TITLE: Pediatric Rhinosinusitis
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: May 31, 2000
RESIDENT PHYSICIAN: Russell D. Briggs, M.D.
FACULTY PHYSICIAN: Norman R. Friedman, M.D.
SERIES EDITOR: Francis B. Quinn, Jr., M.D.
|Return to Grand Rounds Index|
Introduction
The diagnosis and subsequent
treatment of rhinosinusitis in the pediatric population has undergone dramatic
changes in the last twenty-five years.
Even in the early 1970’s, the diagnosis of acute or chronic sinusitis in
the pediatric population was rare (Hopp).
Today, the diagnosis is relatively common, a likely consequence of an
improved understanding of the pathophysiology, etiology, and treatment outcomes
for this disease. Even with its
increased prevalence over the past two decades, controversy still exists
concerning its pathogenesis, presentation, diagnosis, and treatment. As the signs and symptoms of pediatric
rhinosinusitis are often subtle and the fact that the history is often limited
to observations of the parents with a physical examination dependent on the
cooperation of the child, there is greater emphasis on newer diagnostic
modalities in evaluating childhood rhinosinusitis (Kennedy). Indeed, pediatric rhinosinusitis continues
to be a rapidly evolving and controversial topic for the otolaryngologist.
Anatomy
The maxillary sinus is the first of
the paranasal sinuses to begin development in the human fetus. They begin as outgrowths of the lateral nasal
wall about day 65 of gestation. These
sinuses slowly enlarge in utero but are not demonstrated on plain films until
the infant is 4 to 5 months of age.
Growth of these sinuses is biphasic with the first period of
considerable enlargement during the first 3 years and the second phase between
7 and 12 years of age. During this
second phase, the pneumatization extends laterally to the level of the lateral
wall of the orbit and inferiorly into the alveolar process in conjunction with
the eruption of permanent dentition.
Slow expansion of the maxillary sinuses continues until age 18 to reach
adult dimensions with an average capacity of 14.75 mL (Miller). The maxillary sinuses drain into the middle
meatus.
The ethmoid cells begin development
later in the third month of fetal development.
The anterior ethmoids form as evaginations of the lateral nasal wall
with the posterior ethmoids forming in the fourth month of gestation from
outgrowths in the superior meatus. At
birth these cells are fluid filled and are difficult to visualize on
X-rays. By one year of age, the
ethmoids can be detected on plain films and subsequently rapidly enlarge to
reach adult dimensions by age 12. The
cells number 4 to 17 cells on each side with an average total volume of 14-15
mL (Miller). The anterior ethmoid air
cells drain into the middle meatus whereas the posterior cells drain into the
superior meatus.
The frontal sinus begins development
during the fourth month of gestation as an upward extension of the most
anterosuperior ethmoidal cells. The
frontal sinus is rarely visualized radiographically prior to age 5 or 6 after
which it slowly grows to reach an adult size by late adolescence with a total
volume of 6-7 mL. The pneumatization of
the frontal sinus is variable with a developmental failure of one of the sides
in 4-15% of the population. The frontal sinus drains into the frontal recess.
The sphenoid sinuses originate
during the fourth gestational month as paired evaginations of the mucosa in the
superoposterior portion of the nasal cavity.
They remain as small indentations in the sphenoid bone until age 3 when
further pneumatization begins. Growth
becomes rapid to reach the level of the sella turcica by age seven and reach an
adult size by age 18 with a total volume of 7.5 mL (Miller). The sphenoid sinus drains into the superior
meatus along with the posterior ethmoid air cells.
The sinus mucosa consists of
pseudostratified ciliated, columnar epithelial cells, goblet cells, and
submucosal glands that produce a protective mucous blanket. The mucosal blanket traps bacteria and
noxious materials, which are carried by ciliary motion to the ostium and into
the nose for elimination. The orientation
of the cilia within a given sinus is specific as secretions are propelled
towards the natural sinus ostia and from there to the nasopharynx and
oropharynx where they are subsequently cleared by swallowing. This mucosa is similar to that found in the
nose and tracheobronchial tree (Hopp).
Pathophysiology
and Pathogenesis
For normal physiologic function of
the paranasal sinuses, the ostia must be patent, the cilia should be
functioning effectively, and the secretions should be normal (Ott). Retention of secretions in the paranasal sinuses
can be due to one or more of the following: obstruction of the ostia, reduction
in the number or impaired function of the cilia, or overproduction or change in
the viscosity of secretions (Wald).
According to current understanding of sinus physiology, the primary
sinus abnormality for initiation of rhinosinusitis is obstruction of the
osteomeatal complex by mucosal edema or mechanical obstruction (Ott,
Wald). Various local, regional, or
systemic factors may lead to an obstruction of the osteomeatal complex. Local and regional factors include nasal
septal deviation, nasal polyps, anatomic variants such as choanal atresia or
concha bullosa, foreign bodies, edema attributed to viral infections, allergic
inflammation, and nonallergic rhinitis.
Systemic factors can include ciliary dyskinesia syndromes, cystic
fibrosis, and immunological deficiencies.
Other factors that have been attributed to the etiology of pediatric
rhinosinusitis include air pollution, gastroesophageal reflux, day care
attendance, and enlarged adenoids (Lusk).
Although many conditions can lead to obstruction of the natural ostia,
viral upper respiratory tract infections and allergic inflammation are by far
the most frequent causes (Wald).
Obstruction of the natural ostia by any of these predisposing factors
can result in hypoxia of the involved sinus which leads to ciliary dysfunction
and abnormal movement of mucous from the sinus (Ott). Bacteria in the upper respiratory tract are then able to multiply
and invade the mucosa of the obstructed sinus (Ott).
Definitions
The Consensus Panel for the
Management of Rhinosinusitis in Children met in Belgium in 1996 to help
standardize the proper definitions associated with pediatric sinusitis. The preferred term for this disorder is rhinosinusitis
which acknowledges the fact that most sinus infections start in the nasal
passages as a continuum of disease (Clement).
As explained by the Consensus Panel, it is not possible to differentiate
rhinitis from sinusitis based on clinical grounds alone. Isolated rhinitis can exist and is quite
common (i.e. in allergic or specific rhinitis), but isolated sinusitis is rare. (Clement).
Acute rhinosinusitis, as defined by
the Consensus Panel, is a sinus infection that has complete resolution of
symptoms within 12 weeks (based on a clinical basis only). This definition assumes that there is no
intermittent upper respiratory infection during this three month time
(Clement). Acute rhinosinusitis is
further divided into severe or nonsevere forms based on the symptomotology of
the child (Clement). Chronic
rhinosinusitis is defined as a sinus infection with low grade symptoms and
signs that persist for more than 12 weeks, although acute exacerbations can
occur in the setting of a chronic infection. The most common clinical picture
seen in pediatric patients is an acute exacerbation in the setting of chronic
rhinosinusitis (Clement). Recurrent
acute rhinosinusitis consists of repeated acute episodes, with the signs and
symptoms completely resolving between the episodes. In patients who are being treated with antibiotics, it is often
difficult to differentiate on clinical grounds chronic rhinosinusitis from its
acute form (Lusk).
Clinical
Presentation
The diagnosis of rhinosinusitis is
usually based on the clinical evidence and, as discussed earlier, the duration
of the symptoms. The history and
physical examination is vital to the proper diagnosis and subsequent
management. Unfortunately, commonly
recognized symptom complexes apparent in adults such as facial pain, headache,
and fever are uncommon in the pediatric population (Wald). In addition, the symptom complex varies and
in young children, the sinuses are difficult to directly visualize in an office
setting.
The first and perhaps most common
clinical setting is that of a viral upper respiratory tract infection. Also known as the common cold, the signs and
symptoms can mimic those of rhinosinusitis.
According to Lusk, it is virtually impossible to differentiate between
an upper respiratory tract infection and rhinosinusitis during the first 7 to
10 days of symptomotology. Symptoms can
include rhinorrhea which is usually serous but may become mucopurulent . Nasal congestion is common and cough is
usually present. The patient may also
experience low grade fevers, malaise, and headaches. The key to the diagnosis of a viral upper respiratory tract
infection is the brevity of symptoms. A
typical upper respiratory tract infection usually resolves within 10 days
although lingering cough present only at night is a common residual symptom of
an upper respiratory tract infection or an indication of cough-predominant
asthma. Acute nonsevere rhinosinusitis
should be suspected in patients with persistent cold symptoms past ten days. Symptoms are strikingly similar to those of
a viral upper respiratory tract infection and include rhinorrhea of any
quality, cough (dry or wet) which is usually present during the daytime but
often worse at night, low grade fevers, fetid breath, and painless morning
periorbital swelling. The periorbital
swelling is intermittent and painless.
Facial pain is typically absent (Wald, Clement, Ott, Lusk).
A second, less common, presentation
is an upper respiratory tract infection that is more severe than usual. In this setting, a diagnosis of an acute
severe rhinosinusitis should be considered.
Symptoms usually occur after ten days of typical nonsevere symptoms
however the symptoms may occur earlier in the course of the disease. Symptoms of acute severe rhinosinusitis
include high fever (usually over 39.0oC), a purulent and copious
nasal discharge, and associated periorbital swelling and facial pain. The periorbital swelling may involve the
upper or lower eyelids and is most obvious in the early morning after waking. A less common complaint is a headache
usually described as a feeling of fullness or dull ache behind or above the
eyes, most often reported in children over five years of age. Less commonly, there may be dental pain
referred from the sinus infection (Wald, Clement, Ott, Lusk).
Diagnosis
The diagnosis of pediatric
rhinosinusitis is usually based on a combination of the history, physical
examination, laboratory investigations, and radiological findings. The physical examination in pediatric
patients with rhinosinusitis is often unrewarding. The physical examination is limited by the inaccessibility of the
paranasal sinuses as well as the uncooperative nature of the pediatric
patient. Evaluation on anterior
rhinoscopy may reveal a mucopurulent discharge from the osteomeatal complex,
however this assessment is difficult to perform on a child (Younis). Younger patients may tolerate evaluation by
an otoscope which may demonstrate nasal mucosal edema, erythema, or possibly
purulent discharge in the nose.
Examination in the oropharynx may reveal moderate injection of the
oropharyngeal wall with postnasal drainage in the posterior pharynx. Occasionally there may be tenderness with
palpation over the paranasal sinuses.
Assessment of the face may reveal appreciable periorbital edema or dark
discoloration of the lower eyelids.
Flexible and rigid endoscopy may provide a more complete evaluation in
an older, more cooperative child. The
most specific findings for acute rhinosinusitis in a child include
mucopurulence from the middle meatus (after topical vasoconstriction),
periorbital swelling, and facial tenderness (Wald).
Currently utilized diagnostic
procedures for acute rhinosinusitis include transillumination, ultrasonography,
plain radiography, and aspiration of the sinuses. The increased thickness of both the soft tissue and bony vault in
children under age 10 limits the clinical usefulness of sinus
transillumination. As a result, most
authors conclude that transillumination is of no value in diagnosing
rhinosinusitis in children (Lusk, Wald, Ott,).
Controversy still exists concerning the value of ultrasound examination,
however this modality also appears to have little benefit for children (Lusk,
Ott).
Radiography has been traditionally
used to determine the presence or absence of sinus disease. Standard views include the Water's,
Caldwell, lateral, and submentovertex views.
A number of criticisms have been made towards the use of plain
radiographs in diagnosing pediatric rhinosinusitis. First, the ethmoid sinuses on plain radiographs are often poorly
visualized and mucosal disease present in this anatomic location is often
unrecognizable on plain radiography (Ott).
Second, differences of opinion remain concerning what findings on plain
radiography are indicative of disease.
Varying degrees of mucosal thickening (2 to 6 mm) and the presence of
air-fluid levels have been used as criteria for diagnosis (Ott). However, thickening may not be indicative of
bacterial infection, instead it may be the result of allergic or nonallergic
rhinitis. In addition, underdeveloped
sinuses may be misinterpreted as opacification because of the variation of size
and symmetry in children. Mucosal
redundancy can also mimic sinus opacification on plain radiographs. For these reasons, many investigators have
argued that plain radiographs are unreliable in children, especially those
under the age of one (Ott).
McAlister et al. prospectively
compared the usefulness of plain radiographs with coronal CT scans in pediatric
patients with symptoms of chronic rhinosinusitis. Forty-five percent of
children with normal plain films demonstrated abnormalities on CT scans and 34%
of the children with abnormal plain radiographs had normal CT scans. Thus, McAlister concludes not only are plain
radiographs unreliable as screening tools, the radiographs underestimate and
overestimate the amount of sinus disease noted on CT scanning. These findings do not negate the use of
plain radiographs particularly in the event of acute rhinosinusitis where air-fluid
levels may be demonstrated. If air
fluid levels are noted on plain radiographs, these patients have positively
correlated sinus aspirates 75% of the
time (Wald).
Given the problems associated with
plain radiography, many suggest that if the history and physical examination
suggests acute rhinosinusitis, it is reasonable to forego plain radiographs and
treat the condition. However, if the
symptoms and physical examination are inconclusive, plain radiography may play
a role. Criteria have been suggested to
aid in the appropriate use of plain radiographs for assisting in the diagnosis
of pediatric rhinosinusitis. First, it
is suggested not to order radiographs under the age of one. Second, it is important to be familiar with
the normal development of the sinuses in children prior to reading the
films. Third, upright radiographs are
of more benefit than supine. Fourth,
radiographs should be ordered only if symptoms are prolonged and unusually
severe (Ott).
Computed tomography scanning
provides an excellent tool for evaluation of sinus disease, particularly in
cases of chronic rhinosinusitis. The CT
can demonstrate disease that is not shown on routine X-rays. While CT scanning may demonstrate disease
not shown on plain radiographs, the scan may not reveal the extent of disease
actually present (Younis). Nonetheless,
in patients who have failed optimum medical management or are planning for
surgical intervention, computed tomography remains the gold standard for
rhinosinusitis evaluation. CT scans are
not necessary for the management of children with uncomplicated acute bacterial
rhinosinusitis. The indications for
obtaining a CT scan are similar to those for sinus aspirates discussed below.
Confirmation of the diagnosis of
rhinosinusitis can be made by culturing an aspirate of the sinus
secretions. While not completely free
of morbidity as these children typically require a general anesthesia, a
properly performed sinus aspiration allows for precise identification of the
offending pathogen as well as the sensitivities of the organism to appropriate
antibiotics. Indications for sinus
aspiration in children include clinical unresponsiveness to conventional
therapy, sinus disease in an immunosuppressed patient, severe symptoms such as
headache or facial pain, and life threatening complications such as
intraorbital or intracranial suppuration at the time of clinical presentation
(Wald). Unfortunately, nasal,
oropharyngeal, and nasopharyngeal cultures correlate poorly with cultures of
sinus aspirates. Therefore, it is not
recommended to undertake these cultures as guides to the bacteriology and
therapy of acute or chronic rhinosinusitis (Wald). Additionally, there is no consensus on whether middle meatal
cultures can substitute for sinus punctures. (Lusk).
Knowledge of the bacteriology of
sinus aspirates can aid in the proper selection of antibiotics against the
offending organisms. A study of fifty
children with acute maxillary rhinosinusitis has shown that the pathogens found
in sinus secretions were similar to those found in adults. The predominant organisms include
Streptococcus pneumoniae, Moraxella catarrhalis, and nontypeable Hemophilus
influenzae. Rarely, viruses and
anaerobes are isolated from these patients (Wald). These same organisms are also found in cases of chronic
rhinosinusitis with the exception that greater numbers of anaerobes,
Streptococcus, and Staphylococcus species have be isolated.
There is controversy concerning
whether there is normal flora within the paranasal sinuses. Animal data suggest that a noninfected sinus
is sterile, however, similar studies have not been performed in asymptomatic
children. In adults, sinus aspirates
from 12 asymptomatic patients revealed bacteria similar to those pathogens found
in patients with maxillary rhinosinusitis (Ott).
In the past, treatment for acute
maxillary rhinosinusitis consisted of sinus aspiration and irrigation
(Wald). With the current availability
of antimicrobial agents that are effective against the offending pathogens, antibiotic
therapy is considered the standard treatment of rhinosinusitis today. Antibiotic usage should only be considered
for those patients that meet the clinical criteria for bacterial
rhinosinusitis, as a viral upper respiratory tract infection is at least 20-200
times more common than bacterial rhinosinusitis and increasing numbers of drug
resistant bacteria are being isolated.
A recent study revealed that 16.1% and 28.6% of Streptococcus pneumoniae
isolates were penicillin-intermediate and penicillin-resistant respectively
(Academy Guidelines). At UTMB, 35% of
Streptococcus pneumoniae isolates are penicillin resistant. Even when strict clinical criteria are met
approximately 40-60% of rhinosinusitis episodes will resolve without the use of
antibiotics. This is a similar
pathophysiologic picture as patients with acute otitis media (O’Brien). However, the objectives of antibiotic
therapy in treating a bacterial rhinosinusitis include the achievement of a
rapid clinical cure, sterilization of the sinus secretions, prevention of
suppurative complications, and prevention of chronic sinus disease (Wald).
Recommendations by the American
Academy of Otolaryngology for initial therapy for children with acute nonsevere
rhinosinusitis that have not received antibiotics in the past 4-6 weeks include
amoxicillin/clavulanate, amoxicillin (45-90 mg/kg/day), cefpodoxime proxetil,
or cefuroxime axetil. Azithromycin,
clarithromycin, erythromycin, or
TMP/SMX are acceptable if the patient has a known immediate type I hypersensitivity
reaction to beta lactams. These
antibiotics have limited effectiveness against the major pathogens of acute
rhinosinusitis and a failure rate of 25% is possible (Academy Guidelines).
Recommendations for initial therapy
for children with mild disease who have received antibiotics within the
previous 4 to 6 weeks or children with moderate disease without prior
antibiotics includes amoxicillin/clavulanate, high dose amoxicillin (80 to 90
mg/kg/day), cefpodoxime proxetil, or cefuroxime axetil. Clindamycin is appropriate if Streptococcus
pneumoniae is isolated. Moderate
disease in children receiving antibiotics in the previous 4 to 6 weeks should
be treated with amoxicillin/clavulanate or combination therapy (amoxicillin or
clindamycin plus cefpodoxime proxetil or cefixime). Consideration of the side effect profile of any of the
antimicrobial agents should be considered in cases of nonsevere acute
rhinosinusitis as spontaneous resolution can be expected to occur in 40-60% of
cases (Wald). Additionally, knowledge
of local resistance patterns of rhinosinusitis pathogens is important in
selecting the proper initial antimicrobial agent. If no improvements occur in 48 to 72 hours, the antibiotic should
be changed to a beta-lactamase stable agent as there are increasing numbers of
beta-lactamase resistant strains of H. influenzae and M. catarrhalis as well as
resistant Streptococcus pneumoniae species.
Such "switch therapy" for patients without improvement in 72
hours varies depending on the likely pathogen.
Children continuing effective antibiotic therapy and continue to be
symptomatic may need further evaluation and identification of the offending
organism (Academy Guidelines).
An oral beta lactamase stable agent
such as amoxicillin-clavulanate, cefixime, cefuroxime, or cefpodoxime should be
used as initial therapy for acute severe rhinosinusitis. At UTMB, cefixime is no longer an acceptable
second line agent as it is no more beneficial than penicillin for Streptococcus
pneumoniae due to increased resistance patterns. Total therapy length should be from 10-14 days which can be
prolonged to one month if the symptoms have improved but not resolved
completely (Clement). Patients with
severe illness or with suspected or proven suppurative complications should be
treated intravenously with an agent active against beta lactamase producing
pathogens. Cefotaxime or ceftriaxone
with the addition of clindamycin to cover drug resistant Streptococcus
pneumoniae is acceptable.
Clinical improvement is expected
rapidly in most patients with properly selected antimicrobials. If the patient does not improve or worsens
in 48 hours, clinical reevaluation is appropriate. If the diagnosis is unchanged, sinus aspiration may be considered
or a change to a more active antimicrobial agent may be prescribed (Clement).
For chronic rhinosinusitis, a four
to six week course of a beta lactam stable antibiotic is appropriate, with
three weeks of therapy being the minimum (Ott).
The effectiveness of antihistamines
and decongestants (singly or in combination) applied topically or administered
orally in the treatment of acute or chronic rhinosinusitis has not been
adequately studied. Additionally, no
double blind controlled studies have been performed to evaluate the effectiveness
of isotonic saline nose drops, saline sprays or irrigations, steam inhalations,
or nasal steroid medications (Ott). The
reported benefits of topical decongestants such as oxymetazoline or
phenylephrine in shrinking the nasal mucous membrane, improving ostial
drainage, and providing symptomatic relief should be weighed against the
possibility of inhibiting ciliary motion.
By inhibiting ciliary motion, topical decongestants may delay clearance
of infected material. In addition, by
decreasing blood flow to the mucosa, topical decongestants may lower oxygen
tension and impair diffusion of antimicrobials into the sinuses. The use of antihistamines have been
considered mainly in cases of concomitant allergic rhinitis. There use, however, may actually interfere
with the clearance of secretions as these agents are known to dry the mucosal
secretions of the sinuses (Ott).
Reports of benefit from physiologic saline and steam treatments are only
anecdotal. Supposedly, therapeutic
benefit is due to moisturizing the inflamed mucosa, softening the nasal crusts,
and direct removal of purulent material.
The role of nasal steroids in the treatment of rhinosinusitis, likewise,
has also been inadequately addressed.
These agents may have a role for children with chronic, nonpurulent
rhinosinusitis, especially those with an established diagnosis or strong
suspicion of allergic rhinitis (Clement).
The effectiveness of mucolytics such as iodinated glycerol has primarily
been studied on sputum in lower respiratory tract disorders in adults. Although their use in pediatric
rhinosinusitis has not been well studied, the similarities of cough, tenacious
mucous, and recurrent bacterial infections suggests these might have a therapeutic
role. Despite its wide clinical use,
guaifenesin has not been proven efficacious (Zacharisen).
Additional studies may be warranted
in children with recalcitrant rhinosinusitis.
Underlying conditions such as allergy, immunodeficiency, cystic
fibrosis, ciliary immotility disorders, and gastroesophageal reflux must be
considered. Respiratory allergy is the
most frequent of these underlying conditions (Clement). Thus, in children with chronic or recurrent
acute rhinosinusitis with a suggestive history and physical examination,
allergic assessment should be performed for patients who continue to worsen
despite avoidance and simple pharmacological measures. A history of nasal symptoms such as
sneezing, itching of the nose, ears, and eyes coupled with physical examination
findings of an allergic nasal crease, pale swollen turbinates, or other
evidence of atopy such as eczema, urticaria, or asthma should elicit an
allergic assessment (skin prick testing, nasal smear, radioallergosorbent
testing, or a trial of treatment) (Clement).
An immunologic assessment (complete blood cell count, quantitative
immunoglobulin levels, immunoglobulin G subclass level in serum, and
antipneumococcic titers), ciliary dismotility assessment (mucosal biopsy), and
a cystic fibrosis workup (sweat chloride test)is advisable particularly in
cases with children that have recurrent sinopulmonary infections
(Clement). Cystic fibrosis, in
particular, should be considered in any child that is found to have nasal
polyposis. Extended pH probe monitoring
for gastroesophageal reflux and treatment of known gastroesophageal reflux
disease may be warranted in children with recalcitrant rhinosinusitis
(Bothwell).
Patients with acute rhinosinusitis
rarely will ever need surgical intervention except in those cases that are
complicated by orbital or nervous system complications. Subperiosteal abscess, orbital cellulitis,
or intracranial abscess must receive aggressive surgical management
(Stankiewicz). For patients with
nonresponsive recurrent acute or chronic rhinosinusitis that fail to improve
with maximal medical therapy, surgical intervention may be necessary.
In children with rhinosinusitis with
moderate to severe nasal obstruction caused by adenoid hypertrophy,
adenoidectomy has been shown to be beneficial.
However, given the size of the research trials involved, definite
conclusions cannot be drawn as to the efficacy of this form of treatment
(Clement).
Septoplasty is another potential
treatment for the symptoms of rhinosinusitis.
Septal deviation significant enough to nasal obstruction and ipsilateral
sinusitis is an uncommon finding.
However, in selected patients, a limited septoplasty may be a reasonable
surgical procedure.
Antral aspiration and lavage
generally require general anesthesia in children and is indicated in cases of a
severe, unresponsive or complicated condition.
The indications for antral lavage are the same as for sinus puncture
discussed previously. Antral lavage is
usually not a viable therapeutic modality for the treatment of rhinosinusitis
because it involves only the maxillary sinus and not the ethmoid or other
sinuses. The technique does remain a
valuable diagnostic tool in the immunocompromised patient or in select patients
where the disease is limited to the maxillary sinus.
The Caldwell-Luc procedure is an uncommon procedure
for treatment of pediatric rhinosinusitis due to concerns of potential damage
to the unerupted permanent dentition and the uncommon finding of sinus disease
sufficient enough to benefit from removal of the diseased sinus mucosa.
The nasal antral window (inferior
antrostomy) was popularized in the past as a less aggressive and more effective
method of treating rhinosinusitis than the Caldwell-Luc procedure. The nasal antral window is used to promote
sinus drainage and ventilation and is often placed in the inferior meatus. According to Lusk and Stankiewicz, the
inferior antrostomy has not been a successful modality for treating
rhinosinusitis. Reasons cited include
that the cilia continue to beat towards the obstructed natural ostia and the
potentially diseased ethmoid sinuses are not addressed. Additionally, a significant number of
windows have been found to lose patency with a subsequent recurrence of
rhinosinusitis. Exceptions for placing
an inferior antrostomy include cilial dysfunction and cystic fibrosis as
gravity likely plays a larger role in enhancing sinus drainage via the
dependent window thereby increasing its efficacy (Lusk).
The current state of the surgical
technique for treatment of rhinosinusitis is functional endoscopic sinus
surgery (FESS). The technique
frequently involves opening the osteomeatal complex and removal of sinus
disease with minimal manipulation of the surrounding normal tissue. The treatment of pediatric rhinosinusitis by
this method is a very controversial issue and has as many proponents as
opponents. According to the opponents,
pediatric rhinosinusitis is analogous to recurrent acute otitis media and is
actually part of the same disease process.
The surgical equivalence of tubes in recurrent otitis media has none in
rhinosinusitis with some arguing that FESS is equivalent to a mastoidectomy for
acute otitis media. Opponents also
argue that even gross radiographic or extensive mucosal disease has been
repeatedly shown to be reversible. They
contend that the indications for surgery-- unabated rhinorrhea, failure of
maximal medical therapy, and an abnormal CT scan, do not bear scientific
scrutiny. They contend that the precise
population of children most likely to benefit from surgery has not been
delineated. In addition, the small
space of the nasal cavity and the proximity of the lateral nasal wall to the
contents of the orbit and anterior cranial fossa make serious complications a
very real possibility.
Advocates of surgical treatment have a careful
approach that is variable between surgeons.
According to their approach, the patient qualifies for surgery when
medical therapy has failed, as determined by the pediatrician and surgeon. A thorough medical workup is often
undertaken with consideration given to immunologic, allergic, asthmatic, and
reflux disease in the child. Extensive
sphenoethmoidectomy is usually not necessary in children. Typically, an anterior ethmoidectomy with a
maxillary antrostomy is often sufficient.
The proponents often cite excellent results with surgical treatment of
chronic and recurrent acute rhinosinusitis.
A recent study determining the safety and efficacy of FESS in children
with chronic rhinosinusitis reported that 71% of patients were considered
normal by their parents at one year postop (Wald). Additionally, a meta analysis of FESS for chronic and acute
rhinosinusitis revealed an 89% success rate with a complication rate of 0.6%. A preoperative CT scan with coronal sections
is essential in defining the location and extent of the disease as well as the
pertinent anatomy of the proposed endoscopic site.
While many may argue specific indications for or
against surgery, the Consensus Panel for pediatric rhinosinusitis lists the following
for absolute indications for FESS: 1) complete nasal obstruction in cystic
fibrosis due to massive polyposis or closure of the nose by medialization of
the lateral nasal wall, 2) antrochoanal polyp, 3)intracranial complications, 4)
mucocoeles or mucopyocoeles, 5) orbital abscess, 6) traumatic injury in the
optic canal, 7) dacryocystorhinitis due to sinusitis and resistant to
appropriate medical treatment, 8) fungal sinusitis, 9) some
meningoencephaloceles, and 10) some neoplasms (Clement). Possible indications are for children with
chronic rhinosinusitis that persists despite optimal medical management (2-6
weeks of adequate antibiotics and treatment of any concomitant disease) and
after exclusion of any systemic disease (Lusk).
Complications
of Rhinosinusitis
Complications of rhinosinusitis in
children have steadily decreased over the years due to improvements in
diagnostic aids and therapeutic techniques.
Improved radiographic modalities such as CT scanning coupled with newer
surgical techniques have favorably changed the prognosis of patients with
complicated rhinosinusitis.
Nonetheless, the potential severity of complicated sinus disease makes
appropriate recognition and early treatment imperative.
The most common complications in
rhinosinusitis are orbital infections (Gurucharri). Infections from the sinus can spread to the orbit through the
arteries, veins, or lymphatics but most often spread by direct extension
through a dehiscence in the lamina papyracea (Lusk). Chandler has divided the progression of sinusitis-induced orbital
infections into five stages. The
classification aids in the assessment of severity of the disease and the
development of a plan of therapy. Stage
I is a periorbital inflammatory edema, in which cellulitis of the eyelid may
occur with or without edema of the orbital contents. Obstruction of venous channels is usually the cause and there is
no loss of vision or limitation of extraocular mobility.
Stage II is associated with orbital
cellulitis in which diffuse edema, chemosis, proptosis, and pain is present.
There is no abscess formation and opthalmoplegia or globe fixation may occur by
muscle edema or spasm although there is usually no mobility limitation. Visual loss is usually mild due to corneal
edema.
Stage III involves a subperiosteal
abscess, or purulent material between the bony wall of the orbit and the
periorbita. Swelling is generally
circumscribed with displacement of the globe in a lateral or downward direction. Orbital cellulitis is also present and is manifested by a limitation of
extraocular mobility secondary to edema or spasm. Vision is typically decreased.
Stage IV is defined as an orbital
abscess. It is thought to develop
secondary to extension of infection into the orbital site with inflammatory
edema, fat necrosis and abscess formation.
Proptosis and chemosis are severe but the globe is not usually as
displaced as with a subperiosteal abscess.
Opthalmoplegia and visual impairment are usually present with complete
opthalmoplegia and visual loss present in 13% of patients secondary to ischemia
or optic neuritis.
Stage V is cavernous sinus
thrombosis which is due to extension of phlebitis into the cavernous
sinus. This produces a progression of
symptoms initially involving the orbit
and subsequently involving the opposite eye. Marked proptosis and fixation of the eyeball is usually present. Extraocular muscle limitation is typically
caused by involvement of the third, fourth, and sixth cranial nerves. Meningitis may also take place (Gurucharri).
The appropriate diagnosis is based
on an accurate history, physical examination, laboratory results, and
radiographic examinations. Histories
consistent with rhinosinusitis and a physical examination revealing periorbital
or orbital inflammation suggest complicated sinus disease. Opthalmological evaluation is mandatory and
intravenous antibiotics are typically given with ceftriaxone or cefotaxime as
initial first line agents with a consideration given to cover anaerobes and
Staphylococcus species with clindamycin or a combination of oxacillin and
metronidazole. Surgical intervention
should be considered for any patient with abscess formation, worsening visual
acuity, loss of vision, progression of orbital involvement, progression to the
opposite eye, and persistent high-grade fever despite 24 hours of medical
treatment. The surgical procedure
depends on the location of the abscess and the primary site of infection. External ethmoidectomy, endoscopic sinus
surgery, frontal sinus trephines, or Caldwell-Luc procedures may be employed.
Intracranial complications of
rhinosinusitis may be life threatening.
Infection spreads intracranially by extension along anatomic pathways,
retrograde thrombophlebitis, or direct inoculation. Intracranial complications secondary to sinusitis include
meningitis, epidural or subdural abscess, cavernous sinus thrombosis, and
cerebral abscess.
Intracranial complications must be
suspected in patients with histories consistent with rhinosinusitis and
physical examination findings consistent with altered neurologic function. Immediate treatment is similar to that of
orbital complications with the neurosurgeon, ophthalmologist, and infectious
disease specialist playing a prominent role in the child’s initial management.. Of note, a lumbar puncture should not be
performed as this may precipitate brainstem compression.
The main complication of long
standing sinus disease is a mucocoele.
These are destructive masses secondary to local expansion and are
usually identified by CT scan.
Management is surgical with endoscopic or open sinus procedures
indicated depending on the location.
Occasionally, infection in the sinuses may result in osteomyelitis of
the surrounding bony walls. This will
require long term intravenous antibiotic therapy and occasionally surgical
drainage of the infected sinus with debridement of the infected tissues
(Gurucharri).
The
Role of Allergy in Rhinosinusitis
The prevalence of allergy in the
United States has been estimated at 15-30% of the general population. Allergy is a contributing factor in, if not
the primary cause of, recurrent acute rhinosinusitis and chronic rhinosinusitis
in allergic patients. Similar to the
pathophysiology of viral induced rhinosinusitis, allergy evoked sinusitis is
hypothesized to arise from mucosal edema, resulting from the inflammation
induced by the allergic reaction. This
edema leads to obstruction of the sinus ostia, mucostasis, local tissue
hypoxia, and subsequently growth of bacteria within the sinus leading to
rhinosinusitis (Cook).
Differentiation between infectious and allergic
symptomatology is essential in order to correctly diagnose and treat these two
conditions. Symptoms suggesting allergy
include itching mucous membranes of the upper aerodigestive tract, clear
rhinorrhea, and other remote symptoms of allergy including eczema and food
intolerance. Overlap occurs with
infectious rhinosinusitis as both conditions can lead to nasal congestion,
stuffiness, fluctuating rhinorrhea, sneezing, cough, behavioral changes, and
headaches with facial pain or pressure.
Indeed, the two conditions can be present within the same patient,
however in most instances, it is believed that allergic disease with mucosal
edema is the primary etiology with infection occurring secondarily (Cook).
Other historical clues may lead to the diagnosis of
allergy. Infantile colic, numerous
formula changes with vomiting and diarrhea, poor sleeping habits, and
irritability are common occurrences in the allergic infant. Pertinent history also includes a frequently
runny nose or constant cold symptoms, eczema, recurring upper respiratory tract
infections, cough, wheezing, otitis media, and a diagnosis of attention deficit
hyperactivity disorder (Cook).
Physical signs of allergic children can include
“allergic shiners”, characterized by puffy, bluish discoloration of the lower
eyelids. Allergic children also often
display very long silky, uneven eyelashes as well as conjunctivitis. The external nose may frequently display a
supratip horizontal nasal crease owing to the “allergic salute”, a gesture that
is performed by wiping the nose vertically with the palm. The lips are often cracked and chapped
because of chronic open mouth breathing which is the result of nasal
obstruction. The skin of the anterior
cheeks often reveals a rash resembling eczema, often seen with food allergic
children. Examination of the oropharynx
reveal erythema along the faucial arches, edema of the uvula, and hypertrophy in
Waldeyer’s ring. Collections of lymphoid
tissue along the posterior pharyngeal wall is also a prominent finding in
allergic children. Eustachian tube
dysfunction and subsequent otitis media with effusion is common in children
with allergy. Thus, any child requiring
more than one set of tubes should raise the suspicion of allergy as a potential
etiology. Chronic cough and bronchial
asthma are quite common. Indeed, over
85% of these children are allergic to the dust mite (Cook). Feeding irregularities, colic, bloating, and
nocturnal emesis are also potential signs of childhood allergy. Finally, atopic dermatitis, urticaria, and
eczema are also presenting signs of an allergic diathesis in the child.
Diagnostic tests for allergy are
performed to confirm the diagnosis that has been made clinically. Because adverse reactions to food in
children is common, a detailed history about the child’s eating habits helps
direct the diagnostic effort. One of
the most helpful tools is a 2-4 week food diary. Analysis may provide insight into potentially allergy inciting
food products. A double blind placebo
controlled food challenge is considered by many to be the gold standard in the
diagnosis of food hypersensitivity, however the open feeding challenge test with
natural food produces reliable results and is quite effective in the office
setting (Cook).
The use of in vitro diagnostic
testing is helpful in diagnosing inhalant allergies. Radioallergosorbent tests exhibit excellent sensitivity and
specificity for inhalant allergies however their use for food allergies is less
defined. The analysis of nasal smears
can be helpful in confirming the diagnosis of allergy as one may recover
numerous eosinophils in the nasal secretion of the allergic patient. In vivo diagnostic testing via skin testing
remains an excellent confirmatory test for allergy that has a high sensitivity
and specificity.
Treatment for allergic disease
should be prophylactic and regular. The
aim of therapy is to reduce or eliminate the inflammation that is the result of
inflammatory mediators. Theoretically,
avoidance of the antigen should be the only therapy required, however avoidance
of aeroantigens is impractical.
Removing stuffed animals from the bedroom, encasing pillows and
mattresses in allergy proof materials, vacuuming frequently, and using a
high-efficiency particulate air filter system may help decrease the antigenic
load to the child within the house.
Pets should not be allowed in the house of allergic patients and the
rooms of the house should be kept air conditioned with the humidity ideally
between 35%-40%.
Pharmacotherapy via the use of
antihistamines, topical nasal steroids, and mast cell stabilizers remain
important tools in the treatment of allergic disease. The use of certrizine in children as young as two years of age is
quite effective as well as convenient.
Other new antihistamines have proven equally as efficacious. Clemastine (Tavist) may be used in infants
under two years of age (Cook). Cromolyn
can be used safely in children of all ages and is typically used
topically. Topical steroids inhibit
both the early and late stages of inflammation and, as a result, are
exceedingly useful for allergic rhinitis.
Fluticasone has been used safely in children as young as four years of
age showing excellent efficacy and a high therapeutic index. Studies evaluating the safety and efficacy
of nasal steroids in children under the age of four are currently being
performed.
Immunotherapy is also a valuable
tool in the treatment of pediatric allergy and may prevent long-term sequelae
in asthmatic patients as well (Cook).
Immunotherapy is generally applied after allergen avoidance fails and
the patient’s symptoms are not well controlled with pharmacotherapy.
The
Role of Asthma in Rhinosinusitis
Asthma patients probably represent
the largest group of individuals in whom pediatric rhinosinusitis can have a
negative impact on overall health (Manning).
The incidence of asthma has increased dramatically over the last two
decades which has created a large cohort of individuals on high dose steroids
and bronchodilators. Upper respiratory
infections, including rhinosinusitis, may be more prevalent in these
individuals and has been postulated as a trigger for outbreaks of reactive
airway disease. While the association
of asthma and rhinosinusitis has been discussed, the cause-effect relationship
has not been established. The premise
of this association is that sinus mucosal disease effects bronchial
hyperreactivity. Four theories have
been proposed to explain this link. First,
rhinosinusitis causes dripping of mediators into the trachea, a situation that
worsens asthma. Second, nasal-sinus
reflexes in rhinosinusitis exacerbate asthma. Third, cough in patients with
asthma is a major symptom of rhinosinusitis and fourth, antibiotic and surgical
treatment of rhinosinusitis resolves exacerbations of asthma (Ott).
Current evidence refutes the theory
that aspiration of mediators or nasal-sinus reflexes cause rhinosinusitis in
patients with asthma. A recent study
found an absence of pulmonary aspiration of a radionuclide that was previously
placed in the sinuses of patients with asthma and rhinosinusitis. Other studies of nasal challenges with
histamine and methacholine in patients with asthma revealed no increase in
resistance of the lower airway (Ott). A
factor that does support the association of asthma and rhinosinusitis is the
frequent occurrence of cough patients with these diseases. One theory postulates that cough receptors
are present in the paranasal sinuses and the tracheobronchial tree. The literature supports the concept that
cough is the predominant manifestation of cough-variant asthma however there
are a lack of studies separating whether these patients are coughing as result
of the sinus or pulmonary disease processes.
Investigators have suggested that antibiotic
treatment of rhinosinusitis in patients with asthma resolves the symptoms of
asthma. Rachelefsky et al noted a
strong correlation between resolution of sinus disease and the ability to
discontinue bronchdilator therapy in a group of 48 children with rhinosinusitis
and asthma. Friedman et al studied 7
children with poorly controlled asthma and rhinosinusitis and demonstrated
improvements in pulmonary function tests with resolution of the rhinosinusitis
in 5 of the patients. Oliveira et al
demonstrated that bronchial hyperresponsiveness could be improved in children
treated for their concomitant rhinosinusitis.
Finally, numerous studies in adults and children have documented the
effectiveness of controlling asthmatic symptoms and reducing the need for
asthma medications in patients undergoing sinus surgery (Park).
These results certainly support the fact that
aggressive treatment of rhinosinusitis is warranted in patients with difficult
to control asthma. Additional research
needs to be performed to further answer whether sinus disease exacerbates
underlying asthma or is an etiologic factor in the development of asthma in
selected patients.
Conclusion
Pediatric rhinosinusitis remains a
diagnostic dilemma in many children.
Newer technology has helped us diagnosis and allowed us to treat
patients that were previously inadequately or not treated at all. While the management of pediatric
rhinosinusitis is primarily aggressive medical therapy, surgical management is
appropriate for certain patients.
Further inquiry is required to expand our understanding of the etiology
and natural history of sinus disease in children with additional insight into
defining the indications for specific forms of medical and surgical therapy.
Bibliography
Bothwell,
MR, Parsons, DS, Talbot, A, et al.
Outcome of reflux therapy on pediatric chronic sinusitis. Otolaryngology-Head and Neck Surgery, Sept
1999. 121(3): 255-262.
Clement,
PAR, Bluestone, CD, Gordts, F, et al. Management of Rhinosinusitis in Children, Jan 1998. 124:31-34.
Cook,
PR, Nishioka, GJ. Allergic
Rhinosinusitis in the Pediatric Population.
Otolaryngologic Clinics of North America, Feb 1996. 29(1): 39-55.
Friedman,
R, Ackerman, M, Wald, E, et al. Asthma
and bacterial sinusitis in children.
Journal of Allergy and Clinical Immunology, 1984. 74: 185-189.
Gurucharri,
MJ, Lazar, RH, Younis, RT. Current
Management and Treatment of Complications of Sinusitis in Children. Ear Nose and Throat Journal, 1990. 70(2):
107-112.
Hopp,
R, Cooperstock, M. Medical Management
of Sinusitis in Pediatric Patients.
Current Problems in Pediatrics, May/June 1997. 178-186.
Kennedy,
KL. Sinusitis in Children. Dept. of Otolaryngology Grand Rounds. Nov 1, 1995.
Lusk,
RP. Pediatric Rhinosinusitis. In
Bailey, BJ, et al, eds. Head and Neck
Surgery-Otolaryngology. 1(84): 1187-1202.
Lusk,
RP, Stankiewicz, JA. Pediatric
Rhinosinusitis. Otolaryngology-Head and
Neck Surgery, Sept 1997. 117(3):
S53-S57.
Manning,
SC. Pediatric Sinusitis. Otolaryngology Clinics of North America, Aug
1993. 26(4): 623-655.
Manning,
SC. Surgical Management of Sinus
Disease in Children. Annals of Otology,
Rhinology, and Laryngology, 1992. 101:
42-45.
McAlister,
WH, Lusk, RP, Muntz, HR. Comparison of
plain radiographs and coronal CT scans in infants and children with recurrent
sinusitis. American Journal of
Roentgenology, 1989. 153: 1259-1264.
Miller,
AJ, Amedee, RG. Sinus Anatomy and
Function. In Bailey, BJ, et al,
eds. Otolaryngology-Head and Neck
Surgery. 1(31): 413-421.
O’Brien,
KL, Dowell, SF., Schwartz, B. Acute
Sinusitis-Principles of Judicious Use of Antimicrobial Agents. Pediatrics, 1998. Supplement: 174-177.
Oliveira,
CAA, Sole, D, Naspitz, CK, et al.
Improvement of bronchial hyperresponsiveness in asthmatic children
treated for concomitant sinusitis.
Annals of Allergy, Asthma, and Immunology, July 1997. 79: 70-74.
Ott,
NL, O’Connell, EJ, Hoffman, AD, et al.
Childhood Sinusitis. Mayo
Clinics Proceedings, 1991. 66: 1238-1247.
Park,
AH, Lau, J, Stankiewicz, J, et al. The
Role of Functional Endoscopic Sinus Surgery in Asthmatic Patients. The Journal of Otolaryngology, 1998. 27(5): 275-280.
Rachelefsky,
GS, Katz, RM, Siegel, SC. Chronic Sinus
Disease with Associated Reactive Airway Disease in Children. Pediatrics, 1984. 73: 526-529.
Wald,
ER. Sinusitis in Infants and
Children. Annals of Otology, Rhinology,
and Laryngology, Jan 1992. 101(1):
37-41.
Wald,
ER. Sinusitis. Pediatric Annals, Dec 1998. 27(12): 811-817.
Younis,
RT, Lazar, RH. The Approach to Acute
and Chronic Sinusitis in Children. Ear,
Nose, and Throat Journal. 70(1): 35-39.
Zacharisen,
MC, Kelly, KJ. Allergic and Infectious
Pediatric Sinusitis. Pediatric Annals,
Nov 1998, 27(11): 759-766.
Posted 8/4/2000