International Journal of Pediatric Otorhinolaryngology, @ Elsevier/North-Holland Biomedical Press
CONGENITAL
LARYNGEAL
1 (1979)
71-78
71
DEFECTS
P. van den BROEK and W.F.B. BRINKMAN Department of Oto-rhinolaryngology,
University of Nijmegen, Nijmegen (The Netherlands)
(Originally presented at the First World Congress of Pediatric Otorhinolaryngology, in Sirmione, Italy on April 26-30th, 1977)
SUMMARY
Embryologic disorders of the larynx are rare. The main symptoms are stridor and hoarseness, symptoms which in the newborn always necessitate further investigation. Both the laryngotracheo-esophageal cleft and the congenital laryngeal web are discussed in relation to the embryologic development of the larynx and to diagnosis and therapy. The use of the operating microscope is stressed.
INTRODUCTION
Congenital anomalies in the larynx occurrence vary from 1 in 10,000 to can be incompatible with life while only exhibit mild changes in crying cation of these anomalies, especially conditions involved and knowledge conditions of great interest for both EMBRYOLOGIC
are rare, and rough estimations of their 1 in 50,000 births. The major anomalies the minor ones may pass undetected or or breathing. The possible serious implifor the airways, make awareness of the of the means to diagnose and treat these otolaryngologists and pediatricians.
CONSIDERATIONS
Knowledge of the embryonic development of the larynx is necessary to understand the congenital defects which can occur within this structure. Because the most vital parts of laryngeal development take place in early embryonic life, little material is available and only few elaborate studies have been done. This also means that parts of knowledge on the exact mechanism involved in human laryngeal development are still missing. Early descriptions of the stages in human laryngeal development date back to Kallius in 1897 and Soulie and Bardier in France in 1907, who studied laryngeal specimens. More recent and exhaustive studies are from O’Rahilly
72
[6], Tucker [12] and Wind [13]. Both Tucker and O’Rahilly adopted the Carnegie system of embryonic staging, which uses exact morphological criteria, rather than more variable factors such as length or presumed age. The 23 stages of the Carnegie system cover the first 8 weeks of human development. At the end of that time the embryo is about 30 mm in length and enters the actual fetal period. In Table I a schematic representation of the stages of the embryonic development is given. The respiratory primordium derives from the foregut at about 20 days of embryonic life as a ventromedial diverticulum called the median pharyngeal groove. Later the actual laryngotracheal sulcus or ridge forms and the trachea-esophagal septum starts caudally and moves in cranial direction. It should be completed by stage 12, thus separating the laryngotracheal canal and esophagus. At the caudal end of the tracheal canal the lungbuds grow in peripheral direction. The opening of the laryngotracheal canal at this stage is seen as a vertical slit in the anterior wall of the foregut. Three swellings appear at this stage, first the hypopharyngeal eminence (epiglottic eminence) at the cranial end, and on each side condensations of mesenchymal tissue which are to form the arytenoid cartilages. At stages 14 and 15 the laryngeal inlet is altered by the growth of these three masses from a sagittal slit into a more T-shaped opening, with the hypopharyngeal eminence at the top and the arytenoid swellings inferior on each side. Condensation of mesenchymal tissue to form the arytenoid and cricoid cartilages are clearly visible, as are also the first signs of lateral condensation of the thyroid lamina (stage 18). Fig. 1 is a schematic drawing of the most important structures seen at stage 19 in a sagittal section. The first signs of the laryngeal ventricle appear at stage 21 (52 days). At stage 23
TABLE I EMBRYONIC Stage
9
10-11 12-13 14 15-16 17 18 19 20 21 23
STAGING (CARNEGIE
SYSTEM)
Days
Length (mm)
Structures
21 22-26 26-28 32 33-37 41 44 48 51 52 57
1.4 3 5 6 8 11 15 18 21 23 30
median pharyngeal groove laryngotracheal sulcus trachea-esophageal septum hypopharyngeal eminence, arytenoid swellings laryngotracheal canal epiglottis visible, cricoid condensation thyroid lamina hyoid ventricle formation cartilage and muscle identifiable
73
fl6
STA6t 19 Ill,r luck11
Fig. 1. Median section
(8 weeks) marks the present at thelial and CLINICAL
through
larynx
at stage 19 (after Tucker).
most of the laryngeal structures can be recognized as such and this end of the embryonic period proper. Although the rough form is the end of the embryonic period, further differentiation of epimesenchymal tissues is still to take place. IMPLICATIONS
The two most critical developments during this period are, first, the formation of the trachea-esophageal septum at stage 12. Failure in the formation of this septum or arrest of its rostral advancement will leave an open communication between the larynx-trachea complex and the esophagus and is one of the most serious congenital anomalies. The second critical point is the communication to be formed between the laryngeal inlet below the hypopharyngeal eminence (vestibulotracheal canal) and the laryngotracheal canal which are still separated by the epithelial lamina. This epithelial lamina, which is to form the actual vocal cords, will form the glottic opening in a postero-anterior direction. Failure of this to take place will lead to complete atresia of the laryngeal lumen, while a too early arrest in this process will lead to various degrees of web formation (laryngeal diaphragm).
Lmyngotracheo-esophageal
cleft
The laryngotracheo-esophageal cleft caused by an arrest of the formation of the trachea-esophageal septum is a serious anomaly which, depending on its extent, can be life threatening. The first description of this clinical entity dates back to Richter in 1792 who mentioned this anomaly in his thesis “De Infanticide0 in Artis Obstreticae” (quoted in ref. 9). An infant with swallowing difficulties was found to have a common cavity between gullet and larynx. The next descriptions are by Bowman and Jackson in 1934 [l] and in 1949 by Finlay [ 31. Since then a growing number of cases have been reported in the world literature [ 2,9,10]. The diagnosis can be difficult, even if one is familiar with the condition. The most prominent symptoms are aspiration and usually stridor which is present from birth and increases during feeding. Besides the respiratory problems hoarseness during crying may be an important symptom. When the condition is suspected the two most important diagnostic procedure are: (1) X-ray cinematography, by which the swallowing act can be followed and the location of spill of contrast into the trachea can be traced. Although the overflow of contrast is often easily seen, the exact localization where this occurs can be difficult; and (2) direct laryngoscopy under the microscope. The larynx of a normal infant already shows fairly deep indentation between the arytenoids and the correct diagnosis will only be made if a hooked instrument is used to separate the posterior laryngeal wall. Even being aware of the condition it can be difficult to make a correct diagnosis. The first child we saw with this condition was born in 1970. Pregnancy and delivery were normal. Already soon after birth the child was admitted into hospital because of stridor and problems with feeding. On X-rays there was some spilling of contrast into the airways but a cleft or fistula was not observed. A laryngoscopy was performed during which no anomalies were found. After this the patient has been admitted into hospital several times because of pneumonias. When the child was 21 months of age it developed serious stridor and during an attack tracheotomy had to be performed. Only then was a thorough examination possible; during laryngoscopy a deep slit of 4 cm length was found between the arytenoids. After the diagnosis of laryngotracheo-esophageal cleft had been made, surgical repair was anticipated. A lateral pharyngotomy was performed and the cleft was repaired in two layers with interrupted silk. The postoperative course at first was uneventful. About 2 weeks after operation it appeared that the cleft was not entirely closed and a new fistula had developed in the sutured area. A re-suturing was done through a lateral pharyngotomy on the other side. The child has been well since.
75
A second child had a similar history at birth but was diagnosed as having a cleft much sooner. This child was also repaired through a lateral pharyngotomy. The cleft was less deep and the postoperative course was uneventful. As stated before, the condition is relatively rare and diagnosis is only made if one is familiar with the condition. Pettersson from Giiteborg was the first to describe a successful surgical repair of a laryngeal cleft in 1955 [8]. He classified the clefts into three types (Fig. 2) : Type I, the laryngo-esophageal cleft, Type II, partial laryngotracheo-esophageal cleft, Type III, total laryngotracheo-esophageal cleft. Type III is the most serious and probably always incompatible with life. Both other forms can be corrected surgically. The number of reported successfully corrected deformities of this type is rising fast. In our cases we favoured a lateral pharyngotomy as the most desirable approach, also described by Shapiro [ll]. A good view over the lesion is attained by this approach while the risk of damaging the recurrent laryngeal nerves is minimal. A tracheotomy and a gastrostomy are favoured by most authors as auxiliary measures. Jahrsdoerfer [ 51 describes the anterior approach (1 case). The result was called partially successful because the tracheotomy tube could not be plugged. In our opinion this approach should be avoided in young children. Pettersson [9] opens neither the trachea nor esophagus, but divides the esophagus from trachea and opens the cleft between these two structures.
Fig. 2. Types of congenital laryngeal clefts (Pettersson).
76
Fig. 3. Laryngeal diaphragm.
The chance of damaging the recurrent laryngeal nerve is considerable. The operating microscope has proved to be a great aid both in the diagnosis and also for the surgical treatment of these congenital laryngeal clefts.
Laryngeal webs Another condition congenital in origin requires the use of the operating microscope. It is the congenital web or diaphragm. It develops by a failure of the epithelial lamina to open in posterioranterior direction. As a congenital anomaly it is much more rare than webs of traumatic origin (Fig. 3) *. The treatment of webs in young children should be as conservative as possible unless there are complaints of stridor or of serious voice problems. Especially in small children external operations should be avoided if possible because the chance of success is small. Endoscopic treatment under the operating microscope seems to be the treatment of choice. The endoscopic treatment is not new (reviewed by Pennington [7]); in the literature it is generally referred to as by Jackson, who published in 1931 his ideas about treatment.
* Although these webs are usually located at the glottic level, webs in the supraglottic region (ventricular folds) and the subglottic region have also been described.
77
HASLINGER 1823 Fig. 4. Haslinger’s method for correcting a laryngeal web.
He cut the web on one side and performed regular daily laryngeal dilatations. Shortly after Jackson, Iglauer reported his experiences with another technique (see ref. 7), which was derived from the treatment of syhdactylism. This method embodies the principle of producing an epithelial tract as the apex of the web, followed by excision of the web at a later stage. Iglauer used a spring lock from a watch fob. Later Lynch and Le Jeune (1960) (see ref. 7) used the same principle but used a small polyethylene tube. Before these, however, Haslinger of Vienna had already described a method in 1924 (see ref. 7). The principle of this treatment is the translaryngeal introduction of a small keel-shaped prosthesis which is kept in place with wires which are brought exteriorly through the skin (Fig. 4). Jackson’s technique slightly modified was used by us in one case of congenital web with a fair result. In two traumatic cases Haslinger’s technique has been used. The results have been so encouraging as to favour Haslinger’s method. Again in our opinion the treatment of webs in very young children should be approached very conservatively just as other conditions causing congenital stridor, as for instance cricoid stenosis. A careful assessment with the operating microscope is imperative. REFERENCES 1 Bowman, J.E. and Jackson, C.L., Chronic stridor in infancy, J. Pediat., 15 (1934) 476. 2 Cohen, S.R., Cleft larynx. A report of seven cases, Ann. Otol. (St. Louis), 84 (1975) 747-756.
78 3 Finlay, H.V.L., Familial congenital stridor in infancy, Arch. Dis. Childh., 24 (1949) 219. 4 Holinger, P. and Brown, W.T., Congenital webs, cysts, laryngo-celes and other anomalies of the larynx, Ann. Otol. (St. Louis), 76 (1967) 744-752. 5 Jahrsdoerfer, R.A., Kirchner, J.A. and Thaler, S.U., Cleft larynx, Arch. Otolaryng., 86 (1967) 108-113. 6 O’Rahilly, R., Observations on the embryology of the human larynx, Ann. Otol. (St. Louis), 81 (1972) 520-523. 7 Pennington, C.L., The treatment of anterior glottic webs: a re-evaluation of Haslinger’s technique, Laryngoscope (St. Louis), 78 (1968) 728. 8 Pettersson, G., Inhibited separation of larynx and the upper part of the trachea from the esophagus in the newborn: report of a case successfully operated on, Acta chir. stand., 110 (1955) 250. 9 Pettersson, G., Laryngo-trachea-oesophageal cleft, Z. Kinderchir., 7 (1969) 43-48. 10 Pracy, R. and Stell, P.M., Laryngeal cleft: diagnosis and management, J. Laryng., 88 (1974) 483486. 11 Shapiro, M.J., Falla, A. and Irvington, N.J., Congenital posterior cleft larynx, report of a case, Ann. Otol. (St. Louis), 75 (1966) 961. 12 Tucker, J. and Tucker, G.F., Some aspects of fetal laryngeal development, Ann. Otol. (St. Louis), 84 (1975) 49-55. 13 Wind, J.J., On the Phylogeny and the Ontogeny of the Human Larynx, Thesis, Amsterdam, 1969.
CONGENITAL
LARYNGEAL
1 (1979)
71-78
71
DEFECTS
P. van den BROEK and W.F.B. BRINKMAN Department of Oto-rhinolaryngology,
University of Nijmegen, Nijmegen (The Netherlands)
(Originally presented at the First World Congress of Pediatric Otorhinolaryngology, in Sirmione, Italy on April 26-30th, 1977)
SUMMARY
Embryologic disorders of the larynx are rare. The main symptoms are stridor and hoarseness, symptoms which in the newborn always necessitate further investigation. Both the laryngotracheo-esophageal cleft and the congenital laryngeal web are discussed in relation to the embryologic development of the larynx and to diagnosis and therapy. The use of the operating microscope is stressed.
INTRODUCTION
Congenital anomalies in the larynx occurrence vary from 1 in 10,000 to can be incompatible with life while only exhibit mild changes in crying cation of these anomalies, especially conditions involved and knowledge conditions of great interest for both EMBRYOLOGIC
are rare, and rough estimations of their 1 in 50,000 births. The major anomalies the minor ones may pass undetected or or breathing. The possible serious implifor the airways, make awareness of the of the means to diagnose and treat these otolaryngologists and pediatricians.
CONSIDERATIONS
Knowledge of the embryonic development of the larynx is necessary to understand the congenital defects which can occur within this structure. Because the most vital parts of laryngeal development take place in early embryonic life, little material is available and only few elaborate studies have been done. This also means that parts of knowledge on the exact mechanism involved in human laryngeal development are still missing. Early descriptions of the stages in human laryngeal development date back to Kallius in 1897 and Soulie and Bardier in France in 1907, who studied laryngeal specimens. More recent and exhaustive studies are from O’Rahilly
72
[6], Tucker [12] and Wind [13]. Both Tucker and O’Rahilly adopted the Carnegie system of embryonic staging, which uses exact morphological criteria, rather than more variable factors such as length or presumed age. The 23 stages of the Carnegie system cover the first 8 weeks of human development. At the end of that time the embryo is about 30 mm in length and enters the actual fetal period. In Table I a schematic representation of the stages of the embryonic development is given. The respiratory primordium derives from the foregut at about 20 days of embryonic life as a ventromedial diverticulum called the median pharyngeal groove. Later the actual laryngotracheal sulcus or ridge forms and the trachea-esophagal septum starts caudally and moves in cranial direction. It should be completed by stage 12, thus separating the laryngotracheal canal and esophagus. At the caudal end of the tracheal canal the lungbuds grow in peripheral direction. The opening of the laryngotracheal canal at this stage is seen as a vertical slit in the anterior wall of the foregut. Three swellings appear at this stage, first the hypopharyngeal eminence (epiglottic eminence) at the cranial end, and on each side condensations of mesenchymal tissue which are to form the arytenoid cartilages. At stages 14 and 15 the laryngeal inlet is altered by the growth of these three masses from a sagittal slit into a more T-shaped opening, with the hypopharyngeal eminence at the top and the arytenoid swellings inferior on each side. Condensation of mesenchymal tissue to form the arytenoid and cricoid cartilages are clearly visible, as are also the first signs of lateral condensation of the thyroid lamina (stage 18). Fig. 1 is a schematic drawing of the most important structures seen at stage 19 in a sagittal section. The first signs of the laryngeal ventricle appear at stage 21 (52 days). At stage 23
TABLE I EMBRYONIC Stage
9
10-11 12-13 14 15-16 17 18 19 20 21 23
STAGING (CARNEGIE
SYSTEM)
Days
Length (mm)
Structures
21 22-26 26-28 32 33-37 41 44 48 51 52 57
1.4 3 5 6 8 11 15 18 21 23 30
median pharyngeal groove laryngotracheal sulcus trachea-esophageal septum hypopharyngeal eminence, arytenoid swellings laryngotracheal canal epiglottis visible, cricoid condensation thyroid lamina hyoid ventricle formation cartilage and muscle identifiable
73
fl6
STA6t 19 Ill,r luck11
Fig. 1. Median section
(8 weeks) marks the present at thelial and CLINICAL
through
larynx
at stage 19 (after Tucker).
most of the laryngeal structures can be recognized as such and this end of the embryonic period proper. Although the rough form is the end of the embryonic period, further differentiation of epimesenchymal tissues is still to take place. IMPLICATIONS
The two most critical developments during this period are, first, the formation of the trachea-esophageal septum at stage 12. Failure in the formation of this septum or arrest of its rostral advancement will leave an open communication between the larynx-trachea complex and the esophagus and is one of the most serious congenital anomalies. The second critical point is the communication to be formed between the laryngeal inlet below the hypopharyngeal eminence (vestibulotracheal canal) and the laryngotracheal canal which are still separated by the epithelial lamina. This epithelial lamina, which is to form the actual vocal cords, will form the glottic opening in a postero-anterior direction. Failure of this to take place will lead to complete atresia of the laryngeal lumen, while a too early arrest in this process will lead to various degrees of web formation (laryngeal diaphragm).
Lmyngotracheo-esophageal
cleft
The laryngotracheo-esophageal cleft caused by an arrest of the formation of the trachea-esophageal septum is a serious anomaly which, depending on its extent, can be life threatening. The first description of this clinical entity dates back to Richter in 1792 who mentioned this anomaly in his thesis “De Infanticide0 in Artis Obstreticae” (quoted in ref. 9). An infant with swallowing difficulties was found to have a common cavity between gullet and larynx. The next descriptions are by Bowman and Jackson in 1934 [l] and in 1949 by Finlay [ 31. Since then a growing number of cases have been reported in the world literature [ 2,9,10]. The diagnosis can be difficult, even if one is familiar with the condition. The most prominent symptoms are aspiration and usually stridor which is present from birth and increases during feeding. Besides the respiratory problems hoarseness during crying may be an important symptom. When the condition is suspected the two most important diagnostic procedure are: (1) X-ray cinematography, by which the swallowing act can be followed and the location of spill of contrast into the trachea can be traced. Although the overflow of contrast is often easily seen, the exact localization where this occurs can be difficult; and (2) direct laryngoscopy under the microscope. The larynx of a normal infant already shows fairly deep indentation between the arytenoids and the correct diagnosis will only be made if a hooked instrument is used to separate the posterior laryngeal wall. Even being aware of the condition it can be difficult to make a correct diagnosis. The first child we saw with this condition was born in 1970. Pregnancy and delivery were normal. Already soon after birth the child was admitted into hospital because of stridor and problems with feeding. On X-rays there was some spilling of contrast into the airways but a cleft or fistula was not observed. A laryngoscopy was performed during which no anomalies were found. After this the patient has been admitted into hospital several times because of pneumonias. When the child was 21 months of age it developed serious stridor and during an attack tracheotomy had to be performed. Only then was a thorough examination possible; during laryngoscopy a deep slit of 4 cm length was found between the arytenoids. After the diagnosis of laryngotracheo-esophageal cleft had been made, surgical repair was anticipated. A lateral pharyngotomy was performed and the cleft was repaired in two layers with interrupted silk. The postoperative course at first was uneventful. About 2 weeks after operation it appeared that the cleft was not entirely closed and a new fistula had developed in the sutured area. A re-suturing was done through a lateral pharyngotomy on the other side. The child has been well since.
75
A second child had a similar history at birth but was diagnosed as having a cleft much sooner. This child was also repaired through a lateral pharyngotomy. The cleft was less deep and the postoperative course was uneventful. As stated before, the condition is relatively rare and diagnosis is only made if one is familiar with the condition. Pettersson from Giiteborg was the first to describe a successful surgical repair of a laryngeal cleft in 1955 [8]. He classified the clefts into three types (Fig. 2) : Type I, the laryngo-esophageal cleft, Type II, partial laryngotracheo-esophageal cleft, Type III, total laryngotracheo-esophageal cleft. Type III is the most serious and probably always incompatible with life. Both other forms can be corrected surgically. The number of reported successfully corrected deformities of this type is rising fast. In our cases we favoured a lateral pharyngotomy as the most desirable approach, also described by Shapiro [ll]. A good view over the lesion is attained by this approach while the risk of damaging the recurrent laryngeal nerves is minimal. A tracheotomy and a gastrostomy are favoured by most authors as auxiliary measures. Jahrsdoerfer [ 51 describes the anterior approach (1 case). The result was called partially successful because the tracheotomy tube could not be plugged. In our opinion this approach should be avoided in young children. Pettersson [9] opens neither the trachea nor esophagus, but divides the esophagus from trachea and opens the cleft between these two structures.
Fig. 2. Types of congenital laryngeal clefts (Pettersson).
76
Fig. 3. Laryngeal diaphragm.
The chance of damaging the recurrent laryngeal nerve is considerable. The operating microscope has proved to be a great aid both in the diagnosis and also for the surgical treatment of these congenital laryngeal clefts.
Laryngeal webs Another condition congenital in origin requires the use of the operating microscope. It is the congenital web or diaphragm. It develops by a failure of the epithelial lamina to open in posterioranterior direction. As a congenital anomaly it is much more rare than webs of traumatic origin (Fig. 3) *. The treatment of webs in young children should be as conservative as possible unless there are complaints of stridor or of serious voice problems. Especially in small children external operations should be avoided if possible because the chance of success is small. Endoscopic treatment under the operating microscope seems to be the treatment of choice. The endoscopic treatment is not new (reviewed by Pennington [7]); in the literature it is generally referred to as by Jackson, who published in 1931 his ideas about treatment.
* Although these webs are usually located at the glottic level, webs in the supraglottic region (ventricular folds) and the subglottic region have also been described.
77
HASLINGER 1823 Fig. 4. Haslinger’s method for correcting a laryngeal web.
He cut the web on one side and performed regular daily laryngeal dilatations. Shortly after Jackson, Iglauer reported his experiences with another technique (see ref. 7), which was derived from the treatment of syhdactylism. This method embodies the principle of producing an epithelial tract as the apex of the web, followed by excision of the web at a later stage. Iglauer used a spring lock from a watch fob. Later Lynch and Le Jeune (1960) (see ref. 7) used the same principle but used a small polyethylene tube. Before these, however, Haslinger of Vienna had already described a method in 1924 (see ref. 7). The principle of this treatment is the translaryngeal introduction of a small keel-shaped prosthesis which is kept in place with wires which are brought exteriorly through the skin (Fig. 4). Jackson’s technique slightly modified was used by us in one case of congenital web with a fair result. In two traumatic cases Haslinger’s technique has been used. The results have been so encouraging as to favour Haslinger’s method. Again in our opinion the treatment of webs in very young children should be approached very conservatively just as other conditions causing congenital stridor, as for instance cricoid stenosis. A careful assessment with the operating microscope is imperative. REFERENCES 1 Bowman, J.E. and Jackson, C.L., Chronic stridor in infancy, J. Pediat., 15 (1934) 476. 2 Cohen, S.R., Cleft larynx. A report of seven cases, Ann. Otol. (St. Louis), 84 (1975) 747-756.
78 3 Finlay, H.V.L., Familial congenital stridor in infancy, Arch. Dis. Childh., 24 (1949) 219. 4 Holinger, P. and Brown, W.T., Congenital webs, cysts, laryngo-celes and other anomalies of the larynx, Ann. Otol. (St. Louis), 76 (1967) 744-752. 5 Jahrsdoerfer, R.A., Kirchner, J.A. and Thaler, S.U., Cleft larynx, Arch. Otolaryng., 86 (1967) 108-113. 6 O’Rahilly, R., Observations on the embryology of the human larynx, Ann. Otol. (St. Louis), 81 (1972) 520-523. 7 Pennington, C.L., The treatment of anterior glottic webs: a re-evaluation of Haslinger’s technique, Laryngoscope (St. Louis), 78 (1968) 728. 8 Pettersson, G., Inhibited separation of larynx and the upper part of the trachea from the esophagus in the newborn: report of a case successfully operated on, Acta chir. stand., 110 (1955) 250. 9 Pettersson, G., Laryngo-trachea-oesophageal cleft, Z. Kinderchir., 7 (1969) 43-48. 10 Pracy, R. and Stell, P.M., Laryngeal cleft: diagnosis and management, J. Laryng., 88 (1974) 483486. 11 Shapiro, M.J., Falla, A. and Irvington, N.J., Congenital posterior cleft larynx, report of a case, Ann. Otol. (St. Louis), 75 (1966) 961. 12 Tucker, J. and Tucker, G.F., Some aspects of fetal laryngeal development, Ann. Otol. (St. Louis), 84 (1975) 49-55. 13 Wind, J.J., On the Phylogeny and the Ontogeny of the Human Larynx, Thesis, Amsterdam, 1969.
