The para-nasal sinuses form as invaginations
of the mucosa of the nasal cavity and are lined by respiratory
epithelium. They are protected from infection by the muco-ciliary
apparatus, which traps foreign particles in sinus mucous, which
are then removed by ciliary action towards the ostia (openings).
Sinuses are present in the forehead (frontal), cheeks (maxillary)
and "between and behind the eyes" (ethmoid and sphenoid).
Both the ethmoid and maxillary sinuses drain into the nasal cavity
via the "osteo-meatal complex", partial occlusion of
which may predispose to infection.
Infections of the paranasal sinuses are relatively common, affecting
up to 14% of the population in American studies. They typically
follow acute viral upper respiratory infections, which impairs
ciliary function, results in mucosal oedema and epithelial disruption,
which can occlude the osteo-meatal complex. The development of
a sealed sinus cavity impairs sinus drainage and favors the proliferation
of anaerobic bacteria. Barotrauma (from diving) or an infected
dental root can introduce bacteria directly into the sinuses.
Most acute viral infections last less than a week, whereas persistent
symptoms often indicate the development of sinusitis. Symptoms
include purulent nasal discharge or postnasal drip, halitosis,
bad taste in the mouth, sore throat, malaise, fever, and facial
pain / pressure (worse with leaning forward). It is important
to distinguish clinical features of sinusitis from patient's complaints
of "sinus", which may in fact represent other causes
of facial pain, of which facial migraines appear to be the most
common. Symptoms are generally more severe in patients with acute
infections but subtler in those with chronic disease, making definitive
diagnosis more difficult without direct visualization or radiological
imaging. Complications of untreated sinusitis include those of
orbital or facial cellulitis, osteomyelitis, cerebral abscesses,
thrombosis of the cavernous or sagittal sinuses, optic neuropathy
or proptosis.
Diagnosis of rhino-sinusitis may be made in most cases on clinical
grounds, and does not require radiological investigation. When
the diagnosis is uncertain, CT scanning is more sensitive than
sinus x-rays, the latter failing to detect up to 30% of abnormalities.
MRI scanning is generally less sensitive than CT scanning for
this purpose.
Microorganisms implicated in the pathogenesis of sinusitis include
Strep. pneumoniae, Haemophilus influenza,
Moraxella catarrhalis, and anaerobes such as Bacteroides.
Fungal infection may occur, particularly in immunocompromised
hosts. Acute infection will often respond to amoxicillin, but
failure to respond may indicate the presence of beta-lactamase
producing organisms. Under these circumstances, consideration
should be given to switching to amoxicillin/clavulinic acid, cephalosporins
(like cephalohexin or cefaclor) or doxycycline. Where penicillin
allergy is a problem, co-trimoxazole, doxycycline, macrolides
(such as clarithromycin) or cephalosporins (5-10% risk of cross-reactive
allergy) may be used. Patients with long-standing disease may
require the addition of metronidazole to provide anaerobe cover.
Up to 40% of acute infections are estimated to resolve spontaneously
without antibiotics. When symptoms persist, however, management
requires the use of appropriate antibiotics for an adequate duration
(generally at least 2 weeks, following a rule of thumb that the
antibiotics are continued until the patient is well plus an additional
5 days). Ancillary measures include the use of hypertonic saline
douches and steam inhalations. Nasal steroid sprays speed the
rate of clinical resolution, and enhance sinus drainage. Oral
steroids are sometimes useful in chronic disease for the same
reason.
Surgical therapy is indicated in patients with persistent disease
despite adequate medical therapy. Other indications include the
drainage and removal of diseased tissue (e.g. allergic fungal
sinusitis), the correction of impediments to sinus drainage (e.g.
debulking of polyps, opening of the osteo-meatal complex), the
removal of suspected tumours or for the management of complications
such as cerebral abscess.
Patients presenting with recurrent or chronic infections represent
a different group in whom changes in quality of life are comparable
to those observed in CAL, IHD or CCF. It is important to distinguish
between those with a true increased frequency of infection, from
those with chronic disease where antibiotics serve to suppress
rather than eliminate the problem. It is also useful conceptually
to consider predisposing factors as those which will influence
exposure to infection (e.g. child care workers, primary school
teachers), those which will impair sinus drainage, particularly
from the osteo-meatal complex (sepal deviation, concha bullosa,
polyps), and other contributors to mucosal oedema within the nasal
cavity and sinuses, of which allergic rhinitis is the most common.
Non-allergic (vasomotor) rhinitis and rhinitis medicamentosa from
abuse of nasal decongestants may have a similar effect. By contrast,
immunodeficiency is relatively rare, although there is an increased
incidence of immunoglobulin subclass deficiency in those with
recurrent sinusitis. As with hypogammaglobinaemia, patients with
deficiencies of complement components or ciliary dysfunction usually
present with evidence of widespread sinus, chest and middle ear
infection. Other potential contributors include cigarette smoking,
foreign bodies (particularly with unilateral infection in infants)
and nasal tumours.
Treatment of underlying disorders (such as allergic rhinitis)
or correction of anatomical abnormalities (e.g. nasal polyps)
may be required to control the frequency and severity of complicating
infection. Selected patients will benefit from antibiotic prophylaxis
or immunoglobulin replacement where immunological abnormalities
can be identified.
Nasal polyps are benign overgrowths
of the mucosa, and typically arise from the lining of the ethmoid
sinuses and to a lesser extent, from the maxillary or sphenoid
sinuses. Estimated prevalence range from 0.2% to 1% of the population,
although some autopsy studies suggest up to 20% of patients may
develop these during life. Most disease manifests by the age of
40 years, although patients presenting with nasal polyposis before
the age of 16 years should be investigated for associated disorders,
particularly cystic fibrosis.
Polyps are gelatinous in appearance, mobile and insensitive to
manipulation. They are often difficult to distinguish from swollen
turbinates using an auroscope. They rarely bleed, and the bleeding
should raise the suspicion of malignancy. The histology is that
of oedema and an infiltrate consisting of eosinophils, mast cells
and lymphocytes. The cause is unknown, but chronic inflammation
(from allergic disease or infection), and trauma to the lining
of the sinuses appear to be required in experimental models.
Atopy is not a prerequisite for the development
of polyps, but is associated with greater extent of disease and
increased risk of recurrence after surgery. Associated disorders
include asthma, aspirin intolerance, Churg Strauss vasculitis,
cystic fibrosis, allergic fungal sinusitis, and ciliary dysfunction
(such as Kartagener's syndrome and Young's syndrome).
Options for treatment include surgical removal
(around 50% eventually recur), oral corticosteroids (which offer
a rapid but temporary decrease in size) or long term corticosteroid
sprays (which shrink the polyps and slow down their rate of regrowth
once removed). In patients with recurrent disease, nasal steroid
sprays should be considered as "weed killers", which
need to be used continuously to slow down or prevent the regrowth
of polyps. Other modalities include aero-allergen desensitization
in atopic subjects, although it is uncertain whether patients
do better clinically because of control of their rhinitis, their
polyps or both. In patients with the so-called "aspirin triad"
(asthma, rhinitis and polyps), oral aspirin "desensitization"
has been used with some success to decrease polyp size, growth
and the need for surgical intervention. Whether leucotriene inhibitors
have a role to play in this group is yet to be determined.
Aspirin intolerance may manifest as
a number of distinct clinical syndromes, including acute urticaria/anaphylaxis,
an aggravation of chronic urticaria, or the so-called "aspirin
triad" (consisting of rhinitis, asthma and nasal polyps).
Reactions to aspirin are relatively rare in the healthy population
(around 0.3%), and only marginally higher in those with rhinitis
alone (around 1.4%). Prevalence rises to 4 - 20% in patients with
asthma, and occurs in 15 - 40% of those with nasal polyps. The
presence of atopic disease is not a prerequisite for developing
aspirin intolerance.
Some patients with aspirin intolerance will have cross reactive
responses to other NSAIDS. This is particularly common in patients
with the "aspirin triad". Cross reactivity appears to
be related to the potency by which these drugs inhibit cyclooxygenase.
Patients who are intolerant of aspirin or similar drugs may be
able to tolerate relatively weak inhibitors of cyclooxygenase
such as diflunisal or paracetamol, although exceptions occur.
The likelihood of reacting to NSAIDS is dose-related. Five
to 15% of patients who are aspirin intolerant, for example, will
react to paracetamol given in doses of 1,000 mg (2 tablets) or
more at a time.
Cross reactivity between these drugs in acute urticarial or anaphylactic
reactions is relatively rare. Reactions appear to be idiosyncratic
and unrelated either to structural similarities or cyclooxygenase
inhibitory activity. By contrast, aggravation of underlying chronic
urticaria by NSAIDS may occur in up to 40% of patients.
In patients with the "aspirin triad", intolerance appears
to be a marker of disordered leucotriene regulation. Oral "desensitization"
to aspirin decreases the production of, and sensitivity to, some
leucotrienes. In selected patients, this may result in better
asthma control, decreased need for medication and less frequent
recurrence of nasal polyps. Leucotriene inhibitors are also beneficial
in some patients with aspirin-sensitive asthma, but whether they
have a role to play in inhibiting the growth of polyps in this
group is yet to be determined.
Indications for desensitization include the need for aspirin or
similar drugs to treat rheumatological or cardiovascular disease,
or the presence of poorly controlled aspirin-sensitive asthma/polyposis,
despite optimal medical therapy. Patients requiring a NSAID other
than aspirin may be "desensitised" to aspirin first,
and then safely switched to the agent of their choice.
