Diseases of the Nasopharynx: Classification, Causes, Diagnosis, and Treatment

Nasopharyngeal diseases are a common group of pathologies, especially in children. They are associated with impaired function of lymphoid tissue located in this area, and can lead to a significant deterioration in the quality of life, nasal breathing difficulties, sleep disorders, hearing loss and other complications. The most common are hypertrophy of adenoids and adenoiditis, and less commonly hypertrophy of the tubal tonsils. These conditions require timely diagnosis and comprehensive treatment, including both conservative and surgical methods.

Definition of nasopharyngeal diseases

Adenoid hypertrophy is a pathologic overgrowth of the nasopharyngeal tonsils that occurs more often in children.

Hypertrophy of tubal ridges is a pathologic overgrowth of the lymphoid tissue of tubal tonsils located in the area of the opening of the auditory tubes (tubal ridges).

Adenoiditis is an inflammation of the nasopharyngeal tonsil.

Classification of diseases of the nasopharynx

1. Adenoid Hypertrophy:

• 1nd degree hypertrophy;
• 2nd degree hypertrophy;
• 3rd degree hypertrophy;
• 4nd degree hypertrophy.

2. Hypertrophy of the tubal shafts.
3. Inflammation of the adenoids:

• acute adenoiditis;
• chronic adenoiditis.

Etiology

The nasopharyngeal tonsil (adenoids) typically enlarges around the age of 3 years. Hypertrophy occurs in children until puberty, after which regression occurs, and by the age of 20, the tonsil is defined as a small formation.
This condition is quite common—about 35 cases per 1000, accounting for over 50% of all visits to the otorhinolaryngologist. Sometimes adenoids are found in younger children and may persist into adulthood. The tubal tonsil can also enlarge in preschool children, but this is quite rare.

The causes of adenoid and tubal tonsil hypertrophy are identical, as both are composed of lymphoid tissue and located in the nasopharynx. The most common factor is infectious: bacteria, viruses, and fungi cause antigenic stimulation, but immature lymphoid tissue produces insufficient antibodies, leading to compensatory hypertrophy. Subsequently, after immune maturation, tissue size decreases.

Additionally, household and food allergens, as well as gastroesophageal reflux disease (GERD), in which hydrochloric acid vapors irritate nasopharyngeal tissues, contribute to the enlargement of adenoids and tubal tonsils. According to research, the size of the nasopharyngeal tonsils is also affected by parental smoking and genetic predisposition.

Viruses and bacteria play a leading role in the development of adenoiditis. Most common pathogens:

• RS-viruses;
• adenoviruses;
• influenza and parainfluenza viruses;
• herpes viruses (including Epstein-Barr virus);
• streptococci (St. pneumoniae, St. pyogenes);
• staphylococci (S. aureus, S. epidermidis);
• Pseudomonas aeruginosa;
• Moraxella catarrhalis;
• activation of the conditional-pathogenic microflora of the nasopharynx.

Accompanying pathologies, such as recurrent or chronic diseases of the upper respiratory tract (rhinitis, sinusitis, bronchitis), GERD, and allergies can contribute to the development of disease and worsen its course. The presence of hormonal or immune disorders (diabetes mellitus, thyroid pathology, HIV infection) also adversely affects the development of the disease. Lack of a history of breastfeeding and vitamin D deficiency also exacerbate and prolong the course of adenoiditis.

Do not forget about environmental conditions: dry air, inadequate temperature control, cluttered premises, and working in harmful enterprises negatively affect the state of the upper respiratory tract and worsen the disease manifestation.

Anatomy

Adenoids are located in the upper vault of the nasopharynx. They are classified according to their size and projection into the nasopharynx lumen:

• Grade 1 adenoids — located in the upper part of the nasopharynx and cover ⅓ of the vomer;
• Grade 2 adenoids — occupy ½ of the nasopharynx and cover ½ of the vomer;
• Grade 3 adenoids — cover ⅔ of the nasopharynx, leaving small space for breathing;
• Grade 4 adenoids — completely block the nasopharyngeal lumen, descend into the oropharynx, and cover the vomer.

Nasopharyngeal tonsil is a heterogeneous elastic lumpy pink-colored substance, 5–7 mm thick and 20–25 mm in diameter, with longitudinal grooves of varying sizes.

Tubal tonsils are small areas of lymphoid tissue (up to 7 mm) located cranially near the openings of the auditory tubes. If they are hypertrophied, the openings are blocked, and the exit from the eustachian tube is obstructed.

In inflammation of the nasopharyngeal tonsil, its barrier function is compromised, the epithelial cilia are destroyed, adenoid vegetations become hyperemic and infiltrated, covered with fibrinous plaque. A large amount of serous or mucopurulent content is found in the grooves. Mucus drainage is also noted along the posterior pharyngeal wall. Lymphoid follicles enlarge, and hyperemia of the posterior palatine arches and lateral pharyngeal wall is observed. Adenoiditis is divided into catarrhal, exudative-serous, and mucous-purulent based on the nature of the discharge.

Clinical manifestations

Hypertrophied adenoids are characterized by a diverse clinical picture. The most common complaints from parents are constant nasal breathing difficulties, snoring, and noisy breathing. In young children, eating becomes difficult due to impaired nasal breathing. With a pronounced degree of hypertrophy, nasality develops. Due to breathing disorders, children sleep worse at night, wake up frequently, and some experience obstructive sleep apnea syndrome (OSAS), with breathing pauses up to 1 minute. This leads to increased fatigue and reduced ability to perform tasks.

There is also the notion of habitus adenoideus, or adenoid-type face. Such children have a flattened nasal bridge, slightly open mouth, malocclusion (mandibular prognathism), protruding upper incisors, gothic palate, small exophthalmos, and elongated face shape.

Hypertrophied tubal tonsils do not cause clinical manifestations by themselves. Their influence on the airways is mediated by blocking the auditory tube.

Hypertrophied adenoids, like tubal tonsils, obstruct the auditory tube openings, leading to tubotympanitis, recurrent acute otitis, or slow-moving exudative otitis. In some cases, conductive hearing loss develops, which may be the only complaint.

Clinically, adenoiditis is classified as acute (up to 7–10 days), subacute (10 days to 1 month), and chronic (over 1 month). However, in practice, this classification is conditional. Since edema of lymphoid tissue occurs in adenoiditis, the clinical picture resembles that of adenoid hypertrophy. In addition to the abovementioned complaints, mucous or purulent nasal discharge, mucus dripping down the posterior pharyngeal wall, accompanied by coughing, is typical. Deterioration is noted at night.

Acute adenoiditis is characterized by febrile body temperature, general intoxication, pain in the depth of the nose and head with radiation to the eyes and ears. Regional lymph nodes are enlarged, their soreness is noted.

Chronic adenoiditis features subfebrile body temperature, suffocating night cough, and concomitant middle ear pathology, accompanied by conductive hearing loss.

Diagnosis

Initially, complaints are gathered, medical history is clarified, and otorhinolaryngoscopy is performed. To determine the degree of nasopharyngeal obstruction and examine the auditory tube openings, posterior rhinoscopy and nasopharyngeal endoscopy are performed. Manual examination is conducted rarely. To determine the degree of hypertrophy of adenoid vegetations, lateral view nasopharyngeal radiography is performed. In inflammation of the nasopharyngeal tonsil, a microbiological study for microflora and antibiotic sensitivity is conducted.

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Treatment

Conservative therapy is initially given to children with hypertrophied nasopharyngeal or tubal tonsils. Intranasal glucocorticosteroids (mometasone furoate) are prescribed for at least 1 month with follow-up evaluation. If the results are positive, further use of the drug is recommended according to the scheme.

In the absence of effect, and in the presence of complications (OSA, hearing loss, chronic otitis), surgical treatment is recommended. Under local or general anesthesia, an adenotomy is performed, during which the hypertrophied lymphoid tissue is excised with a Beckman adenotome.

Hypertrophied lymphoid tissue of the nasopharyngeal tonsil in adults is subject to mandatory surgical removal with subsequent pathohistologic examination.

The tubal tonsils are subject only to conservative treatment with the use of topical glucocorticosteroids. Their surgical excision is not performed, as in most cases it leads to scarring of the aperture of the auditory tubes. In cases of significant eustachian tube obstruction and presence of exudate in the middle ear, accompanied by hearing loss, balloon dilation is performed.

To treat inflamed nasopharyngeal tonsils, antibacterial drugs are used as topical sprays or systemically, considering the pathogen’s sensitivity. In addition to etiotropic therapy, regular sanitation of the nasal cavity and nasopharynx from pathological contents is recommended with saline or seawater solutions. Vasoconstrictive sprays are used to reduce swelling. It is necessary to carry out general strengthening measures. With recurrent adenoiditis or middle ear complications, surgical treatment should be considered.