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CONGENITAL CHONDROMALACIA OF THE TRACHEA
CONGENITAL CHONDROMALACIA OF THE TRACHEA William L. Cox, Jr., M.D., and Robert R. Shaw, M.D., Dallas, Texas
R
difficulty in the newborn infant is sufficient reason for one to suspect anomaly of the tracheobronchial tree. I t is generally appreciated that some infants have intermittent, loud breathing, but, when the respirations are obstructive and the condition persists, the judgment and experience of the attending physician is taxed to establish the underlying cause. Obstruction of the upper respiratory passage by nondiphtheritic laryngitis, diphtheritic laryngitis, and acute infective laryngotracheobronchitis is well rec ognized. In the older literature, the thymus gland has been cited as a factor causing tracheal obstruction. Recently, emphasis has shifted from the thymus gland to the vascular malformations which may also result in obstruction of the trachea, esophagus, and bronchi. These extraluminal structures that cause the mechanical obstruction syndrome are well known. Evans 3 states that the degree of the mechanical compression syndrome depends upon the pressure exerted by the external mass and the resistance offered by the tracheobronchial tree. It would seem that, for narrowing with obstruction to occur, there must be failure of the supporting architecture which may indicate abnormalities of the supporting cartilages. Congenital chondromalacia of the trachea is a rarity which is poorly rec ognized. Many of the standard textbooks fail to mention this malformation and, when it is mentioned, only a few comments! are offered. The rarity of this con genital anomaly and the opportunity for long-term observation of 2 cases, which we believe represent chondromalacia of the trachea, has prompted this communi cation. ESPIRATORY
CASE REPORTS CASE 1.—A 21-year-old gravida I I I para I I Negro was admitted to the obstetrical service of Parkland Memorial Hospital, where she was delivered, without complications, of a 4 pound 6 ounce premature infant. The past history revealed marked dyspnea on exertion, repeated episodes of hemoptysis, and frequent upper respiratory infections as long as the patient could remember. She also stated that she could not engage in active play, such as running, swimming, and cycling, because of shortness of breath. An interview with her mother confirmed the patient's past From the Thoracic Surgery Department, Southwestern Medical School, Dallas, Texas. Received for publication Jan. 13, 1965. 1033
1034
COX AND SHAW
J. Thoracic and Cardiovas. Surg.
Figr. 1.—Posteroanterior roent&enogram (A) and bronchograms (B and G) of the chest which show narrowing of the trachea.
Vol. 49. No. 6
CONGENITAL CHONDROMALACIA OF TRACHEA
1035
June, 1965 history; she stated that the patient had developed difficult respirations 3 weeks after birth. The history was negative for episodes of cyanosis and stridor. During adolescence, the patient had had several hospital admissions for pneumonia. There had always been absence of cough ing and sputum production. Physical Examination.—The patient was a slender female without respiratory distress. Vital signs were: blood pressure, 120/70 mm. H g ; pulse, 80; respirations 20; temperature, 98.6° F . ; weight, 105 pounds; height, 5 feet 2 inches. There was generalized wheezing through out the lung fields. Other significant findings consisted of right congenital ptosis and absence of the right pectoralis minor muscle. Skin tests were applied for blastomycosis, coccidioidomycosis, histoplasmosis, as well as purified protein derivative ( P P D ) . The intermediate P P B was the only positive skin test. Vitalometry studies produced the following results: forced ventilating capacity, 2.0 liters; forced ventilating capaeity, 0.5 second 0.7 liter; and forced ventilating capacity, 1.0 second 1.0 liter. Roentgenograms of the chest suggested that there was narrowing of the mid-portion of the trachea. A tracheogram revealed malformation of the trachea (Fig. 1 ) . Tracheoscopy showed that, in addition to the stenosis of the mid-trachea, there was stenosis at the level of the cricoid cartilage that would barely admit a 5 mm. bronchoseope. CASE 2.—A full-term, 6 pound 15 ounce, white male infant was born at St. Paul's Hospital, Dallas, Texas, in 1950. Respiratory difficulty was observed during the first day. This was characterized by stridor and retraction of the thoracic cage and periods of cyanosis. Because of persistence of signs of airway obstruction, on the third day the senior author, Eobert R. Shaw, was called in consultation. H e made a tentative diagnosis of "rose petal epiglottis." Since this was in the era when the thymus gland was frequently considered a cause of tracheal compression, roentgen therapy was given to the thymus. Because of persistence of signs of obstruction to breathing, this therapy was repeated 16 weeks later. Observations during the post-irradiation period did not demonstrate any resolution of the obstructive symptoms. I t is interesting to note that later this patient was also diagnosed as having bronchial asthma. This diagnosis resulted in sensitization studies, desensitization, and administration of
Fig. 2.—Posteroanterior roentgenogram (A) and bronchogram (B) of the chest which show narrowing of the trachea with a right tracheal bronchus.
COX AND SHAW
1036
J. Thoracic and Cardiovas. Surg.
antihistaminics without definite improvement in the patient's condition. The interval from 1950 to 1956 was repetitious, with symptoms of respiratory obstruction associated with pul monary infections. These attacks were successfully treated by the family physician. I n 1956 the most severe episode occurred, which required hospital admission. A bronchoscopy was performed and a bronchogram (Fig. 2) was obtained during the patient's convalescence. The x-ray findings readily explained the recurring respiratory infections and the obstructive symptoms. This patient, over an 11 year period, has had 10 hospital admissions. These admissions were necessary for recurring tracheal obstruction associated with respiratory infections. The last hospital admission was in 1961. The mother has stated that many attacks of respiratory distress have occurred since 1961, but the attacks are decreasing in severity. The year 1964 represented the first year without obstructive symptoms. This patient is now playing a musical instrument and his physical activity is not limited. DISCUSSION
There are some who doubt the existence of chondromalacia of the trachea, although chondromalacia is accepted as a primary entity when other structures are involved in the pediatric age group. The dreaded and often fatal complica tion of chondromalacia of the trachea following the removal of compressing masses1 is recognized and accepted as an acquired type. In some cases of con genital lobar emphysema, no abnormality of the cartilaginous rings of the bron chus has been found. However, Overstreet 9 has observed hypoplastic bronchial rings in lobar emphysema of infancy. In other cases, anomalous vessels have accounted for the bronchial obstruction. If chondromalacia can be established in the other structures, why should the cartilaginous rings of the trachea be spared ? In a series of cases of congenital tracheal stenosis reported by Wolman,10 many of the patients failed to have a posterior membrane and the tracheal rings were fused, creating a rigid, fixed tube. Other reported cases of congenital stenosis demonstrated bizarre patterns of the tracheal rings, increased and ab normal numbers of the tracheal rings, and deformity of the rings, such as in complete formation. All of these patients had some other type of defect to explain the stenosis. Gross4 refers to 15 cases of chondromalacia in his presidential address be fore The American Association for Thoracic Surgery. There was no mention of any follow-up observation. I t is interesting that at operation no extrinsic pathology was found to account for the obstructions. DIAGNOSIS
Since this congenital abnormality is diagnosed by roentgen techniques, it is difficult to obtain pathological proof. The diagnosis is made by exclusion, al though there are certain studies that can be obtained which lend supporting evidence. Sgalitzer 11 has shown that with differential intratracheal pressure and proper x-ray technique, the tracheal lumen will change over the area of chon dromalacia. The Mueller maneuver will decrease the lumen size and the Valsalva maneuver will increase the size of the lumen. Another method which has been advocated is cinetracheograms which will show tracheal flutter. I t would appear
Vol. 49, No. 6
CONGENITAL CHONDROMALACIA OF TEACHEA
1037
June, 1965
more desirable and perhaps less hazardous to obtain this information by using the Sgalitzer 11 technique rather than introducing a contrast medium which could produce obstruction.. In Case 1, both air and radiopaque techniques were used. The desired information is obtainable from the air contrast study alone; thus, the possible complication of obstruction and pneumonitis, due to the introduc tion of viscid contrast material, is eliminated. By proper use of the roentgen examination, deviation, displacement, and stenosis of the trachea can be ob served. Information concerning the posterior membrane and innervation of the trachea cannot be obtained without direct visualization. Bronchoscopy is indi cated to exclude laryngeal and intraluminal causes of respiratory distress. Direct observation would also reveal absence of the posterior membrane, foreign bodies, malformation of the tracheal rings, congenital external compression, and tracheal nutter with respirations. Not only is this procedure useful as a diagnostic tool but is also useful as a part of the treatment program. Secretions and plugs are removed, thus relieving obstruction and distal pneumonitis. Bronchoscopy is also necessary to determine accurately the length of involvement which is nec essary to outline the proper program of treatment if surgery is being considered. A short stenotic segment may be amenable to surgery whereas the generalized type might better be treated by medical therapy until better techniques are available for total tracheal replacement. ASSOCIATED ANOMALIES
Congenital anomalies are frequently associated with congenital tracheal stenosis and may involve any system. The following associated anomalies have been reported: congenital absence of the thumbs, 10 imperforate anus, 1 ventricular septal defect,8 truncus arteriosus, 5 atrial septal defect,7 peetus excavatum with absent innominate artery associated with a subclavian artery going posterior to the esophagus.2 In the 2 cases of this report there was absence of the right pectoralis minor muscle and ptosis of the right eyelid in the first patient and a bronchus arising from the distal trachea with an undescended right testicle in the second. CLINICAL COURSE
Tracheal chondromalacia is compatible with life. Holinger 6 reported 3 pa tients who were improved without specific treatment. During the 8 month period of observation, the obstructive symptoms gradually diminished. He concluded that the clinical improvement was due to growth and increase in rigidity of the soft cartilaginous rings. Evans 3 observed a variable rigidity of the tracheal cartilages in infants. He noted a transient stenosis of the cervical thoracic tra chea due to softer cartilages and he stated this would tend to disappear with hardening of the tracheal rings. The 2 reported cases herein certainly support the above observation. The early period of life of these patients was very stormy (as stated by both parents and patients). In retrospect, the parents agreed that the symptoms gradually
COX AND SHAW
1038
J. Thoracic and Cardiovas. Surg.
lessened as the patients advanced in age. The second patient isi now 14 years old and this is his first year to be asymptomatic. In a comparison of our cases with those reported in the literature, one must conclude that the degree of rigidity of the tracheal cartilages necessary to prevent symptoms cannot be pre dicted by age. Some have solidly formed rings of the trachea in the early months of life while others take years to acquire tracheal maturity. The lack of a surgical procedure for the correction of the generalized form of tracheal chondromalacia in an infant or child, with prospect that the recon structed trachea would grow, precludes a dramatic attainment of cure. When this diagnosis is made, the parents should be informed of the potential hazards and the many crises that must be met as the patient and the trachea mature. During these crises the most aggressive medical therapy and supervision must be maintained to protect the individual. The prevention and the treatment of respiratory infection is the single most important phase in the management. Recurrent respiratory infections will lead to scarring, fibrosis, contracture, and thickening of the posterior tracheal membrane, and result in a decrease in the diameter of the tracheal lumen. Other changes may develop in distal bronchi, secondary to recurrent tracheobronchial infections. These distal changes are present in the first of our patients, who has a chronic bronchitis and suffers from repeated hemoptysis. The many problems encountered with congenital chondromalacia of the trachea are not insolvable, and the prognosis can be good. These patients can lead active, useful lives with close observation and medical management. SUMMARY
1. Tracheal chondromalacia should be considered in the differential diag nosis of respiratory obstruction in the newborn. 2. The age of development of tracheal stability is variable and cannot he predicted accurately. 3. Segmental involvement may require surgical reconstruction of the tra chea, but the generalized type will require prolonged conservative therapy. 4. The prognosis is not hopeless, as exemplified by the 2 cases just reported. REFERENCES
1. Bonnier, M.: TJn oas de stenose congenitale de la tractive avec bronche du lobe superieur droite atresie et lobe superieur droite aplasique, imperforation de l'anus, Ann. med.cliir. Hop. Sainte-Justine Montreal 5: 13, 1947. 2. Cantrell, J . R., and Guild, H. G.: Congenital Stenosis of the Trachea, Am. J . Surg. 108: 297, 1964. 3. Evans, W. A., J r . : Congenital Obstructions of the Respiratory Tract. I. Tracheal Mal formations, Am. J . Eoentgenol. 62: 167, 1949. 4. Gross, R. E . : Presidential Address: Thoracic Surgery for Infants, J . THORACIC & CARDIO VAS. SURG. 48: 152,
1964.
5. Heikel, P . E . : Congenital Tracheal Stenosis Combined With Truncus Arteriosus Cordis: A Case Diagnosed I n Vita, Ann. Paediat. Fenn. 3 : 22, 1957. 6. Holinger, P . H., Johnston, K. C , and Basinger, C. E . : Benign Stenosis of the Trachea, Ann. Otol. Rhin. & Laryng. 59: 837, 1950. 7. Houston, I. B., and Mackie, D. G.: Congenital Tracheal Stenosis, Thorax 16: 94, 1961. 8. Moutandon, A.: Stenose congenitale de la traehee et malformations associees, Pract. otorhino-Laryng. 6: 179, 1944.
Vol. 49, No. 6 June, 1965
CONGENITAL CHONDROMALACIA OF TRACHEA
1039
9. Overstreet, R. M.: Emphysema of a Portion of the Lung in the Early Months of Life, Am. J. Dis. Child. 57: 861, 1939. 10. Wolman, I. J.: Congenital Stenosis of the Trachea, Am. J. Dis. Child. 61: 1263, 1941. 11. Sgalitzer, M.: Roentgenological Examination of the Power of Resistance of the Tracheal Wall, Am. J. Roentgenol. 56: 355, 1946.
R
difficulty in the newborn infant is sufficient reason for one to suspect anomaly of the tracheobronchial tree. I t is generally appreciated that some infants have intermittent, loud breathing, but, when the respirations are obstructive and the condition persists, the judgment and experience of the attending physician is taxed to establish the underlying cause. Obstruction of the upper respiratory passage by nondiphtheritic laryngitis, diphtheritic laryngitis, and acute infective laryngotracheobronchitis is well rec ognized. In the older literature, the thymus gland has been cited as a factor causing tracheal obstruction. Recently, emphasis has shifted from the thymus gland to the vascular malformations which may also result in obstruction of the trachea, esophagus, and bronchi. These extraluminal structures that cause the mechanical obstruction syndrome are well known. Evans 3 states that the degree of the mechanical compression syndrome depends upon the pressure exerted by the external mass and the resistance offered by the tracheobronchial tree. It would seem that, for narrowing with obstruction to occur, there must be failure of the supporting architecture which may indicate abnormalities of the supporting cartilages. Congenital chondromalacia of the trachea is a rarity which is poorly rec ognized. Many of the standard textbooks fail to mention this malformation and, when it is mentioned, only a few comments! are offered. The rarity of this con genital anomaly and the opportunity for long-term observation of 2 cases, which we believe represent chondromalacia of the trachea, has prompted this communi cation. ESPIRATORY
CASE REPORTS CASE 1.—A 21-year-old gravida I I I para I I Negro was admitted to the obstetrical service of Parkland Memorial Hospital, where she was delivered, without complications, of a 4 pound 6 ounce premature infant. The past history revealed marked dyspnea on exertion, repeated episodes of hemoptysis, and frequent upper respiratory infections as long as the patient could remember. She also stated that she could not engage in active play, such as running, swimming, and cycling, because of shortness of breath. An interview with her mother confirmed the patient's past From the Thoracic Surgery Department, Southwestern Medical School, Dallas, Texas. Received for publication Jan. 13, 1965. 1033
1034
COX AND SHAW
J. Thoracic and Cardiovas. Surg.
Figr. 1.—Posteroanterior roent&enogram (A) and bronchograms (B and G) of the chest which show narrowing of the trachea.
Vol. 49. No. 6
CONGENITAL CHONDROMALACIA OF TRACHEA
1035
June, 1965 history; she stated that the patient had developed difficult respirations 3 weeks after birth. The history was negative for episodes of cyanosis and stridor. During adolescence, the patient had had several hospital admissions for pneumonia. There had always been absence of cough ing and sputum production. Physical Examination.—The patient was a slender female without respiratory distress. Vital signs were: blood pressure, 120/70 mm. H g ; pulse, 80; respirations 20; temperature, 98.6° F . ; weight, 105 pounds; height, 5 feet 2 inches. There was generalized wheezing through out the lung fields. Other significant findings consisted of right congenital ptosis and absence of the right pectoralis minor muscle. Skin tests were applied for blastomycosis, coccidioidomycosis, histoplasmosis, as well as purified protein derivative ( P P D ) . The intermediate P P B was the only positive skin test. Vitalometry studies produced the following results: forced ventilating capacity, 2.0 liters; forced ventilating capaeity, 0.5 second 0.7 liter; and forced ventilating capacity, 1.0 second 1.0 liter. Roentgenograms of the chest suggested that there was narrowing of the mid-portion of the trachea. A tracheogram revealed malformation of the trachea (Fig. 1 ) . Tracheoscopy showed that, in addition to the stenosis of the mid-trachea, there was stenosis at the level of the cricoid cartilage that would barely admit a 5 mm. bronchoseope. CASE 2.—A full-term, 6 pound 15 ounce, white male infant was born at St. Paul's Hospital, Dallas, Texas, in 1950. Respiratory difficulty was observed during the first day. This was characterized by stridor and retraction of the thoracic cage and periods of cyanosis. Because of persistence of signs of airway obstruction, on the third day the senior author, Eobert R. Shaw, was called in consultation. H e made a tentative diagnosis of "rose petal epiglottis." Since this was in the era when the thymus gland was frequently considered a cause of tracheal compression, roentgen therapy was given to the thymus. Because of persistence of signs of obstruction to breathing, this therapy was repeated 16 weeks later. Observations during the post-irradiation period did not demonstrate any resolution of the obstructive symptoms. I t is interesting to note that later this patient was also diagnosed as having bronchial asthma. This diagnosis resulted in sensitization studies, desensitization, and administration of
Fig. 2.—Posteroanterior roentgenogram (A) and bronchogram (B) of the chest which show narrowing of the trachea with a right tracheal bronchus.
COX AND SHAW
1036
J. Thoracic and Cardiovas. Surg.
antihistaminics without definite improvement in the patient's condition. The interval from 1950 to 1956 was repetitious, with symptoms of respiratory obstruction associated with pul monary infections. These attacks were successfully treated by the family physician. I n 1956 the most severe episode occurred, which required hospital admission. A bronchoscopy was performed and a bronchogram (Fig. 2) was obtained during the patient's convalescence. The x-ray findings readily explained the recurring respiratory infections and the obstructive symptoms. This patient, over an 11 year period, has had 10 hospital admissions. These admissions were necessary for recurring tracheal obstruction associated with respiratory infections. The last hospital admission was in 1961. The mother has stated that many attacks of respiratory distress have occurred since 1961, but the attacks are decreasing in severity. The year 1964 represented the first year without obstructive symptoms. This patient is now playing a musical instrument and his physical activity is not limited. DISCUSSION
There are some who doubt the existence of chondromalacia of the trachea, although chondromalacia is accepted as a primary entity when other structures are involved in the pediatric age group. The dreaded and often fatal complica tion of chondromalacia of the trachea following the removal of compressing masses1 is recognized and accepted as an acquired type. In some cases of con genital lobar emphysema, no abnormality of the cartilaginous rings of the bron chus has been found. However, Overstreet 9 has observed hypoplastic bronchial rings in lobar emphysema of infancy. In other cases, anomalous vessels have accounted for the bronchial obstruction. If chondromalacia can be established in the other structures, why should the cartilaginous rings of the trachea be spared ? In a series of cases of congenital tracheal stenosis reported by Wolman,10 many of the patients failed to have a posterior membrane and the tracheal rings were fused, creating a rigid, fixed tube. Other reported cases of congenital stenosis demonstrated bizarre patterns of the tracheal rings, increased and ab normal numbers of the tracheal rings, and deformity of the rings, such as in complete formation. All of these patients had some other type of defect to explain the stenosis. Gross4 refers to 15 cases of chondromalacia in his presidential address be fore The American Association for Thoracic Surgery. There was no mention of any follow-up observation. I t is interesting that at operation no extrinsic pathology was found to account for the obstructions. DIAGNOSIS
Since this congenital abnormality is diagnosed by roentgen techniques, it is difficult to obtain pathological proof. The diagnosis is made by exclusion, al though there are certain studies that can be obtained which lend supporting evidence. Sgalitzer 11 has shown that with differential intratracheal pressure and proper x-ray technique, the tracheal lumen will change over the area of chon dromalacia. The Mueller maneuver will decrease the lumen size and the Valsalva maneuver will increase the size of the lumen. Another method which has been advocated is cinetracheograms which will show tracheal flutter. I t would appear
Vol. 49, No. 6
CONGENITAL CHONDROMALACIA OF TEACHEA
1037
June, 1965
more desirable and perhaps less hazardous to obtain this information by using the Sgalitzer 11 technique rather than introducing a contrast medium which could produce obstruction.. In Case 1, both air and radiopaque techniques were used. The desired information is obtainable from the air contrast study alone; thus, the possible complication of obstruction and pneumonitis, due to the introduc tion of viscid contrast material, is eliminated. By proper use of the roentgen examination, deviation, displacement, and stenosis of the trachea can be ob served. Information concerning the posterior membrane and innervation of the trachea cannot be obtained without direct visualization. Bronchoscopy is indi cated to exclude laryngeal and intraluminal causes of respiratory distress. Direct observation would also reveal absence of the posterior membrane, foreign bodies, malformation of the tracheal rings, congenital external compression, and tracheal nutter with respirations. Not only is this procedure useful as a diagnostic tool but is also useful as a part of the treatment program. Secretions and plugs are removed, thus relieving obstruction and distal pneumonitis. Bronchoscopy is also necessary to determine accurately the length of involvement which is nec essary to outline the proper program of treatment if surgery is being considered. A short stenotic segment may be amenable to surgery whereas the generalized type might better be treated by medical therapy until better techniques are available for total tracheal replacement. ASSOCIATED ANOMALIES
Congenital anomalies are frequently associated with congenital tracheal stenosis and may involve any system. The following associated anomalies have been reported: congenital absence of the thumbs, 10 imperforate anus, 1 ventricular septal defect,8 truncus arteriosus, 5 atrial septal defect,7 peetus excavatum with absent innominate artery associated with a subclavian artery going posterior to the esophagus.2 In the 2 cases of this report there was absence of the right pectoralis minor muscle and ptosis of the right eyelid in the first patient and a bronchus arising from the distal trachea with an undescended right testicle in the second. CLINICAL COURSE
Tracheal chondromalacia is compatible with life. Holinger 6 reported 3 pa tients who were improved without specific treatment. During the 8 month period of observation, the obstructive symptoms gradually diminished. He concluded that the clinical improvement was due to growth and increase in rigidity of the soft cartilaginous rings. Evans 3 observed a variable rigidity of the tracheal cartilages in infants. He noted a transient stenosis of the cervical thoracic tra chea due to softer cartilages and he stated this would tend to disappear with hardening of the tracheal rings. The 2 reported cases herein certainly support the above observation. The early period of life of these patients was very stormy (as stated by both parents and patients). In retrospect, the parents agreed that the symptoms gradually
COX AND SHAW
1038
J. Thoracic and Cardiovas. Surg.
lessened as the patients advanced in age. The second patient isi now 14 years old and this is his first year to be asymptomatic. In a comparison of our cases with those reported in the literature, one must conclude that the degree of rigidity of the tracheal cartilages necessary to prevent symptoms cannot be pre dicted by age. Some have solidly formed rings of the trachea in the early months of life while others take years to acquire tracheal maturity. The lack of a surgical procedure for the correction of the generalized form of tracheal chondromalacia in an infant or child, with prospect that the recon structed trachea would grow, precludes a dramatic attainment of cure. When this diagnosis is made, the parents should be informed of the potential hazards and the many crises that must be met as the patient and the trachea mature. During these crises the most aggressive medical therapy and supervision must be maintained to protect the individual. The prevention and the treatment of respiratory infection is the single most important phase in the management. Recurrent respiratory infections will lead to scarring, fibrosis, contracture, and thickening of the posterior tracheal membrane, and result in a decrease in the diameter of the tracheal lumen. Other changes may develop in distal bronchi, secondary to recurrent tracheobronchial infections. These distal changes are present in the first of our patients, who has a chronic bronchitis and suffers from repeated hemoptysis. The many problems encountered with congenital chondromalacia of the trachea are not insolvable, and the prognosis can be good. These patients can lead active, useful lives with close observation and medical management. SUMMARY
1. Tracheal chondromalacia should be considered in the differential diag nosis of respiratory obstruction in the newborn. 2. The age of development of tracheal stability is variable and cannot he predicted accurately. 3. Segmental involvement may require surgical reconstruction of the tra chea, but the generalized type will require prolonged conservative therapy. 4. The prognosis is not hopeless, as exemplified by the 2 cases just reported. REFERENCES
1. Bonnier, M.: TJn oas de stenose congenitale de la tractive avec bronche du lobe superieur droite atresie et lobe superieur droite aplasique, imperforation de l'anus, Ann. med.cliir. Hop. Sainte-Justine Montreal 5: 13, 1947. 2. Cantrell, J . R., and Guild, H. G.: Congenital Stenosis of the Trachea, Am. J . Surg. 108: 297, 1964. 3. Evans, W. A., J r . : Congenital Obstructions of the Respiratory Tract. I. Tracheal Mal formations, Am. J . Eoentgenol. 62: 167, 1949. 4. Gross, R. E . : Presidential Address: Thoracic Surgery for Infants, J . THORACIC & CARDIO VAS. SURG. 48: 152,
1964.
5. Heikel, P . E . : Congenital Tracheal Stenosis Combined With Truncus Arteriosus Cordis: A Case Diagnosed I n Vita, Ann. Paediat. Fenn. 3 : 22, 1957. 6. Holinger, P . H., Johnston, K. C , and Basinger, C. E . : Benign Stenosis of the Trachea, Ann. Otol. Rhin. & Laryng. 59: 837, 1950. 7. Houston, I. B., and Mackie, D. G.: Congenital Tracheal Stenosis, Thorax 16: 94, 1961. 8. Moutandon, A.: Stenose congenitale de la traehee et malformations associees, Pract. otorhino-Laryng. 6: 179, 1944.
Vol. 49, No. 6 June, 1965
CONGENITAL CHONDROMALACIA OF TRACHEA
1039
9. Overstreet, R. M.: Emphysema of a Portion of the Lung in the Early Months of Life, Am. J. Dis. Child. 57: 861, 1939. 10. Wolman, I. J.: Congenital Stenosis of the Trachea, Am. J. Dis. Child. 61: 1263, 1941. 11. Sgalitzer, M.: Roentgenological Examination of the Power of Resistance of the Tracheal Wall, Am. J. Roentgenol. 56: 355, 1946.