Dimensions of the Cleft Nasal Airway in Adults: A Comparison With

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1 Dimensions of the Cleft Nasal Airway in Adults: A Comparison With Subjects Without Cleft W. MicHiaAeL HairFieup, D.D.S., M.S. DonaLo W. Warren, D.D.S., Ph.D. The prevalence of mouthbreathing among individuals with cleft lip and palate is significantly higher than in the normal population. This has been attributed to nasal deformities that tend to reduce nasal airway size. The purpose of the present study was to determine how a heterogeneous adult group with cleft lip and palate differs in terms of nasal airway cross-sectional area from an adult > group without cleft during the inspiratory and expiratory phases of breathing. The pressure-flow technique was used to estimate nasal airway size in 15 adults without cleft (15 years or older) and 37 adults with cleft lip, cleft palate, or both. Mean areas and standard deviations for subjects without cleft were 0.63 cm* during inspiration and 0.56 cm' during expiration. This difference is statistically significant (p < 0.01). Mean areas and standard deviations for all subjects with cleft were 0.37 cm' during inspiration and 0.40 cm* during expiration. This difference is not statistically significant (p > 0.15). Twenty-two of the subjects with cleft had nasal areas considered to be impaired (below 0.40 cm*) as compared with only three of the subjects without cleft. A two factor analysis ofvariance (ANOVA) demonstrated that area changes during respiration are different for subjects with and without cleft (p < 0.005), and that cleft nasal areas are smaller than noncleft areas for both phases of breathing (p < 0.001). Inspiratory-expiratory differences between subjects with and without cleft are probably the result of developmental defects, reparative surgery or both. The findings from this study confirm the presence of impairment in a significant proportion of the cleft population and suggest that physiologic responses to impairment may be different. KEY WORDS: upper airway, nasal area, impairment, nasal valve, cleft palate. Nasal airway abnormalities resulting from clefts of the lip and palate, such as septal deformities, atresia of the nostrils, and turbinate and mucosa hypertrophy, diminish airway size (Drettner, 1960; Foster, 1962; Aduss and Pruzansky, 1967; Warren et al, 1969). Warren et al (1969) reported that nasal resistance in the cleft population is about 20 to 30 percent higher in each age group than in the noncleft population. They suggested that abnormally high nasal resistance has important implications for breathing and speech. Hairfield et al (1988) have proposed that the prevalence of mouthbreathing in the cleft population is high. The issue of how impaired nasorespiratory function influences dentofacial growth is more controversial. Harvold et al (1973), on the basis of studies in primates, believe that an open clear nasal airway is a prerequisite to normal facial form and function. Korkhaus' studies (1960) suggest that The authors are affiliated with the University of North Carolina at Chapel Hill. Dr. Hairfield is Assistant Professor, Department of Dental Ecology and Dental Research Center. Dr. Warren is Kenan Professor and - Director, Oral-facial and Communicative Disorders Program, Department of Dental Ecology and Dental Research Center. This paper was supported in part by Grant #s DEOO0129, DEON6957, DEO7105, from the National Institute of Dental Research. maxillary arch form, nasal cavity size, and breathing mode are interrelated in a complex way. Many researchers dispute the contention that nasal airway inadequacy routinely alters dentofacial growth (Humphrey and Leighton, 1950; Leech, 1958; Watson et al, 1968; Warren, 1980; Vig et al 1981). It is true, however, that dentofacial deformities and surgical treatment of velar inadequacy tend to affect nasal respiration adversely (Warren, 1980). We previously reported a method for estimating the smallest cross-sectional area of the nasal passages during quiet respiration (Warren, 1984a; Hairfield et al, 1987). For individuals without cleft we observed that the expiratory nasal cross-sectional area is approximately 10 percent smaller than the inspiratory area. We attributed this finding to expiratory braking at the nasal valve, probably in coordination with laryngeal braking. Expiratory braking acts to allow adequate time for gas exchange at the alveoli (Gautier et al, 1973; Jackson, 1976). There is no comparable information available on individuals with cleft lip and palate. The expiratory-inspiratory size difference in individuals without cleft has been attributed to the nasal valve, a structure located in the region between the upper and lower lateral cartilages and the pyriform aperture just beyond the anterior ends of the inferior turbinates. It is about 1.5 to 2.5 cm posterior to the external aperture (Cole, 1982). The

2 10 Cleft Palate Journal, January 1989, Vol. 26 No. 1 nasal valve is easily compromised by displacements, distortions, or scarring of tissues in this region (Turvey et al, 1984). Additionally, the presence of septal deformities and turbinate hypertrophy may result in the smallest crosssectional area of the nose being shifted from the nasal valve to a more posterior location. When such deformities are present the differences in inspiratory and expiratory size would be minimized. The purpose of the present study was to measure nasal cross-sectional area in a group of subjects with cleft lip and palate and to compare the data with those of a control group of subjects without cleft. More specifically, we wanted to determine if the same size difference observed in the noncleft population between phases of breathing is present in the cleft population. METHODS The minimum cross-sectional area of the nasal airway was measured in a heterogeneous sample of 37 adult (15 years or older) subjects with cleft. Their diagnoses are listed in Table 1. Subjects who had pharyngeal flaps or reported that they were congested, had vasomotor rhinitis, were being managed for allergies, or taking decongestants were excluded from the study. Characteristics of the 15 subjects without cleft were described previously (Hairfield et al, 1987). The pressure-flow technique was utilized as reported previously for normal subjects (Warren et al, 1987a; Hairfield et al, 1987). In brief, a nasal cap that would not distort the nose and would offer only negligible dead space was selected for each patient. The pressure drop across the nose was measured by placing one catheter in the mouth and the other in the nasal cap. Each catheter was attached to a pressure transducer (Validyne model MP45). Airflow was measured by a heated pneumotachograph (Fleish) attached to the nasal cap. The subject was asked to breathe quietly in and out of the nose, and the resulting pressure and airflow data were sent to a 12-bit analog-to-digital converter (Data Translation) to be processed by an IBM/AT microcomputer. Three inspiratory and two expiratory values were averaged separately for each subject. Significant differences between inspiratory and expiratory values for all subjects were determined using the paired t-test. Comparisons were made between subjects with and without cleft using an ANOVA. TABLE 1 Diagnostic Group Code, Diagnosis, and Respective Sample Number for All Subjects Diagnostic Group Code Diagnosis N - 0 Without cleft 15 1 Right or left unilateral complete 11 cleft of the primary and secondary palate 2 Bilateral complete cleft of the 9 primary and secondary palate 3 Secondary palate: velum with or 9 without hard palate involvement 4 Primary palate: unilateral or 5 bilateral involvement 35 Submucous cleft 3 RESULTS Mean nasal cross-sectional area (cm* + S.D.) for normal subg'ects was 0.63 cm* during inspiration and 0.56 cm" during expiration. This difference is statistically significant (paired t-test, p < 0.01). As previously reported, inspiratory areas were significantly greater by almost 10 percent than expiratory areas for subjects without cleft. Nasal cross-sectional areas averaged together for all subjects with cleft during inspiration and expiration were 0.37 cm* and 0.40 cm' , respectively. This difference is not statistically significant (paired t-test, p > 0.15)., Areas for each respiratory phase, paired t-test results, the ratios of inspiratory to expiratory area, and the percentages of subjects with nasal impairment for each diagnostic group are given in Table 2. The only group with cleft with a statistically significant difference between the phases of respiration was bilateral complete cleft of the primary and secondary palate, and the phasic difference was in the opposite direction of subjects without cleft (see Table 2). A two-factor ANOVA with a repeated measure on the respiratory phase demonstrated that inspiratory to expiratory values for subjects without cleft are significantly different from inspiratory to expiratory values for all subjects with cleft averaged together (F = 8.67, p < 0.005). Both inspiratory and expiratory areas for subjects with cleft were found to be smaller than the corresponding area for subjects without cleft (F = 17.0, p < ). A two-factor ANOVA with a repeated measure on the respiratory phase was used to test for differences among all of the diagnostic groups (one without cleft and five with cleft). The respiratory phase by diagnostic group interaction was significant (F = 4.39, p < 0.002). Duncan's multiple range test was used to determine which groups were significantly different from each other. Table 3 lists the diagnostic group, the value of the variable for each group in descending order, and the Duncan grouping for each of the three following variables: inspiratory area, expiratory area, and inspiratory to expiratory area ratio. Inspiratory noncleft areas were significantly different from all cleft areas; however, none of the cleft areas was significantly different from each other (p < 0.05). The other two variables had more complicated groupings as shown in Table 3. The ratio of inspiratory to expiratory area was for all subjects with cleft averaged together as compared with a ratio of for subjects without cleft. These ratios are significantly different (t-test, p < 0.008). Tables 2 and 3 give the ratios and Duncan grouping by diagnostic group, respectively. In previous studies we reported that in adults a nasal area of less than 0.40 cmconstitutes nasal airway impairment (Warren, 1984a, 1987a, 1987b, 1987c). Only three (20 percent) of the 15 subjects without cleft had total nasal crosssectional areas less than 0.40 cm*, whereas 22 (60 percent) of the 37 subjects with cleft had nasal areas less than this value (see Table 2). DIscUssION The data from this study demonstrate that nasal crosssectional area in adults with cleft lip and palate is consid-

3 Hairfield and Warren, DIMENSIONS OF CLEFT NASAL AIRWAY 11 TABLE 2 Comparison of Areas, Phasic Ratios, and Percentages, With Impairment Between Subjects With and Without Clefts Inspiratory- Nasal Area Inspiratory Expiratory Paired Expiratory <0.40 cm Diagnostic Group (cm' + S.D.) (cm' + S.D.) t-test Ratio (% & Ratio) <0.01* % (3/15) > # % (5/11) <0.03* % (6/9) > % (6/9) > % (3/5) > # % (2/3) All Clefts Averaged Together > % (22/37) * Meets our criteria for being significantly different at the p < 0.05 level. erably smaller than in an adult group without cleft. The overall difference was 40 percent during inspiration and 29 percent during expiration. This finding is not unexpected, since Warren et al (1969) reported high nasal resistance in the cleft population, and Hairfield et al (1988) observed a high percentage of mouthbreathing. Septal deformities, turbinate hypertrophy, vomerine spurs, atresia of the nostrils, and maxillary deficits all contribute to nasal airway impairment, and these abnormalities are routinely present in individuals with clefts. Indeed, Siegel et al (1987) reported that septal defects and turbinate hypertrophy are present even in utero. Although a clear difference between inspiration and expiration was noted in the adult group without cleft, the group with cleft did not demonstrate a size difference overall. Hairfield et al (1987) provided strong evidence that, in persons without cleft, the difference can be attributed to nasal valve function. Neither tygon tubing inserts, which enlarged the external aperture, nor a decongestant, which increased area values by 23 percent, affected the relative differences noted between inspiration and expiration. Nasal valve size, however, is modified easily by a variety of factors. Mucosal swelling of the inferior turbinates can diminish valve size (Bridger and Proctor, 1970). The anterior portion of the turbinates impinge on the valve and any engorgement will diminish size, apparently without altering nasal valve phasic behavior. The results of the a posteriori Duncan grouping strongly suggest that the major difference between noncleft and cleft respiration occurs during inspiration. This is consistent with the findings of Strohl et al (1980), who described the acti- vation of the dilator naris during inspiration and its relaxation during expiration. Individuals with cleft may lack adequate dilator naris activity or attachment. During expiration, subjects without cleft differed only from the secondary palate (with or without hard palate involvement) group and the submucous group, which supports our belief that these groups have constrictions posterior to the nasal valve region.» One possible alternative explanation for our failure to observe a phasic difference in the cleft population, except in the group with bilateral complete cleft of the primary and secondary palate, is that in subjects without cleft the technique measures nasal valve size, whereas in subjects with cleft it is influenced by other possible constrictions as well. For example, in individuals with severe septal deformity, the technique may provide a measure or estimate of the composite of two constrictions, and the septal constriction would not be expected to exhibit a phasic difference. Thus, for subjects with cleft we cannot attribute the lack of difference in size between inspiration and expiration to the nasal valve alone. We believe that the phasic difference for the bilateral complete cleft of the primary and secondary: palate group is caused by inspiratory pressure collapsing the unsupported valve and expiratory pressures blowing th valve open. V - The findings from this study also confirm the presence of impairment (i.e., nasal cross-sectional area less than 0.40 cm-*) in a significant proportion (60 percent) of the adult cleft population. Twenty-two of 33 subjects demonstrated nasal area size of less than 0.40 cm. Studies of normal and nasally-impaired adults (Warren et al, 1987a), modeling TABLE 3 A Posteriori Analysis Using Duncan's Multiple Range Test* Inspiration Expiration Ratio Mean Mean Duncan Mean Inspiratory- Duncan Diagnostic Inspiratory Grouping Diagnostic Expiratory Duncan Diagnostic Expiratory Grouping Group Area (p < 0.05) Group Area (p < 0.05) Group Ratio (p < 0.05) A A A B A/B A B A/B A B A/B A/B B B A/B B B B * Groups with the same letter are not significantly different from each other. («= 0.05 df = 46)

4 12 Cleft Palate Journal, January 1989, Vol. 26 No. 1 studies (Warren, 1984a; Warren et al, 1984b), and extrapolation of data from nasal resistance studies (Watson et al, 1968; McCaffrey and Kern, 1979; Warren et al, 1987 ) indicate that airway impairment in adults occurs when the smallest cross-sectional area of the nose is less than 0.40 cm*. Areas greater than 0.40 cm during resting breathing usually meet respiratory requirements without physical constraints imposed by the relationship of area to airflow rate (Warren et al, 1987a). Other studies performed in our laboratory imply that adults with cross-sectional areas less than 0.40 cm" should mouthbreathe to some extent (Warren et al, 1984b; Hinton et al, 1987; Watson et al, 1968). A recent study (Warren et al, 1988) confirms this. These data seem to disagree with recent data from Sandham and Solow (1987); however, there were several major differences between their study and ours. They used decongestants on all subjects, which removes the effects of mucosa and turbinate hypertrophy. Their control group consisted of individuals without cleft who were referred for orthodontic treatment; in our experience this group tends to have a more constricted airway than a nonorthodontic group. The average age of their subjects was 14.4 years; since growth of the nose ceases around 15 years of age, we separated and reported on individuals 15 years or older as adults and those less than 15 years aschildren. Changes in the nasal mucosa and the nasal valve are controlled during inspiration and expiration to provide a sufficient and balanced respiratory lumina in the nasal cavities (Stoksted, 1953). Nasorespiratory balance may be perturbed for individuals with cleft palate who already demonstrate nasal abnormalities and maxillary deficits. Loss of nasal valve patency may lead to respiratory difficulties or to compensatory behaviors elsewhere in the system. For example, we have observed one subject who is lacking cartilaginous support of her nasal valve and therefore inspires through her mouth and expires through her nose. Dynamic changes in the nose can be viewed as being part of a regulation-control system (Warren, 1986). Nasal blood flow, airway dimensions, and the quantity and quality of nasal secretions are all subject to fine adjustment, although the actual reflex arcs are unknown (Proctor and Swift, 1977). Researchers have noted a coordination of pulmonary mechanics and modulation of airway resistance from the nostrils to the alveoli (Cole, 1976, 1982; Drettner, 1970, 1979; Ferris et al, 1964; Lacourt and Polgar, 1971). The nose can compensate to some degree for losses or increases in resistance at the other major resistive segments of the respiratory tract. Nasal and maxillofacial surgery and orthodontic treatment (i.e., rapid maxillary expansion) have been shown to change the course of airflow through the nose (Wertz, 1968; Warren et al, 1987b). Some individuals with cleft lip and palate have been shown to use the nasal airway to compensate for velopharyngeal incompetence (Warren, 1967, 1969). Turvey et al (1984) reported that superior repositioning of the maxilla, with or without involvement of the nasal floor, almost always resulted in decreased nasal airway resistance, in spite of the fact that this procedure reduces nasal cavity volume. They attributed the decrease in nasal airway resistance to widening of the external nares and opening of the nasal valve. Orthodontic and surgical expansion of the maxilla appears to improve airway patency similarly by increasing alar width and nasal valve size (Warren et al, 1987b; Guenthner et al, 1984; Timms, 1986; Hartgerink et al, 1987). Currently, we are investigating other conditions in which alterations of the nose may affect an individual's speech or respiratory capacities. A number of factors could have affected the findings in this study, e.g., sex, age, condition of paranasal sinuses, use of hormonal birth control or antihypertensive medication, or history of septoplasties or closed-open rhinoplastic procedures. However, the purpose of this initial investigation was to document quantifiable differences rather than to establish the etiology of variations in nasal respiratory behavior between subjects with and without cleft. CONCLUSION In this paper we have demonstrated that there are dimensional and physiologic differences in nasal airway size between adults without cleft and adults with surgically repaired cleft lip or cleft palate. Aerodynamic techniques provide a useful tool for estimating the effective cross-sectional area of the nasal airway during both phases of respiration. These findings may provide a more detailed criteria for defining impaired nasorespiratory function. Future studies in our laboratory should allow us to determine whether detrimental compensatory respiratory behaviors are related to the absence of nasal expiratory braking. REFERENCES Apuss H, PrUzZANsKkYy S. (1967). The nasal cavity in complete unilateral cleft lip and palate. Arch Otolaryngol 85: BrRipoGER GP, PROCTOR DF. (1970). Maximum nasal inspiratory flow and nasal resistance. Am J Otol 1970; 79: P. (1976). The extrathoracic airways. J Otolaryngol 5: Core P. (1982). Upper respiratory airflow. In: The nose-upper airway physiology and the atmospheric environment. The Netherlands: Elsevier Biomedical Press, DRETTNER B. (1960). The nasal airway and hearing in patients with cleft palate. Acta Otolaryngol 52: DrETTNER B. (1970). Pathophysiological relationships between upper and lower airways. Am J Otol 79: DRETINER B. (1979). 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