ascites, patent inguinal hernial sacs may become filled and distended with the fluid and may be the presenting feature. On examination the infants are apathetic, and free intraperitoneal fluid can be detected. The temperature and leucocyte count are usually normal and urobilinogen is absent from the urine. The diagnosis is established by abdominal paracentesis, and the bile obtained is sterile on culture. The usual lesion found at exploration is a perforation of the common bile duct close to its junction with the cystic duct. This was present in 13 of the cases reviewed. n the remaining 3 cases no definite perforation could be found. n 9 of these 13 cases with perforation, a distal obstruction was present: in 5 calculi were found, in 3 ampullary or ductal stenosis, and in one inspissated bile. n older children, perforation of the biliary tract by ascaris"" or perforation of a choledochal cyst may cause biliary ascites. The treatment is surgical and the results are excellent. All except 1 of the cases reviewed survived. The 3 infants in whom no definite perforation of the biliary system was found at laparotomy, recovered after simple drainage. The following case of bile ascites operated upon in Rhodesia has been under our care for the past year and is reported to illustrate this condition. Case 5 A female infant, P.S., was born at term by normal delivery and weighed 7 lb. 15 oz. At 11 days of age she started refusing her feeds, became restless and appeared to have abdominal pain. She started to vomit, and over the next 3 weeks the parents noticed her abdomen increasing in size, her urine becoming darker and her stools lighter. At this stage she also developed a swelling in the right groin. Despite these symptoms her weight had increased. She was admitted to the Salisbury Central Hospital in December 1966, aged 5 weeks and weighing 10 lb. 9 oz. Examination showed a mall jaundiced infant with a markedly distended abdomen and umbilical and bilateral inguinal fluid hernias. Free intraperitoneal fluid was detected clinically. Her haemoglobin was 11 G f 100 m!. Paracentesis yielded 125 m!. clear yellow fluid which on analysis consisted of ymphocytes, polymorphs, eosinophils and macrophages, with a protein content of 2 5 G f 100 m!. The total serum protein was 4 3 G /loo ml. with 2 3 Gf 100 ml. albumin. The total serum bilirubin was 8 8 mg.f 100 m!. and the alkaline phosphatase 22 KA units. The rest of the liver-function tests were norma!. During the following 4 days the ascitic fluid reaccumulated and a second paracentesis produced 225 ml. of yellow fluid. Her abdomen again became distended during the ensuing 3 days and at this stage a laparotomy was suggested. Pre-operatively 1,000 m!. of greenish-yellow fluid, resembling bile, was aspirated from the abdominal cavity. At operation a small amount of free fluid was found with greenish fibrin adherent to the serosal surface of the bowel. A small perforation of the cystic duct at its junction with the common bile duct was demonstrated, through which bile was leaking. 0 obstruction to the common bile duct could be found. A cholecystectomy and T-tube drainage of the common bile duct were performed and the gallbladder area was drained. The postoperative course was uncomplicated. AT-tube choledochogram showed free flow of the contrast medium into the duodenum, after which the T-tube was clamped without any untoward effect and removed 3 weeks postoperatively. Since then she has thrived and has been in very good health. HEPATOBLARY DSEASE Ascites in the early weeks of life is a rare complication of neonatal liver disease, and we have found only 5 such cases in the literature. Two were stillborn following abdominal paracentesis to effect delivery-one had portal dysplasia of the liver" and the other an anomaly of the periportal areas." The third case was associated with biliary atresia' and died. n the remaining 2 cases which survived, one had foetal hepatitis complicating maternal infective hepatitis 2 months before delivery; and the other a giant-cell transformation of the liver as seen from a needle liver biopsy." Both of these infants required repeated paracentesis before the ascites eventually disappeared. RUPTURED NTRA-ABDOMNAL CYSTS Another extremely rare cause of ascites in the newborn is rupture of an intra-abdominal cyst. Tietz and Davis" reported a case of ascites due to rupture of an ovarian cyst. DSCUSSON Several other conditions producing abdominal distension have to be differentiated from ascites in the newborn. These are haemoperitoneum," meconium peritonitis," solid or cystic enlargements of intra-abdominal organs, intraabdominal tumours and gaseous distension of the bowel.'" Ascites present at birth may be very gross and most

7 14 September 1968 infants are stillborn or die shortly afterwards. n those born alive, death is usually due to respiratory embarrassment caused by the gross abdominal distension. ntermittent positive-pressure ventilation via an endotracheal tube until the distension has been relieved by paracentesi, may be life-saving." Ascites presenting later in the neonatal period should be investigated to establish the underlying cause. Once free intraperitoneal fluid is detected clinically and radiologically, paracentesis may be advisable in order to determine the nature of the free fluid. The exchange between the ascitic fluid and the plasma occurs so rapidly that the composition of the fluid on analysis is not of great diagnostic value. As the most common cause of ascites in the newborn is urinary obstruction with extravasation of urine from one or other kidney or from the bladder, full urinary investigations are necessary if clear straw-coloured fluid is obtained from the peritoneal cavity. An intravenous pyelogram may show hydronephrosis or a non-functioning kidney. Contrast material in the extravasated urine around a kidney may produce the radiological 'halo' sign: A micturating cysto-urethrogram is required to demonstrate the nature of the obstruction in the lower urinary tract. Dreteric reflux frequently occurs and the leak from the kidney into the perirenal tissues may also be demonstrated by this procedure. n urinary ascites the necessary investigations must be carried out as a matter of urgency, so that surgery can be performed within 24 hours of admission. The waiting period is utilized for rehydration and correction of electrolyte and acid-base disturbances. SUMMARY Ascites in the newborn is rare and, if left untreated, is frequently fatal. The commonest cause is extravasation of urine due to an obstructed urinary tract. Other less common causes of ascites are described. The clinical presentation of these disorders, their diagnosis and management are discussed and the literature on this subject is reviewed. Five cases encountered at the Red Cross War Memorial Children's Hospital are reported, which serve to illustrate some of these conditions. We wish to thank Mr. B. Hammar, F.R.CS., of Salisbury Central Hospital, for the details of case 5; Dr. J. F. W. Mostert, Medical Superintendent of the Red Cross War Memorial Children's Hospital, for permission to use the case records; and the Department of Radiology for their cooperation. REFERENCES. Apert. E. (1895): Bull. Soc. anal. "Paris. 70, Baghdassarian, O. M.. Koehler. P. R. and Schultz. G. (1961): Radiology, S.A. TYDSKRF VR GE EESKU DE CHARMAN OF WORLD MEDCAL ASSOCATON Bellin, L. B. and Baili!. l. W. (1952): J. Pediat.. 40, Craven. C. E.. Goldman. A. S.. Larson. Hendrick, C. K. (1967): bid.. 70, 340. D. L. Paters-on. M. and 5. Cunningham, A. A. (1964): Proc. Roy. Soc. Med., Cy\ves. S. (1967): S. Afr. Med. J Cy\ves, S.. Wynne. J. M. and Louw. J. H. (196): J. Pediat. Surg. (in the press). 8. Davies, P. A. and Elliotl-Smith, A. (1955): Arch. Dis. Childh.. 30, Dockroy; K. T. (1965): J. Amer. Med. Assoc Donald, C. in Paterson. D. and Moncrieff. A.. eds. (1949): Diseases of Children. 4th ed. London: Edward Arnold. 11. Dorland, W. A. N. (1919): Amer. J. Obstet. Dis. Worn.. 79, Easton. L. (1961): J. Obstet. Gynaec. Brit. Emp Ehrlich. J. C., Goodfriend, M. J., Shinohara, Y. and Seki, M. (1964): Pediatrics, 33, Fawcelt, J. and GoldbeTg. H. M. (1958): Brit. J. Surg.. 46, Fletcher, C. B., Eakim, E. L. and Rothman, P. E. (1964): Amer. J. Di,. Child., 108, Fordyce. W. (1894): Terato!ogia,, France,. E. and Back, E. H. (1954): Arch. Dis. Childh., Gribetz, D. and Kanof, A. (1951): Pediatrics, 7, Gross, J. l., Goldenberg, V. E. and Humphreys, E. M. (1961): bid., n, Hoofer, W. D. (1965): J. Pediat., 67, Hunter, R. H. (1932): Lancet, 2, James, U. and Davis, J. A.. (1952): Proc. Roy. Soc. Med., 45, Kelly, M. L. and Butt, H. R. (1960): Gastroenterology, 39, Kelly, M. L. and Logan, V. W. (1961):.Y. Med. J.. 61, Laing, C. R. and ScOlt, R. B. (1954): J. Pediat., Lees, W. and Mitchell, J. E. (1966): Arch. Dis. Childh Linde, N. C. (1966): Acta paediat. scand. 55, Lord, J. M. (1953): Arch. Dis. Childh., 28, Louw, J. H. (1966): Brit. J. Surg. 53, Marx, K. and Dale, W. A. (1961): Pediatrics, 27, Mauriceau, F. (1681): Trairl! des Maladies des Femmes Grasses. ed. 3, p Paris. 32. McKendry, 1. B. J., Lindsay, W. K. and Gerstein, M. C. (1957): Pediatrics, 19, orth, A. F. jnr., E1dredge, D. M. and Talpey, W. B. (1966): Amer. J. Dis. Child., 3, Paterson. D. and Higgins, T. T. in Parsons. L. G. and Barling. S.. eds. (1933): Disease, of nfancy and Childhood, vo\., p London: Oxford University Press. 35. Perrot, R., Barcat, J., Duboi, J. P. and Depondt, M. (1961): Arch. franc. pediat., 18, Radman. H. M. (1962): Obstet. and Gynec., 19, Shinohara, Y. and Seki, M. (1961): Bull. '.Y. Acad. Med., 37, Silver, H. K.. Huffman, P. J. and akashima, l. l. (195): Amer. J. Di3. Child., 96, Swain. V. A. J., Tucker. S.. Stimm.ler, L. and France, E. (1965): Clin. Pediat., 4, Tietz, K. G. and Davis, J. B. (1957): J. Pediat.. S, Wall. L. A. (1959): Amer. J. Obstet. Gynec., Warwick. W. J., Holman, R. T.. Quie, P. G. and Good, R. A. (1959): Amer. J. Dis. Child. 98, Wegner, E. S. (1934): bid., Whittlesey, R. H., ngram, P. R. and Riker, W. L. (1955): Ann. Surg., 142, Whittlesey, R. H.. Heidorn, G. H. and Huntley, W. B. (1960): Arch. Pediat., 77, Williams. D.. and Eckstein, H. B. (1965): J. Uro\. (Baltimore), 93, Wyalt. G. M. and Gross. R. E. (1941): Amer. J. Roentgeno\ At the 22nd General Assembly of the World Medical Association held recently in Sydney, Australia, Dr. Arnold H. Tonkin was elected Chairman of the Council. Dr. Tonkin was first elected as a member of the Council as representative of the African region in After the usual 3-year term of office he was re-elected in the same capacity at the meeting held in the Philippines. He will serve as Chairman until the next meeting in Paris in 1969, when he will have completed the maximum term of office of 6 years on the Council. Dr. Tonkin has been Secretary of the Medical Associa- tion of South Africa since 1945, and he was Secretary of the Steering Committee which was instrumental in establishing the College of Physicians and Surgeons of South Africa. n 1963 he was awarded the Association's Bronze Medal for meritorious service. We at the Journal office feel sure that all colleagues throughout the country join us in congratulating Dr. Tonkin on his election as Chairman of the Council of WMA. Our appreciation also goes to him for having gained this high honour for our country through his long experience and good work.

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