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Cochrane Database of Systematic Reviews Protocol - Intervention

Intranasal corticosteroids for nasal airway obstruction in children with adenoidal hypertrophy

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Abstract

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:

To assess the effects of intranasal corticosteroids for improving nasal airway obstruction in children with adenoidal hypertrophy.

Background

The pharyngeal tonsils (adenoids) are a lobulated mass of lymphoid tissue located on the upper and posterior walls of the nasopharynx. This lymphoid structure is capable of considerable hypertrophy under adverse conditions such as chronic and recurrent infection of the upper respiratory tract, and/or allergies (Brodsky 1993; Javadyan 2003; Raphael 1987). There are few prevalence and incidence data available, but adenoidal hypertrophy is generally considered a common condition of childhood, and represents one of the most frequent indications for surgery in children (Rutkow 1986).

The enlarged adenoids can obstruct the nasopharyngeal airway, particularly at night when the patient is supine. Classically, the symptoms and physical signs considered indicative of adenoidal nasal airway obstruction in children are mouth breathing, hyponasal voice and nocturnal snoring (Kenna 2000; Paradise 1998). In more severe cases, obstructive sleep apnoea may occur potentially causing neurocognitive disturbance, growth failure and cor pulmonale (Guilleminault 1981; Breuillette 1982; Menashe 1965; Gozal 1998). Enlarged adenoids could also obstruct the Eustachian tube orifice resulting in a conductive hearing loss. The presence of fluid in the middle ear (otitis media with effusion) is frequently associated with adenoidal hypertrophy and suggests Eustachian tube dysfunction or chronic adenoidal infection (Kenna 2000; Grimmer 2005).

The diagnosis of adenoidal hypertrophy should be considered when the child presents with signs or symptoms of nasal airway obstruction. The validity of standardised clinical assessment of adenoidal obstruction of the nasopharynx has recently been confirmed by a well‐designed prospective study (Paradise 1998). The degree of a patient's mouth breathing and speech hyponasality were rated by one of eight study‐team nurse practitioners on a 4‐point scale (none = 1; mild = 2; moderate = 3; marked = 4). The two ratings were averaged to obtain a Nasal Obstruction Index (NOI) from 1 to 4. This study demonstrated a high inter‐observer agreement for mouth breathing and speech hyponasality (weighted k 0.84 to 0.91). The overall correlation between NOI and radiological assessment ratings was moderate, however a high correlation was found in children with NOI values at the lower and upper extremes (i.e. 1.0 and 3.5 respectively). Another instrument for the clinical measurement of nasal obstructive symptoms associated with adenoidal hypertrophy was a parent‐administered symptom questionnaire (Demain 1995). This encompassed assessment of a child's nasal congestion, nasal voice, snoring, daytime drowsiness, sleep quality, nasal discharge, ear popping or pain, and bad breath. The degree of each symptom was scored from 0 (never) to 10 (constant) using a visual analogue scale.

As nasal obstruction may be caused by other conditions such as rhinitis, nasal polyps or septal deviation, complementary examinations are needed for a definitive diagnosis of adenoidal hypertrophy. The lateral neck radiograph remains a widely employed investigation, in some countries, for children with suspected adenoidal hypertrophy. The low cost, widespread availability, non‐invasive nature and good correlation with symptoms and rhinoscopy findings are the main advantages of this diagnostic test (Mary 2005; Modrzynski 2005). The following radiological assessment methods have been reported to measure the adenoidal size in children: 1) Cohen and Konak's method (Cohen 1985): the ratio between the soft plate thickness (1 cm below the hard palate or 1/2 cm in children under three years old) and the air column width between the palate and the highest point of convexity of the adenoidal shadow; 2) Fujioka's method (Fujioka 1979): the ratio between the maximal thickness of the adenoidal shadow and the distance measured along a line from the superior/posterior edge of the hard palate to spheno‐occipital synchondrosis on the skull base; 3) Johanneson's method (Johanneson 1968): the distance between the perpendicular line from the pharyngeal tubercle on the skull base and the adenoidal shadow convexity. Of these methods, Cohen and Konak's shows the best correlation with endoscopic findings and clinical symptoms (Wormald 1992; Modrzynski 2005). This method accounts for the relationship between nasopharyngeal and adenoidal size and it is known that it is not the absolute adenoidal size but its ratio to the dimensions of the whole nasopharyngeal cavity which seems crucial in the clinical manifestation of adenoidal hypertrophy (Wang 1994).

Another method for the assessment of adenoidal size is trans‐oral mirror visualisation. A high correlation between mirror examination and fibreoptic nasopharyngeal endoscopy has been demonstrated by a recent prospective and blinded study, however the degree of choanal obstruction may be underestimated by this diagnostic test (Chisholm 2005). Fibreoptic nasopharyngeal endoscopy is considered the gold standard for the diagnosis and evaluation of adenoidal hypertrophy. This diagnostic method allows direct visualisation of the nasal cavity and the nasopharynx providing a dynamic evaluation of the magnitude of nasal airway obstruction (Wang 1992). The diagnostic accuracy of fibreoptic nasopharyngeal endoscopy may be of fundamental importance in establishing suitable indications for adenoidectomy (Wang 1992; Neri 2004), however the requirement of costly equipment and the need for child co‐operation limit this diagnostic approach.

The management of adenoidal hypertrophy in children is dependent on the degree of nasal airway obstruction and any associated morbidity. When obstructive sleep apnoea (OSA) or cardio‐respiratory syndrome occurs, adenoidal and tonsillar hypertrophy are usually implicated and adenoidectomy is generally indicated. However, the effects of surgical intervention in children with OSA attributable to adenoidal hypertrophy have not yet been investigated by randomised controlled trials (Lim 2006). Other potential indications for adenoidectomy include chronic sinusitis and otitis media with effusion (Gates 1992; Paradise 1995). The risk‐benefit ratio of surgical intervention for the individual child needs to be carefully assessed in light of potential anaesthetic complications (cardiac arrhythmia, malignant hyperthermia, vocal cord trauma and aspiration) and postoperative complications (haemorrhage, airway obstruction secondary to oedema, prolonged muscular paralysis and palato‐pharyngeal insufficiency). In less severe cases, non‐surgical interventions may be considered, however few medical alternatives are currently available. Commonly, medical management is limited to the treatment of concurrent infections and the complications of adenoidal enlargement (Sclafani 1998). Recently, the effects of intranasal corticosteroids in children with adenoidal hypertrophy have been assessed by randomised trials (Demain 1995; Criscuoli 2003).

The mechanism by which intranasal corticosteroids would reduce nasal airway obstructive symptoms is unclear, however the following mechanisms have been suggested (Demain 1995): 1) direct reduction of adenoidal size by lympholytic action of corticosteroids on adenoidal tissues; 2) reduction in adenoidal and nasopharyngeal inflammation by anti‐inflammatory effects of corticosteroids; and 3) a reduction in the significance of the adenoids as a reservoir for infection.

Despite the uncertainty of the precise mechanism, establishment of a therapeutic role for intranasal corticosteroids in children with adenoidal hypertrophy may have significant clinical implications. This modality may provide an effective non‐surgical alternative treatment for children with adenoidal hypertrophy. The use of intranasal corticosteroids has been generally considered safe in the paediatric population, despite uncommon reports of some local and systemic adverse events, including epistaxis, nasal mucosal irritation, moderate adrenal suppression and growth retardation (Adamopoulos 1995; Gazis 1999; Skoner 2000). There is a need for a comprehensive systematic review and meta‐analysis of the evidence for the effects of intranasal corticosteroids on reducing nasal airway obstruction associated with adenoidal hypertrophy in children.

Objectives

To assess the effects of intranasal corticosteroids for improving nasal airway obstruction in children with adenoidal hypertrophy.

Methods

Criteria for considering studies for this review

Types of studies

Randomised controlled trials (RCTs).

Types of participants

Children aged up to 12 years with symptoms of nasal obstruction and adenoidal hypertrophy, as demonstrated by fibreoptic nasopharyngeal endoscopy and/or indirect examination (lateral neck X‐ray or intra‐oral mirror visualisation).

Types of interventions

  • Intranasal corticosteroids versus placebo

  • Intranasal corticosteroids versus no intervention

  • Intranasal corticosteroids versus oral corticosteroids

  • Intranasal corticosteroids + other treatment versus placebo + same other treatment

  • Intranasal corticosteroids + other treatment versus same other treatment

Types of outcome measures

Primary outcome measures
Improvement in nasal obstruction assessed by the Nasal Obstruction Index or any other symptom score.

Secondary outcome measures

  • Reduction in adenoid size assessed by fibreoptic nasopharyngeal endoscopy and/or indirect examination (lateral neck X‐ray or intra‐oral mirror visualisation)

  • Improvement in quality of life assessed by validated quality of life questionnaire

  • Adverse events

Search methods for identification of studies

We will search the Cochrane Ear, Nose and Throat Disorders Group Trials Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 2, 2006), MEDLINE (1951 onwards) and EMBASE (1974 onwards). The following databases will also be searched: CINAHL, AMED, LILACS, KoreaMed, IndMED, SIGLE, Cambridge Scientific Abstracts, mRCT (a meta‐database of controlled trials), the National Research Register, ISRCTN and ISI Web of Science.

The Cochrane Central Register of Controlled Trials (CENTRAL) will be searched using the following search terms:

#1 ADENOIDS single term (MeSH)
#2 ADENOID* OR ADENOTONSIL* OR ADENO NEXT TONSIL* OR PHARYN* NEAR TONSIL*
#3 #1 OR #2
#4 HYPERTROPHY single term (MeSH)
#5 HYPERTROPH* OR ENLARGE* OR SWOLLEN OR OVERGROW* OR OVER NEXT GROW*
#6 #4 OR #5
#7 #3 AND #6
#8 STEROIDS explode all trees (MeSH)
#9 ANTI‐INFLAMMATORY‐AGENTS explode all trees (MeSH)
#10 ANTI‐INFLAMMATORY‐AGENTS‐NON‐STEROIDAL explode all trees (MeSH)
#11 #9 NOT #10
#12 GLUCOCORTICOIDS explode all trees (MeSH)
#13 STEROID* OR CORTICOSTEROID*
#14 GLUCOCORTICOID*
#15 BECLOMETHASONE OR BECLAMET OR BECLOCORT OR BECOLMETASONE OR BECOTIDE OR BETAMETHASONE OR CLENIL OR BECLOSOL
#16 BUDESONIDE OR HORACORT OR PULMICORT OR RHINOCORT OR BUDECORT
#17 CORTISONE OR DEXAMETHASONE OR HEXADECADROL OR DECADRON OR DEXASONE
#18 HEXADROL OR METHYLFLUORPREDNISOLONE OR MILLICORTEN OR ORADEXON OR FLUNISOLIDE OR FLUTICASONE OR HYDROCORTISONE OR CORTISOL OR FLIXONASE OR FLIXOTIDE OR PLURAIR
#19 METHYLPREDNISOLONE OR MOMETASONE OR PREDNISOLONE OR PREDNISONE OR NASONEX
#20 TRIAMCINOLONE OR NASACORT OR AIRCLIN
#21 #8 OR #11 OR #12 OR #13 OR #14 OR #15 OR #16 OR #17 OR #18 OR #19 OR #20
#22 #7 AND #21

The MEDLINE and EMBASE databases will be searched using strategies set out in Table 1.

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Table 1. Search Strategies

MEDLINE

EMBASE

1. ADENOIDS.DE.
2. (ADENOID$2 OR ADENOTONSIL$3 OR ADENO ADJ TONSIL$3 OR PHARYN$4 NEAR TONSIL$3).TI,AB.
3. 1 OR 2
4. HYPERTROPHY.DE.
5. (HYPERTROPH$3 OR ENLARGE$4 OR SWOLLEN OR OVERGROW$3 OR OVER ADJ GROW$3).TI,AB.
6. 4 OR 5
7. 3 AND 6
8. STEROIDS#.W..DE.
9. ANTI‐INFLAMMATORY‐AGENTS#.W..DE.
10. ANTI‐INFLAMMATORY‐AGENTS‐NON‐STEROIDAL#.W..DE.
11. 10 NOT 11
12. GLUCOCORTICOIDS#.W..DE.
13. STEROID$2 OR CORTICOSTEROID$2
14. GLUCOCORTICOID$2
15. BECLOMETHASONE OR 4419‐39‐0.RN. OR BECLAMET OR BECLOCORT OR BECOLMETASONE OR BECOTIDE
16. BETAMETHASONE OR 378‐44‐9.RN.
17. BUDESONIDE OR 51333‐22‐3.RN. OR HORACORT OR PULMICORT OR RHINOCORT
18. CORTISONE OR 53‐06‐5.RN.
19. DEXAMETHASONE OR 50‐02‐2.RN. OR HEXADECADROL OR DECADRON OR DEXASONE
20. HEXADROL OR METHYLFLUORPREDNISOLONE OR MILLICORTEN OR ORADEXON
21. FLUNISOLIDE OR 3385‐03‐3.RN.
22. FLUTICASONE OR 90566‐53‐3.RN.
23. (FLUTICASONE ADJ PROPIONATE) OR 80474‐14‐2.RN.
24. HYDROCORTISONE OR CORTISOL OR 50‐23‐7.RN.
25. METHYLPREDNISOLONE OR 83‐43‐2.RN.
26. MOMETASONE OR 105102‐22‐5.RN.
27. PREDNISOLONE OR 50‐24‐8.RN.
28. PREDNISONE OR 53‐03‐2.RN.
29. TRIAMCINOLONE OR 124‐94‐7.RN.
30. FLIXONASE OR FLIXOTIDE OR PLURAIR OR BUDECORT OR NASONEX OR CLENIL OR BECLOSOL OR NASACORT OR AIRCLIN
31. 8 OR 11 OR 12 OR 13 OR 14 OR 15 OR 16 OR 17 OR 18 OR 19 OR 20 OR 21 OR 22 OR 23 OR 24 OR 25 OR 26 OR 27 OR 28 OR 29 OR 30
32. 7 AND 31

1. ADENOID.W..DE.
2. (ADENOID$2 OR ADENOTONSIL$3 OR ADENO ADJ TONSIL$3 OR PHARYN$4 NEAR TONSIL$3).TI,AB.
3. 1 OR 2
4. HYPERTROPHY.W..DE.
5. (HYPERTROPH$3 OR ENLARGE$4 OR SWOLLEN OR OVERGROW$3 OR OVER ADJ GROW$3).TI,AB.
6. 4 OR 5
7. 3 AND 6
8. CORTICOSTEROID#.DE.
9. STEROID$2 OR CORTICOSTEROID$2
10. GLUCOCORTICOID$2
11. BECLOMETHASONE OR 4419‐39‐0.RN.
12. BETAMETHASONE OR 378‐44‐9.RN.
13. BUDESONIDE OR 51333‐22‐3.RN.
14. CORTISONE OR 53‐06‐5.RN.
15. DEXAMETHASONE OR 50‐02‐2.RN.
16. FLUNISOLIDE OR 3385‐03‐3.RN.
17. FLUTICASONE OR 90566‐53‐3.RN.
18. (FLUTICASONE ADJ PROPIONATE) OR 80474‐14‐2.RN.
19. HYDROCORTISONE OR CORTISOL OR 50‐23‐7.RN.
20. METHYLPREDNISOLONE OR 83‐43‐2.RN.
21. MOMETASONE OR 105102‐22‐5.RN.
22. PREDNISOLONE OR 50‐24‐8.RN.
23. PREDNISONE OR 53‐03‐2.RN.
24. TRIAMCINOLONE OR 124‐94‐7.RN.\
25. FLIXONASE OR FLIXOTIDE OR PLURAIR OR BUDECORT OR NASONEX OR CLENIL OR BECLOSOL OR NASACORT OR AIRCLIN
26. 8 OR 9 OR 10 OR 11 OR 12 OR 13 OR 14 OR 15 OR 16 OR 17 OR 18 OR 19 OR 20 OR 21 OR 22 OR 23 OR 24 OR 25
27. 7 AND 26

Strategies for all other databases will be modelled on the CENTRAL version.

References lists of the retrieved articles from electronic searches will be searched. Authors of published trials and other experts in the field will be contacted. Pharmaceutical companies/manufacturers will be contacted for information on unpublished trials. There will be no language, publication year, or publication status restrictions on searching. A search for existing meta‐analyses and non‐Cochrane systematic reviews will be performed and their reference lists scanned for additional trials.

Data collection and analysis

Study selection
Three authors will independently assess the titles and abstracts of all studies identified by the searches. Articles that do not meet the inclusion criteria will be excluded. The full articles will be obtained when they appear to meet the inclusion criteria or there are insufficient data in the title and abstract to make a clear decision. Details of the studies and the reasons for their exclusion will be noted. Any disagreement between the authors about study inclusion will be resolved by discussion.

Assessment of methodological quality
The methodological quality of all included trials will be assessed independently by two authors with a five‐point scoring instrument, proposed by Jadad (Jadad 1996). This instrument evaluates the reported quality of randomisation, blinding and description of withdrawals and drop‐outs. Inter‐rater agreement will be assessed using the kappa statistic, with any disagreement resolved by discussion.

Quality of allocation concealment will also be ranked independently by two reviewers using the Cochrane approach:

Grade A: adequate concealment
Grade B: uncertain
Grade C: clearly inadequate concealment

Data collection
Study details from the included randomised controlled trials will be extracted by two authors independently using a standardised data extraction form and checked by a third reviewer. Any disagreement will be resolved by discussion. Missing information will be sought from authors wherever possible. The extracted data will be entered into RevMan 4.2.8. The following data will be extracted:

  • Study characteristics: publication status, year, country of study and setting;

  • Methods: method of allocation, masking participants and assessment of outcome, exclusion of participants after randomisation, proportion of follow up losses and intention‐to‐treat analysis;

  • Participants: sample size, age, gender, inclusion and exclusion criteria;

  • Intervention: type of intranasal corticosteroids, dosage and treatment duration;

  • Control: placebo, nil, oral corticosteroids, or other treatment;

  • Outcomes: primary and secondary outcomes as described previously.

Data analysis
Data analysis will be on an intention‐to‐treat basis. The Cochrane Ear, Nose and Throat Disorders Group statistical guidelines and plan for assessment of heterogeneity will be followed. Pooling of data will be performed if the data extracted from the included trials are comparable and of sufficient quality. Relative risks (RRs) or odds ratios (ORs) and 95% confidence intervals (CI) will be calculated for all dichotomous data. The number needed to treat to benefit (NNTB) and the number needed to treat to harm (NNTH) will be calculated if possible from the pooled relative risk or odds ratio, applied to appropriate levels of baseline risk. For continuous data, the weighted mean differences (WMDs) or standard mean differences (SMDs) and 95% confidence intervals (CI) will be calculated. Fixed‐effect and random‐effects models will be used to combine the data as appropriate.

If there are sufficient included trials, we plan to conduct sensitivity analyses to assess the impact of potentially important factors on the overall outcomes:

a) Study quality;
b) Differences in the medications used in the intervention and comparison groups;
c) Forms of intranasal corticosteroids (spray and drops);
d) Analysis using random and fixed‐effect models;
e) Analysis by study design ‐ parallel and cross‐over studies.

We will use funnel plots to examine the potential publication bias.

Table 1. Search Strategies

MEDLINE

EMBASE

1. ADENOIDS.DE.
2. (ADENOID$2 OR ADENOTONSIL$3 OR ADENO ADJ TONSIL$3 OR PHARYN$4 NEAR TONSIL$3).TI,AB.
3. 1 OR 2
4. HYPERTROPHY.DE.
5. (HYPERTROPH$3 OR ENLARGE$4 OR SWOLLEN OR OVERGROW$3 OR OVER ADJ GROW$3).TI,AB.
6. 4 OR 5
7. 3 AND 6
8. STEROIDS#.W..DE.
9. ANTI‐INFLAMMATORY‐AGENTS#.W..DE.
10. ANTI‐INFLAMMATORY‐AGENTS‐NON‐STEROIDAL#.W..DE.
11. 10 NOT 11
12. GLUCOCORTICOIDS#.W..DE.
13. STEROID$2 OR CORTICOSTEROID$2
14. GLUCOCORTICOID$2
15. BECLOMETHASONE OR 4419‐39‐0.RN. OR BECLAMET OR BECLOCORT OR BECOLMETASONE OR BECOTIDE
16. BETAMETHASONE OR 378‐44‐9.RN.
17. BUDESONIDE OR 51333‐22‐3.RN. OR HORACORT OR PULMICORT OR RHINOCORT
18. CORTISONE OR 53‐06‐5.RN.
19. DEXAMETHASONE OR 50‐02‐2.RN. OR HEXADECADROL OR DECADRON OR DEXASONE
20. HEXADROL OR METHYLFLUORPREDNISOLONE OR MILLICORTEN OR ORADEXON
21. FLUNISOLIDE OR 3385‐03‐3.RN.
22. FLUTICASONE OR 90566‐53‐3.RN.
23. (FLUTICASONE ADJ PROPIONATE) OR 80474‐14‐2.RN.
24. HYDROCORTISONE OR CORTISOL OR 50‐23‐7.RN.
25. METHYLPREDNISOLONE OR 83‐43‐2.RN.
26. MOMETASONE OR 105102‐22‐5.RN.
27. PREDNISOLONE OR 50‐24‐8.RN.
28. PREDNISONE OR 53‐03‐2.RN.
29. TRIAMCINOLONE OR 124‐94‐7.RN.
30. FLIXONASE OR FLIXOTIDE OR PLURAIR OR BUDECORT OR NASONEX OR CLENIL OR BECLOSOL OR NASACORT OR AIRCLIN
31. 8 OR 11 OR 12 OR 13 OR 14 OR 15 OR 16 OR 17 OR 18 OR 19 OR 20 OR 21 OR 22 OR 23 OR 24 OR 25 OR 26 OR 27 OR 28 OR 29 OR 30
32. 7 AND 31

1. ADENOID.W..DE.
2. (ADENOID$2 OR ADENOTONSIL$3 OR ADENO ADJ TONSIL$3 OR PHARYN$4 NEAR TONSIL$3).TI,AB.
3. 1 OR 2
4. HYPERTROPHY.W..DE.
5. (HYPERTROPH$3 OR ENLARGE$4 OR SWOLLEN OR OVERGROW$3 OR OVER ADJ GROW$3).TI,AB.
6. 4 OR 5
7. 3 AND 6
8. CORTICOSTEROID#.DE.
9. STEROID$2 OR CORTICOSTEROID$2
10. GLUCOCORTICOID$2
11. BECLOMETHASONE OR 4419‐39‐0.RN.
12. BETAMETHASONE OR 378‐44‐9.RN.
13. BUDESONIDE OR 51333‐22‐3.RN.
14. CORTISONE OR 53‐06‐5.RN.
15. DEXAMETHASONE OR 50‐02‐2.RN.
16. FLUNISOLIDE OR 3385‐03‐3.RN.
17. FLUTICASONE OR 90566‐53‐3.RN.
18. (FLUTICASONE ADJ PROPIONATE) OR 80474‐14‐2.RN.
19. HYDROCORTISONE OR CORTISOL OR 50‐23‐7.RN.
20. METHYLPREDNISOLONE OR 83‐43‐2.RN.
21. MOMETASONE OR 105102‐22‐5.RN.
22. PREDNISOLONE OR 50‐24‐8.RN.
23. PREDNISONE OR 53‐03‐2.RN.
24. TRIAMCINOLONE OR 124‐94‐7.RN.\
25. FLIXONASE OR FLIXOTIDE OR PLURAIR OR BUDECORT OR NASONEX OR CLENIL OR BECLOSOL OR NASACORT OR AIRCLIN
26. 8 OR 9 OR 10 OR 11 OR 12 OR 13 OR 14 OR 15 OR 16 OR 17 OR 18 OR 19 OR 20 OR 21 OR 22 OR 23 OR 24 OR 25
27. 7 AND 26

Figures and Tables -
Table 1. Search Strategies