The effects of adenotonsillectomy on growth in young children EDWIN F. WILLIAMS III, MD. PEAK WOO, MD. ROBERT MILLER, MD. and ROBERT M. KELLMAN, MD. Syracuse, New York

A history of poor weight gain can often be elicited In young children with chronic upper airway obstruction resulting from adenotonslllar hypertrophy. A series of 41 consecutive children under 3 years of age. who underwent Inpatient adenotonslllectomy, were reviewed for changes In weight and height. Thirty-seven patients had adequate longterm followup. Of these. many had dramatic Improvements In growth after adenotonslllectomy. Indications for surgery In this group were recurrent Infection In three patients (7%). unilateral tonsillar mass In one patient (3%). and upper airway obstruction In 37 patients (90%).A clear history of sleep apnea was elicited In 59%. At the time of surgery. 19 of 41 patients (46%) were of the fifth percentile or lower for age-corrected weight. The Inpatient hospital stay averaged 3.2 days. The postoperative complication rate was 27'0. with postoperative stridor as the most common complication. After surgery. 28 children (75%)showed a change to a higher percentile for weight. Twenty-four (65%) had percentile changes of 15%or more. This change Is significant according to results of the Wilcoxon signed-rank test (p < 0.001). We conclude that a relationship exists between Improved growth rate and adenotonslllectomy In our study group. The rapid Improvement In growth appears to be most obvious In children with upper airway obstruction resulting from adenotonslllar hypertrophy. Upper airway obstruction (including andenotonslllar hypertrophy) should be suspected as a possible cause In the workUp of children with suboptimum growth. (OTOLARVNGOL HEAD NECK SURG 1991;104:509,)

The deleterious effects of hypertrophic tonsils and adenoids in children that cause intermittent airway obstruction, obstructive sleep apnea, chronic alveolar hyPOventiiation, and subsequent cor pulmonale were first reported more than 20 years ago. 1.2 These reports demonstrated reversible pathophysiology, which generated mUch interest in prevention and early diagnosis of this process. 3-14 Although cardiopulmonary sequelae of pulmonary hypertension-including cor pulmonale and Ultimately death-may develop in only a small number

From the Departments of Otolaryngology and Communicative Sciences and Pediatrics. State University of New York. Health Science Center at Syracuse (Drs, Williams, Woo, Miller, and Kellman), and the Veterans Administration Medical Center (Drs. Woo and Kellman). Presented at the Annual Meeting of the American Academy of Otolaryngology - Head and Neck Surgery. New Orleans. La., Sept. 24-28. 1989. Received for publication Sept. 26. 1989; revision received Sept. 24. 1990; accepted Nov. 21, 1990. Reprint requests: Edwin F. Williams III. MD. Department of Otolaryngology, SUNY Health Science Center at Syracuse, 750 East Adams St.• Syracuse. NY 13210.

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of children, these children appear to be part of a much larger group affected by partial upper ariway obstruction, most commonly resulting from adenotonsillar hyperplasia. This clinical entity, called obstructive sleep apnea syndrome (OSAS), is characterized by sleeprelated airway obstruction resulting in apneic episodes, nocturnal hypoventilation, and carbon dioxide retention. S.12.IS By definition, sleep apnea syndrome is the occurrence of at least 30 apneic episodes of 10 seconds or longer in 7 hours of sleep as recorded by polysomnographic techniques." Additionally, other symptoms often reported include heavy snoring,":" sleep disturbances and daytime hypersornnolence," decreased school performance and personality changes,4.11 recurrent enuresis, II morning cephalgia," oral respiration, 14 hyponasal speech and growth disturbances.t'v-":":" Stool et a1. 5 described OSAS in obese children that resembled a pickwickian syndrome." However, most authors have reported OSAS in association with subnormal or retarded growth.4.12.14.16-18 Lind and Lundell" reported a significant increase in weight and length in 14 Swedish children, first seen with obstructive airway symptoms, who underwent adenotonsillectomy. Most documented improvements, however, had been anecdotal case reports.4.12.14.16-18

50'

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Table 1. Demographics sex distribution Sex

No. of patients

Male Females

27 14

Age Distribution Age

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66% 34%

Table 2. Indications for surgery Symptoms

No. of patients

Obstructive symptoms Recurrent infection Unilateral tonsillar mass

37 3 1

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90% 7% 3%

The purpose of this study was to determine the incidence of growth disturbance and what effect, if any, tonsillectomy and/or adenoidectomy has on subsequent growth in a group of children believed to be at high risk for OSAS .

PATIENT SELECTION AND METHOD OF ASSESSMENT To identify children at high risk for OSAS , a retrospective review was done according to the following criteria: In Syracuse, New York, outpatient adenotonsillectomy is standard practice for otherwise healthy patients over 1 year of age, and only children with OSAS or other medical problems are treated as inpatients. Therefore only charts of inpatient adenotonsillectomies were reviewed for University Hospital and Crouse-Irving Memorial Hospital (private tertiary care hospital) from 1981 to 1989. In addition, because the onset of symptoms is more common in infancy and very early childhood.v" only charts of adenotonsillectomies in children less than 3 years of age were reviewed. Available preoperative data were collected, including sex, age at surgery. symptoms. duration of symptoms, indication for surgery, presence of sleep apnea, additional medical problems, preoperative weight, and preoperative height when available. Preoperative weight and height were plotted on a standard Ross growth and development curve appropriate for sex

(mo.)

No. of patients

0·6 6 - 12 12 - 18 18 - 24 24 - 30 30 - 36

1 7 10 7 8 8

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2.5% 17.0% 24.5% 17.0% 19.5% 19.5%

and age. 19 Age-corrected percentiles taken directly from the growth curve were used for comparison. Follow-up data were collected by obtaining postoperative weight and height or the child's growth curve from the referring primary care physician. Weights and heights were converted to percentiles corresponding to the appropriate age and sex. Percentile values for preoperative and postoperative weights and heights were compared by means of the Wilcoxon signed-rank test.

RESULTS Between January 1981 and June 1989, a total of 41 inpatient adenotonsillectomies were performed in children less than 3 years of age. There were 27 boys and 14 girls (Table I). The age distribution ranged from 6 months to 36 months (Table I). The indications for surgery in this group of patients are shown in Table 2, with the most common indication being upper airway obstruction in 37 patients (90%). A clear history of sleep apnea was elicited in 59%. Thirteen patients (32%) had significant additional medical problems, including seizure disorders in two, prematurity in four, Down's syndrome in two, bronchomalacia in one, recurrent bronchiolitis in one, severe neurologic sequelae as a result of trauma in one, congenital thrombocytosis in one, and asthma in one. At the time of surgery, median weight was below the fifth percentile as plotted on a Ross growth and development curve in 19 of 41 patients (46%), as shown in Fig. 1, A. Preoperative height was obtained in 34 of 41 patients. The median height was below the fifth percentile in 15 of 34 patients (44%) in this category. Surgery included adenotonsillectomy in 32 patients and adenoidectomy alone in nine patients. The inpatient hospital stay averaged 3.2 days. The postoperative complication rate was 27%, with postoperative stridor the most common complication requiring reintubation and monitoring in the intensive care unit in two patients.

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Effects of adenotonsillectomy on growth in young children

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Fig. 1. A, Preoperative age-corrected weight percentile distribution of 41 children less than 3 years of age undergoing adenotonsillectomy as inpatients. B, Postoperative age-corrected weight percentile distribution in 37 follow-up cases.

Postoperative weight percentile followup was obtained in 37 patients, with an average follow-up period of 11.6 months. The postoperative weight distribution histogram is illustrated in Fig, I, B, with individual weight percentile changes shown in Fig. 2. Thirty-one patients (75%) had an increase in the age-corrected weight percentile. Twenty-seven patients (66%) showed a change of 15% or more. This percentile change was significant (p > 0.(01). Postoperative height percentile data were

obtained in only 18 patients. Ten (55%) had an increase in height, as shown in Fig. 3. This increase was not statistically significant (p < 0.(01). DISCUSSION

OSAS, initially described in adults, has become a well-recognized clinical entity in chiidren.4.8·10·14.16 Although the incidence of OSAS in children is currently unknown, Brouillette et at. 14 reported an early onset of

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112 WILLIAMS III at 01.

ADENOTONSILLECTOMY AND WEIGHT tl

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obstructive symptoms in children. In their study, 21 of 22 patients had onset of symptoms before 3 years of age. This suggests a predilection of OSAS in young children and infants. In our study, a high percentage (90%) of young children were undergoing adenotonsillectomy for obstructive symptoms, as shown in Table 2. The age distribution of patients was relatively even (Table I). This suggests that an incidence of OSAS exists beyond 3 years of age, but it was not included in our study. A preponderance of males has been noted in previous studies .:1-4.14 This was also noted in our study, with males representing 66% of the cases, as shown in Table 1.4 The cause of upper airway obstruction resulting in OSAS in children less than 5 years of age is most commonly adenotonsillar hypertrophy. This is supported by other series and by our data.":' The complex nature of this disorder must not be underemphasized. There is a high incidence of patients with coexisting medical problems. Neurologic dysfunction, such as tri-

somy 21, hydrocephalus, cerebral palsy, and Chiari malformation, has been reported by others.Y" We noted a 32% incidence of additional medical problems in our study group. In an attempt to identify the site of obstruction, Richardson et al.' evaluated 15 patients by means of polysomnographic techniques combined with videofluoroscopy. The four areas of obstruction observed were hypopharyngeal collapse, descent of tonsils, posterior tongue displacement, and occlusion of the retropharyngeal sphincter. Although all four of these areas of obstruction were not present in all patients, most patients had multiple areas of obstruction that acted in concert. These findings are in keeping with the hypothesis of Brouillette et al. 14 that anatomic and physiologic factors are important in the pathogenesis of obstructive sleep apnea in children. These investigators proposed that oropharyngeal occlusion occurs whenever the collapsing force of negative pressure exceeds the dilating forces maintaining the pharyngeal airway. These dilat-

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Effects of adenotonsillectomy on growth in young children

513

ADENOTONSILLECTOMY AND HEIGHT 100 PBlCOOILE 80 60

40 20

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ing forces are primarily maintained by sustained muscular contraction and tone. Thus, in addition to the presence of adenotonsillar hypertrophy, neuromuscular Control of the airway is often impaired, thereby resulting in sleep-related obstruction. Fortunately, in patients with no identifiable craniofacial or congenital anomalies adenotonsillectomy is usually effective in relieving the sleep-related obstruction and its associated syrnptoms. 3 .S .7.9 . 13. 14 This was also observed in our series. Adenoidectomy alone was as effective as adenotonsillectomy in relieving symptoms and improving growth When the adenoids were believed to be the primary site of obstruction. Of nine patients undergoing adenoidectomy alone, all but one had an increase in the agecorrected weight percentile. Four of these patients had increases of 20% or more postoperatively. This was statistically significant when compared by means of the Wilcoxon signed-rank test (p < 0.001). In our experience, when obstructive sleep apnea in this population is not relieved by adenotonsillectomy, tracheostomy is

often necesssary to avoid symptoms associated with OSAS, including impaired growth and cardiopulmonary sequelae. In one patient in whom adenotonsillectomy and uvulopalatopharyngoplasty were performed, no improvement in symptoms or weight change was observed. Two months subsequent to the initial procedures, the patient underwent tracheostomy. Symptoms improved dramatically. Over the following 60 days, this patient went from the fifth to the twenty-third age-corrected weight percentile. Diagnosis of OSAS is complicated by its paucity of daytime symptoms. This often results in delay of diagnosis in these children. 6.8 The usefulness of polysomnographic techniques is well accepted in diagnosing significant obstructive sleep apnea and demonstrating improvement postoperatively. 3.6-8. 13 However, these procedures are not readily available to most primary care physicians and are often difficult to perform in young children. Rowe et al. 9 reported a reliable means of determining significant airway obstruction occurring

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OtolaryngologyHead and Neck Surgery

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during sleep in infants by means of transcutaneous electrodes while continuously monitoring P,02 and P,C0 2.9 Brouillette et al. 14 developed a method based on patient history to determine an obstructive sleep apnea score that was thought to be beneficial in identifying those patients who would be helped by surgery. In our experience, an accurate history will generally result in a diagnosis. It is essential to obtain an accurate sleep history. Examination of the patient's oropharynx frequently does not demonstrate enlarged tonsils. Examination of patients while they are sleeping is very desirable. Often children do not have breathing difficulties while they are awake. A tape recording of the first 60 minutes of a child's nighttime sleep is usually very helpful in demonstrating obstructive sleep apnea. The association between growth disturbance and obstructive sleep apnea was first recognized by Guilleminault et al. 4 Five of eight patients in this series were reported to be underweight, and two were considered overweight. Subsequently, Brouillette et al." reported failure to thrive in 27% of 22 infants studied for obstructive sleep apnea. With relief of the upper airway

obstruction, these patients demonstrated a "catch-up" growth pattern. Several case reports in the literature also support a "catch-up" growth pattern, once the upper airway obstruction has been relieved. 16-18 Our data are in agreement with the concept of "catch-up" weight gain after surgery in these children. Two typical cases and their growth curves are shown in Fig. 4. Characteristic of the pattern observed is a dramatic deceleration in growth of these children, many falling off the growth curve. Postoperatively weight gain occurs rapidly, and the child appears to return to his or her premorbid growth curve. A retarded growth pattern was common in our study group. Preoperatively, 46% of 41 patients were below the fifth percentile for weight. Some changes in weight percentiles were dramatic. Seventy-five percent of children demonstrated an increase in age-corrected weight percentiles. Sixty-six percent showed a percentile increase of 15% or more. Height appeared to be less affected in our group. Preoperatively, 44% of patients were below the fifth percentile for age-corrected height. Postoperatively, increases in the age-corrected percentile for height were

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Volume 104 Number 4 April 1991

Effects of adenotonsillectomy on growth in young children

observed. This was not statistically significant. It is important to acknowledge the shortcomings of any retrospective study and conclusions based on these data; however, the dramatic changes in postoperative percentiles appear to support our conclusions. A prospective study designed to randomly assign subjects to surgical and nonsurgical groups would more appropriately determine the effects of adenotonsillectomyon growth rate. Although adenotonsillectomy can be performed safey as an outpatient procedure, we believe strongly that young children undergoing adenotonsillectomy for obstructive symptoms are at increased risk for postoperative complications. Our complication rate was 27%. In the immediate postoperative period, many children have stridor and need close observation. Adenotonsillectomy in young children in which OSAS is suspected should be done in an inpatient hospital setting. The cause of retarded growth in OSAS is not known. SUboptimum growth associated with OSAS may be the result of several factors caused by upper airway obstruction. Results of polysomnographic studies in children with OSAS reveal the highest incidence of hypopnea and apnea during stages I and 2 of sleep. This decreases significantly after adenotonsillectomy.V-" Secretory episodes of growth hormone occur 90 to 120 minutes after the onset of sleep, are associated with Slow-wave sleep, and account for a large proportion of growth hormone secretion.":" It is possible that impaired growth hormone secretion in children with OSAS is a result of interrupted slow-wave sleep, but this has never been demonstrated. Bates et aI. 17 believe that impaired secretion or action of growth hormone is the result of apnea-induced hypercarbia and tissue acidosis. Other mechanisms could include poor appetite and difficulties in feeding, resulting in a lower total caloric intake. In addition, the "work of respiration" in children With OSAS may be increased, thus requiring a greater expenditure of calories. Failure to thrive is defined in the pediatric literature as weight consistently below the third percentile for age or growth that rapidly crosses percentiles downWard.22-24 Although failure to thrive associated with OSAS may be relatively uncommon in comparison to the more common causes of suboptimum growth, it is interesting to note that upper airway obstruction has not been reported as a cause of failure to thrive in any of the larger studies on the subject. 22·24 Sills," in a report On 185 patients with failure to thrive, attributed 58% to nonorganic causes, 18% to organic causes, and 24% to undetermined causes." In those patients for whom the cause was not determined, it is possible that failure

115

to thrive may have been the result of significant sleeprelated intermittent airway obstruction, because many of these children characteristically lack daytime symptoms of obstruction. In children who fail to thrive, OSAS should be considered in the differential diagnosis. In summary, OSAS in children is associated with a suboptimum growth pattern. Early recognition of OSAS is important to avoid delayed growth and other sequelae of this syndrome. Adenotonsillectomy can be effective in relieving upper airway obstruction and restoring a more normal growth pattern in most patients. Because these patients are considered high risk, they should undergo surgery as inpatients. The primary care physician must be aware that obstructive sleep apnea in children, often heralded by snoring, can manifest itself with failure to thrive. This necessitates a high index of suspicion in children less than 5 years of age with history of snoring, apnea, and suboptimum growth. We wish to thank Ms. Joanne Schoonmaker, Ms. Linda Bookman, and Ms. Joanne Chilton for their assistance with statistical analysis, tables. and graphs, and Ms. Dawn Maree Girndt for her patience in the preparation of the manuscript. REFERENCES

1. Noonan JA. Reversible cor pulmonale due to hypertrophied tonsils and adenoids: studies in two cases. Circulation 1965; 31/32:164-8. 2. Menasch V, Farrehi C. Miller M. Hypoventilation and cor pulmonale due to chronic upper airway obstruction. J Pediatr 1965;67:198-203. 3. Richardson MA, Seid A. Cotton RT, Benton C. Kramer M. Evaluation of tonsils and adenoids in sleep apnea syndrome. Laryngoscope 1980;90: 1106-10. 4. Guilleminault C. Eldridge FL, Simmons B. Dement W. Sleep apnea in eight children. Pediatrics 1976;58:23-30. 5. Stool SE. Eavey RD, Stein NL. Sharrar W. The "chubby puffer syndrome." Clin Pediatr 1977;16:43-50. 6. Frank Y, Kravath RE, Pollak CP, Weitzman E. Obstructive sleep apnea and its therapy: clinical and polysomnographic manifestations. Pediatrics 1983;71:737-41. 7. Eliaschar I, Lavie P, Halperin E. Gordon C. Alroy G. Sleep apnea episodes as indications for adenotonsillectomy. Arch 010laryngol Head Neck Surg 1980:106:492-6. 8. Brouillette RT. Ferubach SK. Hunt C. Obstructive sleep apnea in infants and children. J Pediatr 1982;100:31-40. 9. Rowe LD. Hansen TN. Nielson D. Tooley W. Continuous measurements of skin surface oxygen and carbon dioxide tensions in obstructive sleep apnea. Laryngoscope 1980;90:1797-803. 10. Potsic WP. Sleep apnea in children. Otolaryngol Clin North Am 1989;22:537-44. II. Grundfast KM. Wittich DJ. Adenotonsillar hypenrophy and upper airway obstruction in evolutionary perspective. Laryngoscope 1982;92:650-6. 12. Lind MG, Lundell PW. TonsiIlar hyperplasia in children. Arch Otolaryngol Head Neck Surg 1982;108:650-4. 13. Mangat D. Orr WC. Smith R. Sleep apnea. hypersomnolence

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14.

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18.

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and upper airway obstruction secondary to adenotonsillar enlargement. Arch Otolaryngol Head Neck Surg 1977;103:383-6. BrouilletteR. HansonD. RichardD. et al. A diagnosticapproach to suspected obstructive sleep apnea in children. J Pediatr 1984;105:10-4. Guilleminault C. Tilkian A. Dement WC. The sleep apnea syndrome. Am Rev Med 1976:27:465-84. Everett AD. Koch WC, Saulsbury FT. Failure to thrive due to obstructive sleep apnea. Clin Pediatr 1986:26;90-2. Bates TW, Price DA, Home CA. McGucken RB. Short stature caused by obstructive apnoea during sleep. Arch Dis Child 1984;59:78-80. Hodges S. Wailoo MP. Tonsillar enlargement and failure to thrive. Br Med J 1987:295:541-2.

19. Hammill PVV, Drizd TA, Johnson CL, Reed RB, Roche AF, Moore WM. Physicalgrowth: Nationalcenterfor health statistics percentiles. Am J Clin Nutr 1979;32:609-29. 20. Takahushi Y. Kipnis DM, Daughaday WHo Growth hormone secretion during sleep. J Clin Invest 1968;47:2079-90. 21. Honda Y. Takahushi K. Azum K, et al. Growth hormone secretion during nocturnal sleep in normal subjects. J Clin Endocrinol Metab 1969;29:20-5. 22. Sills RH. Failure to thrive. Am J Dis Child 1968:132:967-9. 23. Berwick DM, Levy JC, Kleinderman R. Failure to thrive: diagnostic yield of hospitalization. Arch Dis Child 1982;57:34751. 24. Riley RL. Landnirth J. Kaplan Sa, et al. Failure to thrive. CA Med 1968;103:32-8.

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The effects of adenotonsillectomy on growth in young children.

A history of poor weight gain can often be elicited in young children with chronic upper airway obstruction resulting from adenotonsillar hypertrophy...
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