12
Interaction between the Orthodontist and Medical Airway Specialists on Respiratory and Nonrespiratory Disturbances
Joseph G. Ghafari and Anthony T. Macari
Department of Dentofacial Medicine, American University of Beirut, Beirut, Lebanon
For breath is life, so if you breathe well you will live long on earth.
(Sanskrit proverb)
Breathing is taken for granted as a common behavior essential for life, yet it is seamless, discreet, nonintrusive, and nonscheduled. It has been equated with life itself: it connects the living person to existence by providing oxygen to the body. Breathing also reflects present body status, expressions, and emotions, its tempo changing with relaxation, effort, mood, joy, anger, fear, exercise, and every other beat of life. This core function requires a properly operating inhalation–exhalation system, from nose to lung. Structural interferences, mechanical (e.g. nasal obstruction) or pathological (e.g. cold), compromise the normal air flow, requiring the body to adjust, typically by switching to oral breathing, with variable consequences on local maxillofacial anatomy and general health.
In this chapter, respiratory impairments and their consequences on oral morphology and functions are presented within the perspective of integrated therapy requiring the input of orthodontists and medical airway specialists. The obvious reason for the important interaction between the orthodontist, otolaryngologist, and pulmonary specialist is the critical position of the mouth between the nose, throat, and lungs.
The mouth in relation to the nasopharyngeal airway: Anatomy overview
The posterior boundary of the oral cavity comprises two pairs of folds of mucous membrane that cover two palatal muscles, the palatoglossus and the palatopharyngeus (Figure 12.1). The tonsils lie between these folds, which provide the contour of an opening, the exit from the oral cavity (fauces) to the pharyngeal area. Located in the roof of the nasopharynx, anterior to the basiocciput and inferior to the sphenoid, the adenoids are a mass of lymphoid tissue that merges with the lymphoid tissue of the fossa of Rosenmuller near the opening of the Eustachian tube, which connects to the ear. The tonsils (palatine or faucial tonsils) and the adenoids (pharyngeal tonsils) are part of Waldeyer’s tonsillar ring (or pharyngeal lymphoid ring), which also includes the tubal tonsil where the Eustachian tube opens in the nasopharynx and the lingual tonsils.
Figure 12.1 Anatomical structures in the mouth: oral and pharyngeal soft tissues.
At the gate of the upper respiratory and alimentary tracts where they are constantly exposed to antigens, the tonsils and adenoids are mostly composed of immunologically reactive lymphoid tissue, which contains antibody‐producing lymphocytes, and are related to sounder immune status and the general health of patients, carrying out the functions of humoral and cellular immunity (Hata et al., 1996; Valtonen et al., 2000; Kaygusuz et al., 2009). Inflammation or hypertrophy of the adenoids and tonsils is caused by hypofunction of local and systemic immunity. Although still debated, particularly regarding the timing of surgery relative to the patient’s age, findings indicate that removal of the lymphoid tissues has no adverse effect on immunity (Marcano‐Acuña et al., 2019). Research is not available to support the theory that the adenoids and tonsils initially developed in nonurban, somewhat isolated environments to combat relatively uncommon types of infections, and that these tissues become a health liability because they may not cope with the various viral infections attacking children in urban areas.
The development of the adenoids is unique among major tissues of the body: they increase in size to a peak of approximately twice the adult size around puberty, then decrease to near total regression in most adults (Figure 12.2; Scammon et al., 1930; Linder‐Aronson and Leighton, 1983). The nasopharynx enlarges to accommodate the growing adenoids, thus maintaining a patent nasopharyngeal airway (Macari and Haddad, 2016). Any imbalance between the developing airway and the concomitant adenoid growth may result in nasopharyngeal obstruction or reduced potency. Some reports indicate that the lymphoid tissues do not follow a specific growth curve, but respond individually to different environmental factors (Macari and Haddad, 2016).
Figure 12.2 Scammon’s curves: percentile of adult size of the neural, general, genital, and lymphoid tissues against age.
The nasal cavity extends from the nostrils anteriorly and the choanae posteriorly and is divided into halves by the septum, which is formed by the perpendicular plate of the ethmoid bone above, the vomer bone posteriorly, and an extensive cartilage anteriorly (Figure 12.3). The roof of the nasal cavity is constituted by the ethmoidal cribriform plate, through which olfactory nerves enter the nasal cavity. The lateral walls comprise three bony shelf‐like conchae or turbinates, which are covered with highly vascular mucous membranes (Figure 12.3). Air is heated and humidified past the conchae during breathing.
Beneath each concha is a meatus that opens the nasal cavity to the bilateral paranasal sinuses, which are membrane‐lined cavities within the frontal, maxillary, ethmoid, and sphenoid bones (Figure 12.3). The ethmoid sinus contains a series of small, interconnected air cells instead of a single hollow space. The sinuses communicate with the nasal cavity at the level of the superior and middle meatuses and lateral walls of the cavity. Whereas none of the paranasal sinuses opens into the inferior meatus, the nasolacrimal duct does. Thus, tears produced in the eye by the lacrimal (and other) glands are collected into this duct and enter the nasal cavities.
The function of the paranasal sinuses has been subject to various hypotheses: lightening the housing bones, acting as resonance chambers during speaking, or, as we suggest, being part of the adaptation process to the oropharyngeal capsular matrix, as defined by Moss (Moss and Salentijn, 1969; Macari et al., 2012; see the later section on impaired nasal breathing).
Common sources of airway dysfunction
Tonsils and adenoids present a health problem when they become the nest of continuous infections. Particularly in children, hypertrophy of these tissues is a primary cause of nasal airway obstruction, leading to mouth breathing that in turn may affect facial morphology. Other consequences include nasal voice, snoring, and restless sleep (and associated learning problems if chronic). Considering their critical anatomical position, hypertrophied adenoids may affect nasal function and obstruct the Eustachian tubes, participating in the formation of middle ear effusions. In the rare condition when hypertrophied tonsils touch or meet in the midline, they are called “kissing tonsils.”
Impaired nasal breathing
Enlarged adenoids and tonsils are the most common obstructive agents of the posterior pharyngeal airway. Other causes that raise nasal resistance involve hard tissues, such as a deviated septum; turbinate irregularities; and congenital, traumatic, or therapeutic asymmetries of the nasal cavity; and soft tissues, such as catarrhal and allergic rhinitis and nasal polyps (Figure 12.4; Macari and Haddad, 2016).
Figure 12.3 Anatomical structures in the face. (a) Sagittal near‐midline; (b) lateral; and (c) cross‐sections through oral and nasal hard tissues.
Source: (c) Adapted from Moore (1992), Figure 7, with permission of Lippincott, Williams and Wilkins.
Methods of evaluating airway obstruction
Airway assessment
Tonsillar hypertrophy is readily diagnosed clinically, and its cephalometric determination is only corroborative (Figure 12.4). Cephalometric imaging and the more intrusive endoscopic examination are more common in diagnosing adenoid hypertrophy. Cephalometric assessment of the nasopharyngeal airway may be through subjective rating or direct measurement of defined distances. In one of the various grading systems based on direct observation of the adenoid within the pharyngeal space, three grades were defined by estimating the space that the adenoid occupies between the posterior cranial base and the soft palate:
- Grade 1: less than 50% of the airway is obstructed (Figure 12.5a–c).
- Grade 2: more than 50% but less than 100% of the airway is blocked (Figure 12.5d–f)
- Grade 3: Near total to total obstruction is observed (Figure 12.5g–i).
The adenoids have been evaluated from two‐dimensional (2D) cephalographs that simplify the imaging of three‐dimensional (3D) structures. Moderate to high correlations (0.60 < r <0.88) were reported between cephalometric assessment and the endoscopic evaluation of actual obstruction or the actual size of excised lymphoid tissue (Major et al., 2006). Cephalometric measurements of the shortest distance between adenoid and soft palate (SAD) and the distance between the maximum convexity point and soft palate (CAD) correlated best with actual size (Figure 12.6). A high correlation was reported between SAD and CAD (r = 0.915; Bitar et al., 2010). Moderate to high correlations between the airway grading and SAD and CAD measurements (r = –0.73 and r = –0.79, respectively) account for the correspondence of evaluation in half to two‐thirds of the studied population (Bitar et al., 2010).
The 3D imaging of the nasopharyngeal space and structures yields more accurate information (Major et al., 2014). Visualization and volumetric quantification of the airway are achieved through specialized software applied on computed tomography (CT) and cone beam computed tomography (CBCT) 3D images of the pharyngeal airway space in multiple planes (axial, coronal, and sagittal; Figure 12.7; Major et al., 2014; Brunetto et al., 2014; Tikku et al., 2016; Alsufyani et al., 2017). However, controversies persist, because defining the 3D volume may only be relevant at the “bottle neck,” the narrowest bridge between adenoids and soft palate, corresponding to the most constricted region at the base of the tongue (El and Palomo, 2013). Extending measurements to the limits of the larynx in CBCT studies (Kim et al., 2010; El and Palomo, 2013) may also be clinically impractical, because no statistically significant differences were found between the 3D CBCT and 2D cephalometric groups in the cross‐sectional area (Major et al., 2014). Further research is warranted to correlate diagnostic 3D findings with treatment outcome.
When cephalometric adenoid rating is negative, the ear, nose, and throat (ENT) specialist may resort to other means of assessment (endoscopy) to investigate other obstructive causes (e.g. enlarged turbinates), which is shown more in detail in Chapter 11. In all instances, the decision on the removal of adenoids and tonsils is based on clinical symptoms, not only the assessment of hypertrophy.
Assessment of mouth breathing
Unless it is obvious to the orthodontist or the ENT specialist in the clinical setting, the appraisal of mouth breathing often is based on subjective reporting by the patient or parents, usually figuring on the health history questionnaire, with inquiry on its occurrence during the day, night, or both. The association between mouth breathing and cephalometric measurement of airway clearance (SAD, CAD) indicates the significance of the radiographic record, but does not meet the requirement of validated quantitative evaluation of respiration. Means to generate objective evidence, such as rhinometry, nasal flow, and nasal resistance, have yet to be proven effective or practical for determining mouth breathing (Fujimoto et al., 2009; Ovsenik, 2009). The variation in frequency, duration, and intensity of oral breathing probably accounts for differing outcomes of these quantitative measurements.
Effect of airway obstruction on facial and occlusal morphology
The impact of airway impairment on dentofacial morphology has been evaluated extensively (Linder‐Aronson et al., 1986, 1993; Kerr et al., 1989; Behlfelt et al., 1990; Woodside et al., 1991; Valera et al., 2003; Mattar et al., 2004). In the pioneering days of orthodontics, Edward H. Angle (1907) emphasized the consideration of not only the peculiarities of the occlusion and the relations of the jaws, but also the “condition of the throat and nose [and] habits of the patient.” Angle accounted for mouth breathing in classifying the Class II Division 1 malocclusion as “always accompanied and, at least in its early stages, aggravated, if not indeed caused by mouth breathing due to some form of nasal obstruction,” and the deformities under Class III beginning “at about the age of the eruption of the first permanent molars, or even much earlier, and always associated at this age with enlarged tonsils and the habit of protruding the mandible, the latter probably affording relief in breathing.” Yet the nature of these associations requires further definition.
Figure 12.4 (a) Lateral cephalometric radiograph of a patient 10 years 7 months old, showing the hypertrophied adenoid (yellow arrow) and the posterior extension of the inferior turbinate toward the posterior wall of the nasopharynx (white arrow), causing obstruction of the airway. (b) Bilateral obstruction of the airway by the hypertrophied inferior turbinates (right and left, arrows) shown on a postero‐anterior cephalogram. On endoscopic otolaryngological examination, the diagnosis of inferior turbinate hypertrophy was confirmed, and medication (nasal topical steroids) improved breathing. (c) Hypertrophied tonsils (arrows) in a boy 5 years 6 months old whose adenoids had been removed two years earlier. (d) Septal deviation: S‐shaped deviation of the nasal septum shown on a postero‐anterior cephalograph. (e, f) Cephalometric radiograph (e) of a 14‐year‐old chronic mouth‐breathing patient with hyperdivergent vertical pattern but positive clinical overbite (30%). Note the hypertrophic adenoids, and a unilateral nasal polyp (yellow circle) that contributed to nasal obstruction. A computed tomography scan (f) revealed the extension of the polyp (arrow) from the sinus.
Figure 12.5 Grades of adenoid hypertrophy from less severe (Grade 1) to most severe (Grade 3) are illustrated along with various corresponding types of malocclusion. (a–c) Grade 1; (d–f) Grade 2; (g–i) Grade 3. This variation reflects the individual potentials for adaptation documented in animal (Harvold et al., 1981) and human (Macari et al., 2012) research.
The facial dysmorphology resulting from airway obstruction by adenoid hypertrophy has been termed “adenoid facies” (Angle, 1907), synonymous with “long face syndrome” (LFS; Angle, 1907; Proffit, 2007) and a “high angle” facial pattern. Children who need adenoidectomy have been reported to have a longer facial height, a steeper mandibular plane angle, and a more retrognathic mandible than corresponding controls (Linder‐Aronson et al., 1986; Kerr et al., 1989; Behlfelt et al., 1990; Woodside et al., 1991). Likewise, children with enlarged tonsils were reported to have more retrognathic and superior‐posteriorly inclined mandibles, greater anterior total and lower facial heights, and increased mandibular plane angles (Behlfelt et al., 1990).
Figure 12.6 Cephalometric landmarks, planes, and measurements in the study of craniofacial morphology related to adenoid hypertrophy. Linear measurements of the palatal airway (between the adenoids and soft palate): A is the distance between the most convex contour of the adenoid and soft palate (CAD), and B is the shortest distance between the adenoid and soft palate (SAD). Various hard tissue landmarks (1–20) are used for linear and angular measurements. Key findings included the increased posteroinferior inclination of the palatal plane (PP) relative to the horizontal (H) oriented on natural head position, augmented hyperdivergence between PP and MP (mandibular plane through menton [Me 12] and gonion [Go 11]), as well as increased angle between MP and SN (sella [#2]‐nasion [#1]).
The underlying theory is that chronic mouth breathing leads to narrow maxillary dental arches, anterior open bite, usually through excessive eruption of posterior teeth, and a hyperdivergent skeletal pattern. These symptoms are related primarily to low posturing of the tongue and the subsequent adaptation of other facial muscles. The lips, in repose, have been described as parting, although nasal breathing is possible with incompetent lips if the tongue provides an anterior seal (Macari and Haddad, 2016).
Time and sequence of facial alterations from airway obstruction
Macari et al. (2012) analyzed the cephalographs of 200 Caucasian children who had been diagnosed as chronic mouth breathers by the pediatric otolaryngologist who referred them for cephalometric appraisal of adenoid hypertrophy. Their mean age was 6.00 ± 2.62 years and nearly 50% of them were younger than 5 years. The authors reported posterior‐inferior tilt of the maxilla (average inclination of palatal plane to horizontal –7.68° + 3.44°; norm 0° + 2.5°), apparently the initial response to functional alteration, occurring separately or together with one or all of the following modifications compatible with a hyperdivergent vertical pattern: increased palatal to mandibular plane angle, increased lower face height, steep mandibular plane, mandibular antegonial notching, increased gonial angle, and elongated and thinner symphysis (Figure 12.8). The palatal tilt reached severe levels (8–9°) between the ages of 4 and 5 years. The occlusion ranged from normal with adequate overjet/overbite to malocclusions that contained one or more of these characteristics: posterior crossbite, overjet, Class II, open bite, anterior crossbite (Figure 12.5).
Figure 12.7 (a) Cone beam computed tomography image and (b) three‐dimensional rendition of the skull in which the nasopharyngeal space is mapped in red, illustrating the area (a) and volume (b) of the space.
Figure 12.8 Morphological characteristics of the “long face” syndrome in a girl 10 years, 10 months old with chronic mouth breathing. (a, b) Extraoral photographs reveal lip incompetence, increased lower facial height, narrow nose base width, and shadows under the eyes from chronic venous congestion. (c) Lateral cephalograph of the same patient shows characteristic findings of adenoid facies: palatal plane (ANS–PNS) tipped postero‐inferiorly, steep mandibular plane (MP: menton [Me] to gonion [Go]), mandibular angular notching, reduced inclination of anterior slope of chin (horizontal arrow), and increased lower face height. The upper and lower curved arrows indicate the posterior‐inferior tip of the palatal plane and anterior‐inferior tip of the mandibular plane, respectively. PP, palatal plane.
Accordingly, the following conclusions are drawn regarding growth concepts on the association between airway status and craniofacial morphology:
- Facial dysmorphology related to nasal obstruction starts in structures closest to the obstruction, namely a posterior‐inferior rotation of the maxilla.
- The array of malocclusions differs with the individual respiratory adjustment of the affected child. In this perspective, two observations are made. The occlusal variations join the experimental findings of Harvold et al. (1981) in monkeys at comparable ages. These authors obstructed inspiration, but allowed slight air escape during expiration in growing monkeys (age: 2–6 years), most of them (34/42) in the late deciduous and mixed dentitions (age: 2–4 years). Each animal found its own most convenient way to secure the oral flow, and then develop a dental occlusion in accordance with this new function. Thus, oral respiration induced mesioclusion, maxillary protrusion with distoclusion, open bite, dual bite, and some common cephalometric traits: increased face height, steeper mandibular inclination, and a larger gonial angle. Second, as suggested by Angle (1907) in his theory of Class III genesis and observed in many patients, including those treated for obstructive sleep apnea, forward positioning of the mandible enlarges the airway and enhances breathing through the consequent increase of airflow (Liu et al., 2000). Ghafari (2004) suggested that if the anterior position is sustained in growing children, the ensuing anterior crossbite may induce maxillary retrognathism that otherwise would not exist. This phenomenon reflects intragrowth orthopedics (maxillary retrognathism) generated by the transfer of functional forces through a nontherapeutic occlusal “environmental induction” (anterior crossbite) (Ghafari and Macari, 2013).
- The findings qualify the variable relation between nasal obstruction and facial growth in line with Moss’s functional matrix theory (Moss and Salentijn, 1969). The oropharyngeal space is a primary entity (capsular matrix related to respiration) that influences the position and behavior of the surrounding soft tissues, which in turn shape the associated skeletal units. Impingement on the oropharyngeal space leads to adaptive reorganization of the surrounding structures, beginning with and possibly restricted to the posterior‐inferior maxillary tilt, probably because of its proximity to the obstructed pharynx. The greater amplitude of adaptation occurred at younger ages (<5 years). The adjustment may also start with mandibular remodeling favoring an increase in the gonial angle and mandibular plane inclination.
- As airway obstruction ranges from total to partial, and adaptation to either is an individual response (according to Moss to preserve the oropharyngeal matrix), the variation in malocclusions is not surprising. Conversely, any degree of adaptive morphological change may result in a level of restoration of nasal breathing.
- The association between the amount of blockage and specific signs of malocclusion remains unknown. The severity and extent of dysmorphology would depend on the timing, duration, and rate of oral breathing and associated functional changes, as a percentage of nasal breathing may coexist with mouth breathing (Fields et al., 1991).
Effect of the removal of lymphoid tissues on orofacial morphology
The critical clinical issue is determining the optimal time of lymphoid tissue removal to enhance nose breathing and prevent potential abnormal facial growth, or reverse/minimize developing long face features, possibly aided by orthodontic/orthopedic treatment. Posttreatment studies of adenoidectomy (Linder‐Aronson et al., 1986; Woodside et al., 1991; Bahadir et al., 2006) reveal a more anterior direction of symphyseal growth, reversal of the tendency to posterior mandibular rotation, an increased amount of mandibular growth, and no difference in direction of maxillary growth. The latter is an indication that morphological alterations are not totally irreversible. Additionally, individual growth direction after adenoidectomy was more variable than in control children with clear airways matched for age and sex (Linder‐Aronson et al., 1986). When Harvold et al. (1981) removed the nose plugs in their experimental animals two years after nasal obstruction, nasal breathing returned and some of the dentofacial changes were undone, but facial features and malocclusion were often retained. Research is needed on the extent, scope, and predictability of orofacial counter‐adaptation in relation to age.
Through a recent study, Babakhanian et al. (2021) documented changes (12.92 ± 1.42 years; range 10.16–14.76 years) post adenoidectomy. Long‐term normalization of dentofacial growth in bony bases was found, specifically in the mandible, enhancing more horizontal growth direction and chin projection in the surgical group. Surgery before the age of 6 years resulted in gonial angle closure and more anterior chin projection (Figure 12.9).
Clinical considerations
The findings on airway blockage and dentofacial dysmorphology emphasize the need for pediatricians and pediatric otolaryngologists to examine children for impaired nasal breathing in early childhood and ascertain their breathing mode at night from the parents. Otolaryngologists and orthodontists should appreciate the early impact of enlarged adenoids and tonsils.
From the perspective of otorhinolaryngology, reasons for adenoidectomy often include chronic and recurrent fluid or infections of the ears, chronic or recurrent sinus infections or “rhinosinusitis,” and nasopharyngeal blockage. Tonsillar infection is rarely associated with ear infections and tonsillectomy is usually indicated when tonsils are enlarged. The prevailing practice among otolaryngologists is to delay removal of the pharyngeal lymphoid tissues because of their role in immunological defenses, and the increase in size of the adenoid in preschool and primary grade years followed by a decrease during pre‐ and early adolescence (Figure 12.2; (Linder‐Aronson et al., 1983). Indications for adenotonsillectomy supported by the American Academy of Otolaryngology (2021) include statements related to infections, sleep disorders, malocclusion, and other infectious conditions (Table 12.1).
Adenoidectomy, often conducted using a small mirror and completed on average within 15–20 minutes, involves “shaving” or curetting the adenoid tissue from the back of the nose. Usually, low‐grade bleeding is eliminated by cauterization. Although rare, surgical complications include infection of the surgical site (a source of bad breath), minor bleeding, and infrequently velopharyngeal insufficiency, possibly related to neglect of anatomical considerations. Postsurgical pain is more pronounced with tonsillectomy.
From the perspective of orthodontics, orthodontic correction may be needed to foster adequate tongue posture, such as widening the maxillary arch to maintain an upward position of the tongue at rest. Sometimes the palatal split improves respiration and helps reverse mouth breathing (habitual or from anterior obstruction) to nose breathing, or may even amelioate hearing (Kılıç et al., 2008a, 2008b). However, these responses cannot be predicted. When the mandible is thrust forward for better breathing, and an anterior crossbite follows possibly inducing maxillary retrognathism, early correction of the latter is recommended (Ghafari, 2004) along with the medical/surgical management of the respiratory problem.
Treatment combining orthodontics and orthognathic surgery to correct LFS reverses all characteristics observed in conjunction with sustained chronic mouth breathing during growth; namely, posterior impaction of the maxilla, mandibular advancement, and genioplasty (Figure 12.10). These procedures validate the prior prevention of the symptoms by promoting nasal breathing through the earlier removal of lymphoid tissues.
Orthodontic intervention is confounded by several facts. First, a direct relation between mouth breathing and malocclusion is not established for all mouth breathers (Leiter and Baker, 1989), some of whom may exhibit normal occlusion, possibly because total nasal obstruction is rare. Second, the type and severity of malocclusion are determined by the individual pattern of adaptation to nasal obstruction (e.g. LFS occurring with and without anterior open bite). And last, clearing the nasal airway does not necessarily improve dentofacial relationships, particularly in older children (Ghafari and Macari, 2013).
Figure 12.9 (a) Lateral cephalograph of a boy 4 years 4 months old treated medically for airway obstruction and mouth breathing. (b) Cephalograph of the same subject 13 years later. Although the originally posterior caudal inclination of the palatal plane flattened, the hyperdivergent pattern remained with a very steep mandibular plane. (c) Cephalograph of another boy of a similar age (4 years 2 months) treated for the same conditions with adenoidectomy. Note the hyperdivergent pattern with a posterior‐inferior tip of the palatal plane. (d) The cephalometric record of the second boy taken 14 years later reveals a shift of the morphological pattern to hypodivergence.
The early morphological changes observed with nasal airway obstruction support early surgical intervention (<5–6 years) to avoid a permanent setting of one or more characteristics of LFS that would be difficult to control orthodontically. Thus, adenoidectomy may be recommended in patients found at risk of LFS or based on the severity of some of its characteristics least affected by orthodontic treatment. Linder‐Aronson advocates adenoidectomy in mouth breathers with a small nasopharynx (Linder‐Aronson et al., 1986, 1993; Kerr et al., 1989; Woodside et al., 1991), but this recommendation is not yet supported by clinical trials. To develop operational guidelines, several considerations emerged:
Table 12.1 Summarized statements by the American Academy of Otolaryngology regarding guidelines for adenotonsillectomy.
Source: Adapted from American Academy of Otolaryngology Head and Neck Surgery, https://www.entnet.org/resource/clinical‐indicators‐tonsillectomy‐adenoidectomy‐adenotonsillectomy‐in‐childhood.
| Related to infections | ||
| 1 | Watchful waiting for recurrent throat infection if fewer than 7 episodes in the past year, or fewer than 5 episodes per year in the past 2 years, or fewer than 3 episodes per year in the past 3 years | |
| 2 | Recurrent throat infection with a frequency of at least 7 episodes in the past year, or at least 5 episodes per year for 2 years, or at least 3 episodes per year for 3 years, with documentation for each episode of sore throat and one or more of the following: temperature >38.3 °C, cervical adenopathy, tonsillar exudates, or positive test for Group A β‐hemolytic streptococci (GABHS) | |
| 3 | Tonsillectomy for recurrent throat infection not meeting criteria in Statement 2 for modifying factors, which may include but are not limited to multiple antibiotic allergy/intolerance, PFAPA (periodic fever, aphthous stomatitis, pharyngitis, and adenitis), or history of peritonsillar abscess, parapharyngeal abscess, severe infection with dehydration requiring intravenous fluids, or severe infections that may aggravate comorbid conditions (e.g. seizure disorder). Children at risk for being held back in school due to excessive absences (e.g. over 10 school days per academic year) may also need consideration | |
| Related to sleep disorders | ||
| 4 | ||
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