Author s : Andreas E. These bacteria, mostly Staphylococcus aureus, Haemophilus sp. The recurrent or chronic inflammation of the adenoids and faucial tonsils leads to chronic activation of the cell-mediated and humoral immune response, resulting in hypertrophy of the lymphoid tonsillar tissue. This hypertrophic tissue is the cause for the prominent clinical symptoms: obstruction of the upper airways, snoring, and sleep apnea for adenoiditis or sore throat, dysphagia and halitosis for recurrent tonsillitis. Treatment strategies should target the persisting bacteria within their biofilm or intracellular shelter.
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First, most infections can be linked to the presence of beta-lactamase producing organisms that distort the normal aerodigestive bacterial milieu and can cause commensal organisms to become pathogenic. Second, infections are often polymicrobial in nature and often include anaerobic pathogens. Third, obstruction of tonsillar crypts can serve as a nidus for bacterial stasis and can further perpetuate a condition of chronic infection, suppuration, and fistulae Studies of the bacteriology of adenoid tissue obtained from pathologic postoperative specimens demonstrate the presence of several aerobic species: alpha- and gamma-hemolytic streptococci, Haemophilus influenzae, Staphylococcus aureus, group A beta-hemolytic streptococci GABA , and Moraxella catarrhalis.
Anaerobic species noted include members of Peptostreptococcus, Prevotella, and Fusobacterium. Similar findings have been confirmed in tonsil isolates as well 24 , Due to these findings and the previously mentioned premises, one must conclude that surface cultures have limited utility for identifying the causative organism, especially in chronic inflammation.
Studies have shown that the presence of tonsillopharyngeal exudate and anterior cervical lymphadenitis increase the likelihood that the infectious agent is group A streptococcus The chronicity of adenotonsillar disease may be attributed to multiple overlapping infections caused by different pathogens within fistula and purulent pockets of the tonsil parenchyma even in the absence of clinical symptoms Hypertrophy Although we distinguish between hypertrophy and infectious clinical presentations, it is true that most adenotonsillar hypertrophy is a result of low grade or chronic infectious disease of the involved tissues.
Studies support a bacterial etiology for tonsillar hypertrophy Some authors have argued for an etiologic role for H. Adenoid hyperplasia has been demonstrated to be directly proportional to the number of lymphocytes and the bacterial load of the tissue For the purposes of this discussion, we will consider hypertrophy as a separate clinical entity, one which does not present with the signs and symptoms of acute or chronic infection—erythema, tenderness, lymphadenopathy, or fever.
In practice, many children may have components of both infectious and hyperplastic morbidity. Adenoid hypertrophy is a common cause of nasal obstruction in children. It can present as chronic or recurrent nasal discharge, snoring, SDB, recurrent otitis media, or Eustachian tube dysfunction This development occurs as the result in the changes in head and tongue position and muscular balance secondary to the open mouth breathing that accompanies nasopharyngeal obstruction Recent studies confirm that there are changes in facial growth and development among children with adenoid hypertrophy.
These changes are characterized by increased total and inferior anterior heights of the face, as well as more anterior and inferior position of the hyoid bone Tonsillar hypertrophy can present with dysphagia, SDB at night with gasping for breath, voice changes, and dental malocclusion. The presentation of new onset unilateral tonsillar hypertrophy is most likely due to infection, but the differential should include malignancy. Sudden enlargement of Waldeyer ring should raise suspicion for lymphoma, but actual use of asymmetric hypertrophy without concomitant symptomatology is often of poor predictive value Unusual infections such as atypical mycobacteria, actinomycosis, and lymphoproliferative disease in solid organ transplant children need to be considered with asymmetric enlargement.
Mouth breathing, snoring, and hyponasal speech are common presenting complaints. Rhinorrhea, postnasal drip, and chronic cough are common and nonspecific findings. The aforementioned adenoid facies may be present. Differentiating acute and chronic infections from sinonasal disease can be challenging.
Parents should be made aware that if symptoms persist after adenoidectomy, further investigation and treatment of sinonasal disease may be necessary to fully address the appropriate etiology. A thorough physical exam includes at a minimum anterior rhinoscopy, which is easily facilitated in the cooperative child, with the use of an otoscope and large ear speculum.
This allows the clinician to distinguish possible sources of nasal obstruction within the anterior nasal cavity, such as turbinate hypertrophy, edematous mucosa, or foreign body and to differentiate these from sources within the nasopharynx.
Palatal evaluation should also be undertaken, to ascertain the presence of submucous clefting, bifid uvula, or history of nasal regurgitation. This diminishes the possible complication of postoperative velopharyngeal insufficiency. Children with neuromuscular and central nervous system problems are also at increased risk for velopharyngeal insufficiency following adenoidectomy 32 , Evaluation of the adenoids in an uncooperative child can be difficult and can be accomplished using lateral neck radiographs, although these are often superfluous compliments to physical exam and history.
More recently, an increasing number of children have been evaluated using office nasopharyngoscopy. This technique allows for direct visualization without radiation exposure. Nasopharyngoscopy offers an excellent view of the adenoids and adjacent structures. Parikh et al. Other methods such as video fluoroscopy have been shown to be effective at assessing adenoid size but are less commonly used and carry unnecessary radiation exposure A tongue depressor should be used to depress the tongue with gentle and firm pressure along the oral tongue.
Gagging and tongue extrusion will cause the tonsils to medialize and can produce the appearance of false enlargement. The otolaryngologist must be cognizant of signs of chronic disease, such as peritonsillar erythema, tender cervical lymphadenopathy, tonsilloliths, smooth glistening tonsils, or excessively cryptic tonsils.
Figure Adapted from Brodsky L, Poje C. Tonsillitis, tonsillectomy and adenoidectomy. In: Bailey BJ, ed. Head and neck surgery-otolaryngology, 4th ed. Of note, children at particular risk for the development of SDB secondary to tonsillar hypertrophy include those with craniofacial anomalies, Down syndrome, obesity, and neuromuscular or CNS abnormalities.
These children may have symptoms not necessarily predicted by clinical presentation or tonsillar size. Acute infections need appropriate antibiotic therapy and symptom control. However, the majority of persistent adenotonsillar disease is considered a surgical problem.
Recurrent or chronic adenoiditis due to infection should be treated with an antimicrobial agent effective against beta-lactamase producing microorganisms.
In terms of a durable response from other medical therapies, including inhaled nasal steroids for adenoidal hypertrophy, a Cochrane review 38 has shown only limited short-term benefit. Acute tonsillitis should be managed with a rapid strep antigen screen and culture swab for definitive diagnosis.
Fortunately, group A strep maintains almost universal sensitivity to penicillin. However, given the preponderance of beta-lactamase producing pathogens and their known influence in the development of tonsillar hypertrophy, the clinician may include a clavulanic acid scavenger as well to ensure appropriate antibiotic therapy and response.
Antibiotics have been demonstrated to offer modest benefits to the treatment of sore throat by shortening duration of symptoms by approximately 1 day As previously discussed, a caveat to antibiotic therapy is the management of infectious mononucleosis.
Children known to or suspected of having infectious mononucleosis should not be given amoxicillin or ampicillin containing antibiotics, in order to avoid the development of a rash. When enlarged tonsils and adenoids cause an acute upper airway obstruction, a nasopharyngeal airway with intravenous steroids may be the most effective way to achieve immediate relief. When bacterial infection is suspected, antimicrobial therapy is initiated.
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Adenotonsillar disease. These bacteria, mostly Staphylococcus aureus, Haemophilus sp. The recurrent or chronic inflammation of the adenoids and faucial tonsils leads to chronic activation of the cell-mediated and humoral immune response, resulting in hypertrophy of the lymphoid tonsillar tissue. This hypertrophic tissue is the cause for the prominent clinical symptoms: obstruction of the upper airways, snoring, and sleep apnea for adenoiditis or sore throat, dysphagia and halitosis for recurrent tonsillitis. Treatment strategies should target the persisting bacteria within their biofilm or intracellular shelter. Macrolide antibiotics like clarithromycin are able to modulate the immune system and to interfere in bacterial signaling within biofilms. Clindamycin, quinupristin-dalfopristin, and oritavancin are intracellular high active compounds.
Adenotonsillar Disease in Children