| Adenoid hypertrophy | |
|---|---|
| Other names | Enlarged adenoids |
 | |
| 3D still showing adenoid hypertrophy. | |
| Specialty | Otorhinolaryngology |
Adenoid hypertrophy, also known asenlarged adenoids refers to an enlargement of theadenoid (pharyngealtonsil) that is linked to nasopharyngeal mechanical blockage and/or chronic inflammation.[1] Adenoidhypertrophy is a characterized byhearing loss, recurrentotitis media, mucopurulentrhinorrhea, chronicmouth breathing, nasalairway obstruction, increased infection susceptibility, dental malposition, and dentofacial abnormalities ("adenoid facies" or "mouth breather face").
The exact cause of adenoid hypertrophy in children remains unclear, but it is likely linked to immunological responses, hormonal factors, or genetic components. Adenoid hypertrophy is an immunological abnormality characterized by alteredcytokine production, with children experiencing higher levels of proinflammatory cytokines. Adenoid hypertrophy can also be caused by gastric juice exposure duringgastroesophageal reflux disease,passive smoking, and recurrent bacterial and viral infections. Pathogen colonization can disrupt theimmune system's equilibrium with the adenoid's natural flora. Genetic factors, such as variations inTLR2 andTLR4 genes, also contribute to the condition. Adenoids naturally undergohypertrophy between the ages of 6-10 and atrophy around 16 years old.
A clinical examination andnasoendoscopy are the gold standard for diagnosing adenoid hypertrophy. Visual examinations should be conducted to identify adenoid facies,eczema, and similar signs in diseases like partialchoanal atresia, significant palatine tonsil hyperplasia, nasal airway blockage, endonasal foreign bodies, nasal concha hyperplasia, and allergic or viralrhinitis.Neoplasms, benign or malignant ones, should be ruled out. Screening forjuvenile nasopharyngeal angiofibroma is crucial in male adolescents, while adult patients should be evaluated forcarcinoma andlymphoma.Thornwaldt cysts should also be considered in the differential diagnosis.
Patients with adenoid hyperplasia alone should follow conservative therapy and off-label intranasalcorticosteroids. Patients with significant symptoms and unsatisfactory responses to conservative measures may be candidates foradenoidectomy. Anadenoidectomy can shrink and reduce nasal obstruction in patients. Patients usually experience improved eustachian tube function, reduced obstruction, and decreased nasal discharge. The prevalence of adenoid hypertrophy in the pediatric population is estimated to be 34%.
Enlarged adenoids can become nearly the size of aping pong ball and completely block airflow through the nasal passages. Even if enlarged adenoids are not substantial enough to physically block the back of the nose, they can obstruct airflow enough so thatnasal breathing requires an uncomfortable amount of work, and inhalation occurs instead throughmouth breathing. Adenoids can also obstruct the nasal airway enough to affect the voice without stopping nasal airflow.[2]
Adenoid hypertrophy is characterized by several typical signs and symptoms, includingconductive hearing loss, recurrentotitis media (includingcholesteatoma), mucopurulentrhinorrhea, chronicmouth breathing, nasalairway obstruction, increased susceptibility to infection, and occasionally dental malposition.[1]
If left untreated, adenoid hypertrophy can causepulmonary hypertension, ear issues,obstructive sleep apnea, failure to thrive, andcraniofacial abnormalities.[3][4]
The exact cause of adenoid hypertrophy in children is unclear. Most likely, immunological responses, hormonal factors, or genetic components have some relationship.[5] Contributing environmental factors includeair pollution andsmoking.
One of the immunological abnormalities described is alteredcytokine production. For instance, it was demonstrated thatinterleukin (IL)-32 was upregulated inadenoid tissue. This could potentially impact the progression of adenoid hypertrophy by inducing the production of proinflammatory cytokines and inducingpyroptosis in human nasalepithelial cells, which is mediated by theNOD1/2/TLR4/NLRP3 pathway.[6]
Furthermore, it has been discovered that children with adenoid hypertrophy had higher levels of proinflammatory cytokines, includinginterferon-γ (IFN-γ), high-sensitivityC-reactive protein,IL-1 andIL-10,TNF-α (tumor necrosis factor α), andintercellular adhesion molecule-1.[7]
Adenoid hypertrophy may also be brought on by gastric juice exposure duringgastroesophageal reflux disease, particularly in infants and early toddlers.[8] An additional risk factor for adenoid hypertrophy is passive smoking.[9][5]
Recurrent bacterial and viral infections as well as pathogen colonization might upset the normally stable equilibrium between theimmune system and the natural flora of the adenoid.[10] Hypertrophic processes are frequently brought on by recurrentupper respiratory tract infections orallergies.[9][11] The bacteriaHaemophilus influenza,Streptococcus pneumoniae,Streptococcus pyogenes, andStaphylococcus aureus are most frequently isolated from adenoid tissue. Pathogens that areanaerobic bacteria are also found in chronic infections.[12]
Genetic factors include, for example, variations in the genes encodingTLR2 andTLR4, SCGB1D4, and other genes.[13][14]
The clinical and anatomic basis of hypertrophy is the enlargement of the germinal centers oflymphoid tissue and lymphoid follicles. The fundamental reason is thought to be a vicious cycle ofinflammation,hypertrophy and/orhyperplasia, secretory retention, and recurrent inflammation.[1]
Adenoid is a lymphoid tissue condensation at the back of the nose or on the nasopharyngeal posterosuperior wall. The adenoid is part ofWaldeyer's Ring.[15] In younger children, it seems to play a significant part in the establishment of a "immunological memory."[16] Adenoids naturally undergohypertrophy between the ages of 6 and 10 andatrophy around the age 16.[17]
Thetonsils in the back of the mouth, theadenoid, and the tonsilar tissue at the base of the tongue combine to formWaldeyer's ring, a tissue ring that helps keep toxins,bacteria, andviruses out of the body.B lymphocytes, a kind of blood cell that producesantibodies, make up the majority of the tissues found in the tonsils and adenoid glands. This antibody binds to toxins, germs, and viruses, rendering them inactive, preventing disease-causing agents from entering the body. The adenoid is situated toward the rear of thenasal cavity and up behind thesoft palate, in contrast to the tonsils, which are visible when one looks straight through the mouth. Similar to tonsilar tissue, the adenoid can be affected by both acute and long-terminfections. A persistent infection or inflammation may cause the adenoid to enlarge gradually. Due to its location at the rear of the nasal cavity, its primary symptoms have an impact on nasal function.[15]
During the early years of life, the adenoids expand quickly due to their immunological roles. Its size and form change dramatically during childhood, with dynamic growth occurring between the ages of 3 and 6 years. This may be due to the nasopharyngeal cavity growing more slowly than expected.[10] Under normal circumstances, the adenoid grows less after the age of six, and the nasopharyngeal cavity expands and widens therespiratory tract.[5] Due to the proliferation of fibrous tissue and fattyatrophy, the lymphoid tissue experiencesinvolution later in life.[5] As a result, in the majority of people, adenoid tissue exists in a residual form but never totally vanishes.[18]
Macroscopic changes accompany the microscopic and functional changes within.[10] In humans, these adenoids are most immunologically active between the ages of 4 and 10, and after puberty, they start to involute.[19] The population ofB cells declines and the ratio ofT cells toB cells rises as a result. Inflammation of the crypts due to adenoid infection causes immunologically active cells to become inactive, reducing their capacity to transfer antigens. This, in turn, causes the cells tometaplasia into a multilayered squamous epithelium.[10] Such alterations result in poor cell functioning and ineffectiveantigen uptake.[20]
Currently, a thorough clinical examination combined withnasoendoscopy (NE), notablynasopharyngoscopy, is the gold standard for diagnosing adenoid hypertrophy.[21]
Visual examination should be conducted primarily to determine whether adenoid facies are present. The mouth is usually open, and the tip of the tongue is visible in a patient with an adenoid facies. Furthermore,eczema is frequently seen at the nasal opening.[1]
Similar signs and symptoms can be found in diseases, such as partialchoanal atresia and significant palatine tonsil hyperplasia. Nasal airway blockage can also result from endonasal foreign bodies, nasal concha hyperplasia, and allergic or viralrhinitis. Neoplasms that are benign or malignant in particular need to be ruled out. It is important to screen forjuvenile nasopharyngeal angiofibroma in male adolescents in particular. Adult patients, on the other hand, need to be evaluated particularly forcarcinoma andlymphoma, which typically present with symptoms includingulceration, bleeding, slimy coatings, size increases, andconductive hearing loss. A spherical tumor of the nasopharynx coated in smooth mucosa called aThornwaldt cyst should also be considered in the differential diagnosis.[1]
In patients with adenoid hyperplasia alone without accompanying indications or symptoms, conservative therapy, i.e., cautious waiting, is advised.[1] Furthermore, data is indicating that people with adenoid hyperplasia may benefit from off-label intranasalcorticosteroids.[22]
Patients exhibiting significant symptoms (such as repeatedfever and infections, persistent ear problems) and/or unsatisfactory response to conservative measures (such as topicalcortisone, anti-allergic therapy, and watchful waiting) are candidates foradenoidectomy. Individuals with long-term serous or mucousotitis media frequently have anadenoidectomy,myringotomy, and/or tube insertions performed.[1]
If theadenoid is acutely swollen and responds well to antibiotic and steroid therapy, it will shrink back to a smaller size and cause less nasal obstruction. After undergoing anadenoidectomy, patients usually experience improvements in their eustachian tube function, a reduction in nasal obstruction, and a decrease in excessive nasal discharge. Of children who undergoadenoidectomy for chronic sinus disease, 25% will experience a resolution of their sinus disease.[15]
In the pediatric population, the estimated prevalence of adenoid hypertrophy is 34%.[23]
The structure that is today known as theadenoid was initially described by the German anatomist Conrad Victor Schneider in 1661. But it wasn't until 1868 that the Danish physician Meyer coined the term "adenoid vegetations."[10] In an original research report, Meyer characterized these adenoid vegetations as "soft tumour masses of the nasopharynx that fill the room above the soft palate."[24] He also realized the connection between adenoid hypertrophy, mouth breathing, snoring, nasal obstruction, and hearing loss.[10] In addition, Meyer suggested using a specific knife that is put into thenasopharynx through the anterior nostrils to treat adenoid hyperplasia surgically.[25]