The adenoid in children: out of sight, out of mind?
The adenoid can cause problems when it is acutely or chronically infected or when it is too large for the nasopharyngeal space.
The adenoid is a single clump or pad of lymphatic tissue located in the nasopharyngeal space on the posterior pharyngeal wall about one inch superior to the base of the uvula. Laterally, the adenoid blends with the lymphoid tissue of the fossa of Rosenmuller, near the opening of the Eustachian tube.
The Eustachian tube orifice is located in the lateral adenoid recess an important reason why adenoids are associated with recurrent or chronic middle ear infections. The adenoid develops from a subepithelial infiltration of lymphocytes in the 16th week of gestation. The adenoid pad is fully developed by the eighth month of fetal life, grows during childhood, usually slowly atrophies during adolescence, and is a small remnant in an adult. The adenoid sagital thickness is largest during ages 4 to 5 years and decreases progressively except for a minor increase in size in the preteen years. Unlike the palatine tonsils, the surface of the adenoid is characterized by shallow crypts.
The adenoid performs both known and postulated immunologic functions. The B-lymphocytic cells in the adenoid produce gamma globulins and the T-lymphocytic cells process antigenic material carried to them and produce cytokines. Reports regarding the immunologic consequences of tonsillectomy and adenoidectomy are conflicting, yet it is clear that no major systemic immunologic deficiencies result from these procedures.
The adenoid can cause problems when it is acutely or chronically infected or when it is too large for the nasopharyngeal space and causes obstruction to passage of air through the nose. There is some suggestion that chronic high gastrointestinal reflux can also contribute to adenoid inflammation and hypertrophy. The obstruction can lead to voice, middle ear, paranasal sinuses, posterior nasal passages, posterior choanae, dental arches, senses of taste and smell, appetite, feeding and sleep disorders. A key screening question for the presence of adenoidal hypertrophy is the presence of chronic snoring loud enough to be heard behind a closed door, perhaps associated with cessation of breathing longer than five seconds. Most children with adenoid hypertrophy do not have obstructive sleep apnea, but some do.
Special populations of children including those with Down syndrome, achondroplasia, selected storage diseases, or midface hypoplasia have small nasopharyngeal spaces so that adenoid obstruction is more common and possibly more severe. It is important for the primary care pediatrician to not only be alert to the signs and symptoms of adenoidal hypertrophy but also to be knowledgeable about the intraoral significance of a notched or bifid uvula, absence of the posterior palatal spine, or the presence of a translucent midline palate mucus membrane which may well contraindicate traditional adenoidectomy.
In the operating room, the careful otolaryngologist performs a thorough intraoral examination to assess the integrity of the soft palate prior to adenoidectomy. When excessive nasopharyngeal lymphatic tissue must be removed and the child has a submucous cleft palate with absence of the midline musculus uvulae, the uvulae is recognized preoperatively. The central adenoid pad and the velopharyngeal sphincter are thus preserved. It must be underscored that preoperative clearance of a child with a difficult to detect submucus cleft of the soft palate and subsequent persistent rhinolalia (cleft palate voice) because of emergence of post-adenoidectomy iatrogenic velopharyngeal incompetence has led to successful malpractice litigation against the surgeon and the pediatrician who cleared the child for adenoidectomy.
Acute and chronic adenoiditis
Adenoiditis is typically characterized by nasal stuffiness, secondary symptoms of postnasal drip and frequent snorting noises in an attempt to clear the mucopurulent surface adenoid exudates. It is probably often misdiagnosed as acute sinusitis. Acute adenoiditis is much more common in young children because the adenoids usually shrink during adolescence. Yet, neither acute nor chronic adenoiditis is often mentioned in major pediatric textbooks or in pediatric journals. Acute infection of the adenoids includes the same spectrum of bacteria and viruses that infect the palatine tonsils. These include Streptococcus pyogenes infections, adenoviral adenoiditis, Epstein-Barr virus infections and less common bacterial or viral pathogens, such as Corynebacterium diphtheriae. Recurrent middle ear or paranasal sinus infections are associated with the presence of a biofilm of pathogenic bacteria on the surface of the adenoid but unrelated to adenoid hyperplasia. The adenoid can also be inflamed secondary to gastroesophageal reflux disease (GERD) and or by postnasal drainage of organisms from the nose.
Chronic adenoiditis is a chronic adenoid infection with a mucus biofilm over the surface of the adenoid containing mixed pharyngeal flora intermittently dripping down the posterior pharyngeal wall into the respiratory and digestive passages. These biofilms are not often seen with nasal endoscopy. Surface and core cultures of excised adenoid tissue from children with chronic adenoiditis compared with children in a control group reveals that adenoid specimens from the former group often contain significantly higher percentages of Haemophilus influenzae and Moraxella catarrhalis. Brodsky and Koch cultured more pathogenic bacteria from the adenoids of patients with either recurrent otitis media or persistent otitis media than from the adenoids of patients without such infections. These results occurred regardless of the adenoid size.
Chronic adenoiditis simulates chronic sinusitis with bad breath, chronic cough, mucopurulent rhinorrhea, sounds of snorting or gagging on the mucus throughout the day. Both entities may co-exist. Adenoid facies with open mouth, nasal obstruction, hyponasal voice, and pinched nose may result from chronic adenoidal hypertrophy secondary to chronic adenoiditis.
Adenoid hypertrophy is associated with obstructed nasal breathing, chronic mouth breathing, malodorous breath, snoring, disturbed sleep, obstructive sleep apnea syndrome (OSAS), daytime somnolence, inattention at home and school, persistent middle ear effusion, hyponasal voice, dental deformities, gagging, and chronic posterior rhinorrhea, hyposmia, dysgeusia, appetite suppression, feeding difficulties in young children, and poor weight gain. A simple screening evaluation for snoring and interruptions in the normal respiratory pattern can be obtained inexpensively with the use of audio or audiovisual tape recordings during initial and terminal sleep. The volume of the audio must not be set artificially high. The recorder should be placed several feet away from the sleeping child. Special populations of children with major craniofacial dysmorphology such as those with Down syndrome and those with certain storage diseases may have multiple levels of upper airway obstruction including tonsils, adenoids, macroglossia at the tongue base, soft palate and lateral pharyngeal wall and hypopharyngeal laxness. While adenotonsillectomy is usually very beneficial or curative for these children, a proportion of them continue to have symptoms of obstructive apnea with sequelae of right heart hypertrophy and pulmonary hypertension.
Re-evaluation by endoscopy, repeat polysomnography, or the new imaging technique of cine magnetic resonance imaging can determine the exact site of the airway obstruction. Cine MRI is particularly helpful in children with Down syndrome and other craniofacial anomalies, although it is found only in a few advanced childrens hospitals at this time.
Visualization of the adenoid
The adenoidal-nasopharyngeal ratio (ANR) is a practical noninvasive method to evaluate adenoid hypertrophy. A true lateral cephalometric view roentgenogram can show the size of the adenoid in relationship to the diameter of the posterior nasal air column and any encroachment by hypertrophic adenoids on the nasopharyngeal airway. The X-ray does not show the presence of mucopurulence on the surface of the adenoid, necessary in the evaluation of recurrent purulent rhinorrhea. The X-ray shows the adenoid only in two dimensions. Nasopharyngoscopy provides more accurate three-dimensional data on the nasopharynx and adenoids (see reference for detailed information).
Even in children with symptoms and signs of nasopharyngeal obstruction, further evaluation by an otolaryngologist, pediatric pulmonologist, and/or allergist is recommended prior to surgical intervention. Allergy-induced edema of the nasal turbinates and secondary adenoid hypertrophy from the constant bath of nasal mucus may respond to a trial of inhaled nasal steroids for several weeks. Screening tests for nasal eosinophils, selected prick tests, and/or CAP-Rast tests may help identify those children with an immunological cause for their posterior nasal obstruction. Identification of children with nasal septal deviation (nasal spurs) or turbinate hypertrophy is recommended prior to performing adenoidectomy. Nasopharyngoscopy using a thin pediatric flexible nasal endoscope can sometimes be performed while the child is sitting on a parents lap (see reference). Video documentation of the procedure with hard copies are markers of good clinical practice and helpful to educate the parents to the need for surgery.
The surgical procedure: Adenoidectomy, often combined with tonsillectomy, is usually performed for signs and symptoms of nasopharyngeal obstruction or for middle ear disease, including recurrent acute otitis media and/or chronic middle ear effusion. Recurrent acute or chronic paranasal sinusitis or chronic purulent rhinorrhea is another indication for removal of the adenoids. Preoperative clearance must include careful inquiry about family history of anesthesia complications, drug allergies, and bleeding problems, particularly Von Willibrand disease. Preoperative tests for bleeding diathesis are often not obtained but this varies based on the preference of the surgeon and the surgical center. Children who have an overt or covert cleft palate, or even those with minor defects of the tip of the uvula, should be handled with great care pre-and intra-operatively. Bifid uvula or even small notching or clefting of the uvula tip and a V-shaped midline notch or the posterior border of the hard palate, rather than a smooth curve, are clinical signs of a sub-mucus clefting of the soft palate.
Most commonly, the adenoid is usually removed through an intra-oral approach, after placing an oral retractor to keep the mouth open and retract the palate. The soft palate is palpated for its integrity and then elevated. The adenoid pad is visualized by use of an angulated mirror. Depending on the surgeons preference, curettage, cautery, powered microdebrider or radiofrequency ablation (Coblation) technique may be used to excise the adenoid. The goal of adenoidectomy is complete removal of the midline adenoid pad to achieve a smooth lining of the nasopharynx. Curettage of the lymphatic tissue in Rosenmüllers fossa is performed selectively by the group of pediatric otolaryngologists who advocate that approach. Those who avoid curettage of Rosenmüllers fossa fear scar tissue formation, which may contribute to a patulous eustachian tube and reflux of nasopharyngeal mucus retrograde into the middle ear.
Peri- and post-operative complications from adenoidectomy are unusual but still occur. Although the most common complication of adenoidectomy is postoperative bleeding, the incidence is low, estimated to be about 0.4%. Bleeding is usually noted within the first six hours post-operatively. It is easily controlled in the absence of a bleeding disorder, such as Von Willibrand disease. Other postoperative complications include dehydration, sleep disorders, behavioral problems and postoperative otitis media.
Transient velopharyngeal insufficiency may occur after removal of a large adenoid but resolves quickly in most cases. Persistent velopharyngeal insufficiency is the most feared complication because it requires either prosthesis or a secondary procedure for correction. Most cases of postoperative velopharyngeal insufficiency are caused by an undetected submucous cleft palate. Other craniofacial syndromes (eg, velocardiofacial syndrome, Kabuki syndrome) occasionally remain unrecognized because their features are mild. Children with velocardiofacial syndrome (VCFS) have down-sloping palpebral fissures; bulbous nasal pyramids, small, oval-shaped, fishlike mouths; and pseudohypertelorism. These children unfortunately may be recognized only when they develop prolonged hypernasal speech following adenoidectomy. The carotid arteries often have an anomalous path in children with VCF syndrome and represent a surgical hazard during tonsillectomy or adenoidectomy.
The adenoid appears to be important to pediatricians only when it is implicated in middle ear disease, snoring, recurrent paranasal sinusitis, or obstructive sleep apnea syndrome. It is important to dentists when it is implicated in malocclusion and important to teachers and speech therapists when it is believed to be the cause of difficulties in speech. The adenoid is important to parents when their child has recurrent or persistent middle ear disease, rhinorrhea, or offensive breath. Acute or chronic adenoiditis are under appreciated disease entities that mimic sinusitis. Evidence-based medicine studies have shown a significant improvement in the quality of life after adenoidectomy performed for upper airway obstruction or for obstructive sleep apnea.
For more information:
- Stewart MG, Glaze DG, Friedman EM et al. Quality of life and sleep study findings after adenotonsillectomy in children with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg. 2005;131:308-314.
- Shott SR, Donnelly LF. Cine magnetic resonance imaging: evaluation of persistent airway obstruction after tonsil and adenoidectomy in children with Down syndrome. Laryngoscope. 2004;114:1724-1729.
- Flanary VA. Long-term effects of adenotonsillectomy on quality of life in pediatric patients. Laryngoscope 2003:113:1639-1644.
- Uruma Y, Suzuki K, Hattori, H, et al. Obstructive sleep apnea syndrome in children. Acta Otolaryngol Suppl. 2003;S550:6-10.
- Hayes JT, Houston R. Flexible nasopharyngoscopy. Postgrad Med. 1999;106:107-114.
- Lee D, Rosenfeld RM. Adenoid bacteriology and sinonasal symptoms in children. Otolaryngol Head Neck Surg. 1997;116:301-307.
- Bower CM, Richmond D. Tonsillectomy and adenoidectomy in patients with Down syndrome. Int J Pediatr Otorhinolaryngol. 1995;33:141-148.
- Rosen GM, Muckle RP, Mahowald MW, et al. Postoperative respiratory compromise in children with obstructive sleep apnea syndrome: can it be anticipated? Pediatr. 1994;93:784-788.
- Brodsky L, Koch RJ: Bacteriology and immunology of normal and diseased adenoids in children. Arch Otolaryngol Head Neck Surg. 1993;119:821-829[Medline].
- Paparella, MM, Shumrick DA, Gluckman JL, et al. Otolaryngol, Volume II, 3rd edition, 1990; W.B. Saunders, Philadelphia, PA.
- Potsic WP. Comparison of polysomnography and sonography for assessing regularity of respiration during sleep in adenotonsillar hypertrophy. Laryngoscope. 1987;97:1430-37.
- Cohen D, Konak S: The evaluation of radiographs of the nasopharynx. Clin Otolaryngol. 1985;10:73-8[Medline].
About the authors:
- Richard H. Schwartz, MD, is from the department of pediatrics at Inova Fairfax Hospital for Children, Falls Church, Va.
- Robert A. Bahadori, MD, is a pediatric otolaryngologist in private practice, Fairfax, Va.