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Naso- and oropharyngeal dimensions in children with obstructive sleep apnea
Internotionol Journal of Pediatric Otorhinolaryngology, 17 (1989) l-11 Elsevier POR 00558
Linda Brodsky, Ellen Adler and John F. Stanievich Department of Otola~ngoJogy, State University of New York at Buffalo, School of Medicine ond the Children’s Hospital of &ffrrro, 219 Bvant Street, Buffalo, NY 14222 (U.S.A.) (Received 25 April 1988) (Revised version received 29 August 1988) (Accepted 18 September 1988)
Key words: Obstructive sleep apnea; Adenotonsillar hypertrophy; Oropharyngeal dimension
Sixty children (3-11 years) were evaluated to determine variations in naso- and oropharyngeal dimensions associated with tonsil and adenoid hypertrophy. The subjects were grouped according to tonsil size and a clinical history of chronic upper airway obstruction. Intraoperative measurements included oropharyngead diameter, length of the hard and soft palates, width and arch of the hard palate, nasopharyngeal volume, as well as tonsil and adenoid weights and volumes. A significantly larger oropharyngeal diameter was found in children with small, non-obstructing tonsils (P < 0.01). Children with large, non-obstructing tonsils had a similar oropharyngeal diameter to those children with large, obstructing tonsils. However, tonsil volume, not weight, was increased in the children with large obstructing tonsils as compared to those with large non-obstructing tonsils and small non-obstructing tonsils (P c 0.04). A shorter soft palate was associated with larger, obstructing tonsils (P < 0.004). The length of the hard palate was similar in all patients, however, a trend towards a higher arched palate was seen in patients with larger, obstructing tonsils. The distance from the soft palate to the posterior pharyngeal wall was greater in obstructed patients with adenotonsillar hypertrophy (P < 0.003). In patients requiring adenoidectomy, the nasopharyngeal volume prior to adenoidectomy was significantly smaller in patients with obstructive symptoms (P < 0.001). Postadenoidectomy, no significant difference was found in the nasopharynx volume amongst all subjects. These data indicate that subtle dif-
* Presented at the Scientific Session of the American Society for Pediatric Otolaryngology. Kiaweh Island, South Carolina, U.S.A., April 21-24, 1988. Correspondence: Linda Brodsky, 219 Bryant Street, Buffalo, NY 14222, U.S.A. 01655876/89/$03.50
@ 1989 Elsevier Science Publishers B.V. (Biomedical Division)
2
ferences in orophatyngeal dimensions exist which along with increased lymphoid tissue volume, lead to the development of obstructive symptoms. Etiologic considerations are discussed.
Introduction The development of obstructive sleep patterns in children has been associated with craniofacial abnormalities, cleft palate surgery and most commonly with hypertrophy of the tonsils and adenoids [3,20]. However, not every child with large tonsils and adenoids has symptoms commonly associated with obstructive sleep apnea (OSA). These include loud snoring associated with snorting or apnea, dysphagia with growth retardation, speech abnormalities, hypersomnolence and intellectual/behavioral problems [11,12]. Varying degrees of adenotonsillar hypertrophy may lead to these abnormalities. However, the role of subtle variations in the dimensions of the oropharynx and nasopharynx has not been fully elucidated. Previous studies have assessed morphologic variations in the upper airway in a number of ways. These include cephalometric radiography [3,8,14], fiberoptic endoscopy [6], acoustic reflection techniques [2,4,14], video fluoroscopy awake and asleep [15] and CT scanning with static [7], tine [a] and reconstruction of 3-D images [lo]. The use of direct measurement has previously been reported by Brodsky et al. [l] using direct intrsloperative measurements of bony and soft tissue structures thought to be relevant LO the development of OSA. The oropharyngeal dimensions in children with large obstructing tonsils were compared to children with small non-obsdructing tonsils. They found that the depth of the nasopharynx was increase& while the distance between the lateral pharyngeal walls in the obstructed children was decreased compared to non-obstructed children. In addition, in nonobstructed children an increase in patient height, weight and surface area varied positively to the increase in oropharyngeal dimension, whereas, in the patients with obstructive adenotonsillar hypertrophy, no such correlation existed. Their initial study suggested that subtle structural abnormalities may exist in obstructed patients coincident with adenotonsillar hypertrophy. To further explore these anatomic variations, the present study used direct intraoperative measurements to assess oropharyngeal and nasopharyngeal dimensions in conjunction with adenotonsillar volume and weight in obstructed and non-obstructed children as well as in normal controls.
Materials and Methods Patient population Sixty children between the ages of 3 and 11 years were divided into 4 groups: (I) Control (n = 10). Patients with no history of OSA or tonsillitis were under general anesthesia for unrelated procedures.
3
(2) Smxdl non-obstructed group (SNO) (n = 12). These patients had no history of obstructive symptoms and underwent tonsillectomy for chronic tonsillitis. Preoperatively they had small tonsils from 0 to + 1, less than 20% of the oropharyngeal airway and with no obstructive symptoms. (3) Large non-obstructed group (LNO) (n = 7). These patients had no history of obstructive symptoms and underwent tonsillectomy for chronic adenotonsillitis. Preoperatively they -had large tonsils from + 3 to +4, greater than 75% of the oropharyngeal airway measured with the tongue in the resting position (i.e. no gagging) but with no obstructive symptoms. (4) Large obstructed group (LO) (n = 31). These patients had a long history (> 1 year) of loud snoring associated with snorting or apnea, dysphagia with growth disturbances or speech abnormalities. Preoperatively they had large tonsils from + 3 to +4, greater than 75% of the oropharyngeal airway. Morphologic ana&& Prior to surgery, the patients’ age, height and weight were recorded. While under anesthesia, the patient was placed with the shoulders and neck extended and the Crow- avis mouth gag in place and maximally retracted open. Using calipers with l-mm intervals, string and a ruler the following measurements were taken (Figs. 1, 2, 3): (1) Distance between medial surfaces of the tonsils at mid tonsil (Fig. 1). (2) Distance between the anterior pillars (Fig. 1). (3) Distance between the lateral pharyngeal walls (Fig. 1). (4) The length of the soft palate (excluding the uvula) (Fig. 2). (5) The length of the hard palate from the junction of the hard and soft palate to the central incisors. (6) Width of the hard palate from the right first molar to the left first molar with the string taut (Fig. 3).
Fig. 1. Oropharyngealairway. a, distance between the medial surfaces of the tonsil at mid-tonsil; b, distance between the anterior pillars; and c, distance be?ween the lateral pharyngeal walls.
Fig. 2. Palate and Nasopharynx. d. length of the hard palate; e, anterior-posterior distance from ventral surface of the soft palate to posterior nasophatyngeal wall.
(7) Width of the hard palate from the right first molar to the left first molar with the string following the curvature of the palate. This was used to determine the arch of the hard palate (Fig. 3). (8) Anterior-posterior distance from the ventral surface of the soft palate to the posterior wall at the edge of the soft palate (Fig. 2). The nasopharyngeal volume was determined pre- and postadenoidectomy by threading a Foley catheter into each naris, inflating the balloon and occluding the posterior choana under indirect mirror visualization. The nasopharynx was then
.
I.
Fig. 3. Width and arch of hard palate.
TABLE I Demographic data SNO, small non-obstructed.
LNO, large non-obstructed. LO, large obstructed.
Control SNO LNO LO
Age (months)
Height (cm)
Weight (kg)
74.0 82.6 71.6 67.5
115 122 115 115
21 25 23 24
filled with saline to the edge of the soft palate. The saline was then suctioned into a bronchial suction trap, removed and measured in a syringe with 0.2 ml intervals. The length, width, height and weight of each tonsil was determined posttonsillectomy. The adenoid weight was also recorded. Tonsil and adenoid volume was measured by water displacement in a gradua!d cylinder. Statistical analysis The data rrere statistically analyzed using the Student’s t test for differences of the means, correlation coefficients and analysis of variance.
Demographic data There was no significant difference in mean age, height or weight among the control group, small non-obstructed (SNQ) group, large non-obstructed (LNO) group and large obstructed (LQ) group (Table I). In the control, SNO and LNQ children, age, height and weight correlated positively with all measurements. The LO children showed no correlation between any of t.he parameters measured. Oropharyngeal dimensions As anticipated, the distance between the medial surfaces of the tonsils was significantly greater in the control and the SNO groups than in the LNO and LO groups (P < 0.001). The children with SNO tonsils had a significantly larger pharyngeal diameter, as measured from lateral wall to lateral wall, than either the children with the LNO or LO tonsils (P -C0.05). There was no significant difference in oropharyngeal diameter between the comtrol and SNO groups or between the LNO and NO groups (Table II). Nasopharyngeal dimensions The LNO and LO children had smaller pre-adenoidectomy volumes than the control and SNO children. Postadenoidectomy, there was no significant difference in nasopharyngeal volumes among the groups. (Table III).
TABLE II Oropharyngeal dimensivns P-value
Medial surfaces tonsil9 (mm) 20 20 9 8
Control SNO LNO LO
l
NS -c 0.001 < 0.001
toreralpharyngeal wall diameter (mm)
P-value + *
53 58 48 49
NS‘
-
< 0.001 c 0.001
* In comparison to controls. * * In comparison to SNO. NS = not significant.
Hard and soft palate The total length of the hard and soft palates was found to be longer in the control and SNO patients than in the LNO and LO patients. However, when the hard and soft palates were measured independently there were no significant differences among the groups in the length of the hard palate. Therefore, the LNO
TABLE III Nclsopharyngml (NP) depth and volumes
Control SNO LNO LO
NP depth (mm)
P-value *
21 23 24 26
NS NS < 0.01
NP volume pre-adenoid (ml 40) 5.4 5.1 3.5 3.0
P-value +
NP volume post adenoid. (ml W)
P-value ++
NS < 0.05 C 0.01
5.6 5.1 5.8
NS NS NS
* As compared to controls and SNO groups. * As compared to each group. NS = not significant. Adenoid. = adenoidectomy. l
TABLE IV Dimensiorss of hard und soft palates Total so/l and hard palate length (mm) Control SNO LNO LO
68 70 63 61
P-value *
c 0.05 < 0.01
Soft palate length (mm) 28 28 23 21
* As compared to both control and SNO groups.
P-value +
< 0.05 co.001
Hard palate length (mm) 40 42 39 39
P-vcrlue *
NS NS
TABLE V
Width /arch of hard palate Hard palate width (mm) 30 28 30 28
Control SNO LNO LO
P-value
Hard palate arch (mm)
P-value
8.8 8.7 6.8 9.4
NS NS NS
NS NS NS
NS = not significant.
and LO groups demonstrated a shorter soft palate than the control and SNO groups. In addition, it was noted that there was a tendency for the LO group to have the shortest palates (‘Fable IV). Measurements of the width and arch of the hard palate revealed no difference in palatal width among the groups, but a trend towards a higher arch was seen in the LO group as compared to the LNO group (Table V). These results, however, did not attain statistical significance. The distance between the soft palate and the posterior pharyngeal wall was greatest in the LO group. It also coincides with the short soft palate found in this group documenting the larger oropbaryngeal airway at this level of the pharynx in children presenting with large clinically obstructing tonsils and adenoids. Tonsil and adenoid dimensions The volume of the LO tonsils was significantly greater than the LNO and SNO tonsils, although there was no difference between the weight of the LO and LNO tonsils. Small non-obstructing tonsils weighed significantly less, as expected. The LO tonsils had the greatest length, width and height which went along with the larger volumes determined by the water displacement method (Table VI).
TABLE VI
Tonsil weight and volume Tonsil P-va!ue * Vohune P-value * Length P-value * Width P-value * Height P-vaIue * weight displace(mm) (mm) (mm1 ment (gl (ml) Control _ _ _ _ _ 24 39 53 8.1 SNO 6.4 LNO LO
8.9 8.6
c 0.05 < 0.05
8.9 11.2
* Compared to SNO group. NS = not significant.
NS < 0.05
54 59
NS < 0.05
43 46
NS < 0.01
28 30
NS -z 0.01
8
Adenoids in the LO group demonstrated a trend toward a larger adenoid volume and weight than in the LNO group. The lack of statistical significance may have been due to the small number of children evaluated for adenoid dimensions.
Discussion Anatomical and physiological differences in the upper airways of patients with obstructive sleep apnea have received much attention, particularly in the adult population. The anatomical abnormalities which have been identified in the adult population include the following: reduced upper airway diameter, increased pharyngeal collapsibility, elongated soft palate, shallower palatal arch, enlarged tongue base, and reduced mandible size [2,4,6,13,15,19]. Most of the data on anatomical changes in adult patients with OSA appear to contradict findings in the present study in children ‘with OSA. The data from the present study indicate that children with obstructing tonsils and significan
9
to open up the pharyngeal aperture in response to decreased air flow and possibly chronic hypoxia [3]; or (3) they may represent alterations in facial growth from the abnormal mouth and jaw posturing which is associated with mouth breathing. Mouth breathing may result in high-arched palates through a number a! possible mechanisms as stated previously [18]. Furthermore, anatomical variations from birth may also play role. It is possible that patients born with a small decrease in lateral oropharyngeal dimension may be predisposed to obstruction by large tonsils and adenoids [IT]. It is interesting to note that the volumes of the tonsils in the SNO and LNO group were similar, suggesting that oropharyngeal dimension rather than tonsil size may be the difference between these two groups. The finding of a narrower oropharyngeal diameter in the large non-obstructed, and large obstructed children fit this congenital predisposition theory. In this instance the postulated mechanism is as follows: children are born with a small diameter oropharynx at the level of the palatine tonsils. They then develop low density/high volume tonsillar hypertrophy. During sleep, their tonsils undergo inferior and posterior displacement into the airway (as demonstrated by Brouilette et al. [3]) and they develop obstructive symptoms. In addition, children with OSA may have pharyngeal muscle hypotonia as demonstrated in adults with OSA [2], and the pharyngeal airway may actually collapse against the voluminous tonsils as they are displaced posteriorly during the negative pressure of inspiration. What is not understood at this time is why certain children develop various types of tonsillar hypertrophy (i.e. low density/high volume). Although the numbers of children studied are small, obstruction from adenoid hypertrophy at the level of the nasopharynx may be related more to the size of the adenoids rather than to the size of the nasopharynx. This is evidenced by the similarities in nasopharyngeal volume measured after adenoidectomy amongst all groups. However, in light of the similar preadenoidectomy volumes between the large obstructed and large non-obstructed groups, it can be stated that in this study, the obstruction is not at the nasopharyngeal level. The low density tonsils may play a greater role in the development of symptoms. In conclusion, this study demonstrates that subtle abnormalities exist in nasoand oropharyngeal dimensions as well as differences in tonsil volume and weights among children with varying degrees of adenotonsillar hypertrophy. These abnormalities give us some insight into why certain children with large tonsils and adenoids have obstructive symptoms while others do not. While the data from this study reveal some significant findings about children with obstructive sleep patterns, certain issues remain unclear. First, the children in the study were placed in obstructive or non-obstructive groups by subjective determination of symptoms instead of polysomnographic studies. Second, the study is limited by the necessarily static position for measurements which neglects the functional aspects of the muscle and soft tissue structures involved. Third, the number of patients in the LNO group was smaller than in the other groups.This affected the statistical significance of some of the parameters measured. However, the low number in the LNO group probably represents the rarity of having large tonsils without obstructive symptoms. Finally, and perhaps most importantly, a
10
separation of the influence of tonsillar versus adenoid hypertrophy was not undertaken and therefore the exact etiologic role of these related but separate areas has not been determined. While this study’s data indicate that children with large obstructing tonsils tend to have adenoids of greater weight and volume than children with large non-obstructing tonsils the numbers were too small to arrive at firm conclusions. Further research is underway to arrive at more precise clinical and radiological correlation of these anatomical findings as well as to further elucidate the role of the tonsils separately from the adenoids in the development of OSA in children.
Acknowledgements
Marilyn Smistek provided the fine technical preparation of the manuscript. Elena Greco prepared the drawings.
References 1 B&sky, L., Moore, L. and Stanievich, J., A comparisonof tonsillar size and oropharyngeal dimension in children with obstructive adenotonsillar hypertrophy, nt. J. Pediatr. Otorhinolaryngol., 13 (1987) 149-156. 2 Bradley, T.D., Brown, LG., Grossman, R.F., Zamel, N., Martinez, D., Philipson, E.A. and Hoffstein, V., Pharyngeal size in snorers, nonsnorers and patients with obstructive sleep apnea, N. Engl. J. Med., 315 (1986) 1327-1331. 3 Brouillette, R.T., Fembach, SK. and Hunt, C.E., Obstructive sleep apnea in infants and children, J. Pediatr., 100 (1982) 31-40. 4 Brown, LB., McClean, P.A., Boucher, R., Zamel, N. and Hoffstein, V., Changes in pharyngeal cross-sectional area with posture and application of continuous positive airway pressure in patients with obstructive sleep apnea, Am. Rev. Respir.’Dis., 136 (1987) 628-632. 5 Coccaro, P.J. and Coccaro Jr., P.J., Dental development and the pharyngeal lymphoid tissue, Otolaryngol. Clin. N. Am., 20 (1987) 241-257. 6 Crumley, R.L., Stein, M., Golden, J., Gamsu, G. and Dermon, S., Determination of obstructive site in obstructive sleep apnea Laryngoscope, 98 (1987) 301-308. 7 Haponik, E.F., Smith, P.L., Bohlman, M.E., Allen, R.P., Goldman, S.M. and Bleecker, E.R., Computerized tomography in obstructive sleep apnea, Am. Rev. Respir. Dis., 127 (1983) 221-226. 8 Jamieson, A., Guilleminault, C., Partinen, M. and Quera-Salva, M.A., Obstructive sleep apneic patients have craniomandibular abnormalities, Sleep, 9 (1986) 469-477. 9 Klein, J.C., Nasal respiratory function and craniofacial growth, Arch. Otolaryngol. Head Neck Surg., 112 (1986) 843-849. 10 Lowe, A.A., Gionhaku, N., Takeuchi, K. and Fleethan, J.A., Three-dimensional CT reconstruction of tongue and airway in adult subjects with obstructive sleep apnea, Am. J. Orthod. Dentofac. Orthop., 90 (1986) 364-374. 11 Mauer,K.W.,Staats, B.A. and Olsen, K.D., Upper airway obstruction and disordered nocturnal breathing in children, Mayo Clin. Proc., 58 (1983) 349-353. 12 Richardson, M.A., Seid, A.B., Cotton, R.T., Benton, C. and Kramer. M., Evaluation of tonsils and adenoids in sleep apnea syndrome, Laqngoscope, 90 (1980) 1106-1110. 13 RfhY, P., Guilleminault, C., Heman, J. and Powell, N., Cephalometric analysis and flow-volume loops in obstructive sleep apnea patients, Sleep, 6 (1983) 303-311.
11 14 Rivlin, J., Hoffstein. B., Kalbfleisch, J., McNicholas, W., Zamel. N. and Bryan, A.C., Upper airway morphology in patients with idiopathic obstructive sleep apnea, Am. Rev. Respir. Dis., 129 (1984) 355-360. 15 Rojewski, T.E., Schuller, D.E., Schmidt, H.S., Clark, R.W. and Potts, R.E., Synchronous video recording of the pharyngeal airway and polysomnograph in patients with obstructive sleep apnea, Laryngompe, 92 (1982) 246-249. 16 Suratt, P.M., Dee, P., Atkinson, R.L., Armstrong, P. and Wilhoit, SC., Fluoroscopic and computed tomographic features of the pharyngeal airway in obstructive sleep apnea, Am. Rev. Respir. Dis., 127 (1983) 487-492. 17 Thach, B.T., Pediatric aspects of the sleep apnea syndrome, Ear, Nose Throat J., 63 (1984) 214-221. 18 Watson, R.M., Warren, D.W. and Fischer, N.D., Nasal resistance, skeletal classification and mouth breathing in orthodontic patients, Am. J. Orthodont., 54 (1968) 367-379. 19 Wilms, D., Popovich, J., Fujita, S., Conway, W. and Zorick, F., Anatomic abnormalities in obstructive sleep apnea, Ann. Otol. Rhino]. Laryngol., 91 (1982) 595-596. 20 Yonkers, A.J. and Spaur, R.C., Upper airway obstruction and the pharyngeal lymphoid tissue, Otolaryngol. Clin. N. Am., 20 (1987) 235-239.
Linda Brodsky, Ellen Adler and John F. Stanievich Department of Otola~ngoJogy, State University of New York at Buffalo, School of Medicine ond the Children’s Hospital of &ffrrro, 219 Bvant Street, Buffalo, NY 14222 (U.S.A.) (Received 25 April 1988) (Revised version received 29 August 1988) (Accepted 18 September 1988)
Key words: Obstructive sleep apnea; Adenotonsillar hypertrophy; Oropharyngeal dimension
Sixty children (3-11 years) were evaluated to determine variations in naso- and oropharyngeal dimensions associated with tonsil and adenoid hypertrophy. The subjects were grouped according to tonsil size and a clinical history of chronic upper airway obstruction. Intraoperative measurements included oropharyngead diameter, length of the hard and soft palates, width and arch of the hard palate, nasopharyngeal volume, as well as tonsil and adenoid weights and volumes. A significantly larger oropharyngeal diameter was found in children with small, non-obstructing tonsils (P < 0.01). Children with large, non-obstructing tonsils had a similar oropharyngeal diameter to those children with large, obstructing tonsils. However, tonsil volume, not weight, was increased in the children with large obstructing tonsils as compared to those with large non-obstructing tonsils and small non-obstructing tonsils (P c 0.04). A shorter soft palate was associated with larger, obstructing tonsils (P < 0.004). The length of the hard palate was similar in all patients, however, a trend towards a higher arched palate was seen in patients with larger, obstructing tonsils. The distance from the soft palate to the posterior pharyngeal wall was greater in obstructed patients with adenotonsillar hypertrophy (P < 0.003). In patients requiring adenoidectomy, the nasopharyngeal volume prior to adenoidectomy was significantly smaller in patients with obstructive symptoms (P < 0.001). Postadenoidectomy, no significant difference was found in the nasopharynx volume amongst all subjects. These data indicate that subtle dif-
* Presented at the Scientific Session of the American Society for Pediatric Otolaryngology. Kiaweh Island, South Carolina, U.S.A., April 21-24, 1988. Correspondence: Linda Brodsky, 219 Bryant Street, Buffalo, NY 14222, U.S.A. 01655876/89/$03.50
@ 1989 Elsevier Science Publishers B.V. (Biomedical Division)
2
ferences in orophatyngeal dimensions exist which along with increased lymphoid tissue volume, lead to the development of obstructive symptoms. Etiologic considerations are discussed.
Introduction The development of obstructive sleep patterns in children has been associated with craniofacial abnormalities, cleft palate surgery and most commonly with hypertrophy of the tonsils and adenoids [3,20]. However, not every child with large tonsils and adenoids has symptoms commonly associated with obstructive sleep apnea (OSA). These include loud snoring associated with snorting or apnea, dysphagia with growth retardation, speech abnormalities, hypersomnolence and intellectual/behavioral problems [11,12]. Varying degrees of adenotonsillar hypertrophy may lead to these abnormalities. However, the role of subtle variations in the dimensions of the oropharynx and nasopharynx has not been fully elucidated. Previous studies have assessed morphologic variations in the upper airway in a number of ways. These include cephalometric radiography [3,8,14], fiberoptic endoscopy [6], acoustic reflection techniques [2,4,14], video fluoroscopy awake and asleep [15] and CT scanning with static [7], tine [a] and reconstruction of 3-D images [lo]. The use of direct measurement has previously been reported by Brodsky et al. [l] using direct intrsloperative measurements of bony and soft tissue structures thought to be relevant LO the development of OSA. The oropharyngeal dimensions in children with large obstructing tonsils were compared to children with small non-obsdructing tonsils. They found that the depth of the nasopharynx was increase& while the distance between the lateral pharyngeal walls in the obstructed children was decreased compared to non-obstructed children. In addition, in nonobstructed children an increase in patient height, weight and surface area varied positively to the increase in oropharyngeal dimension, whereas, in the patients with obstructive adenotonsillar hypertrophy, no such correlation existed. Their initial study suggested that subtle structural abnormalities may exist in obstructed patients coincident with adenotonsillar hypertrophy. To further explore these anatomic variations, the present study used direct intraoperative measurements to assess oropharyngeal and nasopharyngeal dimensions in conjunction with adenotonsillar volume and weight in obstructed and non-obstructed children as well as in normal controls.
Materials and Methods Patient population Sixty children between the ages of 3 and 11 years were divided into 4 groups: (I) Control (n = 10). Patients with no history of OSA or tonsillitis were under general anesthesia for unrelated procedures.
3
(2) Smxdl non-obstructed group (SNO) (n = 12). These patients had no history of obstructive symptoms and underwent tonsillectomy for chronic tonsillitis. Preoperatively they had small tonsils from 0 to + 1, less than 20% of the oropharyngeal airway and with no obstructive symptoms. (3) Large non-obstructed group (LNO) (n = 7). These patients had no history of obstructive symptoms and underwent tonsillectomy for chronic adenotonsillitis. Preoperatively they -had large tonsils from + 3 to +4, greater than 75% of the oropharyngeal airway measured with the tongue in the resting position (i.e. no gagging) but with no obstructive symptoms. (4) Large obstructed group (LO) (n = 31). These patients had a long history (> 1 year) of loud snoring associated with snorting or apnea, dysphagia with growth disturbances or speech abnormalities. Preoperatively they had large tonsils from + 3 to +4, greater than 75% of the oropharyngeal airway. Morphologic ana&& Prior to surgery, the patients’ age, height and weight were recorded. While under anesthesia, the patient was placed with the shoulders and neck extended and the Crow- avis mouth gag in place and maximally retracted open. Using calipers with l-mm intervals, string and a ruler the following measurements were taken (Figs. 1, 2, 3): (1) Distance between medial surfaces of the tonsils at mid tonsil (Fig. 1). (2) Distance between the anterior pillars (Fig. 1). (3) Distance between the lateral pharyngeal walls (Fig. 1). (4) The length of the soft palate (excluding the uvula) (Fig. 2). (5) The length of the hard palate from the junction of the hard and soft palate to the central incisors. (6) Width of the hard palate from the right first molar to the left first molar with the string taut (Fig. 3).
Fig. 1. Oropharyngealairway. a, distance between the medial surfaces of the tonsil at mid-tonsil; b, distance between the anterior pillars; and c, distance be?ween the lateral pharyngeal walls.
Fig. 2. Palate and Nasopharynx. d. length of the hard palate; e, anterior-posterior distance from ventral surface of the soft palate to posterior nasophatyngeal wall.
(7) Width of the hard palate from the right first molar to the left first molar with the string following the curvature of the palate. This was used to determine the arch of the hard palate (Fig. 3). (8) Anterior-posterior distance from the ventral surface of the soft palate to the posterior wall at the edge of the soft palate (Fig. 2). The nasopharyngeal volume was determined pre- and postadenoidectomy by threading a Foley catheter into each naris, inflating the balloon and occluding the posterior choana under indirect mirror visualization. The nasopharynx was then
.
I.
Fig. 3. Width and arch of hard palate.
TABLE I Demographic data SNO, small non-obstructed.
LNO, large non-obstructed. LO, large obstructed.
Control SNO LNO LO
Age (months)
Height (cm)
Weight (kg)
74.0 82.6 71.6 67.5
115 122 115 115
21 25 23 24
filled with saline to the edge of the soft palate. The saline was then suctioned into a bronchial suction trap, removed and measured in a syringe with 0.2 ml intervals. The length, width, height and weight of each tonsil was determined posttonsillectomy. The adenoid weight was also recorded. Tonsil and adenoid volume was measured by water displacement in a gradua!d cylinder. Statistical analysis The data rrere statistically analyzed using the Student’s t test for differences of the means, correlation coefficients and analysis of variance.
Demographic data There was no significant difference in mean age, height or weight among the control group, small non-obstructed (SNQ) group, large non-obstructed (LNO) group and large obstructed (LQ) group (Table I). In the control, SNO and LNQ children, age, height and weight correlated positively with all measurements. The LO children showed no correlation between any of t.he parameters measured. Oropharyngeal dimensions As anticipated, the distance between the medial surfaces of the tonsils was significantly greater in the control and the SNO groups than in the LNO and LO groups (P < 0.001). The children with SNO tonsils had a significantly larger pharyngeal diameter, as measured from lateral wall to lateral wall, than either the children with the LNO or LO tonsils (P -C0.05). There was no significant difference in oropharyngeal diameter between the comtrol and SNO groups or between the LNO and NO groups (Table II). Nasopharyngeal dimensions The LNO and LO children had smaller pre-adenoidectomy volumes than the control and SNO children. Postadenoidectomy, there was no significant difference in nasopharyngeal volumes among the groups. (Table III).
TABLE II Oropharyngeal dimensivns P-value
Medial surfaces tonsil9 (mm) 20 20 9 8
Control SNO LNO LO
l
NS -c 0.001 < 0.001
toreralpharyngeal wall diameter (mm)
P-value + *
53 58 48 49
NS‘
-
< 0.001 c 0.001
* In comparison to controls. * * In comparison to SNO. NS = not significant.
Hard and soft palate The total length of the hard and soft palates was found to be longer in the control and SNO patients than in the LNO and LO patients. However, when the hard and soft palates were measured independently there were no significant differences among the groups in the length of the hard palate. Therefore, the LNO
TABLE III Nclsopharyngml (NP) depth and volumes
Control SNO LNO LO
NP depth (mm)
P-value *
21 23 24 26
NS NS < 0.01
NP volume pre-adenoid (ml 40) 5.4 5.1 3.5 3.0
P-value +
NP volume post adenoid. (ml W)
P-value ++
NS < 0.05 C 0.01
5.6 5.1 5.8
NS NS NS
* As compared to controls and SNO groups. * As compared to each group. NS = not significant. Adenoid. = adenoidectomy. l
TABLE IV Dimensiorss of hard und soft palates Total so/l and hard palate length (mm) Control SNO LNO LO
68 70 63 61
P-value *
c 0.05 < 0.01
Soft palate length (mm) 28 28 23 21
* As compared to both control and SNO groups.
P-value +
< 0.05 co.001
Hard palate length (mm) 40 42 39 39
P-vcrlue *
NS NS
TABLE V
Width /arch of hard palate Hard palate width (mm) 30 28 30 28
Control SNO LNO LO
P-value
Hard palate arch (mm)
P-value
8.8 8.7 6.8 9.4
NS NS NS
NS NS NS
NS = not significant.
and LO groups demonstrated a shorter soft palate than the control and SNO groups. In addition, it was noted that there was a tendency for the LO group to have the shortest palates (‘Fable IV). Measurements of the width and arch of the hard palate revealed no difference in palatal width among the groups, but a trend towards a higher arch was seen in the LO group as compared to the LNO group (Table V). These results, however, did not attain statistical significance. The distance between the soft palate and the posterior pharyngeal wall was greatest in the LO group. It also coincides with the short soft palate found in this group documenting the larger oropbaryngeal airway at this level of the pharynx in children presenting with large clinically obstructing tonsils and adenoids. Tonsil and adenoid dimensions The volume of the LO tonsils was significantly greater than the LNO and SNO tonsils, although there was no difference between the weight of the LO and LNO tonsils. Small non-obstructing tonsils weighed significantly less, as expected. The LO tonsils had the greatest length, width and height which went along with the larger volumes determined by the water displacement method (Table VI).
TABLE VI
Tonsil weight and volume Tonsil P-va!ue * Vohune P-value * Length P-value * Width P-value * Height P-vaIue * weight displace(mm) (mm) (mm1 ment (gl (ml) Control _ _ _ _ _ 24 39 53 8.1 SNO 6.4 LNO LO
8.9 8.6
c 0.05 < 0.05
8.9 11.2
* Compared to SNO group. NS = not significant.
NS < 0.05
54 59
NS < 0.05
43 46
NS < 0.01
28 30
NS -z 0.01
8
Adenoids in the LO group demonstrated a trend toward a larger adenoid volume and weight than in the LNO group. The lack of statistical significance may have been due to the small number of children evaluated for adenoid dimensions.
Discussion Anatomical and physiological differences in the upper airways of patients with obstructive sleep apnea have received much attention, particularly in the adult population. The anatomical abnormalities which have been identified in the adult population include the following: reduced upper airway diameter, increased pharyngeal collapsibility, elongated soft palate, shallower palatal arch, enlarged tongue base, and reduced mandible size [2,4,6,13,15,19]. Most of the data on anatomical changes in adult patients with OSA appear to contradict findings in the present study in children ‘with OSA. The data from the present study indicate that children with obstructing tonsils and significan
9
to open up the pharyngeal aperture in response to decreased air flow and possibly chronic hypoxia [3]; or (3) they may represent alterations in facial growth from the abnormal mouth and jaw posturing which is associated with mouth breathing. Mouth breathing may result in high-arched palates through a number a! possible mechanisms as stated previously [18]. Furthermore, anatomical variations from birth may also play role. It is possible that patients born with a small decrease in lateral oropharyngeal dimension may be predisposed to obstruction by large tonsils and adenoids [IT]. It is interesting to note that the volumes of the tonsils in the SNO and LNO group were similar, suggesting that oropharyngeal dimension rather than tonsil size may be the difference between these two groups. The finding of a narrower oropharyngeal diameter in the large non-obstructed, and large obstructed children fit this congenital predisposition theory. In this instance the postulated mechanism is as follows: children are born with a small diameter oropharynx at the level of the palatine tonsils. They then develop low density/high volume tonsillar hypertrophy. During sleep, their tonsils undergo inferior and posterior displacement into the airway (as demonstrated by Brouilette et al. [3]) and they develop obstructive symptoms. In addition, children with OSA may have pharyngeal muscle hypotonia as demonstrated in adults with OSA [2], and the pharyngeal airway may actually collapse against the voluminous tonsils as they are displaced posteriorly during the negative pressure of inspiration. What is not understood at this time is why certain children develop various types of tonsillar hypertrophy (i.e. low density/high volume). Although the numbers of children studied are small, obstruction from adenoid hypertrophy at the level of the nasopharynx may be related more to the size of the adenoids rather than to the size of the nasopharynx. This is evidenced by the similarities in nasopharyngeal volume measured after adenoidectomy amongst all groups. However, in light of the similar preadenoidectomy volumes between the large obstructed and large non-obstructed groups, it can be stated that in this study, the obstruction is not at the nasopharyngeal level. The low density tonsils may play a greater role in the development of symptoms. In conclusion, this study demonstrates that subtle abnormalities exist in nasoand oropharyngeal dimensions as well as differences in tonsil volume and weights among children with varying degrees of adenotonsillar hypertrophy. These abnormalities give us some insight into why certain children with large tonsils and adenoids have obstructive symptoms while others do not. While the data from this study reveal some significant findings about children with obstructive sleep patterns, certain issues remain unclear. First, the children in the study were placed in obstructive or non-obstructive groups by subjective determination of symptoms instead of polysomnographic studies. Second, the study is limited by the necessarily static position for measurements which neglects the functional aspects of the muscle and soft tissue structures involved. Third, the number of patients in the LNO group was smaller than in the other groups.This affected the statistical significance of some of the parameters measured. However, the low number in the LNO group probably represents the rarity of having large tonsils without obstructive symptoms. Finally, and perhaps most importantly, a
10
separation of the influence of tonsillar versus adenoid hypertrophy was not undertaken and therefore the exact etiologic role of these related but separate areas has not been determined. While this study’s data indicate that children with large obstructing tonsils tend to have adenoids of greater weight and volume than children with large non-obstructing tonsils the numbers were too small to arrive at firm conclusions. Further research is underway to arrive at more precise clinical and radiological correlation of these anatomical findings as well as to further elucidate the role of the tonsils separately from the adenoids in the development of OSA in children.
Acknowledgements
Marilyn Smistek provided the fine technical preparation of the manuscript. Elena Greco prepared the drawings.
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