Добрый день, Игорь.
Эта методика не входит в рекомендации по лечению хронического полипозного риносинусита утвержденные минздравом Украины, институтом отоларингологии. Рекомендации европейских ринологов (EPOS) доступны в интернете
CONTENTS
1 Introduction 3
2 Definition of rhinosinusitis and nasal polyps 4
2-1 Introduction 4
2-2 Clinical definition 4
2-3 Definition for epidemiology/General Practice 5
2-4 Definition for research 5
3 Chronic rhinosinusitis and nasal polyps 6
3-1 Anatomy and (patho)physiology 6
3-2 Rhinosinusitis 6
3-3 Nasal polyps and chronic rhinosinusitis 6
4 Epidemiology and predisposing factors 8
4-1 Introduction 8
4-2 Acute bacterial rhinosinusitis 8
4-3 Factors associated with acute rhinosinusitis 9
4-4 Chronic rhinosinusitis (CRS) 9
4-5 Factors associated with chronic rhinosinusitis (CRS) 9
4-6 Nasal polyps 12
4-7 Factors associated with NP 13
4-8 Epidemiology and predisposing factors for
rhinosinusitis in children 14
4-9 Conclusion 15
5 Inflammatory mechanisms in acute and chronic
rhinosinusitis and nasal polyposis 16
5-1 Introduction 16
5-2 Acute rhinosinusitis 16
5-3 Chronic rhinosinusitis 16
5-4 Nasal polyps 17
5-5 Conclusion 19
6 Diagnosis 20
6-1 Assessment of rhinosinusitis symptoms 20
6-2 Examination 21
6-3 Quality of Life 24
7 Management 27
7-1 Treatment of rhinosinusitis with corticosteroids 27
7-2 Treatment of rhinosinusitis with antibiotics 32
7-3 Other medical management for rhinosinusitis 36
7-4 Evidence based surgery for rhinosinusitis 42
7-5 Surgical treatment vs. medical treatment
in CRS /NP 45
8 Complications of rhinosinusitis and nasal polyps 47
8-1 Introduction 47
8-2 Epidemiology of complications 47
8-3 Orbital complications 47
8-4 Endocranial complications 48
8-5 Cavernous sinus thrombosis 49
8-6 Osseous complications 49
8-7 Unusual complications of rhinosinusitis 50
8-8 Complications of surgical treatment 50
9 Special considerations: Rhinosinusitis in children 53
9-1 Introduction 53
9-2 Anatomy 53
9-3 Epidemiology and pathophysiology 53
9-4 Symptoms and signs 53
9-5 Examination 54
9-6 Systemic disease and chronic rhinosinusitis 54
9-7 Management 55
10 Socio-economic cost of chronic rhinosinusitis
and nasal polyps 58
10-1 Direct Costs 58
10-2 Indirect Costs 58
11 Outcomes measurements in research 60
12 Evidence based schemes for diagnostic
and treatment 61
12-1 Introduction 61
12-2 Level of evidence and grade of recommendation 61
12-3 Evidence based diagnosis and management
scheme for GP’s 63
12-4 Evidence based diagnosis and management
scheme for Non-ENT specialist for adults
with CRS/NP 64
12-5 Evidence based diagnosis and management
scheme for ENT specialists 65
12-6 Evidence based schemes for therapy in children 69
13 Research needs and priorities 70
14 References 70
15 Appendix 85
15-1 Survey of published olfactory tests 85
15-2 Source of some olfactory tests 87
European Position Paper on Rhinosinusitis and Nasal Polyps
Participants:
Wytske Fokkens, Chair
Valerie Lund, Co-Chair
Claus Bachert
Peter Clement
Peter Hellings
Mats Holmstrom
Nick Jones
Livije Kalogjera,
David Kennedy
Marek Kowalski
Henrik Malmberg
Joaquim Mullol
Desiderio Passali
Heinz Stammberger
Pontus Stierna
2 Supplement 18
European Position Paper on Rhinosinusitis and Nasal Polyps 3
Rhinosinusitis is a significant health problem which seems to
mirror the increasing frequency of allergic rhinitis and which
results in a large financial burden on society (1-3). The last
decade has seen the development of a number of guidelines,
consensus documents and position papers on the epidemiology,
diagnosis and treatment of rhinosinusitis and nasal polyposis
(4-6).
Data on (chronic) rhinosinusitis is limited and the disease entity
is badly defined. Therefore, the available data is difficult to
interpret and extrapolate. Although of considerable assistance,
the available consensus documents on chronic rhinosinusitis
and nasal polyps do not answer a number of relevant questions
that would unify the information and current concepts that
exist in epidemiology, diagnosis, treatment and research. To
add to this, none of these documents are evidence based.
There is considerable interest in guidelines as tools for implementing
health care based on proof of effectiveness.
Guidelines should be informative, simple and easy to use and
in a form that can be widely disseminated within the medical
community in order to improve patient care.
Evidence-based medicine is an important method of preparing
guidelines (7, 8). Moreover, the implementation of guidelines
is equally important.
The European Academy of Allergology and Clinical
Immunology (EAACI) has created a Taskforce to consider
what is known about rhinosinusitis and nasal polyps, to offer
evidence based recommendations on diagnosis and treatment,
and to consider how we can make progress with research in
this area. The EP3OS document is also approved by the
European Rhinologic Society (ERS).
The present document is intended to be state-of-the art for the
specialist as well as for the general practitioner:
• to update their knowledge of rhinosinusitis and nasal polyposis;
• to provide an evidence-based documented revision of the
diagnostic methods;
• to provide an evidence-based revision of the available treatments;
• to propose a stepwise approach to the management of the
disease;
• to propose guidance for definitions and outcome measurements
in research in different settings.
Table 1-1. Category of evidence (8).
Ia Evidence from meta-analysis of randomised controlled trials
Ib Evidence from at least one randomised controlled trial
IIa Evidence from at least one controlled study without
randomisation
IIb Evidence from at least one other type of quasi-experimental
study
III Evidence from non-experimental descriptive studies, such as
comparative studies, correlation studies, and case-control
studies
IV Evidence from expert committee reports or opinions or
clinical experience of respected authorities, or both
Table 1-2. Strength of recommendation.
A Directly based on category I evidence
B Directly based on category II evidence or extrapolated
recommendation from category I evidence
C Directly based on category III evidence or extrapolated
recommendation from category I or II evidence
D Directly based on category IV evidence or extrapolated
recommendation from category I, II or III evidence
1. Introduction
4 Supplement 18
2-1 Introduction
Rhinitis and sinusitis usually coexist and are concurrent in
most individuals; thus, the correct terminology is now rhinosinusitis.
The diagnosis of rhinosinusitis is made by a wide variety
of practitioners, including allergologists, otolaryngologists,
pulmonologists, primary care physicians and many others.
Therefore, an accurate, efficient, and accessible definition of
rhinosinusitis is required. A number of groups have published
reports on rhinosinusitis and its definition. In most of these
reports definitions are based on symptomatology and duration
of disease and one definition aims at all practitioners (4-6, 9).
In 2001 the WHO put together a working group on rhinitis and
its impact on asthma (ARIA)(10). In this group rhinitis was
classified according to duration and severity.
Table 2-1. Classification of allergic rhinitis (10).
1- “Intermittent” means that the symptoms are present:
• Less than 4 days a week,
• And for less than 4 weeks.
2- “Persistent” means that the symptoms are present:
• More than 4 days a week,
• Or for more than 4 weeks. (should it be “and”, not or?)
3- “Mild” means that there are none of the following items:
• No sleep disturbance,
• No impairment of daily activities, leisure and/or sport,
• No impairment of school or work,
• Symptoms are not troublesome.
4- “Moderate-severe” means that there are one or more of the
following items:
• Sleep disturbance,
• Impairment of daily activities, leisure and/or sport,
• Impairment of school or work,
• Troublesome are symptoms.
Until recently rhinosinusitis was usually classified based on the
duration into acute, subacute, chronic and acute on chronic
(see figure 1). Yet this division does not correlate with the classification
of rhinitis. Moreover it does not incorporate the
severity of the disease. Also due to the long timeline of 12
weeks in chronic rhinosinusitis it can be difficult to discriminate
between recurrent acute rhinosinusitis and chronic rhinosinusitis
with or without exacerbations.
Figure 2-1. Former classification of Rhinosinusitis (11).
Due to the large differences in technical possibilities to diagnose
and treat rhinosinusitis/nasal polyps by various professions,
the need to differentiate between subgroups varies. On
one hand the epidemiologist wants a workable definition that
does not impose too many restrictions to study larger populations.
On the other hand researchers in a clinical setting are in
need of a set of clearly defined items that describes their
patient population accurately and avoids the comparison of
‘apples and oranges’ in studies that relate to diagnosis and
treatment. The taskforce tried to accommodate these different
needs by giving definitions that can be applied in appropriate
studies. In this way the taskforce hopes to improve the comparability
of studies and thus enhance the evidence based diagnosis
and treatment of patients with rhinosinusitis and nasal
polyps.
2-2 Clinical definition
2-2-1 Clinical definition of rhinosinusitis/nasal polyps
Rhinosinusitis (including nasal polyps) is defined as:
• Inflammation of the nose and the paranasal sinuses characterised
by two or more symptoms:
- blockage/congestion;
- discharge: anterior/post nasal drip;
- facial pain/pressure,
- reduction or loss of smell;
and either
• Endoscopic signs:
- polyps;
- mucopurulent discharge from middle meatus;
- oedema/mucosal obstruction primarily in middle meatus,
and/or
• CT changes:
- mucosal changes within ostiomeatal complex and/or
sinuses.
2. Definition of rhinosinusitis and nasal polyps
European Position Paper on Rhinosinusitis and Nasal Polyps 5
2-2-2 Severity of the disease
The disease can be divided into MILD and MODERATE/
SEVERE based on total severity visual analogue scale (VAS)
score (010 cm):
MILD = AS 0-4
MODERATE/SEVERE = VAS 5-10
To evaluate the total severity the patient is asked to indicate
on a VAS the question:
How troublesome are your symptoms of rhinosinusitis?
2-2-3 Duration of the disease
Acute/Intermittent
< 12 weeks
Complete resolution of symptoms.
Chronic/Persistent
>12 weeks symptoms
No complete resolution of symptoms.
2-3 Definition for epidemiology/General Practice
For epidemiological studies the definition is based on symptomatology
without ENT examination or radiology.
Acute/Intermittent Rhinosinusitis is defined as
sudden onset of two or more of the symptoms:
blockage/congestion;
discharge anterior/post nasal drip;
facial pain/pressure;
reduction/loss of smell;
for 12 weeks,
with validation by telephone or interview.
Questions on allergic symptoms i.e. sneezing, watery rhino
rhea, nasal itching and itchy watery eyes should be included.
Also include questions on intermittent disease (see definition
above).
2-4 Definition for research
For research purposes Chronic Rhinosinusitis (CRS) is the
major finding and Nasal Polyposis (NP) is considered a subgroup
of this entity. For the purpose of a study, the differentiation
between CRS and NP must be based on out-patient
endoscopy.
The research definition is based on the presence of polyps and
prior surgery.
2-4-1 Definitions when no earlier sinus surgery has been performed
Polyposis: bilateral, endoscopically visualised in
middle meatus
Chronic rhinosinusitis: bilateral, no visible polyps in middle
meatus, if necessary following decongestant
This definition accepts that there is a spectrum of disease in
CRS which includes polypoid change in the sinuses and/or
middle meatus but excludes those with polypoid disease presenting
in the nasal cavity to avoid overlap.
2-4-2 Definitions when sinus surgery has been performed
Once surgery has altered the anatomy of the lateral wall, the
presence of polyps is defined as pedunculated lesions as
opposed to cobblestoned mucosa > 6 months after surgery on
endoscopic examination. Any mucosal disease without overt
polyps should be regarded as CRS .
2-4-3 Conditions for sub-analysis
The following conditions should be considered for sub-analysis:
• aspirin sensitivity based on positive oral, bronchial or nasal
provocation or an obvious history;
• asthma/bronchial hyper-reactivity /COPD based on symptoms,
respiratory function tests;
• allergy based on specific serum IgE or SPTs;
• finding of purulent discharge/pus.
2-4-4 Exclusion from general studies
Patients with the following diseases should be excluded from
general studies on chronic rhinosinusitis and/or nasal polyposis:
• cystic fibrosis based on positive sweat test or DNA alleles;
• gross immunodeficiency (congenital or acquired);
• congenital mucociliary problems e.g. primary ciliary dyskinesia
(PCD);
• non-invasive fungal balls and invasive fungal disease;
• systemic vasculitic and granulomatous diseases.
Not troublesome Most troublesome imaginable
10 cm
6 Supplement 18
3-1 Anatomy and (patho)physiology
The nose and paranasal sinuses constitute a collection of airfilled
spaces within the anterior skull. The paranasal sinuses
communicate with the nasal cavity through small apertures.
The nasal cavity and its adjacent paranasal sinuses are lined by
pseudostratified columnar ciliated epithelium. This contains
goblet cells and nasal glands, producers of nasal secretions that
keep the nose moist and form a “tapis roulant” of mucus.
Particles and bacteria can be caught in this mucus, rendered
harmless by enzymes like lysozyme and lactoferrin, and be
transported down towards the oesophagus. Cilia play an
important role in mucus transport. All paranasal sinuses are
normally cleared by this mucociliary transport, even though
transport from large areas of sinuses passes through small
openings towards the nasal cavity.
A fundamental role in the pathogenesis of rhinosinusitis is
played by the ostiomeatal complex, a functional unit that comprises
maxillary sinus ostia, anterior ethmoid cells and their
ostia, ethmoid infundibulum, hiatus semilunaris and middle
meatus. The key element is the maintenance of optimal sinus
ventilation and clearance. Specifically, ostial patency significantly
affects mucus composition and secretion; moreover, an
open ostium allows mucociliary clearance to easily remove particulate
matters and bacteria eventually come in contact with
the sinusal mucosa.
Problems occur if the orifice is too small for the amount of
mucus, if mucus production is increased, for instance during
an upper respiratory tract infection (URI), or if ciliary function
is impaired. Stasis of secretions follows and bacterial export
ceases, causing or exacerbating inflammation of the mucosa
whilst aeration of the mucosa is decreased, causing even more
ciliary dysfunction. This vicious cycle can be difficult to break,
and if the condition persists, it can result as chronic rhinosinusitis.
In chronic rhinosinusitis the role of ostium occlusion
seems to be less pronounced than in acute rhinosinusitis.
3-2 Rhinosinusitis
Rhinosinusitis is an inflammatory process involving the
mucosa of the nose and one or more sinuses. The mucosa of
the nose and sinuses form a continuum and thus more often
than not the mucous membranes of the sinus are involved in
diseases which are primarily caused by an inflammation of the
nasal mucosa. Chronic rhinosinusitis is a multifactorial disease
(12). Factors contributing can be mucociliary impairment (13,
14), (bacterial) infection (15), allergy (16), swelling of the
mucosa for another reason, but only rarely physical obstructions
caused by morphological/anatomical variations in the
nasal cavity or paranasal sinuses (17, 18). A role in the pathogenesis
of rhinosinusitis is certainly played by the ostiomeatal
complex, a functional unit that comprises maxillary sinus ostia,
anterior ethmoid cells and their ostia, ethmoid infundibulum,
hiatus semilunaris and middle meatus. The key element is the
maintenance of the ostial patency. An in depth discussion on
factors contributing to chronic rhinosinusitis and nasal polyps
can be found in chapter 4-4 and 4-6.
3-3 Nasal polyps and chronic rhinosinusitis
Nasal polyps and chronic rhinosinusitis are often taken together
as one disease entity, because it seems impossible to clearly
differentiate between them (19-21). Nasal Polyposis is therefore
considered a subgroup of Chronic Rhinosinusitis (fig. 1).
The question remains as to why “ballooning” of mucosa develops
in polyposis patients and not in all rhinosinusitis patients.
Nasal polyps have a strong tendency to recur after surgery
even when aeration is improved (22). This may reflect a distinct
property of the mucosa of polyp patients which has yet to
be identified. Some studies have tried to divide chronic rhinosinusitis
and nasal polyps based on inflammatory markers (23-
27). Although these studies point to a more pronounced
eosinophilia and IL-5 expression in nasal polyps than that
found in patients with chronic rhinosinusitis, these studies also
point to a continuum in which differences might be found at
the ends of the spectrum but at the moment no clear cut division
can be made.
Figure 3-1. The spectrum of chronic rhinosinusitis and nasal polyps.
3. Chronic rhinosinusitis and nasal polyps
European Position Paper on Rhinosinusitis and Nasal Polyps 7
Nasal polyps appear as grape-like structures in the upper nasal
cavity, originating from within the ostiomeatal complex. They
consist of loose connective tissue, oedema, inflammatory cells
and some glands and capillaries, and are covered with varying
types of epithelium, mostly respiratory pseudostratified epithelium
with ciliated cells and goblet cells. Eosinophils are the
most common inflammatory cells in nasal polyps, but neutrophils,
mast cells, plasma cells, lymphocytes and monocytes
are also present, as well as fibroblasts. IL-5 is the predominant
cytokine in nasal polyposis, reflecting activation and prolonged
survival of eosinophils (28).
The reason why polyps develop in some patients and not in
others remains unknown. There is a definite relationship in
patients with ‘Samter triad’: asthma, NSAID sensitivity and
nasal polyps. However, not all patients with NSAID sensitivity
have nasal polyps, and vice-versa. In the general population,
the prevalence of nasal polyps is 4% (29). In patients with asthma,
a prevalence of 7 to 15% has been noted whereas, in
NSAID sensitivity, nasal polyps are found in 36 to 60% of
patients (30, 31). It had long been assumed that allergy predisposed
to nasal polyps because the symptoms of watery rhinorrhoea
and mucosal swelling are present in both diseases, and
eosinophils are abundant. However, epidemiological data provide
no evidence for this relationship: polyps are found in 0.5
to 1.5% of patients with positive skin prick tests for common
allergens (31, 32).
8 Supplement 18
4-1 Introduction
The incidence of acute viral rhinosinusitis (common cold) is
very high. It has been estimated that adults suffer 2 to 5 colds
per year, and school children may suffer 7 to 10 colds per year.
The exact incidence is difficult to measure because most
patients with common cold do not consult a doctor. More reliable
data are available on acute rhinosinusitis. As mentioned
earlier acute non-viral rhinosinusitis is defined as an increase of
symptoms after 5 days or persistent symptoms after 10 days
after a sudden onset of two or more of the symptoms: blockage/
congestion, discharge, anterior/post nasal drip, facial
pain/pressure and/or reduction/loss of smell. It is estimated
that only 0.5% to 2% of viral URTIs are complicated by bacterial
infection; however, the exact incidence is unknown given
the difficulty distinguishing viral from bacterial infection without
invasive sinus-puncture studies. Bacterial culture results in
suspected cases of acute community-acquired sinusitis are positive
in only 60% of cases (33). Signs and symptoms of bacterial
infection may be mild and often resolve spontaneously (34, 35).
In spite of the high prevalence and significant morbidity of
chronic rhinosinusitis and nasal polyps, there is only limited
accurate data on the epidemiology of these conditions. This
observation mainly relates to the lack of a uniformly accepted
definition for CRS. In addition, patient selection criteria greatly
differ between epidemiologic studies complicating comparison
of studies.
When interpreting epidemiologic data, one should be aware of
a significant selection bias of the different studies presented
below. The purpose of this section of the EPOS document is
to give an overview of the currently available epidemiologic
data on rhinosinusitis and nasal polyps, and illustrate the factors
which are believed to predispose to the development.
4-2 Acute bacterial rhinosinusitis
When describing the incidence of acute bacterial rhinosinusitis
there has been a lot of debate about the definition of acute
bacterial rhinosinusitis. For example in the Cochrane Review
on antibiotics for acute sinusitis, studies were included if
sinusitis was proven by a consistent clinical history, and radiographic
or aspiration evidence of acute sinusitis (36).
However, most guidelines on the diagnosis of acute bacterial
rhinosinusitis base the diagnosis on symptoms and clinical
examination. However, if the diagnosis is based on clinical
examination alone, the rate of false positive results is high. In
patients with clinical diagnosis of acute rhinosinusitis less than
half have significant abnormalities at X-ray examination (37).
Based on sinus puncture/aspiration (considered diagnostically
the most accurate), 49-83% of symptomatic patients had acute
sinusitis (38). Compared with puncture/aspiration, radiography
offered moderate ability to diagnose sinusitis Using sinus opacity
or fluid as the criterion for sinusitis, radiography had sensitivity
of 0.73 and specificity of 0.80 (38).
An average of 8.4% of the Dutch population reported at least
one episode of acute rhinosinusitis per year in 1999 (39). The
incidence of visits to the general practioner for of acute sinusitis
in the Netherlands in 2000 was 20.0 per 1,000 men and 33.8
per 1,000 women (40). According to National Ambulatory
Medical Care Survey (NAMCS) data in the USA rhinosinusitis
is the fifth most common diagnosis for which an antibiotic is
prescribed. Rhinosinusitis accounted for 9% and 21% of all
paediatric and adult antibiotic prescriptions, respectively, written
in 2002 (5).
4-3 Factors associated with acute rhinosinusitis
4-3-1 Pathogens
Superinfection of bacteria on mucosa damaged by viral infection
(common cold) is the most important cause of acute rhinosinusitis.
The most common bacterial species isolated from
the maxillary sinuses of patients with acute rhinosinusitis are
Streptococcus pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis, the latter being more common in children
(41, 42). Other streptococcal species, anaerobic bacteria
and Staphylococcus aureus cause a small percentage of cases.
Resistance patterns of the predominant pathogens vary considerably
(43, 44). The prevalence and degree of antibacterial
resistance in common respiratory pathogens are increasing
worldwide. The association between antibiotic consumption
and the prevalence of resistance is widely assumed (45).
4-3-2 Ciliary impairment
Normal mucociliary flow is a significant defence mechanism in
the prevention of acute rhinosinusitis. Viral rhinosinusitis
results in the loss of cilia and ciliated cells, with a maximum
around one week after the infection. Three weeks after the
beginning of the infection the number of cilia and ciliated cells
increases to nearly normal. However, as a sign of regeneration,
immature short cilia (0.7 to 2.5 microns in length) were often
seen (46). The impaired mucociliary function during viral rhinosinusitis
results in an increased sensitivity to bacterial infection.
Also in animal experimental work it was shown that early after
exposure to pathogenic bacteria, like Streptococcus pneumoniae,
Hemophilus influenzae, Pseudomonas aeruginosa, a significant
loss of ciliated cells from sinus mucosa and a corresponding
disruption of normal mucociliary flow was found (47).
4. Epidemiology and predisposing factors
European Position Paper on Rhinosinusitis and Nasal Polyps 9
4-3-3 Allergy
Review articles on sinusitis have suggested that atopy predisposes
to rhinosinusitis (48). This theory is attractive given the
popularity of the concept that disease in the ostiomeatal area
contributes to sinus disease in that the mucosa in an individual
with allergic rhinitis might be expected to be swollen and more
liable to obstruct sinus ostia, reduce ventilation, lead to mucus
retention that might be more prone to become infected.
Furthermore there has been an increase in the body of opinion
that regard the mucosa of the nasal airway as being in a continuum
with the paranasal sinuses and hence the term rhinosinusitis
(49). The number of studies determining the occurrence
of acute rhinosinusitis in patients with and without allergy
is very limited.
Savolainen studied the occurrence of allergy in 224 patients
with verified acute rhinosinusitis by means of an allergy questionnaire,
skin testing, and nasal smears. Allergy was found in
25% of the patients and considered probable in another 6.5%.
The corresponding percentages in the control group were 16.5
and 3, respectively. There were no differences between allergic
and non-allergic patients in the number of prior acute sinusitis
episodes or of previously performed sinus irrigations.
Bacteriological and radiological findings did not differ significantly
between the groups (50). Alho showed that subjects
with allergic IgE-mediated rhinitis had more severe paranasal
sinus changes in CT scans than nonallergic subjects during
viral colds. These changes indicate impaired sinus functioning
and may increase the risk of bacterial sinusitis (51).
In conclusions: although an attractive hypothesis we can repeat
the statement made a decade ago, there remain no published
prospective reports on the incidence of infective rhinosinusitis
in populations with and without clearly defined allergic rhinosinusitis
(52).
4-4 Chronic rhinosinusitis (CRS)
CRS is one of the most common health care problems, with
significant direct medical costs and severe impact on lower airway
disease and general health outcomes (53, 54). The paucity
of accurate epidemiologic data on CRS and nasal polyps contrasts
with the more abundant information on microbiology,
diagnosis and treatment options for these conditions. When
reviewing the current literature on CRS, it becomes clear that
giving an accurate estimate of the prevalence of CRS remains
speculative, because of the heterogeneity of the disorder and
the diagnostic imprecision often used in publications. In a survey
on the prevalence of chronic conditions, it was estimated
that CRS, defined as having ‘sinus trouble’ for more than 3
months in the year before the interview, affects 15.5% of the
total population in the United States (55), ranking this condition
second in prevalence among all chronic conditions. Later,
the high prevalence of CRS was confirmed by another survey
suggesting that 16% of the adult US population has CRS (56).
However the prevalence of doctor diagnosed CRS is much
lower; a prevalence of 2% was found using ICD-9 codes as an
identifier(57).
Of note, the prevalence rate of CRS was substantially higher in
females with a female/male ratio of 6/4 (55). In Canada, prevalence
of CRS, defined as an affirmative answer to the question
‘Has the patient had sinusitis diagnosed by a health professional
lasting for more than 6 months?’ ranged from 3.4% in male
to 5.7% in female subjects (58). The prevalence increased with
age, with a mean of 2.7% and 6.6% in the age groups of 20-29
and 50-59 years respectively. After the age of 60 years, prevalence
levels of CRS levelled off to 4.7% (58). In a nationwide
survey in Korea, the overall prevalence of chronic sinusitis,
defined as the presence of at least 3 nasal symptoms lasting
more than 3 months along with the endoscopic finding of a
nasal polyp and/or mucopurulent discharge within the middle
meatus, was 1.01% (59), without differences neither in age
groups nor in sexes. By screening a non-ENT population,
which may be considered representative of the general population
in Belgium, Gordts et al. (60) reported that 6% of subjects
suffered from chronic nasal discharge and 40% had signs of
mucosal swelling of more than 3 mm on MRI .
Notwithstanding the shortcomings of epidemiologic studies on
CRS, it represents a common disorder of multifactorial origin.
A list of factors will be discussed in the following chapter
which are believed to be etiologically linked to CRS.
4-5 Factors associated with chronic rhinosinusitis (CRS)
4-5-1 Ciliary impairment
As may be concluded from the section on anatomy and pathophysiology,
ciliary function plays an important role in the
clearance of the sinuses and the prevention of chronic inflammation.
Secondary ciliary dyskinesia is found in patients with
chronic rhinosinusitis, and is probably reversible, although
restoration takes some time (61) It will be clear that in patients
with Kartagener’s syndrome and primary ciliary dyskinesia,
chronic rhinosinusitis is a common problem. These patients
usually have a long history of respiratory infections. In patients
with cystic fibrosis (CF), the inability of the cilia to transport
the viscous mucus causes ciliary malfunction and consequently
chronic rhinosinusitis. Nasal polyps are present in about 40%
of patients with CF (62). These polyps are generally more neutrophilic
than eosinophilic in nature but may respond to
steroids as well, as inhaled steroids in patients with CF reduce
neutrophilic inflammation (63-65).
4-5-2 Allergy
Review articles on rhinosinusitis have suggested that atopy
predisposes to its development (48, 66). It is tempting to speculate
that allergic inflammation in the nose predisposes the
atopic individual to the development of CRS. Both conditions
share the same trend of increasing prevalence (67, 68) and are
frequently associated.
10 Supplement 18
It has been postulated (69) that swelling of the nasal mucosa in
allergic rhinitis at the site of the sinus ostia may compromise
ventilation and even obstruct sinus ostia, leading to mucus
retention and infection. Furthermore, there has been an
increase in the body of opinion that regard the mucosa of the
nasal airway as being in a continuum with the paranasal sinuses
and hence the term ‘rhinosinusitis’ was introduced (49).
However, critical analysis of the papers linking atopy as a risk
factor to infective rhinosinusitis (chronic or acute) reveal that
whilst many of the studies suggest a higher prevalence of allergy
in patients presenting with symptoms consistent with
sinusitis than would be expected in the general population,
there may well have been a significant selection process,
because the doctors involved often had an interest in allergy
(27, 70-74). A number of studies report that markers of atopy
are more prevalent in populations with chronic rhinosinusitis.
Benninger reported that 54% of outpatients with chronic rhinosinusitis
had positive skin prick tests (75). Among CRS
patients undergoing sinus surgery, the prevalence of positive
skin prick tests ranges from 50 to 84% (50, 76, 77), of which the
majority (60%) have multiple sensitivities (77). As far back as
1975, Friedman reported an incidence of atopy in 94% of
patients undergoing sphenoethmoidectomies (78).
However, the role of allergy in CRS is questioned by other epidemiologic
studies showing no increase in the incidence of
infectious rhinosinusitis during the pollen season in pollensensitized
patients (52). In a small prospective study, no difference
in prevalence of purulent rhinosinusitis was found
between patients with and without allergic rhinitis (79).
Furthermore, allergy was found in 31.5% of patients with verified
acute maxillary sinusitis and there were no differences
between allergic and non-allergic patients in the number of
prior acute sinusitis episodes (50). Newman et al. reported that
whilst 39% of patients with CRS had asthma, raised specific
IgE or an eosinophilia, only 25% had true markers to show
they were atopic (80). Finally, Emanuel et al. (77)found relatively
lower percentages of allergic patients in the group of
patients with the most severe sinus disease on CT scan and
Iwens et al. (81) reported that the prevalence and extent of
sinus mucosa involvement on CT was not determined by the
atopic state.
Taken together, epidemiologic data show an increased prevalence
of allergic rhinitis in patients with CRS, but the role of
allergy in CRS remains unclear.
Radiological studies are unhelpful in unravelling the correlation
between allergy and rhinosinusitis. High percentages of
sinus mucosa abnormalities are found on radiological images
of allergic patients, e.g. 60% incidence of abnormalities on CT
scans among subjects with ragweed allergy during the season
(82). However, one should interpret this data with caution in
view of the fact that high percentages of incidental findings are
found on radiological images of the sinus mucosa in individuals
without nasal complaints, ranging from 24.7% to 49.2% (83-
86), that the normal nasal cycle induces cyclical changes in the
nasal mucosa volume (87), and that radiological abnormalities
contribute minimally to the patient’s symptoms (82).
Notwithstanding the lack of hard epidemiologic evidence for a
clear causal relationship between allergy and CRS, it is clear
that failure to address allergy as a contributing factor to CRS
diminishes the probability of success of a surgical intervention
(88). Among allergy patients undergoing immunotherapy,
those who felt most helped by immunotherapy were the subjects
with a history of recurrent rhinosinusitis, and about half
of the patients, who had had sinus surgery before, believed
that the surgery alone was not sufficient to completely resolve
the recurrent episodes of infection (88).
4-5-3 Lower airway involvement
Recent evidence suggests that allergic inflammation in the
upper and lower airways coexist and should be seen as a continuum
of inflammation, with inflammation in one part of the
airway influencing its counterpart at a distance. The arguments
and consequences of this statement are summarized in the
ARIA document (10). Rhinosinusitis and lower airway involvement
are also frequently associated in the same patients, but
their interrelationship is poorly understood. The evidence that
treatment of rhinosinusitis improves asthma symptoms and
hence reduces the need for medication to control asthma
mainly results from research in children and will be discussed
below (Chapter 7-6). In short, improvements in both asthma
symptoms and medication have been obtained after surgery
for rhinosinusitis in children with both conditions (89-91).
Studies on radiographic abnormalities of the sinuses in asthmatic
patients have shown high prevalences of abnormal sinus
mucosa (92, 93). All patients with steroid dependant asthma
had abnormal mucosal changes on CT compared to 88% with
mild to moderate asthma (94). Again caution should be exercised
in the interpretation of these studies. Radiographically
detected sinus abnormalities in sensitized patients may reflect
inflammation related to the allergic state rather than to sinus
infection.
4-5-4 Immunocompromised state
Among conditions associated with dysfunction of the immune
system, congenital immunodeficiencies manifest themselves
with symptoms early in life and will be dealt with in the paediatric
CRS section (see Chapter 7-6). However, dysfunction of
the immune system may occur later in life and present with
CRS. In a retrospective review of refractory sinusitis patients,
Chee et al. found an unexpectedly high incidence of immune
dysfunction (95). Of the 60 patients with in vitro T-lymphocyte
function testing, 55% showed abnormal proliferation in
response to recall antigens. Low immunoglobulin G, A and M
European Position Paper on Rhinosinusitis and Nasal Polyps 11
titres were found in respectively 18, 17 and 5% of patients with
refractory sinusitis. Common variable immunodeficiency was
diagnosed in 10% and selective IgA deficiency in 6% of
patients. Therefore, immunological testing should be an integral
part of the diagnostic pathway of patients with CRS not
responding to conservative treatment. In a cross-sectional
study to assess the overall prevalence of otolaryngologic diseases
in patients with HIV-infection, Porter et al. (96) reported
that sinusitis was present in more than half of the HIV-positive
population, ranking this condition one of the most prevalent
diseases in HIV-positive persons. However, the relevance of
these data is questioned as there was no difference in sinonasal
symptom severity between HIV-positive and AIDS patients
nor was there a correlation between CD4+ cell counts and
symptom severity. In a more detailed study, Garcia-Rodrigues
et al. (97) reported a lower incidences of rhinosinusitis (34%),
but with a good correlation between low CD4+ cell count and
the probability of rhinosinusitis. It should also be mentioned
here that atypical organisms like Aspergillus spp,
Pseudomonas aeruginosa and microsporidia are often isolated
from affected sinuses and that neoplasms such as non-
Hodgkin lymphoma and Kaposi’s sarcoma, may account for
sinonasal problems in patients with AIDS (98).
4-5-5 Genetic factors
Although chronic sinus disease has been observed in family
members, no genetic abnormality has been identified linked to
CRS. However, the role of genetic factors in CRS has been
implicated in patients with cystic fibrosis (CF) and primary ciliary
dyskinesia (Kartagener’s syndrome). CF is one of the most
frequent autosomal recessive disorders of the Caucasian population,
caused by mutations of the CFTR gene on chromosome
7 (99). The most common mutation, DF508, is found in
70 to 80% of all CFTR genes in Northern Europe (100, 101).
Upper airway manifestations of CF patients include chronic
rhinosinusitis and nasal polyps, which are found in 25 to 40%
of CF patients above the age of 5 (102-105). Interestingly,
Jorissen et al. (106) reported that DF508 homozygosity represents
a risk factor for paranasal sinus disease in CF.
4-5-6 Pregnancy and endocrine state
During pregnancy, nasal congestion occurs in approximately
one-fifth of women (107). The pathogenesis of this disorder
remains unexplained, but there have been a number of proposed
theories. Besides direct hormonal effects of oestrogen,
progesterone and placental growth hormone on the nasal
mucosa, indirect hormonal effects like vascular changes may
be involved. Whether pregnancy rhinitis predisposes to the
development of sinusitis, is not clear. In a small prospective
study, Sobol et al. (108) report that 61% of pregnant women
had nasal congestion during the first trimester, whereas only
3% had sinusitis. In this study, a similar percentage of nonpregnant
women in the control group developed sinusitis during
the period of the study. Also in an earlier report, the incidence
of sinusitis in pregnancy was shown to be quite low, i.e.
1.5% (109).
In addition, thyroid dysfunction has been implicated in CRS,
but there is only limited data on the prevalence of CRS in
patients with hypothyroidism.
4-5-7 Local host factors
Certain anatomic variations such as concha bullosa, nasal septal
deviation and a displaced uncinate process, have been suggested
as potential risk factors for developing CRS (110).
However, Bolger et al. (111) found no correlation between
CRS and bony anatomic variations in the nose. Also in the
survey by Min et al. (112), no correlation was found between
septal deviation and the prevalence of CRS. However, one
should mention here that no study has so far investigated
whether a particular anatomic variation can impair drainage of
the ostiomeatal complex per se. Whilst some authors have
postulated that anatomical variations of the paranasal sinuses
can contribute to ostial obstruction (113) there are several
studies that show the prevalence of anatomical variations is no
more common in patients with rhinosinusitis or polyposis than
in a control population (17, 18, 114, 115). One area where conjecture
remains is the effect of a deviated septum. Whilst there
is no recognised method of objectively defining the extent of a
deviated septum, some studies have found a deviation of more
than 3mm from the midline to be more prevalent in rhinosinusitis
(116, 117)whilst others have not (18, 118). Taken
together, there is no evidence for a causal correlation between
nasal anatomic variations in general and the incidence of CRS.
In spite of the observation that sinonasal complaints often
resolve after surgery, this does not necessarily imply that
anatomic variation is etiologically involved.
CRS of dental origin should not be overlooked when considering
the aetiology of CRS. Obtaining accurate epidemiologic
data on the incidence of CRS of dental origin is not possible as
the literature is limited to anecdotal reports.
4-5-8 Micro-organisms
4-5-8-1 Bacteria
Although it is often hypothesized that CRS evolves from acute
rhinosinusitis, the role of bacteria in CRS is far from clear. A
number of authors have described the microbiology of the
middle meatus and sinuses. However if and which of these
pathogen are contributory to the disease remains a matter of
debate.
Arouja isolated aerobes from 86% of the middle meatus samples
CRS patients, anaerobes were isolated in 8%. The most
frequent microorganisms were Staphylococcus aureus (36%),
coagulase-negative Staphylococcus (20%), and Streptococcus
pneumoniae (17%). Middle meatus and maxillary sinus cultures
presented the same pathogens in 80% of cases. In healthy
12 Supplement 18
individuals, coagulase-negative Staphylococcus (56%), S.
aureus (39%), and S. pneumoniae (9%) were the most frequent
isolates. (119).
Some authors suggest that as chronicity develops, the aerobic
and facultative species are gradually replaced by anaerobes
(120, 121). This change may result from the selective pressure
of antimicrobial agents that enable resistant organisms to survive
and from the development of conditions appropriate for
anaerobic growth, which include the reduction in oxygen tension
and an increase in acidity within the sinus. Often polymicrobial
colonisation is found; the contribution to the disease of
the different pathogens remains unclear.
4-5-8-2 Fungi
Fungi have been cultured from human sinuses with many different
ramifications (122). Their presence may be relatively
benign, colonizing normal sinuses or forming saprophytic
crusts. They also may cause a range of pathology, ranging from
non-invasive fungus balls to invasive, debilitating disease (123).
There is an increasing interest in the concept that the most
common form of sinus disease induced by fungus may be
caused by the inflammation stimulated by airborne fungal antigens.
In 1999 it was proposed that most patients with CRS
exhibit eosinophilic infiltration and the presence of fungi by
histology or culture (124). This assertion was based on finding
positive fungal culture by using a new culture technique in 202
of 210 (96%) patients with CRS who prospectively were evaluated
in a cohort study. No increase in type I sensitivity was
found in patients as compared with controls. The term
‘‘eosinophilic chronic rhinosinusitis’’ was proposed to replace
previously used nomenclature. Using this new culture technique,
the same percentage of positive fungi cultures was also
found in normal controls (125).
A broad array of fungi has been identified in the sinus cavities
of patients with sinusitis through varied staining and culture
techniques (124, 125).
As with the isolation of bacteria in sinus cavities in these
patients, the presence of fungi does not prove that these
pathogens directly create or perpetuate disease.
4-5-9 “Osteitis”—the role of bone
Areas of increased bone density and irregular bony thickening
are frequently seen on CT in areas of chronic inflammation
and may be a marker of the chronic inflammatory process.
However, the effect during the initial phases of a severe chronic
rhinosinusitis frequently appears as rarefaction of the bony
ethmoid partitions. Although to date bacterial organisms have
not been identified in the bone in either humans or animal
models of chronic rhinosinusitis, it has been suggested that
that this irregular bony thickening is sign of inflammation of
the bone. This inflamed bone might maintain mucosal inflammation
(126).
In rabbit studies it was demonstrated that not only the bone
adjacent to the involved maxillary sinus become involved, but
that the inflammation typically spreads through the Haversian
canals and may result in bone changes consistent with some
degree of chronic osteomyelitis at a distance from the primary
infection (127, 128). It is certainly possible that these changes,
if further confirmed in patients, may at least in part, explain
why chronic rhinosinusitis is relatively resistant to therapy.
4-5-10 Environmental factors
Cigarette smoking was associated with a higher prevalence of
rhinosinusitis in Canada (58), whereas this observation was not
confirmed in a nationwide survey in Korea (59). Other
lifestyle-related factors are undoubtedly involved in the chronic
inflammatory processes of rhinosinusitis. For instance, low
income was associated with higher prevalence of CRS (58). In
spite of in vitro data on the toxicity of pollutants on respiratory
epithelium, there exists no convincing evidence for the etiologic
role of pollutants and toxins such as ozone in CRS.
4-5-11 Iatrogenic factors
Among risk factors of CRS, iatrogenic factors should not be
forgotten as they may be responsible for the failure of sinus
surgery. The increasing number of sinus mucocoeles seems to
correlate with the expansion of endoscopic sinus surgery procedures.
Among a group of 42 patients with mucocoeles, 11
had prior surgery within 2 years before presentation (129).
Another reason for failure after surgery can be the recirculation
of nasal mucus out of the natural maxillary ostium and
back through a separate surgically created antrostomy resulting
in an increased risk of persistent sinus infection (130).
4-6 Nasal polyps
In the light of epidemiologic research, a distinction needs to be
made between clinically silent NP, or preclinical cases, and
symptomatic NP. Asymptomatic polyps may transiently be
present or persist, and hence remain undiagnosed until they
are discovered by routine examination. On the other hand,
polyps that become symptomatic may remain undiagnosed,
either because the patient is not investigated properly or
because they are missed on anterior rhinoscopy. Endoscopy of
the nasal cavity makes it possible to visualize NP and to give a
reliable estimate of the prevalence of NP.
In a population-based study in Skövde, Sweden, Johansson et
al. (131) reported a prevalence of nasal polyps of 2.7% of the
total population. In this study, NP were diagnosed by nasal
endoscopy and were more frequent in men (2.2 to 1), the
elderly (5% at 60 years of age and older) and asthmatics. In a
nationwide survey in Korea, the overall prevalence of polyps
diagnosed by nasal endoscopy was 0.5% of the total population
(112). Based on a postal questionnaire survey in Finland,
Hedman et al. (29) found that 4.3% of the adult population
European Position Paper on Rhinosinusitis and Nasal Polyps 13
answered positively to the question as to whether polyps had
been found in their nose. However, nasal endoscopy appears
to be a prerequisite for an accurate estimate of the prevalence
of NP, as 1.4% of the sample population studied by Johansson
et al. (131) said to have NP, did not actually have any polyps
on nasal endoscopy. From autopsy studies, a prevalence of 2%
has been found using anterior rhinoscopy (132). After removing
whole naso-ethmoidal blocks, nasal polyps were found in 5
of 19 cadavers (133), and in 42% of 31 autopsy samples combining
endoscopy with endoscopic sinus surgery (134). The
median age of the cases in the 3 autopsy studies by Larsen and
Tos ranged from 70 to 79 years. From these cadaver studies,
one may conclude that a significant number of patients with
NP do not feel the need to seek medical attention or that the
diagnosis of NP is often missed by doctors.
It has been stated that between 0.2 and 1% of people develop
nasal polyps at some stage (135). In a prospective study on the
incidence of symptomatic NP, Larsen and Tos (136) found an
estimated incidence of 0.86 and 0.39 patients per thousand per
year for males and females respectively. The incidence
increased with age, reaching peaks of 1.68 and 0.82 patients
per thousand per year for males and females respectively in the
age group of 50-59 years. When reviewing data from patient
records of nearly 5000 patients from hospitals and allergy clinics
in the US in 1977, the prevalence of NP was found to be
4.2% (137), with a higher prevalence (6.7%) in the asthmatic
patients.
In general, NP occur in all races (138-141) and becomes more
common with age. The average age of onset is approximately
42 years, which is 7 years older than the average age of the
onset of asthma (142-144). NP are uncommon under the age of
20 (145) and are more frequently found in men than in women
(29, 136, 146), except in the population studied by Settipane
(137).
4-7 Factors associated with NP
4-7-1 Allergy
0.5-4.5% of subjects with allergic rhinitis have NP (31, 32, 147),
which compares with the normal population (135). In children
the prevalence of NP has been reported to be 0.1% (31) and
Kern found NP in 25.6% of patients with allergy compared to
3.9% in a control population (148). On the other hand, the
prevalence of allergy in patients with nasal polyps has been
reported as varying from 10% (149), to 54% (150) and 64%
(151). Contrary to reports that have implicated atopy as being
more prevalent in patients with NP, others have failed to show
this (31, 147, 152-154). Recently, Bachert at al. (155) found an
association between levels of both total and specific IgE and
eosinophilic infiltration in nasal polyps. These findings were
unrelated to skin prick test results. Positive intradermal tests to
food allergies have been reported in 81% of polyp patients
compared to 11% of controls (156). Food and drug sensitivities
have been reported in 31% of patients with nasal polyposis and
this was more common in men (43% vs. 24%) (140).
4-7-2 Asthma
In patients with asthma 7% have nasal polyps (31) with a prevalence
of 13% in non-atopic asthma (skin prick test and total
and specific IgE negative) and 5% in atopic asthma (145). Late
onset asthma is associated with the development of nasal
polyps in 10-15% (31). Asthma develops first in approximately
69% of patients with both asthma and NP and NP take
between 9 and 13 years to develop. Ten percent develop both
polyps and asthma simultaneously and the remainder develop
polyps first and asthma later that (between 2 and 12 years)
(138). However, not all patients with nasal polyps have lower
respiratory tract symptoms (157).
Generally NP are twice as prevalent in men although the proportion
of those with polyps and asthma is twice that in
women than men. Women that have nasal polyps are 1.6 times
more likely to be asthmatic and 2.7 times to have allergic rhinitis
(141).
4-7-3 Aspirin sensitivity
In patients with aspirin sensitivity 36-96% have nasal polyps
(32, 145, 158-163) and up to 96% have radiographic changes
affecting their paranasal sinuses (164). Patients with aspirin
sensitivity, asthma and nasal polyposis are usually non-atopic
and the prevalence increases over the age of 40 years.
The children of probands with asthma, nasal polyps and
aspirin sensitivity had nasal polyps and rhinosinusitis more
often than the children of controls (165). Concerning hereditary
factors, HLA A1/B8 has been reported as having a higher
incidence in patients with asthma and aspirin sensitivity (166).
4-7-4 Genetics
An interesting observation is that NP are frequently found to
run in families, suggestive of an hereditary or shared environmental
factor. In the study by Rugina et al. (140), more than
half of 224 NP patients (52%) had a positive family history of
NP. The presence of NP was considered when NP had been
diagnosed by an ENT practitioner or the patients had undergone
sinus surgery for NP. A lower percentage (14%) of familial
occurrence of NP was reported earlier by Greisner et al. in
smaller group (n = 50) of adult patients with NP (59). Thus,
these results strongly suggest the existence of a hereditary factor
in the pathogenesis of NP. In this regard, recent genetic
studies found a significant correlation between certain HLA
alleles and NP. Luxenberger et al. (167) reported an association
between HLA-A74 and nasal polyps, whereas Molnar-Gabor et
al. (168) report that subjects carrying HLA-DR7-DQA1*0201
and HLA-DR7-DQB1*0202 haplotype had a 2 to 3 times odds
ratio of developing NP.
14 Supplement 18
Of note, studies of monozygotic twins have not shown both
siblings always develop polyps, indicating that there are likely
to be environmental factors influencing their development
(169, 170). Nasal polyps have been described in identical twins
but given the prevalence of nasal polyps it might be expected
that there would be more than a rare report of this finding
(171).
4-7-5 Environmental factors
The role of environmental factors in the development of NP is
unclear. No difference in the prevalence of NP has been found
in the patient’s habitat or pollution at work (140). One study
found that a significantly smaller proportion of the population
with polyps were smokers compared to an unselected population
(15% vs. 35%) (140) whilst another found an association
between the use of a woodstove as a primary source of heating
and the development of NP (172).
4-8 Epidemiology and predisposing factors for rhinosinusitis in
children
4-8-1 Epidemiology
Since the introduction of CT scanning, it has become clear
that a runny nose in a child is not only due to limited rhinitis
or adenoid hypertrophy, but that in the majority of the cases
the sinuses are involved as well. Van der Veken in a CT scan
study showed that in children with a history of chronic purulent
rhino rhea and a nasal obstruction 64% showed involvement
of the sinuses (173). In a MRI study of a non-ENT paediatric
population (60) it was shown that the overall prevalence
of sinusitis signs in children is 45%. This prevalence increases
in the presence of a history of nasal obstruction to 50%, to 80%
when bilateral mucosal swelling is present on rhinoscopy, to
81% after a recent upper respiratory tract infection (URI), and
to 100% in the presence of purulent secretions. Kristo et al.
found a similar overall percentage (50%) of abnormalities on
MRI in 24 school children (174). They included, however, a
follow-up after 6 to 7 months, and found that about half of the
abnormal sinuses on MRI findings had resolved or improved
without any intervention.
Unfortunately, most studies in the paediatric ENT literature
deal with patient populations (children with nasal complaints
attending outpatient clinics) and few involve normal populations.
Very few prospective studies are available and practically
no documentation exists on the natural history of the disease.
The first prospective epidemiologic and long-term longitudinal
study was performed by Maresh and Washburn (175) (see
Table 4.1). It was started in 1925 and these authors followed on
a regular basis 100 healthy children from birth to maturity,
looking at the history, and performing a physical examination
and routine postero-anterior radiograph of the paranasal sinuses
4 times a year (a total of 3,501 roentgenograms). The oldest
children underwent over 50 radiographs. It was noted that
there existed a relatively constant percentage (30%) of “pathologic”
antra in the films taken between 1 and 6 years of age,
the range being 23% to 35%. From 6 to 12 years, this percentage
dropped steadily to approximately 15%. Interestingly, the
authors noted that variations in size of the sinuses occur frequently,
without any demonstrable relation to the amount or
frequency of infections as seen on the radiographs and without
following any definitive pattern. When there was a recent
upper respiratory tract infection (“URI”) (in the previous 2
weeks), less than 50% showed clear sinuses. Tonsillectomy had
no demonstrable effect on the radiographic appearance of the
sinuses.
Although this is one of the only long term follow-up studies
one has to realize that a postero-anterior standard X-ray of the
sinuses in a child gives only information about the maxillary
sinuses and gives little information about the ethmoids so it
may well be that the prevalence of sinusitis was under- or overestimated.
In an MRI study of 60 children (mean age 5.7 years) with
symptoms of uncomplicated URI for an average of 6 days,
Kristo et al. found in 60% major abnormalities in maxillary and
ethmoidal sinuses, 35% in sphenoidal sinuses, and 18% in the
frontal sinuses (174). The MRI scores correlated significantly
with the symptom scores, especially nasal obstruction, nasal
discharge and fever. Of the 26 children with major abnormalities
in the first MRI, these findings subsequently (after 2
weeks) improved significantly, showing that these abnormalities
after an URI do not need antimicrobial therapy.
Therefore, it seems from all these studies that in younger chil-
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