Paper - Congenital malformations of the oesophagus
|Embryology - 15 Apr 2021 Expand to Translate|
|Google Translate - select your language from the list shown below (this will open a new external page)|
العربية | català | 中文 | 中國傳統的 | français | Deutsche | עִברִית | हिंदी | bahasa Indonesia | italiano | 日本語 | 한국어 | မြန်မာ | Pilipino | Polskie | português | ਪੰਜਾਬੀ ਦੇ | Română | русский | Español | Swahili | Svensk | ไทย | Türkçe | اردو | ייִדיש | Tiếng Việt These external translations are automated and may not be accurate. (More? About Translations)
Guthrie KJ. Congenital malformations of the oesophagus. (1945) J. Pathol. Back. 57: 363-373.
|Historic Disclaimer - information about historic embryology pages|
|Embryology History | Historic Embryology Papers)|
Congenital Malformations of the Oesophagus
Katharine J. Guthrie
From the Department of Pathology of the Royal Hospital for Sick Children, Glasgow (1945)
Congenital atresia of the oesophagus with tracheal ﬁstula—the commonest type of oesophageal malformation-—has been regarded in the past as an inoperable condition invariably fatal within a few days of birth. The increasing scope of thoracic surgery now renders the prognosis more hopeful ; ‘in fact surgical repair has been undertaken in a number of cases in America (Richter, 1913; Leven, 1936-37,. 1940-41 ; Lanman, 1940; Carter, 1941 ; Haight and Towsley, 1943 ;: Ladd, 1944). Grey Turner (1943-45) described the pioneer attempt. in this country at direct suture of the oesophageal segments after closure of the ﬁstula. He found four examples of (esophageal atresia. in 10,543 deliveries (1935-42) at the British Postgraduate School of Medicine—a ratio of approximately 1 in every 2650 births. This incidence is sufficient to justify increasing attention to the condition.
The post-mortem records of the Royal Hospital for Sick Children, Glasgow, furnish 38 examples of oesophageal malformation in 69161 autopsies between 16th February 1915 and 25th September 1944. These cases, which form the subject matter of this paper, are classiﬁed as follows :—
|Congenital atresia with tracheal ﬁstula||23|
|Congenital atresia without tracheal ﬁstula||1|
Congenital Atresia With Tracheal Fistula
The lesion in all 23 cases was essentially obliteration of the middle portion of the gullet, blind ending of the upper segment and communication of the lower with the trachea in the region of the bifurcation. In one instance the ﬁstula opened about g in. above this point. The proximal segment of the oesophagus was generally dilated to form a. small, rather thick-walled pouch approximately 1-1% in._ long; the distal part was generally of narrow calibre, especially at its origin, and the gap, of variable length, averaged 1-2 cm. In several cases the two portions, though contiguous, were entirely separate. Five cases showed slight variation from the usual pattern in that the absent portion of the oesophagus was represented by an impermeable cord 1 cm. or more in length.
Not all patients dying in hospital come to autopsy, so the clinica records from 1915 onwards were searched for further examples of cesophageal atresia and 6 more cases with suggestive clinical ﬁndings were discovered. The series thus totals 29 cases—18 male, 11 female.
In these infants the typical history, dating from birth, is one of coughing, choking and cyanosis on attempting to swallow, since milk overﬂowing from the upper blind pouch enters the air passages. As a rule much frothy mucoid ﬂuid is present in the nasopharynx. Frequently the upper part of the abdomen is tympanitic owing to the presence of air in the stomach. Nothing but meconium is passed per rectum. The presence of oesophageal atresia is readily conﬁrmed by X-ray examination after the passage of a catheter which is held up generally about 9-12 cm. from the teeth. The practice of giving barium sulphate by mouth is contra-indicated (Lanman, Ladd) since it acts as a toxic irritant if aspirated ; they regard iodised poppy-seed oil as safer. However, in Lanman’s opinion simple X-ray examination after the passage of a soft rubber catheter is adequate for diagnosis.
Since infants thus affected are unable to swallow, they would die of starvation ; but aspiration bronchopneumonia generally supervenes. Carter remarks that copious secretion pours from the upper pouch when it is brought to the surface for drainage.
Of the 23 infants coming to autopsy, none had healthy lungs. Aspiration pneumonia, generally extensive, was present in 18, patchy collapse in 3, hypostatic congestion in 1 and streptococcal empyema with pulmonary collapse in 1. Other developmental defects were associated with the cesophageal atresia in 4 instances. In one there was congenital atresia of part of the small bowel and the middle lobe of the right lung was missing. Another infant had severe congenital malformation of the heart and malformations of the spleen and right hand. In a third, dextrocardia was diagnosed on X-ray examination. The fourth had rectal atresia, the rectum forming a large cul—de-sac distended with meconium. There was no communication with the anal canal, which was patent though narrow. The remaining 18 cases examined post mortem were free from associated congenital defects and there was no mention of any external abnormality in the other 6 ; 24 infants died within 8 days of birth, I survived for 12 days and the remaining 4 for slightly shorter periods. Gastrostomy was performed in 7 cases but all died shortly after. This operation alone is useless, since, owing to the tracheal ﬁstula, the stomach contents regurgitate upwards into the air passages and induce bronchopneumonia. In the case with a defect of the small bowel gastrostomy was combined with anastomosis between duodenum and colon.
Other Abnormalities of the Oesophagus
The 15 remaining autopsy cases presented a variety of oesophageal malformations. In some instances the anatomical anomaly appeared slight in view of the severity of the symptoms——persistent dysphagia and vomiting, often with great emaciation. In such patients cardio-spasm probably played a part. A short description of the individual cases is given, since most of them presented features of interest. The single example of muscular hypertrophy of the (esophagus with associated hypertrophy of the pylorus and small bowel—a condition of extreme rarity~will form the subject of a separate report.
Oesophageal atresia without tracheal fistula
In a male infant surviving for 19 days the proximal segment of the oesophagus, comprising about two-thirds of the total length, had a smooth blind lower end. The short distal portion, blind above, extended only about 0.5 in. above the diaphragm so that the gap between the segments was considerable. Death resulted from marasmus and bronchopneumonia. The infant, though able to suck at birth, regurgitated milk through the nose. Bougies were held up at the lower end of the oesophagus.
The severity of the lesion in the 6 cases forming this group is graded from virtually complete atresia to slight localised narrowing.
Case 1, female, 6 days, had a tight stricture with slight pouching of the gullet above it. Although the condition amounted practically to atresia, the case is placed in this group since a minute lumen existed, allowing the passage of a ﬁne probe. Bronchopneumonia was present. The infant, who had been unable to swallow from birth, was greatly emaciated. A sister died in this hospital seven years previously at the age of 13 days. At autopsy no oesophageal lesion was found, though there was a history of inability to swallow from birth.
Case 2, male, 5 months, very marasmic, had marked stenosis due to an -encircling band of ﬁbrosis with pouching of the mucosa above. The infant had been healthy at birth. Regurgitation began at the age of 6 weeks on weaning, with increasing dysphagia and progressive emaciation.
Case 3, female, 3.5 years, showed a stricture about 1 in. in length high up in the oesophagus, which was slightly. dilated above it. The constricted portion of the wall was smooth and free from disease. Absence of scarring was suggestive of a congenital origin. In addition a small semicircular diaphragm was present at the pharyngo-oesophageal junction. The child had been healthy prior to an attack of severe emesis at the age of 3 years. Thereafter attacks of vomiting increasing in severity recurred at ever shorter intervals and emaciation became pronounced. On admission a stomach tube could be passed only 6 in. from the teeth and X-ray showed oesophageal stenosis. Gastrostomy was performed but the child died next day.
Case 4, female, 5 years, showed deﬁnite oesophageal narrowing at the level of the tracheal bifurcation. Below this the wall was much thickened. There was also a “ thoracic stomach ”. The child, a microcephalic, was much emaciated. Feeding had been difficult from birth and she had never been able to swallow solids. The passage of bougies gave only temporary relief. Death followed a prolonged period of persistent vomiting.
Case 5, female, 5 months, showed considerable narrowing of the oesophagus below the tracheal bifurcation with dilatation above. Bronchopneumonia was present. There was a history of dysphagia with vomiting since birth, slight at first but recurrent and increasing in severity. Thick mucus was vomited along with the feeds.
Case 6, male, 4 months, had a slight stricture at the level of the tracheal bifurcation combined with localised hypertrophy affecting the last 3 cm. of the oesophagus and ceasing abruptly at the cardia. In hospital oesophageal obstruction was conﬁrmed by a barium meal. Vomiting had been present since birth. The passage of bougies aﬂbrded relief so that the child was able to retain feeds but fatal gastro-enteritis supervened.
In this group of 6 cases the anatomical lesion was again relatively slight, consisting of simple dilatation, localised or diffuse, unassociated with stricture. There was slight muscular hypertrophy of the gullet wall in some instances.
Case 1, female, 14 weeks, a twin, showed merely dilatation at the lower end of the oesophagus. Bronchopneumonia affected both lungs. The child had dysphagia with partial regurgitation. A test feed in hospital showed ability to swallow, but the feed was returned. X-ray examination after a barium meal suggested cardiospasm.
Case 2, male, 16 weeks, a mongol, had a fusiform dilatation of the oesophagus with thickening of its wall. The mucous membrane, which was red and smooth, was thrown into prominent transverse ridges. Bronchopneumonia was present and the child was jaundiced and much emaciated. There was no history of vomiting or dysphagia. The oesophageal lesion was an accidental post-mortem ﬁnding.
Case 3, male, 10 months, showed combined hypertrophy and dilatation of the oesophagus, most marked in the middle third where the diameter was about twice the normal. At the lower end there was present a shallow oval acute ulcer which had given rise to repeated severe haematemesis shortly before death ; the stomach and duodenum contained blood at autopsy. Early broncho-pneumonia and double otitis media were present. There was a history of ' vomiting at least once daily since birth. Latterly emesis had been more severe. and there had been great loss of weight.
Case 4, male, 8 months, had a funnel-shaped oeophagus broadest at the lower end. Bronchopneumonia was present. The infant throve till the age of 5 months, when vomiting began and continued. Slight haematemesis occurred before death.
Case 5, female, 5 months, had dilatation and hypertrophy of the last inch. of the oesophagus. Several small acute ulcers were present about the junction of the normal and dilated portions. There was a history of vomiting from birth with progressive emaciation. Repeated haematemesis occurred before: death.
Case 6, female, 9 years, showed considerable dilatation with slight muscular hypertrophy of the whole gullet, which was of approximately constant width except for a slight constriction about ;- in. in length at the level of the tracheal bifurcation. The child was breast-fed and -throve till the age of 18 months, when an attack of “ congestion of the lungs ” was followed by severe persistent vomiting of all food and even of water. She was admitted at the age of 2 years and 9 months when an oesophagoscope passed readily along the whole length of the gullet, which was normal except for slight dilatation at the cardiac end. The passage of bougies improved but did not entirely cure the dysphagia. The child was not seen again for nearly six years, during which time the condition remained stationary. After a severe prolonged attack of vomiting, which began immediately after the death of her mother to whom she was much attached, she was readrnitted greatly emaciated, 57 per cent. underweight. A barium meal was completely held up at the level of the bifurcation. Death occurred shortly after admission.
This condition was represented in a female infant aged 9 days, who showed a large thick-walled diverticulum 1.5 in. long in the anterior gullet wall at the upper end, extending down behind the trachea. The oesophagus itself was patent throughout and there was no communication with the trachea. Broncho-pneumonia was present. Feeding from birth had been attended with great difficulty, as the child choked and turned blue on taking food. Gastrostomy was performed but death occurred some hours later.
Abel (1929) has classiﬁed congenital malformation of the oesophagus into seven types—total absence, doubling, oesophago-tracheal ﬁstula, partial obliteration, diverticulum, simple congenital stricture and stricture due to a membrane or valve. The present series represents all but the ﬁrst two varieties, both extremely rare, and includes an example of an additional abnormality consisting of muscular hypertrophy of the oesophagus.
Esophageal atresia with tracheal fistala
According to published ﬁgures approximately 70 per cent. of all congenital malformations of the oesophagus are of this type. Fischer (1926) gives the average duration of life as 2-7 days. In the exceptional case reported by Schmidgall (1915) life was prolonged for 28 days.
Surgical repair offers the one slender chance of survival to these infants, many of whom suck eagerly and are well nourished and vigorous at birth, though liable to the early onset of pneumonia as in 18 of the 23 cases coming to autopsy in the present series. Various types of operation, described in detail by the authors quoted, have been devised to surmount the great technical difficulties inherent in the problem of reconstruction of the infantile oesophagus. Another factor which must be taken into account in deciding whether to operate is the presence of associated congenital malformations. These occurred only in 4 of our 23 cases, but the recorded incidence is generally much higher (Plass, 1919; Fischer, 1926; Ladd, 1944). Atresia ani is the most frequent single concomitant defect. Multiple errors of development in the same patient are recorded in the papers of Meusburger (1910), Harris (1922-23), Marcus (1923) and Gruenwald (1941).
The genesis of oesophago-tracheal ﬁstula should be explicable on embryological grounds since it is a typical malformation, Le. it is of frequent occurrence and standard pattern though not of uniform severity, since gradations exist between mild and severe forms (Gruenwald, 1940). Atypical abnormalities on the other hand may arise erratically from some such accidental cause as amniotic adhesions. Gruenwald found the usual combination of oesophageal atresia and tracheal ﬁstula already well developed in a 9 mm. human embryo. In his opinion the essential cause of the malformation lies in the premature lengthening of the respiratory tract before separation of the oesophagus is complete, so that the rapidly growing respiratory tube draws out the corresponding portion of the oesophagus into a narrow strip of tissue incorporated into its own dorsal wall. This process results in atresia of the oesophagus and tracheo~—oesophageal ﬁstula. From the lower end of this composite tube arises the normal distal portion of oesophagus. The upper pouch, he assumes, develops from the part of the primitive tube attached to the pharynx. On the extent of oesophageal separation depends the level of the ﬁstulous opening into the trachea, the severest type of malformation occurring when the lower portion of oesophagus communicates with the tracheal bifurcation.
As regards aetiology, Pearson (1914) and Still (1927) associate certain congenital defects and diseases with order of birth. Thus Still found that among 400 cases of congenital pyloric stenosis, 48-5 per cent. were ﬁrst-born (including still—births and miscarriages) and there was a steep fall from ﬁrst to second and subsequent children. Mongolism, on the other hand, occurred in high proportion in later born children. He attributes congenital deformity at the extremes of reproductive life to imperfect function and failing function respectively. Other congenital defects, e.g. cardiac and cerebral, he found occurring with undue frequency among ﬁrst—born children. In a series of 160 varied malformations, including 5 congenital obliterations of the oesophagus or bowel and 5 of the bile~ducts, 41-8 per cent. were first-born, a proportion indicative in his opinion of some special liability in the ﬁrst pregnancy to anomalies of development under the inﬂuence of toxaemia, to which primagravidae are particularly prone. Pearson also gives evidence, based on large series of ﬁgures, that ﬁrst—born infants reaching term are physically inferior to those of later sequence.
The present series affords no evidence in support of this contention. Of the 12 cases of cesophageal atresia with tracheal ﬁstula in which order of birth is mentioned only 1 was a ﬁrst-born child. In the group of 15 subjects with varied oesophageal defects, order of birth was stated in 12, of whom only 2 were ﬁrst—born children.
Oesophageal atrcsia without fistula
In this rare condition there is simple obliteration of the lumen of the oesophagus. In a single example occurring in the present series the long proximal portion had a smooth blind end and the short distal segment formed a minute cul-de-sac closed above. The condition recalled Thomas Gibson’s classical 17th century description of one of the earliest recorded cases of oesophageal atrcsia (Gibson, 1697, p. 239): “ The isthmus (between the oesophageal segments) did not seem ever to have been hollow, for in the bottom of the upper and top of the lower cavity there was not the least print of any such thing but the parts were here as smooth as the bottom of an acorn cup ”. Particular interest attaches to this ancient report, not only because the clinical and pathological ﬁndings are described with precision, but also on historical grounds, since the author was the grandson of Oliver Cromwell and Physician-General of the Army.
Morell Mackenzie (1884, vol. ii, p. 156) deﬁnes simple stenosis as “ Abnormal narrowness of a limited portion of the oesophagus, without any morbid change in any of its component tissues at the site of stricture ”. Six cases of the present series fall into this group. In the one with the greatest degree of constriction the channel, though present, was very minute, admitting only -a ﬁne probe. In a second, marked stenosis was due to an encircling ﬁbrous band apparently of congenital origin, as regurgitation began at the age of six weeks. Reduction in calibre was relatively slight in the other 4 and there was no apparent disease of the wall. In 3 of these four cases some other (esophageal abnormality was present. In one this took the form of localised muscular hypertrophy at the lower end of the gullet well below the stricture, in another of a semicircular valve-like fold of mucosa projecting into the lumen and forming a partial diaphragm, in the third of “ thoracic stomach ”. This case was no. 7 of the series reported by Findlay and Brown Kelly (1930-31).
Obstruction by an annular membrane more or less complete or in the shape of a semicircular valve, though rare, is recorded by various authors (Morell Mackenzie, 1884, vol. ii, p. 219; Beatty, 1928; Abel, 1929). In Abel’s patient—a 42-hour-old infant—mere pressure with the endoscope suﬂiced to rupture the thin membrane. Abel makes the important observation that the symptoms in all types of congenital malformation of the oesophagus are almost identical; hence without a complete examination by all available methods cases amenable to operation may be missed. Simple atresia and stenosis are attributed by embryologists to developmental anomalies. According to Harris (1928-29) the oesophagus and duodenum in early embryonic life act as parent tubes which give rise to daughter tubes-—trachea and lungs in the former; pancreas, liver and bile-ducts in the latter. Such parent tubes are liable to become weakened at the expense of the normally developing daughter tubes. Consequently proliferation of the mesoderm cells is defective and compensatory hyperplasia of the epithelium occurs, leading to complete occlusion of the lumen. It is to these two factors—deﬁcient growth of mesoderm and overgrowth of epithelium—that these parent tubes owe their “ pathological predestination ”. The muscle coats arising in the deﬁcient mesoderm are liable to be weakened or to be partially replaced by ﬁbrous tissue, thus encouraging diverticulosis. Normally, after undergoing partial atrophy the solid epithelial core is canalised by the development of intra-epithelial cysts which become conﬂuent. Atresia, stenosis or intra-epithelial cyst formation may result from interference with the normal course of evolution.
This condition occurred in 6 cases. Here, as in some of the patients with slight stricture, the insigniﬁcance of the morbid change was surprising in view of the severe dysphagia, vomiting and emaciation which had directed attention to the oesophagus during life. Lust (1923-24) found the same discrepancy between the autopsy and clinical ﬁndings in some of his cases. These minor anatomical lesions appeared insufﬁcient per se to account for the clinical symptoms, particularly in view of the fact that a spindle-shaped dilatation of the whole gullet in one case of the present series had shown no clinical symptoms. Likewise D’Silva (1944) discovered gross oesophagectasia accidentally at post-mortem in an adult. Simple stenosis also may exist without causing dysphagia, as in the case reported by Brown Kelly (1931) of a 35-year-old man dying of cerebral haemorrhage in whom marked stenosis at the entrance to the oesophagus had not been suspected during life. An additional factor must be sought to explain the clinical severity, and this is probably of spastic nature. According to Brown Kelly (1936) cardiospasm is not uncommon in young children. It varies in severity and duration, sometimes passing off and at others causing complete obstruction. This author describes a primary type, due apparently to congenital predisposition of which the fundamental cause is unknown. The intermittent, variable nature of the symptoms in such cases suggests transient spasm of the cardiac sphincter as a result of stimulation of the sympathetic nerves under the inﬂuence of emotional disturbance. This has a profound eﬂ'ect, inhibiting spasm in health but exciting it when the child is ailing or thwarted. In one of the present cases severe intractable vomiting began after the death of the child’s mother. Faulkner at all. (1941) are convinced by their radiological experience that emotional stimulus has a marked inﬂuence on oesophageal function. Ashby (1920) and Lust (1923~24) mention that (esophageal spasm is frequently induced in susceptible infants on changing the diet, and particularly on introducing solids which they resent. A slight anatomical defect such as simple localised stenosis or dilatation probably acts as a locus resistentice minoris where spasm tends to originate in susceptible subjects. A minute scar left after swallowing corrosive in a case of Lust’s probably had the same effect.
That spasm of the oesophagus may date from birth is proved by the reports of Langmead (1919-20), Segar and Stoefﬂer (1930) and Negus (1936). Sudhues (1932) is of the opinion that 70 per cent. of these cases originate within the first year, and half of them within the ﬁrst ten days of life. This author expresses the opinion that some infantile cases of cardiospasm may be due to inhibition of vagal inﬂuence owing to injury of the vagi at birth. Examination by the usual methods, however, generally reveals no organic cause for the oesophageal spasm. It is very improbable, according to Hurst and Rake (1929-30), that this temporary disability could ever produce gross dilatation like that seen in achalasia. I-Iere persistent closure of the sphincter occurs owing to failure of relaxation resulting from nervous imbalance, the essential cause of which Hurst regards as vagal inhibition from ﬁbrous involvement and progressive destruction of Auerbach’s nerve plexus in the wall of the oesophagus. Other workers (Cameron, 1927 ; Rake, 1927; Etzel, 1937) also found ﬁbrosis of the nerve elements of Auerbach’s plexus in such cases.
Two members of the group with dilatation of the oesophagus showed an acute ulcer at the lower end and gave a history of repeated severe haematemesis before death. In another patient slight ante- mortem haematemesis had occurred though no ulcer was found at autopsy. Burghard (1926) also described ulceration of the oesophagus with haematemesis in a four-months-old infant with cardiospasm and spindle-shaped dilatation. He comments on the extreme rarity of oesophageal ulcer in infancy.
Abel states that congenital diverticula with a complete muscular investment, which occur generally at the pharyngo-oesophageal junction, are extremely rare in man though found in the hog and other animals. The single example in the present series had a thick-walled pouch of the anterior wall of the oesophagus, the lumen of which was patent throughout and did not communicate with the trachea. Yet the symptoms present at birth were indistinguishable from those of ordinary atresia with tracheal ﬁstula. The child died from broncho-pneumonia. In cases of this type simple drainage of the pouch might save life. This type of case diﬂers from the commoner pharyngeal pouch at the lower border of the inferior constrictor.
Atresia with tracheal ﬁstula is the most frequent congenital malformation of the (esophagus. In the present autopsy series 23 of 38 cases were of this nature. The condition in the past has always proved fatal within a few days of birth, but surgical repair is nowadays coming to be regarded as feasible in the absence of bronchopneumonia —-the most common complication—and of severe associated congenital defects such as atresia ani or duodeni.
Since certain rare oesophageal malformations—e.g. simple atresia, membranous or valvular stenosis and diverticula—which require relatively simple surgical treatment bear a close clinical resemblance to the ordinary ﬁstulous type with atresia, the use of all available methods, including X—ray and endoscopic examination, should be employed for exact diagnosis. Barium is contra-indicated.
In simple idiopathic stenosis and dilatation of the oesophagus (12 cases in the present series), the anatomical lesion found at autopsy is often comparatively slight in view of the severe persistent dysphagia with vomiting and progressive wasting Which, during life, had suggested a grave cesophageal malformation. In such cases a spastic element is frequent, possibly originating in a defective area of the gullet wall through stimulation of the sympathetic nerves under the inﬂuence of emotional disturbance.
It is a pleasure to acknowledge my indebtedness to Professors C. H. Browning, H. A. Harris and G. Grey Turner for their advice and criticism and to the clinicians at the Royal Hospital for Sick Children, Glasgow, for access to the case records.
ABEL, A. L. 1929. (Esophageal obstruction, London and New York, pp. 50-57.
ASHBY, H. T. 1920. Brit. J. Child. De?s., xvii, 195.
BEATTY, C. C. 1928. Ib<aId., xxv, 237.
BURGHARD, E. 1926. Arch. Kindcrheilh, lxxix, 292.
CAMERON, J. A. M. 1927. Arch. Dis. 0hz'ld., ii, 358.
CARTER, B. N. 1941. Surg. Gynec. 0bstet., lxxiii, 485.
D’SILVA, J. L. 1944. Brit. Med. J., i, 750.
ETZEL, E. . . . . 1937. Guy’s Hosp. Rep, lxxxvii, 158.
FAULKNER, W. B., JR., RoDENBAUGH, F. H., AND O’NEILL, J. R. 1941. Radiology, xxxvii, 443.
FINDLAY, L., AND KELLY, A. BROWN 1930-31. Proc. Roy. Soc. Med., xxiv, 1561.
FISCHER, W. 1926. In Henke and Lubarsch’s Handbuch der speziellen pathologischen Anatomic und Histologie, vol. iv, pt. i, Berlin, .p. 86.
GIBSON, T. 1697. The anatomy of humane bodies epitomized, 5th ed., London, p. 239.
GRUENWALD, P. 1940. Anat. Rec., lxxviii, 293.
- 1941. Illinois Med. J ., Ixxix, 55.
HAIGHT, 0., AND TOWSLEY, H. A. 1943. Surg. Gynec. 0bstet., lxxvi, 672. 1922-23. J.-Anat., lvii, 76.
HARRIS, H. A. 1928-29. Proc. Roy. Soc. Med., xxii, 1341.
HURST A. F., AND RAKE, G. W. 1929-30. Quart. J. Med., Xxiii, 491.
KELLY, A. BROWN 1931. J . Laryngol. and Otol., xlvi, 521. 1936. Ibid., Ii, 78.
LADD, W. E. 1944. New England J . M ed., cexxx, 625.
LANGMEAD, F. 1919-20. Proc. Roy. Soc. Med., xiii, Sect. Dis. Child., 43.
LANMAN, T. H. 1940. Arch. Surg., xli, 1060.
LEVEN, N. L. 1936-37. J . Thoracic Surg., vi, 30.
- 1940-41. Ib’id., X, 648.
LUST, F. 1923-24. Mschr. K2Inderhe?Ilk., xxvii, 9.
MACKENZIE, MORELL 1884. Diseases of the throat and nose, London, vol. ii, pp. 156 and 219.
MARCUS, J . H. 1923. New York Med. J., cxviii, 374.
MEUSBURGER, K. 1910. Arch. path. Anat., cxcix, 401.
NEGUS, V. E. 1936. J . Laryngol. and Otol., li, 100.
PEARSON, K. 1914. On the handicapping of the ﬁrst-born, London, pp. 2 and 23.
PLASS, E. D. 1919. Johns Hopkins Hosp. Rep, xviii, 259.
RAKE G.W. 1927. Guy’s Hosp. Rep., lxxvii, 141.
RICHTER, H. M. 1913. Surg. G3/nec. 0bstet., xvii, 397.
SCHMIDGALL, G. 1915. Arch. Klnderheilhx, Ixiv, 74.
SEGAR, L. H., AND STOEFFLER, W. 1930. Amer. J . Dis. 0h'tld., xxxix, 354.
STILL, G. F. 1927. Lancet, ii, 795 and 853.
SUDHUES, M. 1932. Arch. Kinderheilla, xcvi, 65.
TURNER, G. GREY 1943-45. Newcastle Med. J ., xxii, 32.
|Historic Disclaimer - information about historic embryology pages|
|Embryology History | Historic Embryology Papers)|
Cite this page: Hill, M.A. (2021, April 15) Embryology Paper - Congenital malformations of the oesophagus. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Paper_-_Congenital_malformations_of_the_oesophagus
- © Dr Mark Hill 2021, UNSW Embryology ISBN: 978 0 7334 2609 4 - UNSW CRICOS Provider Code No. 00098G