Academic literature on the topic 'Chronic adenotonsillar disease'

BACKGROUND: Adenotonsillar hypertrophy is a common disorder in the children’s population that can lead to growth disorders. Chronic adenotonsillar hypertrophy can cause a break in the normal growth of children, weight loss, and decreased growth hormone secretion. AIM: The purpose of this study was to evaluate adenotonsillar hypertrophy in the growth rate of children with height, weight, and body mass index (BMI). METHODS: In this descriptive-analytical cross-sectional study, after examining 312, 3–10-year-old children with adenotonsillar hypertrophy, who met the inclusion criteria, growth scales were evaluated and entered into the patient evaluation form. RESULTS: There was a significant relationship between BMI, height, weight, and severity of tonsillar hypertrophy at Brodsky’s scale (P <0.001). Our studies showed well that with increasing severity of adenotonsillar hypertrophy disease, the growth indicators are also decreased in children. CONCLUSION: Adenotonsillar hypertrophy decreases growth indicators in children. There was also a relationship between growth indicators and severity of adenotonsillar hypertrophy in patients.

We sought to investigate the prevalence of potentially pathogenic bacteria in secretions and tonsillar tissues of children with chronic adenotonsillitis hypertrophy compared to controls. Prospective case-control study comparing patients between 2 and 12 years old who underwent adenotonsillectomy due to chronic adenotonsillar hypertrophy to children without disease. We compared detection of Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Pseudomonas aeruginosa, and Moraxella catarrhalis by real-time PCR in palatine tonsils, adenoids, and nasopharyngeal washes obtained from 37 children with and 14 without adenotonsillar hypertrophy. We found high frequency (>50%) of Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, and Pseudomonas aeruginosa in both groups of patients. Although different sampling sites can be infected with more than one bacterium and some bacteria can be detected in different tissues in the same patient, adenoids, palatine tonsils, and nasopharyngeal washes were not uniformly infected by the same bacteria. Adenoids and palatine tonsils of patients with severe adenotonsillar hypertrophy had higher rates of bacterial coinfection. There was good correlation of detection of Moraxella catarrhalis in different sampling sites in patients with more severe tonsillar hypertrophy, suggesting that Moraxella catarrhalis may be associated with the development of more severe hypertrophy, that inflammatory conditions favor colonization by this agent. Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, and Moraxella catarrhalis are frequently detected in palatine tonsils, adenoids, and nasopharyngeal washes in children. Simultaneous detection of Moraxella catarrhalis in adenoids, palatine tonsils, and nasopharyngeal washes was correlated with more severe tonsillar hypertrophy.

ABSTRACT Recurrent or chronic adenotonsillar infections mainly affect children and frequently involve otherwise healthy subjects. Therefore, having excluded systemic immunological deficiencies, this disease may be due to a local dysfunction of the epithelial structures at either the rhino or oropharyngeal level. The aim of the present investigation was to analyze structural and immunological aspects of tonsils and adenoids in subjects who underwent adenotonsillectomy because of recurrent inflammatory episodes with fever. Histological studies and analyses of the cytokine patterns were carried out in palatine tonsils and adenoid samples from 105 patients who underwent adenoidectomy and bilateral extracapsular tonsillectomy for chronic inflammatory hypertrophy of these organs; 46 of the 105 cases examined presented hyperkeratosis of the crypt epithelium; in the remaining 59, the epithelium was hyperplastic with no signs of keratosis. Scanning electron microscopy revealed a continuous epithelial surface of polygon-shaped flattened cells with fissures towards the cryptic depressions. Titration of interleukin-1β and tumor necrosis factor alpha in serum and tissues demonstrated higher concentrations in the adenotonsillar specimens, whereas the rise in interleukin-6 was more modest.

Obstructive sleep apnea (OSA) in children is one of the most common problems encountered by the otolaryngologist. It was described frequently in adults but was not clearly defined as of true medical significance in children until 19761. Since then, rapid advances in technology and increasing recognition have propelled pediatric sleep apnea into both fame and notoriety. Snoring is the hallmark of sleep disordered breathing. It occurs in up to 27% of school aged children 2-10 and peaks at 2-8 years. This is coincident with the peak in size and degree of immunologic activity of the tonsils 11. The reported prevalence of sleep apnea in this age group is 2-3 % 10, 12. Snoring again increases in children 15 years and above with nearly half the males and a third of the females snoring habitually13. Characteristics of pubertal children with OSA closely mimic adult patterns and are usually addressed as such. Airway collapse in OSA is dictated by many factors. Anatomic obstruction caused by adenotonsillar hypertrophy is the most readily recognizable etiology. Certain craniofacial characteristics also result in a smaller airway. Moreover, functional pharyngeal muscle tone varies in response to sleep state, pressure-flow airway mechanics and respiratory drive to determine the cross sectional area of the upper airway14. In children with primary snoring, narrowing occurs at the level of the soft palate. In those with OSA, collapse is at the level of the tonsils and adenoids 12. Interestingly several researches have failed to demonstrate significant correlation between adenotonsillar size and OSA14-18. This discrepancy is now being attributed primarily but not solely to the increased incidence of childhood obesity. Upper airway, neck, chest and abdominal fat deposition give rise to upper airway narrowing, increased mass loading, decreased chest and diaphragmatic excursions14. These result in an obstructive as well as restrictive pattern of respiratory compromise. Although obese children may have concomitant adenotonsillar hypertrophy, addressing this exclusively rarely leads to resolution of OSA. The consequences of untreated childhood OSA encompass a broad range of morbidities including behavioral disturbances and learning deficits, cardiovascular disease, metabolic disturbances, somatic growth compromise, decreased quality of life and psychiatric illness14. Mouth breathing is a clinical presentation worthy of special mention. It has been known that adenoid hypertrophy resulting in chronic mouth breathing leads to “adenoid facies”. This is characterized by an incompetent lip seal, narrow upper dental arch, increased anterior face height, steep mandibular plane angle, and a retrognathic mandible 19-20. Craniofacial development progresses rapidly and retains its plasticity until early puberty (12 or 13 years). Thereafter, growth slows down as the adult face begins to set21. If mouth breathing is left untreated by this age the probability that the child will eventually develop adult-pattern OSA is greater. Fortunately not all children develop these complications. Environmental exposure and genetic susceptibility certainly play a role in making a child more vulnerable to the effects of OSA. On the other hand, some of these morbidities may not be completely reversible despite treatment 14, 22. Therefore timely and appropriate management of OSA is crucial in ensuring conditions for optimal development. . Tonsillectomy and adenoidectomy remain the primary mode of treatment for childhood OSA. Fear of rheumatic fever and its complications traditionally prompted immediate removal of the tonsils and adenoids. In 1978, OSA was not documented as an indication for tonsillectomy. An increasing trend was demonstrated such that in 1986 19% of cases were due to OSA22. By 2003, upper airway obstruction was the reason for surgery in 96% of tonsillectomies performed in children less than 36 months over a period of 2 years in a tertiary center23. A meta-analysis of 14 studies reporting polysomnographic outcomes of tonsillectomy and adenoidectomy showed a summary success rate of 82.9% 24. Significant improvement in quality of life based on validated questionnaires measuring sleep disturbance, physical symptoms, emotional symptoms, hyperactivity and daytime functioning without supporting polysomnographic results have also been reported25-30. However, this still leaves a number of children with residual disease. Readily identifiable risk factors for surgical failure are untreated nasal obstruction, maxillomandibular deficiency, obesity and a high respiratory index 14,31,32. Further treatment using medications, additional surgery or positive airway pressure therapy is usually necessary for this group of patients. The first 24 hours after surgery is probably the most critical time for developing complications. Patients have deeper sleep due to chronic poor sleep quality and sedation or may be placed in supine position37. OSA as an operative diagnosis automatically increases the risk of the patient. Other factors are low weight, obesity especially those with associated co-morbidities (hypertension, asthma and type II diabetes), age less than 3 years and those with severe pulmonary hypertension33-37. Identified problems are supraglottic obstruction, breath holding, desaturation on induction and emergence37. In children less than 6 years 6.4% experienced morbidities which were primarily respiratory. More than half of these children (57.7%) had desaturations necessitating use of an artificial airway via nasopharyngeal airway or endotracheal intubation and 18% had significant chest findings on radiograph particularly atelectasis, infiltrates and pulmonary edema36. Children less than 3 years old have nearly a 2-fold increased risk for respiratory complications36. Risk-assessment prior to surgery is essential in achieving a safe perioperative outcome. Close coordination with other concerned physicians particularly pediatric subspecialists and anesthesiologists is fundamental. The hospital wherein the procedure will be conducted should have provisions for thorough intra- and post-operative monitoring. The decision to admit to the ICU after surgery is dictated by severity of illness, the presence of co-morbidities and young age. Pediatric obstructive sleep apnea is an entity in evolution. Heterogenous patient profiles especially in the face of rising obesity, changing syndrome definitions and polysomnographic parameters, innovations in treatment and even legal issues will continue to challenge every otolaryngologist. Notwithstanding, otolaryngology should remain in the foreground in treating pediatric OSA. Despite attendant risks and limitations, pediatric sleep surgery in the hands of the informed otolaryngologist is still the most useful tool in helping children recover from sleep disordered breathing.

Background: Allergic diseases are among the most common chronic conditions in pediatrics. Objectives: This study aimed to evaluate the relative frequency of allergic rhinitis (AR) in children with adenotonsillar hypertrophy. Methods: In this descriptive study, 175 patients with adenotonsillar hypertrophy referred to the Imam Khomeini hospital of Ahvaz from March 2019 to March 2020 were enrolled. Allergic rhinitis was diagnosed based on the Score for AR (SFAR) questionnaire. The questionnaire, including the expert-designed SFAR, has eight main components that evaluate eight quantitative features of AR, and each was designated with a specific weighted score based on previous clinical studies. The total score could vary from 0 to 16. Frequency and percentage were used to describe the data. The chi-square test and Fisher's exact test were used to analyze the data. Results: One hundred seventy-five patients with adenotonsillar hypertrophy in the age range of 1 to 17 years were studied. Ninety-one patients (52%) were male, and 84 patients (48%) were female. Based on the score obtained from the questionnaire, 146 patients (83.4%) had a score of less than seven, indicating susceptibility to AR. Twenty-nine patients (16.6%) had a score equal to or higher than 7, confirming the diagnosis of AR. The Chi-square test showed that AR was significantly associated with all the components of the questionnaire, except for cigarette smoking (P-value < 0.001). Conclusions: This study showed the strong association of AR with some demographic factors. Allergic rhinitis could potentially increase the risk of adenotonsillar hypertrophy in children.

Aims: Cardiopulmonary diseases may be seen in patients with chronic adenotonsillar hypertrophy that lead to severe obstructive sleep apnea (OSA), among which pulmonary hypertension is the most well-known. Here we compared the oxygen saturation in children who underwent tonsilo-adenoid resection (TAR) or tonsilar resection. Fifty patients Materials and Methods: diagnosed with chronic tonsillitis and adenoid hypertrophy was studied in the Department of Otorhinolaryngology and head and neck surgery. All the patients have undergone TAR or tonsilar resection and oxygen saturation was recorded by pulse oximeter pre and post surgery. Male Results: preponderance was observed (72%). Postoperative oxygen saturation (97.27±0.096) was signicantly higher to preoperative oxygen saturation (96.42±0.123) (p<0.001). Among 50 patients, 15 underwent tonsilar resection and 35 TAR, 29 (58%) patient had risen in oxygen saturation postoperatively, 19 (38%) patient had same saturation as prior to saturation, 2 (4%) patient had fallen in saturation after the surgery. Conclusion: TAR is an important surgery to improve oxygen saturation in children having chronic tonsilitis. This also improves other associated complains of snoring, mouth breathing, ear infections

Objective: Pediatric obstructive sleep apnea (OSA) can have both acute and chronic consequences when untreated. We hypothesize that a link exists between childhood obesity and OSA at nationwide level, with race, gender, and socioeconomic status conferring their own risk for pediatric OSA. Methods: This study examined nationwide discharges in 2016 using the Kids’ Inpatient Database (KID). The International Classification of Diseases, 10th revision, Clinical Modification (ICD-10-CM) codes for obesity (E66.0) and OSA (G47.33) were used. Prevalence rates and odds ratios (ORs) were used to quantify associations between the obesity and OSA groups in the general pediatric inpatient population. Multiple binary logistic regression was utilized to compare cohorts of pediatric inpatient admissions. Results: There were 36 266 285 weighted discharges in the 2016 KID. Among patients included in our dataset, 0.426% (26 684) were diagnosed with obesity and 0.562% (35 242) had OSA. Obesity was independently associated with a significantly increased risk of OSA (OR = 22.89; 95% C.I. = 21.99-23.84). Within the OSA inpatient population, obesity was associated with non-Hispanic black race, Hispanic ethnicity, and Native American race/ethnicity (OR = 1.45, 1.32, 2.51; 95% C.I. = 1.33-1.58, 1.21-1.44, 1.73-3.63). Conclusions: Obesity is independently associated with OSA in children after controlling for adenotonsillar hypertrophy. Non-Hispanic black race and Hispanic ethnicity are independent risk factors for OSA and are associated with obesity in the OSA inpatient population, which suggests that obesity may play a role in the increased risk of OSA within these groups.

Rinovírus (RV) é freqüentemente detectado nos tecidos tonsilares e nas secreções de nasofaringe de pacientes com doença adenotonsilar crônica, sem sintomas de infecção respiratória aguda (IRA). O objetivo deste estudo foi investigar a infecção por rinovírus em tonsilas humanas, com base em dois aspectos: infecção in vivo de células linfóides de tonsilas humanas naturalmente infectadas; e infecção ex vivo de células dissociadas desses tecidos inoculadas com rinovírus, visando a contribuir para elucidar possíveis mecanismos de infecção em amígdalas palatinas e adenóides humanas. De um total de 104 pacientes com doenças adenotonsilar crônicas, 21.1% (22/104) e 42.3% (44/104) apresentaram respectivamente amígdalas palatinas e adenóides positivas para RV por PCR. A replicação viral foi confirmada por hibridização in situ com sonda para intermediário replicativo nas regiões internas e externas aos folículos linfóides de amígdalas e adenóides, bem como em porções do epitélio ciliado de adenoides, e apenas raramente nas células epiteliais escamosas de tonsilas palatinas. A presença e distribuição de proteína estrutural do capsídeo viral foi detectada por imunohistoquímica (IHQ), utilizando anticorpos contra proteínas estruturais virais VP1 e VP2 nas tonsilas positivas para RV por qPCR. Os resultados indicaram marcação positiva tanto na superfície (epitélio), quanto em regiões extrafoliculares e centros germinativos. Em seguida, foi possível verificar a co-localização da marcação positiva da proteína estrutural VP2 de RV com marcadores linfocitários de membrana. Células CD4 + e CD20 + apresentaram marcação positiva para VP2 verificada usando estratégia de \'sequential immuno-peroxidase labelling and erasing\' (SIMPLE). Culturas primárias de células linfomononucleares (CLMN) de tonsilas sabidamente negativas para RV por PCR, foram infectadas in vitro, com RV (MOI=1). A replicação de RV foi titulada por TCID50, mostrando aumento inicial (24 h) e subsequente queda após 48 horas. Por IF observamos que os fenótipos de CLMN infectadas com RV in vitro foram células T CD4 + e B, mas também com células CD8 +, CD56 + e CD33 +. RV não infectou células CD123 +. RV foi isolado em WI- 38 e HeLa a partir de tecidos e secreções de nasofaringe de pacientes com hipertrofia tonsilar sem sintomas de infecção respiratória aguda. Nossos resultados confirmam que tonsilas de pacientes sem sintomas respiratórios agudos podem ser reservatórios de RV, que infecta não somente epitélio, mas também CLMN (frequentemente linfócitos T CD4 + e linfócitos B). A detecção de RNA intermediário replicativo e proteínas estruturais VP1 e VP2 nas tonsilas hipertróficas, além do isolamento de vírus infeccioso a partir de tecidos e secreções nasofaríngeas, classificam tonsilas hipertróficas como sítios de infecção e replicação de RV, e sugerem que esses indivíduos hipertróficos são portadores assintomáticos de RV persistente, e podem ser importantes fontes de transmissão de RV na comunidade.
The chronic adenotonsillar diseases are frequent otorhinolaryngologic conditions caused by chronic inflammation of adenoids and palatine tonsils. Rhinovirus (RV) is highly frequently detected in secretions, and tonsillar tissues from patients experience chronic tonsillar hypertrophy without symptoms of ARI, and our goal is to full understanding of viral infections in hypertrophic tonsillar tissues by RV. Of 104 enrolled patients with adenotonsillar chronic diseases, 21.1% (22/104) and 42.3% (44/104) had palatine tonsils and adenoids positive for RV by qPCR, respectively. RV Viral replication was confirmed by in situ hybridizations. Minus-strand RNA were detected in all tested samples (7 tonsils and 9 adenoids), and positive reactions were seen inside and outside of lymphoid follicles from tonsils and adenoids, in the ciliated epithelium of the adenoids and rarely in positive squamous epithelium cells from tonsils. The presence of viral structural protein VP1 and VP2 was detected within and outside of the lymphoid follicles from tonsils and adenoids, and also in epithelial cells from adenoids by immunohistochemistry (IHC). Later, by sequential immuno-peroxidase labelling and erasing protocol (SIMPLE), we saw co-localization of RV VP2 capsid protein staining with CD4 positive cells and CD20 positive cells. We confirmed that RV could infect primary culture of tonsilar mononuclear cells (TMNCs). Additionally, intracellular replication of RV in TMNCs, measured by TCID50 in HeLa cells, had an initial increase in the first 24 hours, and dropped at 48 hours post infection. Immunolocalization staining with anti-RV and TMNCs surface markers indicated that phenotypes of susceptible cells were T-cells both CD4+ and CD20+, but also, we saw co-localization of VP-2 protein with CD8+ cells, CD56+ cells and CD33+ cells. RV-16 couldn\'t infect CD123+ cell in our experiments. Finally, we were able to recover 4 rhinoviruses by inoculating WI-38 fibroblast cells and HeLa cells, confirming by the cytopathic effect and immunofluorescence positive staining with anti-VP1 antibody. Taken together, our results indicate that tonsils and adenoids of patients without ARI may be reservoirs of replicating human rhinovirus, infecting manly Tcells CD4+ and CD20+ B-cells. The high-frequency detection of RNA (-) and VP1 expression in tissues from patients with chronic adenotonsillar diseases, plus the isolation of infectious viral particles, suggests that these detected agents replicate in the adenotonsillar tissues and this specific sites may be important sources of transmission of RV in the community.