Paper - Dystocia due to distension of the urinary bladder of the fœtus (1909)
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Spicer JE. Dystocia due to distension of the urinary bladder of the fœtus, with remarks on renal secretion in utero. (1909) Proc R Soc Med. 2(Obstet Gynaecol Sect): 1–24. PMID 19973800
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Dystocia due to Distension of the Urinary Bladder of the Foetus, with Remarks on Renal Secretion in utero
By Joun Evan Spicer, M.D.
- Part of a thesis on ‘‘ Malformation of the Urethra in the Foetus as a Cause of Dystocia,’’ read at Cambridge for the M.D. degree, 1908.
Difficult labour as the result of morbid enlargement of the foetal bladder is referred to in most works on obstetrics, and imperforate urethra is the cause assigned. At the beginning of 1907 a case occurred in the maternity charity of the London Hospital, while I was resident accoucheur, and it became my duty to deal with it.
I propose to give some details of this case in the present paper and to discuss certain of the problems which have arisen during my investigation of the foetus.
Clinical History of the Case
Mary H., aged 29, 3-para, a short but well-built woman. The patient was in good health and working as usual in her home, when labour pains unexpectedly began about the sixth month. She had had three previous confinements at full term, delivery being normal in each case. The children, who are alive and well, show no signs of malformation or disease. No history or signs of syphilis in either parent. No symptoms of tuberculosis. No history of maternal impression during pregnancy.
The only unusual points concerning the present pregnancy noticed by the mother were that her abdomen was larger than usual and that she had not quickened. Pains began in the morning of January 5, but continued slow and weak throughout the day. At 11 p.m. there was slight hemorrhage. At 9 a.m. on January 6 my assistant was called to the case. The os uteri was by this time fully dilated, the membranes already ruptured, the vertex engaged in the brim and the cord prolapsed beside the head. The occiput was posterior. No exact information can be given as to the amount of liquor amnii, but from the appearance of the bed it was not excessive. If hydramnios was present, it cannot have been severe. The abdomen appeared nearly as large as at full term, but the foetal parts could not be made out; the foetal heart was not heard and the cord was pulseless.
On being summoned to the case at 10 a.m. I found the head in the pelvis and the other signs as above, but, in spite of the fact that the head was not large, the effect of the pains on the position of the foetus was nil. I anesthetized the patient and tried the effect of forceps. Traction on the head failed to deliver the body, and, instead, the head came off. By inserting the hand into the vagina and past the child’s chest it was now easy to detect that the delay resulted from a fluid enlargement of the child’s abdomen. Making use of a “ perforator,” therefore, I thrust the instrument through the chest wall and punctured the diaphragm. Immediately a considerable quantity of nearly clear ascitic fluid escaped from the peritoneal cavity, and I anticipated that delivery would forthwith be possible. But it was not so: the shoulders advanced only slightly. On passing the finger into the abdominal cavity through the opening made by the perforator in the chest and diaphragm, a large tense cystic swelling, which afterwards proved to be the enormously distended bladder, could be felt practically filling up the cavity, and it was not until this had also been punctured that delivery was accomplished. At once a far larger quantity of clear fluid gushed out. I greatly regret that I did not contrive means to measure the amount of this fluid and have it analysed. There was no further difficulty in extracting the child. The placenta followed in due course and the uterus contracted well. The puerperium was perfectly normal and the patient made a good recovery.
Cases such as the one just described are rare, but a considerable
number have now been recorded, and their importance is well recognized. Until the abdomen of the foetus has been opened it is quite impossible, however, to tell whether the enlargement is due to distension of the bladder, to ascites, or both. In my own specimen, as in some others, both were present. In any case the points in diagnosis are precisely similar, and from the purely obstetric point of view the result is the same.
Diagnosis is difficult, chiefly because the abnormality is so rare that it is not suspected. Asa rule it has not been discovered until prolonged delay has occurred. It seems from the history of the other cases to be found in the literature that an abnormally large percentage of the cases occur in primigravida, though by no means all—multipara of all degrees have been affected. As a recurrence it is of extreme rarity ; I have only been able to find one recorded case, and of this there is some lack of detail. Breech presentation is relatively frequent, though the vertex generally presents. Labour is premature as a rule. The uterus is abnormally distended for the period of pregnancy reached, but foetal parts can seldom be recognized. Where the point is mentioned in the records, ‘‘hydramnios”’ or “twins” seems almost always to have been the diagnosis previous to the rupture of the membranes. It must be noticed, however, that ballottement, which is so characteristic in hydramnios, is generally absent. Hydramnios has been known to accompany the condition, and oligohydramnios is reported in a few cases, but neither the one nor the other is constant. After rupture of the membranes the uterus remains distended, and still no foetal parts can be made out satisfactorily. Labour is prolonged, the pains are weak, and little or no advance is made by the presenting part. In vertex cases the head is felt to be not abnormally large, and “ excessive size of the shoulders ”’ becomes the favourite diagnosis. If this diagnosis had never been accepted without at once excluding fluid enlargement of the abdomen by passing up the hand in front of the child’s chest, much time would have been saved and less damage done. Frequently the true diagnosis has not been arrived at until the patient has been exhausted by long and unsuccessful methods of delivery, and more than one case of rupture of the uterus has supervened.
There can be no doubt as to the best form of treatment in cases of dystocia from fluid distension of the abdomen from whatever cause. In minor degrees delivery may perhaps be effected by traction on the head, and several such cases are reported, though very few have survived for more than an hour or two. But if the enlargement is great and this method does not succeed quickly, the foetal abdomen should be tapped. It is not a very difficult procedure, and, if performed carefully, always leads to eminently satisfactory results at once. The “ perforator” is perhaps the most useful instrument for the purpose. One or two cases are said to be on record where the child has been born alive after the use of a trocar and cannula, but I have not been able to trace these. I should recommend the use of this instrument on purely scientific grounds, for we need a more careful analysis of the fluid found; but a satisfactory form of trocar ard cannula is usually not immediately at hand, and delay must under no circumstances be permitted. As the conditions found in these severe cases are incompatible with extra-uterine life, at any rate for more than a few hours, one should not hesitate to perforate at once, remembering to destroy the medulla at the same time if there is any likelihood of the child breathing.
One of the first cases to be published where fluid enlargement of the abdomen led to dystocia appeared in 1681, in F. Mauriceau’s Traité d. mal. des femmes grosses, third edition, Paris. The author there gives a most graphic account of the delivery, which has been translated into English by Fordyce’ and quoted by Ballantyne in his “ Ante-natal Pathology.” ? This is a very interesting case and in many ways quite characteristic. The following cases of dystocia arising from distension of the foetal bladder I have found in the literature :—
AHLFELD, figured in Norris’s ‘‘ Text-book of Obstetrics.’’ Arch. f. Gyn., 1873, iv, p. 161.
BaLuantyNngE. ‘‘ Ante-natal Pathology ’’ (‘‘ The Foetus ’’), 1902, pp. 379, &c.
BrtuarpD. ‘ Traité des maladies des nouveau-nés,’’ 1828.
Bruce, reported by Duncan. Edin. Med. Journ., 1870-1, xvi, p. 163.
Cormack. Month. Journ. Med. Sci., Lond. and Edin., 1844, iv, p, 660.
CovuvetarRE, Bull. Soc. Anat. de Paris, 1900, Ixxv, p. 287.
DELBOVIER. Canstati’s Jahresb., 18438, i, p. 77.
Depaun. Bull. d’Acad. de Méd., Par., 1850, xv; ‘‘De la rétention d’urine pendant la vie foetale,’’ Par., 1860.
Ibid. Gaz. hebd. de Méd. et Chir., Par., 1860, vii, pp. 824, 842, 371.
Devine. Bull. de la Soc. Anat. de Paris, 1846, xxi, p. 103.
Duncan, MattHews. Edin. Med. Journ., 1870-1, xvi, p. 1683 (two cases).
Duparqum. ‘‘ Des maladies des femmes et des enfants,’’ Ann. d’Obstet., 1842.
Fasris, quoted by Bannantyng. ‘‘ Ante-natal Pathology ’’ (“ The Foetus”), 1902, p. 380.
Fearn. Lancet, 1834-5, ii, p. 178.
Forpycre. Teratologia, 1894, i, pp. 61, 143 (several cases quoted).
GaLaBIN. Obstet. Journ., Lond., 1877-8, v, p. 192.
Gaupon. (Three cases.) See DevinuE and DEpauL,
Hay. Med. Chir. Trans, 1835, xix, p. 289.
Howsuir. ‘ Urinary Diseases,’’ 1823, p. 374.
KENNEDY, see Cormack. Journ. Med. Sci., Dubl., 1840.
1 Teratologia, 1894, i, p. 61. 2 «The Foetus,’’ p. 356. Or
Obstetrical and Gynecological Section
Kine. Guy’s Hosp. Reports, 1837, Ser. 1, ii, p. 508; museum specimen, 2551/47.
Ler. Med. Chir. Trans., 1835, xix, p. 238.
Lerour. Le Progrés méd., Par., 1877, 2 Sér., v, p. 413.
Léwe. Prag. med. Wochenschr., 1898, xviii, p. 343.
Lusk. Trans. N. Y. Obstet. Soc., 1879, i, p. 899, and Amer. Journ. Obstet., 1878, xi, p. 781. . ‘
Marswatt and Linpsay. Trans. Glasg. Obstet. and Gyn. Soc., 1900-2, iii, p. 81.
Moreau. Bull. Acad. de Méd., Par., 1851, 2 Sér., xvii, pp. 904, 909.
MvusEtuer. Arch. f. Gyn., Berl., 1894, xlvii, p. 130.
OusHavusEeN. Arch. f. Gyn., Berl., 1871, ii, p. 280.
O’Mrara. Trans. Obstet. Soc. Lond., 1887, xxix, p. 54.
Parrerson. Brit. Med. Journ., 1904, i, p. 190.
Porakx. Arch. de Tocol., Par., 1885, xii, p. 1073, and’ France méd., Par., 1885, ii, p. 1441.
PortaL, see DEPAUL and BALLANTYNE. ‘‘ La pratique des accouchements,’’ 1685.
Rayner. Brit. Med. Journ., 1892, ii, p. 1384.
Rosertson. Glasg. Med. Journ., 1889, xxxii, p. 113.
Ross, quoted by Dienst. Arch. f. path. Anat., Berl., 1898, cliv, pp. 81-138.
ScuwyzER. Arch. f. Gyn., Berl., 1893, xliii, p. 333.
SILBERMANN. Wien. med. Presse, 1890, xxxi, p. 332.
WattHer. Zeitschr. f. Geburts. wu. Gyn., 1893, xxvii, p. 333.
Cases and reports in works to which I have not had access :—
Detoieng. Ann. Soc. de Méd. de Liege, 1847, i, pp. 76, 95.
Derivavux. St. Louis Cour. of Med., 1900, xxiii, pp. 167, 200.
Frascani. Di un caso de grande distensione della vescica urinaria in un aborto di cinque mesi e mezzo,”’ Pisa, 1891.
Freunp. Klin. Beitr. zur Gyn., Bresl., 1862-5, ii, p. 240.
Guéniot, quoted by A. Herreorr. ‘Des maladies foetales qui peuvent faire obstacle & l’accouchement,’’ Thése d’Agrég., Par., 1878.
Herreorr. Mém. Soc. de Méd. de Nancy, 1882-3, p. 90.
Howirz. Hosp. Tid. Kjobenk., 1862, v, p. 57.
Janny. Klin. Beitr. zur Gyn., Bresl., 1864, ii, p. 240.
JiupEn. ‘Ein Fall von Geburtshindernis in Folge iibermissiger Ausdehnung der kindlichen Harnblase,’”” Wiirzburg, 1890.
Kovatcuerr. ‘‘ Dystocie fostale par rétention d’urine,”’ Lille, 1901.
KRIsTELLER. Monatschr. f. Geburtsk., 1866, xxvii, p, 165, and Verhandl. d. Gesells: f. Geburtsh. in Berl., 1866-7, xix, p. 5.
Mavricrau. ‘‘Traité d. mal. des femmes grosses,’ 3rd ed., Par., 1681
Patorr. Bull. méd. dw Nord, Lille, 1881, xxi, p. 581, and Journ. de Sages-Femmes, Par., 1882, x, p. 43. : ,
Puinomenow. Vrach, St. Petersb., 1880, i, p. 337.
ScuroperR. ‘‘ Lehrbuch der Geburtshiilfe,’’ 1891.
VERMEIL. France méd., Par., 1881, ii, p. 482, and Arch. de Tocol., Par., 1882, ix, p. 93.
Vernues, Journ. gén. de Méd., Chir., et Pharm., Par., 1808, xxxiii, pp. 172-178.
WesrrHaL. ‘Ein Fall von Geburtshindernis bedingt durch die iibermissig ausgedehnte kindliche Harnblase,”’ Kénigsberg i./Pr., 1896.
Wotczynsky. Wien. med. Presse, 1882, xxxvi, p. 1135.
Other instances of distended foetal bladder are found among the cases of imperforate urethra quoted elsewhere, but dystocia is not actually recorded, although probable in several of them. 6 Spicer: Dystocia due to Distension of Fetal Bladder
The external appearances of the foetus are well seen in the accompanying photographs.’ It is a male child of about six months development, between 13 in. and 14 in. in total length, and nearly 10 in. (25 cm.) from vault of skull to coccyx. It appears to consist for the most part of abdomen. The girth could not be accurately measured, but it was not less than 26 in. The head and face show signs of intra-uterine pressure, but there are no abnormal developments such as hare-lip, cleft palate, or supernumerary auricles. The chest appears small in comparison with the rest of the body, but with the exception of the lower ribs, which have been spread out a little by the abdominal distension, there is nothing amiss. The limbs are normal, but the feet are tucked up under the abdomen, crossed, and in a position of extreme talipes equino-varus ; this is probably only the result of pressure. The fluid having been
1 (Figs. 1 and 2 from photos. by Mr. E. E. Wilson, Photographer, London Hospital.) Obstetrical and Gynecological Section 7
evacuated, the abdominal walls are flabby, soft, and remarkably thin. Surrounding the insertion of the umbilical cord is a translucent membranous area, oval in shape, 34 in. long by 24 in. wide, through which the umbilical vessels and contents of the abdomen could be seen (see fig. 3). It forms a window in the anterior abdominal wall. Before the abdomen was tapped this must have protruded as a large hernia. The veins of the abdominal wall are dilated, as can also be seen in the photograph. The penis and scrotum appear well developed ; no epi- or hypo-spadias ; preputial and meatal orifices not obliterated ; testes undescended. There is no exstrophy of the bladder. The anus is imperforate; there is no trace of an opening, not even a dimple. No spina bifida or other external malformation. The cord was of the usual length and appearance ; placenta and membranes seemed normal.
Fia. 38. The Umbilical Ring.
Through the membrane can be seen: (a) the attachment of the bladder and its upper limit ; (b) the umbilical vein ; (c) the right hypogastric artery.
The foetus has been added to the Museum of the Royal College of Surgeons, where no such specimen previously existed.
The result of an exhaustive dissection of the foetus may be summed up shortly as follows: On opening the abdomen, the most noticeable feature was the urinary bladder. This was of enormous size (as can be seen in the drawing, fig. 4), and before puncture must have occupied
Fig. 4. . General view on opening the abdomen. 10 Spicer: Dystocia due to Distension of Fetal Bladder
most of the abdominal cavity and reached the diaphragm. An exact estimate of its capacity was impossible. The enlargement was eccentric, owing to hypertrophy of its walls in some parts and thinning and stretching in others. The wall measured nearly 3 in. in its thickest parts. The interior was fairly smooth, but with wrinkling and puckering in parts as if by scar tissue contraction. The anterior wall was firmly
Belly: wallet ke ee eee ek
Upper edge of umbilical ring oo opi. .cse sisantingesees wisne se
Transparent membrane -. ~-,..-.. Distended pouch of the bladder_____-___-_— - UPR ON Mee Sin eG
Upper edge of firm attachment . 1% oo oo. of bladder lif
Bladder cavity:- -.-. 0...
Bladder wallcercatly hyper: 2 trophied and firmly attached
Lower cage of umbilical Ting. 2-620.
Belly wall -----. - enen-ece 2 2 ee ene eee ee 2 eee
To show attachment of bladder to abdominal wall, urachus, eccentric hypertrophy’ of bladder, and the relation of parts at the umbilicus.
attached to the abdominal wall (fig. 5). The gut, which ended in a distended cul-de-sac, opened into the posterior wall through a pin-point opening. Both ureters were hugely dilated and thrown into tortuous coils. Obstetrical and Gynexcological Section 11
The kidneys were in a state of hydronephrosis. The urethra showed, on microscopic examination, a general malformation of the spongy portion, with an obstruction in two parts. These obstructions I believe to have been complete. To investigate the point I made serial sections of the whole urethra, after failure to pass both air and water through the canal from either end. The placenta, chorion, and amnion appeared normal to the naked eye, but were unfortunately not retained, so that microscopic and other detailed examination has been impossible. This serves to remind one again of the importance of reserving the placenta, membranes and cord as part of every foetus. The cord, on section, was found to contain one artery only and one vein (fig. 6). The vein pursued its normal course to the liver; the artery proved to be the right hypogastric artery, which was a direct extension of the right common iliac trunk. The left hypogastric artery was entirely absent (fig.7).
Fig. 6. Transverse section of the umbilical cord showing one artery and one vein.
What is the Result of Imperforate Urethra?
It seems to be assumed by writers of obstetric books and some others who have described specimens more or less like my own that the condition of dilatation and hypertrophy of the bladder, most commonly met with in such specimens, and the accumulation of a large quantity of fluid in that bladder, is the natural result of imperforate urethra in the foetus. But is it?
Many infants have been born alive and at full term with an imperforate urethra. In.itself atresia of the urethra in no way interferes with the general growth of a fetus, nor does it of necessity create other 12 Spicer: Dystocia due to Distension of Fetal Bladder
complications in wtero which render the life of the new-born infant impossible. It is more often found without enlargement of the bladder than with. It is an arrest of development comparable with hare-lip, cleft palate, or imperforate anus, with which, indeed, it is sometimes associated , but it may be found in an otherwise perfectly normal child. It is only when the renal function is stimulated and excessive secretion takes place that the malformation begins to assert itself and trouble ensues. Now, it has always been a matter of dispute whether the renal function is established 77 utero or not, and to this I am about to refer. Suffice it
Right renal artery -------.--.----.-+. ----- ... Left renal artery
Inferior mesenteric. -...2.0.2...022..0000 00.
Right common iliac ...... .......----- 2... seeeee- + Left common iliac
Internal iliac.....2....2..2..000 2. ---. Internal iliac
External iliac. -..---- 2. 1.22. cess -- External iliac
Small branches... -.......... 00020... a
No definite anterior and posterior trunks
«++ Posterior trunk coos Anterior trunk
--- Small branches lost on the der wall
No left hypogastric artery
Right hypogastric ......-.--~......
Fic. 7. The abdominal aorta and its branches.
to say for the moment that a large number of children have been born alive with atresia of the urethra, and that apparently primary and complete, in whom no accumulation of fluid was manifest in the bladder until some hours, or even a day or two, after birth, and in whom the abnormality was not observed until absence of micturition drew attention to the condition of the genito-urinary organs. Whether or not renal secretion had taken place at all in wtero, birth fully established the function, and within a very short time operative procedure was rendered imperative. That this has often proved satisfactory will be seen from the records. An artificial opening has been made into the bladder by several routes (forcing a passage through the length of the penis, suprapubic puncture, perineal cystotomy), and in not a few cases the patient has not only recovered from the effects of the immediate operation but, in the terms of a popular phrase, lived happily ever after. The following cases, chosen from many in the literature, will suffice to prove this point :—
Apams. Brit, Med. Journ., 1891, i, p. 221.
Autumn. Med. Record, New York, 1896, xlix, p. 801.
Brake. Boston Med. and Surg. Journ., 1856, lv, p. 508.
CamMPBELL. Brit. Med. Journ., 1891, i, p. 460.
Davis. Med. Record, New York, 1896, 1, p. 354.
Durray. Ashhurst, Internat. Encyc. Surg., Lond., vi, p. 485.
Epis. Lancet, 1874, i, p. 898.
Forster. Brit. Med. Journ., 1885, i, p. 17.
Gruss. Lancet, 1874, ii, p. 857.
Jacguart. L’ Union méd., Par., 1875, xix, p. 351.
Lanneavu. New Orleans Med. and Surg. Journ., 1889-90, N.S. 17, i, p. 22. WHITEHEAD. Med. Times, Lond., 1847, xvi, p. 594.
I can find no accurate observations on the mode of death in similar cases where operation was not performed, but I presume the bladder would rupture or that death would ensue from suppression of urine.
Cases of imperforate urethra therefore fall into the two classes: (1) those accompanied, and (2) those unaccompanied by excessive secretion of fluid into the bladder; and imperforate urethra becomes dangerous in utero only when accompanied by excessive secretion. With this condition morbid results are bound to follow, which, I take it, will differ according to the amount of fluid secreted, the rate at which it is poured into the bladder, and the date when it begins. Four possible results of such a secretion suggest themselves :—
(1) In the earliest stages, exstrophy of the bladder—a theory advanced by Andrew Duncan in 1805, and fully set forth in the Edinburgh Medical and Surgical Journal, 1805, i, pp. 43 and 182. This theory has been revived again lately and deserves much consideration.
(2) Urinary fistula at the umbilicus. This certainly occurs where no obstruction is evident, and indeed it is not mentioned in a single case of imperforate urethra that I can find in the literature.
(3) Distension and rupture of the bladder into the peritoneum. (See specimen in Guy’s Hospital Museum, 2551/47, described by King.’)
1 Guy’s Hosp. Reports, 1837, Ser. 1, ii, p. 508. 14 Spicer: Dystocia due to Distension of Fatal Bladder
(4) Dilatation and hypertrophy of the bladder, with other complications.
In the present paper I shall refer only to the last suggestion, namely, dilatation and hypertrophy.
Firstly, can a bladder which has no “ exit,’ hypertrophy? In adult life hypertrophy of the bladder follows not complete, but partial obstruction of the urethra, and it is universally recognized as indicating repeated attempts by the organ to overcome a difficulty. It is a development of slow degrees. The bladder of the foetus reacts in a precisely similar way if it is called upon to eject urine in the presence of congenital narrowness or partial obstruction of the urethra. This is exemplified in cases recorded by Macan, Walther, Seuvre, Commandeur, and others :— ,
CommanDEuR. Lyon méd., 1898, lxxxvii, p. 359. Macan. Brit. Med. Journ., 1887, i, p. 513.
SruvkE. Bull. Soc. Anat. de Paris, 1874, p. 174. WattHer. Zeitschr. f. Geburts. u. Gyn., Stuttg., 1898, xxvii, p. 333.
But does it dilate and hypertrophy in the presence of atresia? Ballantyne, in his work on ‘“ Ante-natal Pathology,” states that it is necessary to divide cases of enlargement of the bladder in the foetus into two classes: (a) simple dilatation ; (6) dilatation and hypertrophy.
After studying the reports of a large number of cases, however, I am convinced that although there may be a necessity for distinction, it is not possible from the description alone to classify the recorded cases according to this plan. The text is often far too indefinite. Even in the cases of simple dilatation quoted by Ballantyne himself, I cannot satisfy myself that hypertrophy can be excluded.
I may mention especially two of these cases—those of Fabris and Schwyzer — in neither of which is the fact clearly stated. Indeed, Fabris’s note that the bladder walls were thick when contrasted with the thinned-out abdominal parietes is suggestive that hypertrophy may have existed. The dilatation is so striking a feature that hypertrophy is liable to escape mention. Moreover, one would expect cases of simple dilatation to end in rupture long before the bladder attained anything like the proportions given either in Fabris’s or Schwyzer’s case.
There is an admirable specimen of a four months’ foetus in St. Thomas’s Hospital Museum (No. 2691), described by Shattock,’ in which dilatation is the most marked feature. But Shattock says in this case :
Trans. Path. Soc. Lond., 1887-8, xxxix, p. 185. Obstetrical and Gynecological Section - 15
“The post surface of this dilated bladder presents faint transverse ridges like those due to the muscular hypertrophy seen in most cases of ordinary vesical or urethral obstruction.”
Hypertrophy does not take place in the bladders of young animals after the urethra has been completely obstructed by artificial means. Guyon? demonstrated this repeatedly. After tying a ligature round the urethra in dogs, for instance, he found that rupture of the bladder ensued in fifty to seventy hours. Dilatation takes place and rupture follows. Hypertrophy is usually the result of repeated contractions under difficulty. It is true that a muscle can contract without its points of origin and insertion coming nearer together, but it is difficult to think that it would persist in this for long and hypertrophy as the result, especially if it were being progressively stretched all the time by an opposing force.
It is quite as difficult to believe that a hollow viscus, distended and further distending with fluid, can persist in its efforts to contract and thereby hypertrophy to an enormous degree unless some of the fluid contained in it can escape.
It seems to me, therefore, that hypertrophy of the bladder wall is not a result that might be expected in a case of imperforate urethra. How, then, does it come about? Only, I believe, by means which entail an actual or virtual escape of the urine from the bladder, and again four possibilities occur to me to explain the cases in the literature :— .
(1) Incorrect diagnosis. What is reported complete atresia of the urethra would, if serial sections had been made, have proved in reality partial obstruction only ; and part of the fluid has been ejected into the liquor amnii with every contraction of the bladder.
(2) A partial or slowly increasing obstruction, which only became complete shortly before the child was born.
(3) That contractions of the bladder have produced a pouch or hernia capable of accommodating part of the fluid during contvaction of the rest of the viscus.
(4) That regurgitation into the ureters has taken place, with a reciprocating action between these and the bladder during contraction and relaxation of the latter.
Secondly, is the dilatation’ of the bladder with copious sccretion a natural result of imperforate urethra ? It has long been a matter of dispute whether or not urine is secreted physiologically during foetal life, and
1“ Maladies des vices urinaires,” 1903. 16 Spicer: Dystocia due to Distension of Fetal Bladder
even now, although a vast amount of literature may be found on the subject, the matter is not finally settled. Reasons which follow lead me to think that a physiological secretion does take place as a rule, but only to a very small extent, save at the very end of pregnancy. I do not believe that this is of excretory purport, but that it is a simple filtration of watery elements designed to clear the many tubules and ducts of which the urinary passages are composed. I hold that the specific function of the kidney, like that of most other organs, remains more or less in complete abeyance during fcetal life. Throughout the whole of this time (normally ten lunar months) development is slowly progressing, and although it is perfected about the seventh or eighth lunar month to a sufficient extent to enable the organs to carry on a post-natal existence of a sort should the necessity arise, they only take on true activity in utero as the result of some process which must be called “ pathological.” I suggest that the large amount of secretion in the case of the foetus under consideration and others like it was an evidence of a pathological and not a physiological process.
(A) Fetal life can undoubtedly be supported and normal development of other parts of the body proceed in the entire absence of urinary organs.
Arthur E. Giles* records a case of malformation of the rectum and bladder, absence of both kidneys and ureters, imperforate anus, and absence of the right hypogastric artery. The child was born alive. A similar case was described by Rissman, of Hanover,” in which the child was born alive shortly before full term; and another by Bonn? Straussman ‘ reports two others, one a living child at eight months, the other at “ nearly full term.’’ Mayer ° records the birth of a stillborn fullterm male infant in which kidneys, ureters, bladder, renal arteries, and external genitals were all absent, as well as sigmoid, rectum, and anus, though the other organs were fully developed. Berry Hart® records a specimen sent him by Mr. Miles of an eight months’ foetus with no external or internal genitals, no bladder, ureters, or kidneys. Absence of both kidneys is not rare in sympodial monsters, two of which are referred to by Shattock.! In both of these the bladder was normal, but there was no trace of kidneys or ureters.
' Trans. Obstet. Soc. Lond., 1892, xxxiv, p. 129.
Centrailbl. f. Gyn., Leipz., 1892, xxvi, p. 497. See Connell, Journ. Amer. Med. Assoc., Chicago, 1907, xxxvi, p. 637. ‘ Zeitschr. f. Geburts: u. Gyn., Stuttg., 1894, Ser. 1, xxviii, p. 181.
° Zeitschr. f. Physiol., Heidelb., 1827, ii, p. 36.
° «A Contribution to the Morphology of the Human Urino-genital Tract,” Journ. Anat. and Physiol., xxxv, 1901, p. 330. Obstetrical and Gynecological Section 17
If renal excretion and secretion were necessary to foetal life and development, no child could have been born alive without kidneys or reached a period of development anything like full term.
(B) The fetal kidneys do not always secrete an appreciable quantity of fluid, for in a child born alive with atresia of the urethra there may be no external evidence of distension of the bladder at birth. Ifa large quantity of urine is normally excreted during intra-uterine life (1.e., a quantity anything approaching that found in my own specimen and others like it) the absence of such in these cases, provided, of course, that the occlusion is primary and complete—and there is no reason to doubt it in many cases—must be explained either by: (1) inhibition of normal excretion, which is unlikely, since these children are frequently well developed in other respects, or by (2) reabsorption of fluid from the bladder. It is difficult to prove conclusively that the latter cannot occur in the foetus; many experiments have been performed? which make it certain that absorption does not take place from the bladder in animals, and we can safely conclude that the same holds good in man and in the foetus.
If foetal life and development can be supported in the absence of the urinary system, and if foetal kidneys may be present and yet not secrete appreciably, it is obvious that the renal functions of excretion of urea and other catabolic products must be carried out, at any rate in these cases, by some other organ. As a matter of fact, it is now well recognized that throughout foetal life excretion is normally carried out, at any rate for the most part, by way of the placenta. Innumerable experiments have been performed which show the possibility of transference of various substances from foetus to mother and vice versa, and there is no doubt that all the foetal toxins can be passed by this route into the blood of the mother and by her excreted. All this depends, however, on the integrity of the combined circulation. Providing that the circulatory arrangements of the mother and child are undisturbed, it is possible for a foetus to carry on a parasite existence with a minimum exertion of its own organs, and, in the case of the genito-urinary organs, to live without them. This does not prove conclusively that under normal circumstances the foetus does not use the urinary system, if it has one ; but taken with the following facts concerning the other systems it provides a strong argument that it uses it very little. Thus anencephalic foetuses are frequently born alive and well developed, and, indeed, the central nervous system may be entirely absent and yet life persist. Malformations which completely discount the use of the digestive tract wn utero do not interfere with the life and growth of the foetus. For instance, cases of atresia of the cesophagus have not infrequently been reported, and I have myself recorded three such cases which occurred in my own experience.’ These three children were all well developed and were born alive ; in fact, they lived one, six, and nine days respectively. The liquor amnii contains so little albumin that even if it were swallowed (and there is evidence that it sometimes is) it could not sustain the life of the child.
e ' Trans. Path. Soc., xxxix, p. 10. > « Hixperiments by L. Lewin and H. Goldschmidt,” Archiv. f. exper. Path. u. Pharmacol., Leipz., 1896, xxxviii, p. 60, and Archiv. f. path. Anat. (Virchow), 1898, cxxxiv, p. 1.
It seems almost beyond dispute that the placenta is the most important, and probably the only channel by which nutriment reaches the foetus. Again, while means of respiration are provided by the mother through the placenta, why should the child attempt to use its own immature organs? A foetus is capable of using its lungs at seven months or even less, but it does not, because its mother supplies abundant oxygen. The respiratory centres remain at rest during the whole intra-uterine life, and ante-natal respiratory movements must be considered abnormal phenomena.
Doubtless the development of the lungs is more complete at nine months than at seven; but as soon as the maternal circulation is cut off or severely interfered with, stimulus is given to the infant’s respiratory centres, whether it be at full term or not, im utero or not, and for the first time it puts its own lungs-into action. In this particular case we know from experiments on animals that unless the placental circulation is actually disturbed, foetal respiration will not be attempted.
Runge, Cohnstein, and Zuntz” experimented on the sheep, in which there is no fear of disturbing the placenta when incising the uterus. In the sheep at term they exposed to the air the head and forepart of the foetus. Pinching, pricking the skin, tickling the pharynx and nasal mucous membrane provoked no respiration. The foetus was then extracted bodily from the uterus and placed on the belly of the mother, without the cord being pulled on. The stimuli were continued again for several minutes. Insufflations of air into the nasal fossa had no effect ; there were only general reflex movements. The foetus sucked
1 Journ, Anat. and Physiol., Lond., 1906, xli, p. 52, and Lancet, 1907, i, p. 157. 2+ Foetus,’’ Richet, Dict. de Physiol., 1904, vi, p. 548. Obstetrical and Gynecological Section 19
and bit the finger when this was introduced into its mouth and pharynx; following that, it executed spontaneous movements which altered its position ; but only after the cord had been tied did the foetus attempt to respire. These experiments were repeated later by Runge,’ with the same results. Cohnstein and Zuntz demonstrated the same results in the rabbit and, by exercising great care, in the guinea-pig. Heinricius® laid bare the muzzle of the foetus in a bitch at full term, and introduced into the nasal fossee a mixture of water and ammonia in equal parts; it produced violent reflex movements of the face, but no respirations. He opened the mouth and put some drops of the solution into the mouth and pharynx; the animal made movements of deglutition, opened and shut its mouth, put out its tongue, but did not breathe. It was only when he disturbed the placental circulation in withdrawing the foetus from the uterus that he saw respiration commence.
A phenomenon which in some ways upholds the preceding results is seen when a foetus born in the caul makes respiratory movements and succumbs to asphyxia, though it has never left the liquor amnii or been exposed to cutaneous stimuli. Engstrém came to a similar conclusion, that arrest of the placental circulation provokes respiratory movements in the foetus, without the necessary addition of cutaneous stimuli. It may also be mentioned that Heinricius proved by further experiment that premature respiration could be produced without disturbing the placental circulation, by diminishing the flow of blood to the medulla of the foetus by ligature of the carotid arteries. By thus causing an insufficient supply of oxygen to the bulb, the respiratory centre was stimulated.
From all the evidence at our disposal it is beyond doubt that the allimportant factor to the intra-uterine life of the child is the mother’s circulation and its own. By this means respiration, nutrition, and excretion are all so perfectly provided for that its own major organs are not essential to the foetus for life and growth; in fact, it is possible for them to be dispensed with. Even its own heart is unnecessary, provided a satisfactory circulation can be borrowed from a neighbouring twin; and its lungs are never used.
It is reasonable, therefore, to conclude that under normal conditions excretion by the foetal kidney is unnecessary and improbable. If the mother is capable of carrying off the toxins efficiently, why burden the kidneys of the foetus with work which they are less prepared to perform at, say, seven months than nine ?
Arch. f. Gyn., Berl., 1894, xlvi, p. 512.
Zeitschr. f. Biol., Miinch. u. Leipz., 1889, xxvi, p. 137.
Now in the case of the lungs we have seen that a premature stimulus may be given to respiration by an interference with the normal circulatory arrangements in utero. It is easy to understand that the same may be true of excretion. The nature and degree of interference are probably somewhat different in the two cases, but I venture to contend that only as the result of a breakdown in the normal mechanism of excretion provided for through the placental circulation will the foetal kidney take on excretory responsibility im utero. Should such a breakdown occur, previous filtration processes will be exaggerated and excretory efforts made. The immediate result will depend on the stage of development of the kidney and a free passage through the lower urinary tracts. Foetal uremia is a subject about which very little is at present known, but it is possibly not an uncommon sequel and cause of death.
Although excretion of toxins is amply provided for through the placenta, a reasonable purpose may be suggested for the filtration of small quantities of water in the washing away of epithelial debris which might be expected to accumulate in the multitude of tiny tubules developing in the kidney. The presence of such debris may account for the albumin noted in the analysis of the first water passed after birth. That the kidneys may secrete copiously during the last hour or two at any rate of intra-uterine life cannot be disputed, and is what one would expect if the previous theories are correct. The onset of labour—if not earlier circumstances, such as changes in the placenta preparatory to labour, but insufficient to stimulate respiration—brings about the beginning of a breakdown in the previous arrangements of excretion ; a stimulus is given to the kidney and it starts work. Often enough perfectly normal infants micturate freely within a few minutes of birth, and in the case of breech birth not uncommonly during delivery. This fluid must be secreted im utero. It is not always present at birth, however, and the amount varies greatly when it is. In seventy-five cases of new-born children, Dohrn found urine in the bladder of 69 per cent. Schaller found the bladder empty in ten cases out of twenty-four. This variation in quantity may, of course, depend on whether or not the foetus has evacuated the contents of its bladder into the amniotic cavity shortly before or during delivery. Analysis shows that the first water passed by the new-born infant is different from that which follows an hour or two later. It is watery and very little charged with extractives.
It is pale and nearly as clear as water. It has the specific gravity of 1009 to 1010, and is acid or neutral in reaction. According to the figures found in Richet’s Dictionnaire de Physiologie (‘ Foetus,” p. 618), it contains 0°245 per cent. urea immediately after birth, 0°360 per cent. urea in the first twelve hours, and 0°921 per cent. urea in the following twelve hours. Albumin in small quantity seems to be frequent, and according to Virchow very nearly constant. These figures support the view that excretion of toxins is not a normal duty of the kidneys until after birth. The child’s kidneys will excrete certain chemical substances given to the mother during pregnancy and parturition. Thus, methylene blue given to the mother during labour has been found in the first urine passed by the child.
L. Schaller’ gave pregnant women phloridzin, a glucoside which produces glycosuria, and always found sugar present as the result in the urine of the new-born child. This proves the transference of chemicals between mother and child and activity of the foetal kidneys shortly before birth, but nothing more.
The bladder is found to contain urine in some human fetuses and occasionally even at an early date. This proves renal filtration (unless it be a secretion from the bladder—-see later), though it does not necessarily prove a physiological secretion or excretion, and it may have taken place only with the onset of abortion. Nagel? found, on four occasions, foetuses of three to four months with the bladder in the form of a transparent vesicle the size of a bean, full of clear liquid. On the other hand, five or six other foetuses of the same age had the bladder empty. Similar observations are published by other writers.
But we must not forget that there is unfortunately always an initial difficulty in accepting statistics drawn from observations on the human foetus. We can seldom be sure that we are dealing with a physiological specimen. But for pathological circumstances, very few embryos or foetuses would be in our hands. There is a specific cause for every abortion and for every foetal death, although in most cases we omit to trace them and treat the product as normal. A normal foetus, provided, of course, we consider the whole foetus (including placenta, cord, &c.), is probably much less common on our dissecting tables than we think. The very fact that a foetus is there should lead us to suspect its apparent normality.
' Centralbl. f. Gyn., Leipz., 1898, xxii, p. 321. 2 Arch. f. Gyn., Berl., 1889, xxxv, 131.
Slow pathological changes, which act through interference with the combined circulation and ultimately kill the child or precipitate abortion, probably create, meanwhile, sufficient stimulus to call the kidneys into premature use. In regard to the presence of urine in the foetal bladder, I believe that experimental research on pregnant animals has led to somewhat similar results. The bladder occasionally contains a little secretion—usually not. Some writers have suggested that when fluid is found in the bladder it is due to the secretion of the bladder wall itself. There are several reasons to contraindicate this theory, and there is no proof at present that the foetal bladder is provided with the necessary secreting mechanism. It was at one time commonly supposed that the liquor amnii was entirely composed of foetal urine. That it often contains foetal urine is probable, but that it is composed entirely, or even mostly, of this fluid can be no longer accepted. In cases of complete absence of genito-urinary organs, and in cases of imperforate urethra, liquor amnii is often found in normal quantity, and, indeed, hydramnios has been reported. Oligohydramnios is quite as rare in these as in other pregnancies... Liquor amnii was certainly present in my own case of imperforate urethra.
In cases where the kidneys are stimulated into the production of a pathological excess of fluid (and I have elsewhere suggested an abnormality of the circulation as cause), and where no obstruction to the urinary passages exists, it is probable that the urine is ejected into the liquor amnii, and it may in this way take a share sometimes in producing hydramnios. If that is so we can suppose that in certain cases, my own included, well-marked hydramnios might have been present but for the atresia of the urethra.
- In itself, imperforate urethra is not antagonistic to foetal life.
- It is not necessarily accompanied by distension of the bladder, nor does it render dystocia inevitable.
- It becomes dangerous in utero only in. the presence of a large secretion of fluid by the foetal kidney, and such secretion is pathological.
- The foetal kidney normally allows the filtration of a small quantity of watery fluid, but the amount is insignificant. The kidney is not employed as an excretory organ im utero, unless a breakdown occurs in the normal mechanism by which the mother performs the whole of the necessary excretory function of her child.
- The kidney, like the other major organs, though capable of carrying on post-natal functions of a sort at an earlier date than the tenth lunar month, if necessity demands, remains in abeyance during foetal life.
- The effects of accumulation of fluid in the foetal bladder depend on the amount, the rate, and the date of secretion, and especially also on the possibility of evacuation.
- Hypertrophy and dilatation of the bladder can only arise where there is an actual or virtual means of exit for the contained fluid.
- See case by Ballantyne, Hdin. Med. Jouwrn., 1895, x1, p. 858. Obstetrical and Gynecological Section 23
The PRESIDENT (Dr. Herbert Spencer) said that the Section was much indebted to the author for his valuable paper, which contained a great number of facts. Until he had had time fully to consider those facts he did not feel able to give up the view he had held for many years that the foetus normally secreted urine and passed it into the liquor amnii during pregnancy. He had met with at least half a dozen cases of stenosis of the ureters in stillborn children in which the ureters were distended with urine above the obstruction ; in one case the distended ureters gave rise to dystocia. In these cases urine had evidently been secreted during long periods and not merely during the act of birth, and it was much more reasonable to suppose that the obstruction interfered with the normal outflow of urine than that the obstruction, or an associated pathological condition which was not observed, was itself the cause of the secretion. When the kidneys were absent the liquor amnii had been observed to be very scanty. With regard to the statement that foetal secretion remained in abeyance till birth, it was certainly not true of the vaginal or the uterine secretion, for he had found the vagina and the body of the uterus greatly distended when the outflow of mucus was obstructed by stenosis or by tumours.
Mr. ALBAN DoRAN observed that quite recently a case of oligohydramnios had been reported where both kidneys were absent in the foetus and the bladder was empty. The suprarenal bodies were hypertrophied. The absence of the kidneys was held to support the theory that the liquor amnii was mainly supplied by the foetus, but Mr. Doran doubted if Dr. Spicer or any other competent obstetrician would be convinced on the evidence of a single case.
' Hauch: ‘“‘ Oligohydramnios : Foetus sans reins,” L’Obstétrique, August, 1908, p. 373.
Dr. W. 8. A. GRIFFITH stated that Dr. Spicer’s admirable paper was one of great interest and raised points which were of great importance. The records of these cases showed that imperforate urethra was not necessarily followed by distension of the foetal bladder, and Dr. Griffith was prepared to accept Dr. Spicer’s view that interference with the normal secretory apparatus of the foetus through the placenta was the cause of the renal activity before birth, and that this activity during intra-uterine life was therefore pathological. The class of cases which he believed Dr. Spicer had not referred to in his paper was that of distension of the foetal bladder without stenosis of the urethra, and he (Dr. Griffith) pointed out that, although the view that a foetus could empty its bladder into the closed amniotic sac was commonly held, no one had brought forward any evidence that this was possible ; and it appeared to be very unlikely, although cases of great hypertrophy, such as that reported by Dr. Spicer, in which the contracted bladder measured 4 in. in thickness, appeared to show that under certain conditions it might be possible. From some work he did in the investigation of this subject some years ago, with the help of the lecturer on chemistry at St. Bartholomew’s Hospital, in the examination of the fluid found in the bladder at birth, he was able to agree with Dr. Spicer’s statement that the small amount of fluid found in the bladder at birth was little more than a watery filtration, and that the secretion was the same until the ingestion of food began to give it the ordinary urine characteristics.
Dr. SPICER, in answer to a remark by the President that hydronephrosis in a case of congenital narrowing of the ureter found in a stillborn foetus proved physiological secretion by the foetus, suggested that the foetus would not have died in utero but for some pathological process. That process, ending as it did in death and abortion of the foetus, was probably: acting in the meantime as a stimulus to pathological secretion of urine, which happened to be retained owing to the malformation of the tract.
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