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Congenital absence of the epiglottis
International Journal of Pediatric Otorhinolaryngology 45 (1998) 237 – 241
Case report
Congenital absence of the epiglottis Jeffrey A. Koempel a,*, Lauren D. Holinger b b
a Uni6ersity of Southern California, CA, USA The Children’s Memorial Hospital and Northwestern Uni6ersity, Chicago, IL, USA
Received 18 February 1998; received in revised form 17 June 1998; accepted 20 June 1998
Abstract The congenital absence of the epiglottis is a very rare anomaly. We present a patient who has a complete absence of the epiglottis, illustrated with an endoscopic photograph, review the literature and discuss the management of patients with this condition. © 1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Epiglottis; Congenital anomaly; Absence; Laryngeal abnormalities
1. Introduction Congenital absence of the epiglottis is a very rare anomaly. Failure of the epiglottis to develop results from an event occurring during the period of organogenesis, the period extending from conception through the eighth week of intrauterine life and involving both the third and fourth branchial arches. Such an event might also result in a number of other laryngeal abnormalities and would offer the opportunity to provide some in* Corresponding author. Present address: Division of Pediatric Otolaryngology, Mailstop 58, Children’s Hospital of Los Angeles, 4650 Sunset Blvd, Los Angeles, CA 90027, USA. Tel.: + 1 213 6692145; fax: + 1 213 6647327.
sight into the function of the epiglottis. We describe our experience with a patient who has a congenitally absent epiglottis.
2. Case report A 3-month-old boy was admitted to the general pediatric floor of the Children’s Memorial Hospital in Chicago in January 1997, with a several week history of increased difficulty of breathing. The child was born full-term without a history of any significant pre or post-natal events and left the hospital with his mother shortly after birth taking all feeds by mouth. Except for routine well-baby visits, there had been no other hospital
0165-5876/98/$ - see front matter © 1998 Elsevier Science Ireland Ltd. All rights reserved. PII S0165-5876(98)00082-2
238
J.A. Koempel, L.D. Holinger / Int. J. Pediatr. Otorhinolaryngol. 45 (1998) 237–241
admissions, emergency room or office visits prior to this admission. In the course of the work-up for his difficulty breathing, posterio-anterior and lateral soft tissue radiographs of the neck were obtained, which were interpreted as demonstrating a large epiglottis (Fig. 1). This finding prompted an otolaryngology consultation. On examination, the child had a mild biphasic stridor but no signs of respiratory distress. The mandible was noted to be slightly smaller than average for a baby of this age, but no other obvious dysmorphic features were present. The remainder of the routine head and neck examination was unremarkable. Flexible laryngoscopy, performed at the bedside, demonstrated enlarged cuneiform and arytenoid cartilages bilaterally, edema of the posterior larynx and complete absence of the epiglottis (Fig. 2). The vocal folds
demonstrated full adduction and abduction. Complete evaluation of the tracheobronchial tree was recommended to rule out other structural abnormalities. Direct laryngoscopy confirmed the findings of the flexible exam. Direct laryngoscopy and bronchoscopy disclosed a larynx of normal size and no subglottic stenosis or other abnormalities of the trachea or main bronchi. Esophagogastroduodenoscopy was normal and an esophageal mucosal biopsy showed no evidence of inflammation. A rehabilitation swallow study confirmed that he aspirated both solids and liquids. The baby was discharged home without supplemental oxygen or monitors but was restricted to nasogastric tube feeding. One month later, the child was admitted to the intensive care unit with increased work of breathing. Chest radiograph showed an infiltrate consistent with an aspiration pneumonia. The child was intubated on admission and treated with a 10-day course of intravenous antibiotics and chest physiotherapy. He failed the first attempt at extubation but was successfully extubated after a total of 7 days. The nasogastric tube was replaced with a nasojejunal tube and the child was discharged on ranitidine and cisapride. As a result of the aspiration pneumonia, Nissen fundoplication and gastrostomy tube placement were performed 1 month later. The child was last seen in the otolaryngology office at the age of 17 months. The child’s mother reported no respiratory problems and that the child had not yet tried to vocalize. The child had several visits with the speech and swallowing therapist, including a few rehabilitation swallow studies which were not able to be completed secondary to an inability to even attempt to swallow. The child continues to receive all nutrition through his gastrostomy tube and is growing well.
3. Discussion
Fig. 1. Lateral soft tissue radiograph of the neck demonstrating a large soft tissue mass (arrow) which was interpreted as a large epiglottis.
Congenital absence of the epiglottis is a rare anomaly. In our review of the English literature, Holinger and Brown were the first to report this occurrence in 1967 [1]. They presented two cases
J.A. Koempel, L.D. Holinger / Int. J. Pediatr. Otorhinolaryngol. 45 (1998) 237–241
239
Fig. 2. Endoscopic photograph demonstrating enlarged cuneiform and arytenoid cartilages bilaterally, edema of the posterior larynx and lymphoid tissue at the base of the tongue anteriorly but no epiglottis.
and found that each was associated with severe glottic stenosis. Constantinides and Cywes reported the case of a 6-day-old girl who was referred to their intensive care unit for respiratory distress and cyanotic episodes, with attempts to feed in the supine or sitting position [2]. The initial physical exam was significant only for the absence of the median portion of the mandible. Direct laryngoscopy revealed an absent epiglottis. No other laryngeal abnormalities were noted. A few weeks after a tracheostomy and gastrostomy, the child experienced an anoxic episode and died. Reyes et al. have the longest follow-up, 8 years, of a patient with a rudimentary epiglottis [3]. They reported a 3-month-old girl who was referred for evaluation of inspiratory stridor but
had no feeding difficulties. A flexible bronchoscopy revealed a rudimentary epiglottis and prominent arytenoid cartilages. This child never had signs or symptoms of aspiration over 8 years, but did develop daytime somnolence, loud snoring and shortness of breath with exercise. She was an obese girl at age 8 and a polysomnogram was consistent with obstructive sleep apnea. The hypopharynx and larynx were unchanged. A few cases of an absent or rudimentary epiglottis associated with other congenital anomalies outside of the head and neck have been described. Meinecke and Hayek reported a newborn baby boy with orofaciodigital syndrome type IV (Mohr–Majewski syndrome) which has multiple anomalies including microcephaly, hypertelorism, cleft lip and palate, choanal stenosis,
240
J.A. Koempel, L.D. Holinger / Int. J. Pediatr. Otorhinolaryngol. 45 (1998) 237–241
anal atresia, hexadactyly (six nails), brachydactyly and syndactyly [4]. The infant died shortly after birth and necropsy revealed hypoplasia of the larynx and epiglottis. The vocal folds were absent. Knapp et. al. have reported the case of a 3-dayold infant with short rib polydactyly syndrome which includes a rudimentary epiglottis, polydactyly of the hands and feet, shortened ribs and a small chest [5]. This baby died of respiratory causes after 47 days of life. Lastly, Chen and Holinger presented the serial sections of a larynx from a patient with orofaciodigital syndrome, type II, which demonstrated an abnormal hyoid bone and only a trace of a piece of cartilage in the area of the epiglottis. There was no evidence of subglottic stenosis [6]. No clinical information was provided. The events which result in the congenital absence or hypoplastic development of the epiglottis are thought to occur during the period of organogenesis, the period extending from conception through the eighth week of intrauterine life. The Carnegie staging system divides this period into 23 stages [7]. The epiglottic swelling first becomes visible in the region of the hypobranchial eminence by stage 15, day 33 of life. Both the epiglottis and larynx are clearly identifiable by stage 17, day 41 of life. By stage 19, day 48 of life, the epiglottis is well-demarcated from the tongue but does not become chondrified until about the fifth month of fetal life. Interestingly, the limbs also develop at this same time which accounts for the concurrent limb abnormalities found in the orofaciodigital syndromes. Although the embryological development of the epiglottis has been described in detail, its function remains unclear. Some physicians have proposed that the epiglottis helps to protect the airway and prevent aspiration [8,9], while others have suggested that it is a vestigial organ which aided in olfaction [10]. Unfortunately, most of the patients with this rare anomaly do not survive long enough to provide any insight into the problems that result from the absence of the epiglottis. The patient from the report of Reyes et al., did not develop signs or symptoms of aspiration over a period of 8 years, but did develop obstructive sleep apnea providing some evidence to suggest
that the epiglottis may play a role as a support structure of the airway such that its absence might increase the patient’s risk of obstructive apnea through lateral collapse of the surrounding soft tissues. It is interesting to note that our patient, who had similar findings on direct laryngoscopy, did not develop any signs or symptoms of obstructive apnea but did develop significant signs and symptoms of aspiration, eventually requiring a Nissen fundoplication and gastrostomy. Our follow-up period is only 17 months, however, compared to 8 years in Reyes’ case report. When one review reports of the minimal complications which follow epiglottectomy in adults, more evidence is provided that suggests that the epiglottis does not play a significant role in airway protection or prevention of aspiration. Davis et al. were among the first to report their results of patients who had undergone an epiglottectomy.[11] In a group of 20 patients, all had minimal aspiration postoperatively but the longest period lasted only 5 days. Woo reported a series which included five patients [12]. Only one patient had aspiration for 1 week. Lastly, Zeitels et al. reported the largest series with 51 patients [13]. Unfortunately, the number of patients with aspiration postoperatively are not specifically stated. They indicate that those patients who had any pre-existing problems with aspiration, due to the presence of an interfering mass, were improved. However, they noted that aspiration worsened if there were underlying neuromuscular defects, other loss of glottic tissue or upward restriction of the laryngotracheal complex. No one reported any airway compromise postoperatively. Since the events resulting in the congenital absence of the epiglottis occur at a time during organogenesis, when other parts of the larynx are developing as well, the absence of the epiglottis may or may not be associated with other laryngeal anomalies. Therefore, direct laryngoscopy and bronchoscopy are recommended for complete evaluation of the larynx and tracheobronchial tree to assess for other abnormalities such as subglottic stenosis which may affect the management of these patients. A rehabilitation swallow study is undertaken to assess for aspiration. Lastly, the patient is followed for symptoms of obstructive
J.A. Koempel, L.D. Holinger / Int. J. Pediatr. Otorhinolaryngol. 45 (1998) 237–241
sleep apnea. Polysomnogram is considered if these develop.
References [1] P.H. Holinger, W.T. Brown, Congenital webs, cysts, laryngoceles and other anomalies of the larynx, Ann. Otol. Rhinol. Laryngol. 76 (1967) 744–752. [2] C.G. Consantinides, S. Cywes, Complete median cleft of the mandible and aplasia of the epiglottis, SA Med. J. 64 (1983) 293 – 294. [3] B.G. Reyes, J.E. Arnold, L.J. Brooks, Congenital absence of the epiglottis and its potential role in obstructive sleep apnea, Int. J. Ped. Otorhinolaryn. 30 (1994) 223–226. [4] P. Meinecke, H. Hayek, Orofaciodigital syndrome type IV (Mohr – Majewski syndrome) with severe expression expanding the known spectrum of anomalies, J. Med. Genet. 27 (1990) 200–202. [5] C.H. Knapp, A. Satin-Hodges, R.R. Cole, Laryngeal findings in short rib polydactyly syndrome: case report and embryological correlations, Laryngoscope 100 (1990) 579 – 582.
.
241
[6] J. Chen, L.D. Holinger, Congenital laryngeal lesions: pathology study using serial macrosections and review of the literature, Ped. Path. 14 (1994) 301 – 325. [7] J.A. Tucker, R. O’Rahilly, The early development of the larynx in staged human embryos, Ann. Otol. Rhinol. Laryngol. 82 (Suppl.7) (1973) 3 – 27. [8] G.M. Ardran, F.H. Femp, The mechanism of the larynx, Br. J. Radiol. 40 (1994) 372 – 389. [9] I.A. Bowman, Historical perspective, in: O.P. Matthew (Ed.), Function of Upper Airway, vol. 35, Marcel Dekker, New York, 1980, p. 23. [10] V.E. Negus, The mechanism of the larynx, J. Anat. 1 (1929) 62. [11] R.K. Davis, S.M. Shapshay, M.S. Strong, V.J. Hyams, Transoral partial supraglottic resection using the CO2 laser, Laryngoscope 93 (1983) 429 – 432. [12] P. Woo, Acquired laryngomalacia: epiglottis prolapse as a cause of airway obstruction, Ann. Otol. Rhinol. Laryngol. 101 (1992) 314 – 320. [13] S.M. Zeitels, C.W. Vaughan, G. F. Domanowski, N.S. Fuleihan, G.T. Simpson II, Laser epiglottectomy: endoscopic technique and indications, Otolaryngol. Head Neck Surg. 103 (1990) 337 – 343.
Case report
Congenital absence of the epiglottis Jeffrey A. Koempel a,*, Lauren D. Holinger b b
a Uni6ersity of Southern California, CA, USA The Children’s Memorial Hospital and Northwestern Uni6ersity, Chicago, IL, USA
Received 18 February 1998; received in revised form 17 June 1998; accepted 20 June 1998
Abstract The congenital absence of the epiglottis is a very rare anomaly. We present a patient who has a complete absence of the epiglottis, illustrated with an endoscopic photograph, review the literature and discuss the management of patients with this condition. © 1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Epiglottis; Congenital anomaly; Absence; Laryngeal abnormalities
1. Introduction Congenital absence of the epiglottis is a very rare anomaly. Failure of the epiglottis to develop results from an event occurring during the period of organogenesis, the period extending from conception through the eighth week of intrauterine life and involving both the third and fourth branchial arches. Such an event might also result in a number of other laryngeal abnormalities and would offer the opportunity to provide some in* Corresponding author. Present address: Division of Pediatric Otolaryngology, Mailstop 58, Children’s Hospital of Los Angeles, 4650 Sunset Blvd, Los Angeles, CA 90027, USA. Tel.: + 1 213 6692145; fax: + 1 213 6647327.
sight into the function of the epiglottis. We describe our experience with a patient who has a congenitally absent epiglottis.
2. Case report A 3-month-old boy was admitted to the general pediatric floor of the Children’s Memorial Hospital in Chicago in January 1997, with a several week history of increased difficulty of breathing. The child was born full-term without a history of any significant pre or post-natal events and left the hospital with his mother shortly after birth taking all feeds by mouth. Except for routine well-baby visits, there had been no other hospital
0165-5876/98/$ - see front matter © 1998 Elsevier Science Ireland Ltd. All rights reserved. PII S0165-5876(98)00082-2
238
J.A. Koempel, L.D. Holinger / Int. J. Pediatr. Otorhinolaryngol. 45 (1998) 237–241
admissions, emergency room or office visits prior to this admission. In the course of the work-up for his difficulty breathing, posterio-anterior and lateral soft tissue radiographs of the neck were obtained, which were interpreted as demonstrating a large epiglottis (Fig. 1). This finding prompted an otolaryngology consultation. On examination, the child had a mild biphasic stridor but no signs of respiratory distress. The mandible was noted to be slightly smaller than average for a baby of this age, but no other obvious dysmorphic features were present. The remainder of the routine head and neck examination was unremarkable. Flexible laryngoscopy, performed at the bedside, demonstrated enlarged cuneiform and arytenoid cartilages bilaterally, edema of the posterior larynx and complete absence of the epiglottis (Fig. 2). The vocal folds
demonstrated full adduction and abduction. Complete evaluation of the tracheobronchial tree was recommended to rule out other structural abnormalities. Direct laryngoscopy confirmed the findings of the flexible exam. Direct laryngoscopy and bronchoscopy disclosed a larynx of normal size and no subglottic stenosis or other abnormalities of the trachea or main bronchi. Esophagogastroduodenoscopy was normal and an esophageal mucosal biopsy showed no evidence of inflammation. A rehabilitation swallow study confirmed that he aspirated both solids and liquids. The baby was discharged home without supplemental oxygen or monitors but was restricted to nasogastric tube feeding. One month later, the child was admitted to the intensive care unit with increased work of breathing. Chest radiograph showed an infiltrate consistent with an aspiration pneumonia. The child was intubated on admission and treated with a 10-day course of intravenous antibiotics and chest physiotherapy. He failed the first attempt at extubation but was successfully extubated after a total of 7 days. The nasogastric tube was replaced with a nasojejunal tube and the child was discharged on ranitidine and cisapride. As a result of the aspiration pneumonia, Nissen fundoplication and gastrostomy tube placement were performed 1 month later. The child was last seen in the otolaryngology office at the age of 17 months. The child’s mother reported no respiratory problems and that the child had not yet tried to vocalize. The child had several visits with the speech and swallowing therapist, including a few rehabilitation swallow studies which were not able to be completed secondary to an inability to even attempt to swallow. The child continues to receive all nutrition through his gastrostomy tube and is growing well.
3. Discussion
Fig. 1. Lateral soft tissue radiograph of the neck demonstrating a large soft tissue mass (arrow) which was interpreted as a large epiglottis.
Congenital absence of the epiglottis is a rare anomaly. In our review of the English literature, Holinger and Brown were the first to report this occurrence in 1967 [1]. They presented two cases
J.A. Koempel, L.D. Holinger / Int. J. Pediatr. Otorhinolaryngol. 45 (1998) 237–241
239
Fig. 2. Endoscopic photograph demonstrating enlarged cuneiform and arytenoid cartilages bilaterally, edema of the posterior larynx and lymphoid tissue at the base of the tongue anteriorly but no epiglottis.
and found that each was associated with severe glottic stenosis. Constantinides and Cywes reported the case of a 6-day-old girl who was referred to their intensive care unit for respiratory distress and cyanotic episodes, with attempts to feed in the supine or sitting position [2]. The initial physical exam was significant only for the absence of the median portion of the mandible. Direct laryngoscopy revealed an absent epiglottis. No other laryngeal abnormalities were noted. A few weeks after a tracheostomy and gastrostomy, the child experienced an anoxic episode and died. Reyes et al. have the longest follow-up, 8 years, of a patient with a rudimentary epiglottis [3]. They reported a 3-month-old girl who was referred for evaluation of inspiratory stridor but
had no feeding difficulties. A flexible bronchoscopy revealed a rudimentary epiglottis and prominent arytenoid cartilages. This child never had signs or symptoms of aspiration over 8 years, but did develop daytime somnolence, loud snoring and shortness of breath with exercise. She was an obese girl at age 8 and a polysomnogram was consistent with obstructive sleep apnea. The hypopharynx and larynx were unchanged. A few cases of an absent or rudimentary epiglottis associated with other congenital anomalies outside of the head and neck have been described. Meinecke and Hayek reported a newborn baby boy with orofaciodigital syndrome type IV (Mohr–Majewski syndrome) which has multiple anomalies including microcephaly, hypertelorism, cleft lip and palate, choanal stenosis,
240
J.A. Koempel, L.D. Holinger / Int. J. Pediatr. Otorhinolaryngol. 45 (1998) 237–241
anal atresia, hexadactyly (six nails), brachydactyly and syndactyly [4]. The infant died shortly after birth and necropsy revealed hypoplasia of the larynx and epiglottis. The vocal folds were absent. Knapp et. al. have reported the case of a 3-dayold infant with short rib polydactyly syndrome which includes a rudimentary epiglottis, polydactyly of the hands and feet, shortened ribs and a small chest [5]. This baby died of respiratory causes after 47 days of life. Lastly, Chen and Holinger presented the serial sections of a larynx from a patient with orofaciodigital syndrome, type II, which demonstrated an abnormal hyoid bone and only a trace of a piece of cartilage in the area of the epiglottis. There was no evidence of subglottic stenosis [6]. No clinical information was provided. The events which result in the congenital absence or hypoplastic development of the epiglottis are thought to occur during the period of organogenesis, the period extending from conception through the eighth week of intrauterine life. The Carnegie staging system divides this period into 23 stages [7]. The epiglottic swelling first becomes visible in the region of the hypobranchial eminence by stage 15, day 33 of life. Both the epiglottis and larynx are clearly identifiable by stage 17, day 41 of life. By stage 19, day 48 of life, the epiglottis is well-demarcated from the tongue but does not become chondrified until about the fifth month of fetal life. Interestingly, the limbs also develop at this same time which accounts for the concurrent limb abnormalities found in the orofaciodigital syndromes. Although the embryological development of the epiglottis has been described in detail, its function remains unclear. Some physicians have proposed that the epiglottis helps to protect the airway and prevent aspiration [8,9], while others have suggested that it is a vestigial organ which aided in olfaction [10]. Unfortunately, most of the patients with this rare anomaly do not survive long enough to provide any insight into the problems that result from the absence of the epiglottis. The patient from the report of Reyes et al., did not develop signs or symptoms of aspiration over a period of 8 years, but did develop obstructive sleep apnea providing some evidence to suggest
that the epiglottis may play a role as a support structure of the airway such that its absence might increase the patient’s risk of obstructive apnea through lateral collapse of the surrounding soft tissues. It is interesting to note that our patient, who had similar findings on direct laryngoscopy, did not develop any signs or symptoms of obstructive apnea but did develop significant signs and symptoms of aspiration, eventually requiring a Nissen fundoplication and gastrostomy. Our follow-up period is only 17 months, however, compared to 8 years in Reyes’ case report. When one review reports of the minimal complications which follow epiglottectomy in adults, more evidence is provided that suggests that the epiglottis does not play a significant role in airway protection or prevention of aspiration. Davis et al. were among the first to report their results of patients who had undergone an epiglottectomy.[11] In a group of 20 patients, all had minimal aspiration postoperatively but the longest period lasted only 5 days. Woo reported a series which included five patients [12]. Only one patient had aspiration for 1 week. Lastly, Zeitels et al. reported the largest series with 51 patients [13]. Unfortunately, the number of patients with aspiration postoperatively are not specifically stated. They indicate that those patients who had any pre-existing problems with aspiration, due to the presence of an interfering mass, were improved. However, they noted that aspiration worsened if there were underlying neuromuscular defects, other loss of glottic tissue or upward restriction of the laryngotracheal complex. No one reported any airway compromise postoperatively. Since the events resulting in the congenital absence of the epiglottis occur at a time during organogenesis, when other parts of the larynx are developing as well, the absence of the epiglottis may or may not be associated with other laryngeal anomalies. Therefore, direct laryngoscopy and bronchoscopy are recommended for complete evaluation of the larynx and tracheobronchial tree to assess for other abnormalities such as subglottic stenosis which may affect the management of these patients. A rehabilitation swallow study is undertaken to assess for aspiration. Lastly, the patient is followed for symptoms of obstructive
J.A. Koempel, L.D. Holinger / Int. J. Pediatr. Otorhinolaryngol. 45 (1998) 237–241
sleep apnea. Polysomnogram is considered if these develop.
References [1] P.H. Holinger, W.T. Brown, Congenital webs, cysts, laryngoceles and other anomalies of the larynx, Ann. Otol. Rhinol. Laryngol. 76 (1967) 744–752. [2] C.G. Consantinides, S. Cywes, Complete median cleft of the mandible and aplasia of the epiglottis, SA Med. J. 64 (1983) 293 – 294. [3] B.G. Reyes, J.E. Arnold, L.J. Brooks, Congenital absence of the epiglottis and its potential role in obstructive sleep apnea, Int. J. Ped. Otorhinolaryn. 30 (1994) 223–226. [4] P. Meinecke, H. Hayek, Orofaciodigital syndrome type IV (Mohr – Majewski syndrome) with severe expression expanding the known spectrum of anomalies, J. Med. Genet. 27 (1990) 200–202. [5] C.H. Knapp, A. Satin-Hodges, R.R. Cole, Laryngeal findings in short rib polydactyly syndrome: case report and embryological correlations, Laryngoscope 100 (1990) 579 – 582.
.
241
[6] J. Chen, L.D. Holinger, Congenital laryngeal lesions: pathology study using serial macrosections and review of the literature, Ped. Path. 14 (1994) 301 – 325. [7] J.A. Tucker, R. O’Rahilly, The early development of the larynx in staged human embryos, Ann. Otol. Rhinol. Laryngol. 82 (Suppl.7) (1973) 3 – 27. [8] G.M. Ardran, F.H. Femp, The mechanism of the larynx, Br. J. Radiol. 40 (1994) 372 – 389. [9] I.A. Bowman, Historical perspective, in: O.P. Matthew (Ed.), Function of Upper Airway, vol. 35, Marcel Dekker, New York, 1980, p. 23. [10] V.E. Negus, The mechanism of the larynx, J. Anat. 1 (1929) 62. [11] R.K. Davis, S.M. Shapshay, M.S. Strong, V.J. Hyams, Transoral partial supraglottic resection using the CO2 laser, Laryngoscope 93 (1983) 429 – 432. [12] P. Woo, Acquired laryngomalacia: epiglottis prolapse as a cause of airway obstruction, Ann. Otol. Rhinol. Laryngol. 101 (1992) 314 – 320. [13] S.M. Zeitels, C.W. Vaughan, G. F. Domanowski, N.S. Fuleihan, G.T. Simpson II, Laser epiglottectomy: endoscopic technique and indications, Otolaryngol. Head Neck Surg. 103 (1990) 337 – 343.