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The purpose of our review was to synthesize the existing literature about the prevalence of adenoid hypertrophy (AH) in children and adolescents confirmed by the reference standard - the nasoendoscopy (NE). Six electronic databases and partial grey literature were searched. Studies were included if they reported the prevalence of AH confirmed via NE. Studies involving participants with associated comorbidities and/or fully diagnosed sleep apnea in their sample were excluded. The MAStARI tool assessed the potential risk of bias (RoB) among the studies, while the GRADE approach determined the level of evidence. A total of 5248 patients were included. Seventeen studies were included in the meta-analysis showing an AH prevalence of 49.70% (confidence interval (CI): 39.92 to 59.50). The studies were then divided into 3 groups based on the RoB assessment and patient selection method. The AH prevalence for group 1 (studies having low RoB) was 42.18% (CI: 34.93 to 49.60; n = 2794), for group 2 (studies having moderate RoB) was 70.02% (CI: 40.102 to 92.690; n = 538), and finally for group 3 (studies with randomly collected samples) was 34.46% (CI: 10.507 to 63.742; n = 1446). High heterogeneity between the studies was found. The GRADE approach classified the quality of evidence as moderate. In summary, in a randomized representative sample the prevalence of AH was 34.46%; however, in convenience samples the prevalence ranged from 42 to 70%., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The paper presents the results of comprehensive survey and orthodontic treatment of 40 children with dentoalveolar anomalies and nasopharyngeal tonsil hypertrophy aged 7-9 years. The linear parameters obtained by cone beam CT and TWH in the lateral projection were analyzed. The study revealed changes, indicating that the presence of nasopharyngeal tonsil hypertrophy, leads to pathology of the dental system and estimated the efficiency of muscle training and combined use of functional devices and elastopositioner «Corrector» for the treatment of anomalies of dentition and the formation of physiological occlusion in the process of permanent teeth eruption.

Velo-cardio-facial syndrome is the most common contiguous gene disorder in humans and constitutes 8% of patients with clefts of the secondary palate. Speech disorders, including severe hypernasality and articulation impairment have been documented as among the most common clinical manifestations of the disorder. A series of 36 consecutive patients with VCFS ranging in age from 3 to 14 years, all confirmed to have a 22q11.2 deletion, were studied to determine specific risk factors associated with VPI and articulation impairment. Factors studied included palatal clefting, hypotonia, platybasia, and adenoid size. The factor that correlated most strongly with speech disorders was adenoid hypoplasia or absence, a common manifestation in the syndrome. It is hypothesized that early identification of the absence or hypoplasia of the adenoids can result in the implementation of appropriate therapy plans to avoid severe disorders of speech intelligibility.

The obstructive sleep apnoea syndrome (OSAS) in children is a clinical syndrome resulting from complete or partial obstruction of the upper respiratory tract during sleep. The pathogenesis is multifactorial; clear risk groups are children with anatomical anomalies of the upper airways, neurological abnormalities and genetic syndromes (including craniofacial syndromes). The clinical symptoms of OSAS in children vary. In partial obstructions, the most frequent forms, the patients may snore and have impaired respiration during sleep. Polysomnography contributes to definite confirmation and specification of the clinical diagnosis. Standard values should be interpreted with respect to age. Adenotonsillectomy is the most frequent treatment of children with OSAS. In persistent symptoms, continuous positive pressure therapy is often successful. The natural evolution and the long-term prognosis of OSAS in children are still unknown.

In children and adolescents there have been only few reports dealing with Obstructive Sleep Apnea (OSA) associated with morbid obesity. We report here on sleep-associated breathing disorders in morbidly obese children and the effect of adenoidectomy and tonsillectomy on sleep-associated breathing disorders. The subjects were 31 children with morbid obesity. The mean patient age was 7.9 years ranging from 2 to 14 years. The percentage of expected body weight ranged from 130% to 260%. All of them had adeno-tonsillar hypertrophy. We undertook the study during the period of natural sleep. Percentage of sleeping period with irregular breathing was determined by means of respisomnogram and the percentage of sleeping period with SpO(2) > or = 90% with a pulse oximeter. The percentage of sleeping period with irregular breathing ranged from 10% to 85% before the operation. In all cases, the irregular breathing period decreased almost to zero after the adenoidectomy and tonsillectomy. The percentage of sleeping period with SpO(2) > or = 90% ranged from 1.7% to 95%. The percentage was related to reduction of body weight and it increased gradually as a result of a diet given as therapy. Our studies reveal that weight control may result in partial cure of sleep-associated breathing disorders. Operations, such as adenoidectomy and tonsillectomy, were remarkably effective in treating sleep-associated breathing disorders of severely obese children with large adenoids and tonsils, even if the severe obesity remained.

A simplified method for the diagnosis of sleep respiratory disorders in children was explored on the basis of visual inspection. The subjects were 31 children suffering from symptoms of upper airway constriction. Polysomnography was carried out on all patients to measure the mesopharyngeal pressure amplitude (MPA). The patients were divided into the following four groups: Group A (degree I hypertrophy at rest), Group B (degree II hypertrophy both at rest and during pharyngeal reflex), Group C (degree II hypertrophy at rest and degree III hypertrophy during pharyngeal reflex), and Group D (degree II hypertrophy at rest, accompanied by forward protrusion from the anterior faucial pillar). The MPA values were 26.0 +/- 13.7, 39.2 +/- 18.3, 86.9 +/- 36.4 and 84.6 +/- 16.3 cmH(2)O in Groups A, B, C and D, respectively. The MPA values in Groups C and D were significantly higher than those in Groups A and B. The result of this study suggest that the MPA values are high and sleep respiratory disorders severe in cases from Groups C and D. The severity of sleep respiratory disorders in children was estimated to a considerable extent by checking these parameters.

To define the role of adenotonsillar hypertrophy and facial morphology in obstructive sleep apnea (OSA) in children we performed a cephalometric analysis of an OSA group and an age-matched control group. Adenotonsillar hypertrophy was remarkable in OSA children at every age level. Maxillary protrusion expressed by SNA was significantly smaller in the OSA group than in the control group for elderly children (5-9 years old). Mandibul protrusion expressed by SNB was significantly smaller in the OSA group even at younger ages (1-2 years). The hyoid bone was significantly lower in the OSA group than in the control group who were from 3 to 6 years. Environmental factors due to upper airway obstruction as well as genetic factors are suspected to cause abnormal facial morphology in OSA children.

Beckwith-Wiedemann syndrome is a congenital disorder manifested by organomegaly, omphalocele, hypoglycemia, and macroglossia. We have found a significant number of these children to be at risk for upper airway obstruction during infancy or childhood. In this review of 13 children, 2 required tracheotomy during infancy for cor pulmonale caused by macroglossia. Seven of nine children older than 1 year required tonsillectomy and adenoidectomy to relieve upper airway obstruction. Although macroglossia can be a cause of airway obstruction in infants with Beckwith-Wiedemann syndrome, we have found that airway obstruction during childhood is related to tonsillar and adenoidal hypertrophy and not to macroglossia. Anterior tongue reduction is reserved for the correction of malocclusion, articulation errors, or cosmesis, whereas tonsillectomy and adenoidectomy may be curative of obstructive symptoms.

A prospective study was performed to evaluate the effects of adenotonsillar hypertrophy on snoring in children. Thirty male patients were grouped with respect to the severity of snoring and were evaluated in terms of the noise level of the snoring sound, the lowest arterial oxygen saturation, degree of palatine tonsillar hypertrophy, body mass index and cephalometric findings that included the adenoidal-nasopharyngeal ratio, the angle between the lines sella turcica/nasion and most posterior point of anterior maxilla/nasion, the angle between the lines sella turcica/nasion and most posterior point of anterior mandible/nasion, the posterior airway space, the distance from the sella to the nasion, lower face height and the distance from the basion to the posterior nasal spine. The noise level of the snoring sound, the lowest arterial oxygen saturation and the adenoidal-nasopharyngeal ratio showed a significant correlation with the severity of snoring, but the degree of palatine tonsillar hypertrophy and the body mass index failed to disclose any significant relationship.

In this paper, the Authors propose a new method of cephalometric visualization of adhaenoids, in order to verify the amount of them as cause of an obstructive pathology. In this evaluation, related to a group of 100 individuals, was found an inversely proportional relation between adhaenoid's volume and angolar value of FHBoPA angle.

The authors examined four children with substantial adenotonsillar enlargement that caused intermittent severe upper airway obstructive episodes, documented by all-night polygraphic monitoring of sleep and respirations. Previously unreported complications of severe adenotonsillar enlargement that were demonstrated included prolonged obstructive apneic episodes and disturbed sleep patterns. The children also exhibited daytime hypersomnolence. Polygraphic sleep studies after adenotonsillectomy confirmed improved sleep patterns and relief of the obstructive episodes. None of our patienqs had developed pulmonary hypertension, cor pulmonale, or other reported complications of prolonged upper airway obstruction, all of which may have been averted by early diagnosis and treatment.

A case of cardiorespiratory syndrome secondary to chronic upper airway obstruction from hypertrophied tonsils and adenoids, involving a three-year-old boy, is presented. The haemodynamic changes were verified by heart catheterization. The possible role of steroids in the treatment of the syndrome is suggested.

A three year old with sleep apnea due to adenotonsillar hypertrophy is presented. The picture improved after treatment with antibiotics and corticosteroids, and disappeared after adenotonsillectomy. The symptomatology is studied in relation to primary alveolar hypoventilation and the "sudden death" syndrome in infants. The need of an early diagnosis is emphasized to avoid onset of an irreversible "cor pulmonale". It is suggested that aside from a probable predisposing "central" and constitutional factor in children with this syndrome, apparently there are heterogeneous electroencephalographic sleep patterns.