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The roles of the anterior tonsillar pillar and previous tonsillectomy on sleep-disordered breathing.


We conducted a study to determine if there is a correlation between inadequate anterior tonsillar pillar support and sleep-disordered breathing. We examined 11 patients with a history of tonsillectomy to ascertain the structural and functional integrity of their anterior tonsillar pillars. All 11 demonstrated a loss of anterior pillar support and collapse of their soft palate to the extent that the soft palate passively pressed against the posterior pharyngeal wall. We conclude that a deficiency of anterior tonsillar pillar support does indeed predispose patients to obstructive sleep apnea syndrome. Knowledge of this correlation can help guide the method of surgical treatment and should reinforce the need to maintain the integrity of the anterior tonsillar pillars.


Obstructive sleep apnea syndrome (OSAS) is a serious condition that has been associated with an increased prevalence of stroke, motor vehicle accidents, systemic and pulmonary hypertension, congestive heart failure, and arrhythmias. (1-3)

Efforts have been made to identify anatomic abnormalities that produce obstructive sleep apnea, and treatment has addressed these structures accordingly. (4) Some investigators have suggested that the ability to precisely determine the site of airway collapse can predict the outcome of surgery for OSAS. (5) In children, the physical finding of adenotonsillar hypertrophy is correlated with OSAS. In adults, the pattern of collapse in OSAS is poorly understood, although we know that it usually occurs at multiple levels. According to most studies, uvulopalatopharyngoplasty (UPPP), which addresses only the retropalatal area, is successful in approximately 50% of cases. (6) There is no widely established cause of UPPP failure, although multilevel obstruction is thought to be the primary reason. Endoscopy and manometry of the upper airway have identified the velopharynx as a primary location of obstruction (20 to 45% of cases), but only infrequently is it the only site. (7) Even when UPPP successfully addresses the retropalatal area, other blockage can remain and OSAS can therefore persist. For instance, identification of an obstruction at the tongue base is virtually predictive of UPPP failure (90%). (8) Unfortunately, UPPP is not always successful even when lower pharyngeal obstruction is not present, which underscores the point that multiple factors contribute to OSAS. Because of the complicated pathophysiology of OSAS, anatomy is not always a reliable predictor of surgical outcome, and few guidelines exist to assist us with surgical planning. (9)

A history of tonsillectomy was investigated as a predictor of outcome in UPPP by McGuirt et al. (10) They observed that tonsillectomy, which is often performed on patients with anatomic predilections to OSAS, may not completely address their disease. The integrity and function of the anterior tonsillar pillars may be compromised, which can result in a weakening of the anterior suspension of the soft palate.

The soft palate is supported in part by the anterior and posterior tonsillar pillars, and it has been identified as a major site of airway obstruction in OSAS. The importance of the posterior tonsillar pillar has been addressed in traditional surgery for OSAS. It has been implicated in such postoperative complications as velopharyngeal insufficiency and nasopharyngeal stenosis. However, the role of the anterior tonsillar pillar has largely been ignored.

In this article, we describe our study of a group of patients who were characterized by the presence of sleep-disordered breathing, posterior collapse of the soil palate, and a history of tonsillectomy. Their symptoms and physical findings appear to have occurred as a result of a loss of support by the anterior tonsillar pillars. By highlighting the anatomic importance of the anterior tonsillar pillar, we hoped to attain an objective finding on physical examination that can help guide appropriate therapy for OSAS and to alert surgeons to the importance of preserving anterior tonsillar pillar integrity and function.

Patients and methods

Our study group was made up of 11 patients--7 men and 4 women, aged 18 to 79 years (mean: 51; mean body mass index [BMI]: 28 kg/[m.sup.2])--who had previously undergone tonsillectomy and who were known to have a deficiency of the anterior tonsillar pillars that contributed to sleep-disordered breathing. Between January 1998 and September 2001, we evaluated these patients for snoring and obstructive sleep apnea at a tertiary care academic medical center.

Each patient underwent a thorough history-taking, physical examination, fiberoptic laryngoscopy, and photographic documentation of their distal soft palate collapse. Polysomnography was offered to all patients; 3 declined. Based on the sleep study results, appropriate treatment was initiated. Surgery was offered to those patients who did not tolerate continuous positive airway pressure or were not candidates for it. Most underwent septoplasty with turbinate surgery and UPPP. The intent was not only to trim the soft palate but to restructure and advance it in order to prevent its collapse against the posterior pharyngeal wall.

Standard septoplasty and turbinate surgery were performed when indicated. Our emphasis was on achieving maximal patency of the nasal passages without compromising nasal function.

Our UPPP technique was a modification of the technique introduced by Fujita et al in 1981. (11) An incision was made on the ventral soft palate, and muscle and soft tissue were removed, with care taken to preserve the nasopharyngeal mucosa. Deep suspension sutures were then placed at the angles of the palate overlying the pterygoid hamulus. The nasopharyngeal mucosa was advanced, rotated anteriorly, and sutured to the oropharyngeal mucosa in order to restructure the soft palate. Advancing the soft palate during UPPP may increase the success rate in those patients with a predisposition to posterior palatal collapse.


Seven patients were diagnosed with OSAS, and their mean apnea-hypopnea index (AHI) was 19.8 events per hour (table). Five of these patients underwent corrective UPPP; 3 of them also underwent concomitant septoplasty and 1 underwent septorhinoplasty. All patients who underwent surgery reported symptomatic improvement with regard to their snoring and OSAS postoperatively, and their self-reports were corroborated by their bed partners. Postoperative polysomnography was offered to all patients, but all declined.

Photographic documentation of the collapse of their distal soft palate was recorded. All 11 patients demonstrated a loss of anterior pillar support and collapse of their soft palate to the extent that the soft palate passively pressed against the posterior pharyngeal wall (figure 1).



Some studies have examined the posterior tonsillar pillar and its role in velopharyngeal insufficiency (12) and nasopharyngeal stenosis, (13) but to our knowledge, no study has heretofore addressed the clinical relevance of the anterior pillar in the development of obstructive sleep apnea. We believe that our preliminary report forms the basis for further studies.

Posterior collapse of the soft palate may be the result of a loss of anterior tonsillar pillar support. This phenomenon can occur as either a primary condition or a secondary condition associated with previous tonsillectomy. Stevenson et al suggested that previous tonsillectomy could be used as a prognostic indicator of UPPP success. (14) In their study, 92% of patients with no history of tonsillectomy experienced improvement in their AHI, compared with only 67% who had previously undergone tonsillectomy.

McGuirt et al confirmed these results when they found response rates of 88% in patients who had not undergone previous tonsillectomy and 59% in those who did. (10) They suggested that tonsils represent excess oropharyngeal tissue that contributes to obstruction. Patients with a history of tonsillectomy do not benefit from the removal of this extra oropharyngeal tissue at the time of UPPP. This implies that their persistent obstruction could be the result of either surgical failure or simply a predisposition toward OSAS. We favor the latter explanation and suggest that the reason for the posterior collapse in our group of patients with previous tonsillectomy was attributable at least in part to a loss of anterior tonsillar pillar support. Our findings of a clinical correlation and our photographic documentation of this process provide further evidence to support this theory.

The role of the anterior tonsillar pillar is not clearly defined in patients with normal function or in patients with sleep-disordered breathing (figure 2). It clearly plays a role in drawing the soft palate anteriorly and preventing its collapse against the posterior pharynx, especially in the supine position. The vector forces of the palatoglossus muscle lend support to this observation; histologic studies by Kuebn and Azzam have demonstrated that the elastic layer of the anterior tonsillar pillar is oriented in a mostly craniocaudal direction between the tongue and the soft palate. (15) This anatomic arrangement serves to move the soft palate in an anteroposterior dimension relative to the posterior pharyngeal wall. Moreover, the muscle of the anterior pillar contains more elastin and collagen than do other muscles in the oropharynx, which provides additional evidence that the pillars play an important role in restoring a neutral palatal position. (15) When these pillars are compromised during surgery, as they are during tonsillectomy, scarring and a loss of elasticity ensue. This prevents the palate from adequately drawing forward (figure 3).


Mortimore et al wrote that upper airway obstruction at the retropalatal level is related to the imbalance between the activity of the levator and tensor veli palatini muscles, which elevate and tense the soft palate, and the activity of the palatoglossus and palatopharyngeus muscles, which depress the soft palate anteroinferiorly. (16) They concluded that in the supine position, the palatoglossus muscle attempts to maintain palatal position against gravity by increasing its motor activity. Without palatoglossal support, the soft palate tends to fall backward and narrow the airway at the nasopharyngeal introitus.

Electromyographic studies by Mathur et al revealed that palatoglossus muscle activity does not always increase in the supine position. (17) When muscle activity does not increase, an imbalance between the levator and the palatoglossus muscles results in posterior displacement of the soft palate and obstruction at the retropalatal level. An additional factor that can lead to this imbalance is an absence or deficiency of the anterior tonsillar pillars, further supporting its role in maintaining a patent airway. When anterior tonsillar pillar support is absent or inadequate, the soft palate collapses against the posterior pharyngeal wall. Our study provides a clinical correlation with these earlier findings. We suggest that patients who have lost the integrity of the palatoglossus muscle as a result of tonsillectomy are at increased risk for snoring and obstruction of their upper airway. This risk is present even in patients who would otherwise not appear to be at increased risk, such as those who are not morbidly obese.

Our study has important clinical implications. For one, our findings indicate that surgeons who perform tonsillectomies must attempt to preserve the integrity of the anterior tonsillar pillars. Also, the ability to identify a posterior collapse of the soft palate may provide a physical finding that can lead to modifications of the techniques employed during UPPP (figure 4). Awareness of such a physical finding enables surgeons to correct a defective anterior pillar support mechanism and possibly increase the chance of UPPP success. In our study, patients who lost anterior support exhibited snoring, and their polysomnographic findings were conclusive for mild obstructive sleep apnea. These were not obese patients. The identification of such patients preoperatively can dissuade surgeons from selecting a surgical technique (i.e., laser-assisted uvuloplasty or radioffequency ablation) that we believe may lower the likelihood of a successful outcome. Although further study of this subject is necessary, we believe that such e patients would benefit from more definitive soft palate restructuring procedures.

Table. Characteristics of the 11 study patients

Pt. Age/Sex AHI BMI Surgery

1 35/F 3.3 36.6 None

2 55/M 40.0 * 33.5 UPPP, septoplasty

3 68/M 10.3 * 23.7 UPPP

4 43/F 7.3 * 20.0 None

5 56/M 12.0 * 30.0 None

6 18/M None 18.6 Septorhinoplasty

7 79/M None 22.7 None

8 59/F 12.2 * 40.4 UPPP, septorhinoplasty

9 56/M 50.7 * 30.0 UPPP, septoplasty

10 40/M 6.4 * 31.4 UPPP, septoplasty

11 54/F None 22.0 None

* This patient's AHI value indicates the presence of obstructive sleep
apnea syndrome.

Key: AHI = apnea-hypopnea index; BMI = body mass index (expressed
as kg/[m.sup.2]); UPPP = uvulopalatopharyngoplasty.


The authors are grateful to illustrator Mark Sabo for the use of his artwork.


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(9.) Woodson BT. Predicting which patients will benefit from surgery for obstructive sleep apnea: The ENT exam. Ear Nose Throat J 1999;78:792-800.

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(11.) Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomie abnormalities in obstructive sleep apnea syndrome: Uvulopalatopharyngoplasly. Otolaryngol Head Neck Surg 1981;89:923-34.

(12.) Jackson IT, Kennedy D. Surgical management of velopharyngeal insufficiency following uvulopalatopharyngoplasty: Report of three cases. Plast Reconstr Surg 1997;99:1151-3.

(13.) Krespi YP, Kacker A. Management of nasopharyngeal stenosis after uvulopalatoplasty. Otolaryngol Head Neck Surg 2000;123: 692-5.

(14.) Stevenson EW, Turner GT, Sutton FD, et al. Prognostic significance of age and tonsillectomy in uvulupalatopharyngoplasty. Laryngoscope 1990;100:820-3.

(15.) Kuehn DP, Azzam NA. Anatomical characteristics of palatoglossus and the anterior faucial pillar. Cleft Palate J 1978;15:349-59.

(16.) Mertimore IL, Mathur R, Douglas NJ. Effect of posture, route of respiration, and negative pressure on palatal muscle activity in humans. J Appl Physiol 1995;79:448-54.

(17.) Mathur R, Mortimore IL, Jan MA, Douglas NJ. Effect of breathing, pressure and posture on palatoglossal and genioglossal tone. Clin Sci (Lond) 1995;89:441-5.

From the Department of Otolaryngology and Communicative Disorders, the Cleveland Clinic.

Reprint requests: James Chan, MD, The Cleveland Clinic Foundation, A71, 9500 Euclid Ave., Cleveland, OH 44195. Phone: (216) 445-5972; fax: (216) 444-7927; e-mail:

Originally presented at the annual meeting of the American Academy of Otolaryngology--Head and Neck Surgery; Sept. 23, 2002; San Diego.
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Author:Eliachar, Isaac
Publication:Ear, Nose and Throat Journal
Geographic Code:1USA
Date:Jun 1, 2004
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