46  Acute Rhinosinusitis:

Pathogenesis, Treatment,
and Complications
Michael S. Benninger  |  Janalee K. Stokken

Key Points
■ Understanding the pathogenesis of rhinosinusitis depends on defining the specific types of
rhinosinusitis.
■ Acute bacterial rhinosinusitis (ABRS), chronic rhinosinusitis (CRS), and acute exacerbation of

chronic rhinosinusitis (AECRS) are three distinct entities.
■ A number of environmental and host factors predispose to the development of rhinosinusitis; these
include allergy, infection, and environmental exposures.
■ Acute rhinosinusitis is usually the result of a viral infection, whereas ABRS occurs primarily with

Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus.
■ The treatment of acute rhinosinusitis has changed with the emergence of resistance to the
common pathogens and the routine use of S. pneumoniae and H. influenzae immunizations.
■ After thorough reviews of the literature, multiple guidelines have been proposed that now suggest

amoxicillin with clavulanic acid as a first-line treatment; this is due to the growing emergence of
β-lactamase–producing organisms, particularly H. influenzae. High-dose amoxicillin-clavulanate is
recommended in individuals or environments where levels of S. pneumoniae resistance are high.
■ AECRS is a sudden worsening of symptoms in a patient with CRS. It is often associated with an
increase in the bacteria prominent in the exacerbation. Although an increase is seen in the
organisms typically associated with ABRS—S. pneumoniae, H. influenzae, M. catarrhalis, and
Staphylococcus aureus—a high percentage of anaerobic organisms are also identified.

DEFINITIONS OF ACUTE AND
CHRONIC RHINOSINUSITIS
In order to understand the pathogenesis and pathophysiology
of rhinosinusitis, it is important to realize that different types
of rhinosinusitis have been defined, and the inciting mecha-
nism may vary dramatically among the different subtypes.
Although sinusitis is the term commonly used for any inflam-
mation or infection of sinuses, this term has largely been
replaced by rhinosinusitis, because the nose is almost always
involved with the infection or inflammation at the same time
as the sinuses.1 Because many potential factors can contribute
to rhinosinusitis, some debate has ensued concerning the exact
definition. In general terms, rhinosinusitis is defined as “a group
of disorders characterized by inflammation of the mucosa of
the paranasal sinuses.”2 In 1997, the Rhinosinusitis Task Force
of the American Academy of Otolaryngology–Head and Neck
Surgery3 developed a now well-accepted classification of rhino-
sinusitis, and this was reported by Lanza and Kennedy.1 This
classification relies on the identification of symptoms to make
a diagnosis. The symptoms are broken into major symptoms—
purulent nasal drainage, nasal congestion, facial pressure or
pain, decreased smell, and posterior purulent drainage—and
various minor symptoms.1 When a patient describes two major
criteria or one major and two minor criteria, rhinosinusitis can
be diagnosed (Table 46-1). The classification of rhinosinusitis
types was based primarily on time frames from the onset of
symptoms. More recently, a stricter division for chronic rhino-
sinusitis (CRS) has been described based on endoscopic find-
ings. These include CRS with nasal polyps (CRSwNP) and
without nasal polyps (CRSsNP). The 2012 European position
paper on rhinosinusitis and nasal polyps (EPOS 2012)4 further
defines the disease process for both the adult and pediatric
populations (Box 46-1).
An inflammatory response is an expected sequela of an
infectious process. Sinonasal inflammation can result from a
variety of elements that result in sinus ostia obstruction and
predispose patients to infection. Many factors have been
described that play a role in the development of acute bacterial
rhinosinusitis (ABRS).1,4-6 These include factors related to the
host: genetic factors such as immotile cilia syndrome or cystic
fibrosis; certain systemic diseases or medical treatments that
predispose individuals to infections; neoplasms; and allergic or
immune disorders. Although anatomic abnormalities such as
large septal spurs and large paradoxic turbinates have been
suggested to be associated with rhinosinusitis, it is not currently

724

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 46  |  ACUTE RHINOSINUSITIS: PATHOGENESIS, TREATMENT, AND COMPLICATIONS 725
TABLE 46-1.  Rhinosinusitis Symptoms
Major Minor
Facial pain/pressure Headache
Facial congestion/fullness Fever (nonacute)
Nasal obstruction/blockage Halitosis
Nasal discharge/purulence, Fatigue
discolored posterior drainage Dental pain
Hyposmia/anosmia Cough
Purulence on nasal exam Ear pain, pressure,
Fever (acute rhinosinusitis only) and/or fullness
Diagnosis of rhinosinusitis requires two major or one major and two
minor symptoms.
clear whether a relation exists. Rhinosinusitis may also develop
in relationship to environmental factors that include bacterial,
viral, or fungal infections or inflammation that occurs second-
ary to fungal or bacterial colonization2,7; trauma; primary or
secondary tobacco smoke exposure8; chronic or acute irritants
or noxious chemicals; or iatrogenic factors such as surgery,
medications, nasal packing, or nasogastric tube placement.9
Evidence shows that individuals with allergic rhinitis have a
higher incidence of developing both acute and chronic rhino-
sinusitis, and an association of ABRS with asthma has also been
suggested, although this may also relate to the presence of
allergic rhinitis.6-8
The distinctions between acute rhinosinusitis (ARS), recur-
rent acute rhinosinusitis (RARS), subacute rhinosinusitis
(SARS), and CRS and acute exacerbation of CRS (AECRS) are
based on the temporal differences in the presentation and in
some cases on the clinical presentation. Each of these subcat-
egories may be associated with different pathophysiologic pro-
cesses, and the predisposition to their development may vary
from patient to patient. Given these differing etiologies, the
pathogenesis will be described based on this classification.
ACUTE RHINOSINUSITIS
Acute rhinosinusitis (ARS) is a very common disorder that at
one time or another impacts most people. From a temporal
standpoint, acute rhinosinusitis lasts for up to 4 weeks1 and
results from interactions between a predisposing condition—
such as allergic rhinitis, immune deficiency, or inflammatory
Box 46-1.  CLINICAL DEFINITION OF RHINOSINUSITIS
IN ADULTS
Inflammation of the nose and the paranasal sinuses characterized by
two or more symptoms:
• Either nasal blockage/obstruction/congestion or anterior/posterior
nasal discharge:
• ± Facial pain/pressure
• ± Reduction or loss of smell (± cough in children)
And either:
• Endoscopic signs of:
• Nasal polyps, and/or
• Mucopurulent discharge primarily from middle meatus and/or
• Edema/mucosal obstruction primarily in the middle meatus
And/or:
• CT changes that include:
• Mucosal changes within the ostiomeatal complex and/or the
sinuses
From Fokkens W, Lund V, Meullo J, et al: The European Position Paper on
rhinosinusitis and nasal polyps. Rhinology 2012;23:1-299.
CT, computed tomography.
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response from a viral infection. The inflammation then leads
to edema and obstruction of the sinus ostium, the normal 
ventilation and drainage of the sinus is then impaired, and a
secondary bacterial infection ensues (Fig. 46-1).
Viruses account for the majority of cases of ARS and include
rhinovirus, coronavirus, influenza, respiratory syncytial virus
(RSV), and parainfluenza. Attempts have been made at estimat-
ing the prevalence of ARS. It is estimated that children have
between six and eight upper respiratory tract infections (URTIs)
per year, whereas adults average two to three.9 If an assumption
is made that 90% of patients with colds have sinusitis (bacterial
or viral), it can be estimated that in the United States, more
than 1 billion cases of viral and bacterial rhinosinusitis occur
annually (4 episodes per person × 260 million people).10
Acute bacterial rhinosinusitis (ABRS) has been defined as
sudden in onset and with duration of less than 4 weeks.1 Because
most cases of rhinosinusitis are from a self-limited viral infec-
tion, and bacterial infections usually occur following a viral
URTI, ABRS is diagnosed after at least 7 to 10 days of symptoms
or in patients whose symptoms worsen after 5 to 7 days.1,4,10 ARS
becomes a bacterial infection in only about 0.5% to 2% of cases,
a distinction endorsed in most of the guideline development
for the treatment of ABRS.5 The diagnosis may be more diffi-
cult in children, because they often have difficulty describing
their symptoms.
In ABRS, Streptococcus pneumoniae (20% to 45%), Haemophilus
influenzae (20% to 43%), and Moraxella catarrhalis (14% to
28%) are the predominant organism.4,11,12 Although previously
thought to be a contaminant, Staphylococcus aureus is now being
considered a real pathogen in ABRS and accounts for 8% to
11% of cases.13 Methicillin-resistant S. aureus (MRSA).14,15
Because M. catarrhalis is largely a self-limited pathogen, and
because MRSA is becoming a bigger health care issue, S. aureus
may be more important to treat, and it is also well recognized
in both CRS and in AECRS.10,11,16
ABRS is a self-limited disease in many cases. Evaluation of
placebo-controlled antibiotic trials has shown a high self-
resolution rate.4,10,17  M. catarrhalis is most likely to resolve without
antibiotic treatment and, to a lesser extent, so is H. influenzae;
Streptococcus pneumoniae is least likely to resolve without treat-
ment, therefore, it can be important to identify which patients
FIGURE 46-1.  Sagittal computed tomography scan from a patient with
acute bacterial rhinosinusitis and forehead swelling reveals dehiscence of the
anterior table of the frontal sinus and opacification of the frontal, ethmoid,
and sphenoid sinuses.
726 PART IV  |  SINUS, RHINOLOGY, AND ALLERGY/IMMUNOLOGY
have which organism. The most reliable way is to obtain sinusitis
cultures, and a maxillary sinus tap is the traditional method of
obtaining these; however, the invasiveness of this test and the
advancement of endoscopically guided selective middle meatal
cultures have resulted in a shift to this latter method in clinical
practice.16,18 An evidence-based review has revealed that endo-
scopic middle meatal cultures are as sensitive and specific as
those obtained by maxillary sinus taps.18 In clinical practice,
however, cultures are often only obtained when treatment has
failed. The severity of the symptoms and radiographic findings
may help to identify different pathogens, in that patients
infected with S. pneumoniae have been found to have more
significant symptoms and worse radiographic findings than
those infected with H. influenzae.11
With the widespread utilization of pneumococcal 7-valent
conjugate vaccination, an apparent shift has occurred in the
overall distribution of pathogens in ABRS. In a recent study
that assessed ABRS pathogenesis, the proportions of the recov-
ery of pathogens obtained by endoscopic-directed cultures in
adults with acute maxillary sinusitis were compared between
the 4 years prior to and the 5 years after introduction of the
pneumococcal conjugate vaccine (PCV). H. influenzae increased
from 36% to become the most common pathogen at 43%. At
the same time, S. pneumoniae was found to decrease, from being
the most common pathogen at 46% of isolates to 35% after the
use of the vaccine; but an increase was also seen in the cases
caused by M. catarrhalis and Staphylococcus aureus.14 In a similar
study, nasopharyngeal cultures were obtained in children with
acute maxillary sinusitis before and after widespread use of
PCV. Streptococcus pneumoniae decreased from 43% of isolates to
25%, and H. influenzae increased from 35% to 41%; M. catarrha-
lis remained stable at 13% to 14%. Streptoccoccus pyogenes
increased from 7% to 12%, and Staphylococcus aureus increased
from 4% to 8%.12
Following widespread pneumococcal vaccination, an appar-
ent change was observed in the serotypes of Streptococcus pneu-
moniae responsible, not only for ABRS but also for acute otitis
media (AOM), with an increase in serotypes not found in the
vaccine.15,19,20 However, some speculate that this serotype
replacement may reduce the long-term efficacy of the pneumo-
coccal 7-valent conjugate vaccine.20 Multiple studies have shown
a reduction in both the nonsusceptible and high-level resistant
strains of S. pneumoniae cultured in AOM and, to a lesser extent,
in ABRS.21-25 Whitney and colleagues22 showed a reduction of
35% in strains not susceptible to penicillin. High-level resis-
tance of S. pneumoniae to penicillin also appears to have dropped
and was reported to have decreased from 15% to 5%.24 An
associated increase has been reported in the β-lactamase–
producing strains of H. influenzae.25 Although the data related
to the shift in pathogens are less well supported in ABRS than
in AOM, a clear shift has occurred in the pathogens associated
with both diseases, and this shift is parallel between the two
groups. This is not unexpected, because the pathogenic organ-
isms are similar for ABRS and AOM, and the shift in the micro-
biology of ABRS has been suggested to have occurred because
of the involvement of the same pathogens in AOM and ABRS.26
The mechanism by which the inflammation of a viral URTI
can lead to ABRS has been suggested in a number of reports.5,27
As mentioned above, ARS typically develops in conjunction
with an acute viral URTI. The propensity to develop a viral
URTI may occur more commonly in predisposed individuals.
The viral infection can result in swelling of the mucosa of the
nose or sinuses, and the resultant swelling and engorgement
can result in occlusion or obstruction of the sinus ostia. A
reduction in oxygen tension occurs, which can reduce muco-
ciliary transport and transudation of fluid into the sinuses.6 The
inflammation also results in changes in the mucus, such that it
becomes more viscous, and alterations in cilia beat frequency
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often occurs. These changes in the nasal sinus environment
lead to reduced clearance, stasis of the mucus, and bacterial
colonization. If the sinuses remain obstructed, or the mucocili-
ary transport system does not return to normal, a bacterial
infection can ensue. The ability of the body to respond to the
viral challenge and reduce the inflammation may, in part,
determine whether a secondary bacterial infection occurs.
The role of allergies in the development of rhinosinusitis
has been strongly suggested but not proven.6-8 Antigen-antibody
reactions result in an immunoglobulin E (IgE)–mediated
hypersensitivity that results in mast cell degranulation and the
release of histamine and other mediators of inflammation.
These mediators cause changes in vascular permeability, desta-
bilization of lysosomal membranes, and other reactions that
produce inflammation, mucosal swelling, and ostia obstruc-
tion.6 Although infectious agents can be the primary cause of
sinus inflammation, they may also represent a secondary infec-
tion. The type and magnitude of the reaction may be related
to the host response and how it relates to the disease process
and progression. Limited studies have been done on the effects
of topical nasal steroids, allergen avoidance, or immunotherapy
in preventing recurrent ABRS.
Recurrent acute rhinosinusitis (RARS) is defined by four or
more episodes per year, with each lasting longer than 7 to 10
days, and an absence of intervening signs or symptoms that
would suggest an ongoing or chronic rhinosinusitis.1 Although
recurrent viral respiratory tract infections are common, in
general, it is rare for someone to develop true recurrent episodes
of ABRS that meet the criteria for a diagnosis of recurrent ABRS.
When they do, it is expected that the bacteriology and patho-
physiology would be similar to individual episodes of ABRS.
Although ABRS is a common disorder, the criteria used to
make the diagnosis are fairly well established, and the treat-
ment is relatively straightforward, the definitions and subse-
quent treatment for CRS have been particularly difficult to
establish as a result of the wide variety of potential contribut-
ing factors that have been associated with CRS. Although the
role of bacteria and antibiotic therapy is well established in
ABRS, the role of bacteria in CRS is not well supported; 
therefore the use of symptoms to try to define CRS is not as
effective as in ABRS.2,28
DIAGNOSIS
The diagnosis of ABRS is based upon a set of clinical criteria
that are often difficult to distinguish from those of a viral URTI
or viral rhinosinusitis. Available diagnostic testing methods are
cumbersome and are rarely used in clinical practice. The diag-
nosis of ABRS is usually based on clinical presentation, such as
symptoms of a viral URTI that persist for more than 10 days or
that have worsened after 5 to 7 days.29 Common signs and
symptoms of ABRS include nasal and/or postnasal drainage,
nasal congestion, facial pressure/pain, hyposmia or anosmia,
fever, cough, fatigue, maxillary dental pain, and ear pressure
and/or fullness. The most recent guidelines from the Infec-
tious Disease Society of America (IDSA) acknowledge that diag-
nosis can be made on clinical grounds and physical examination.
Diagnostic tests, such as radiographs, computed tomography
(CT) scans, and magnetic resonance imaging (MRI) provide
little if any additional information over that provided by the
clinical presentation, and therefore they do not advocate their
routine use in the diagnosis of ABRS, except when complica-
tions are suspected.30 These observations and recommenda-
tions are identical to those of the American Academy of
Pediatrics (AAP),31 which published guidelines for the manage-
ment of pediatric rhinosinusitis in 2001.
Sinus aspirate and culture, considered the gold standard in
diagnosing ABRS, is an invasive, potentially painful procedure
 46  |  ACUTE RHINOSINUSITIS: PATHOGENESIS, TREATMENT, AND COMPLICATIONS 727
that is time consuming and requires the expertise of an otolar-
yngologist. Consequently, it is not used in the primary care
setting, where a significant proportion of patients with ABRS
receive care. It is more appropriately used in diagnosing
patients whose symptoms of ABRS persist despite appropriate
antibiotic therapy—a population more likely to seek treatment
from a specialist.29,31 Recent data strongly support the use of
selective endoscopic middle meatal cultures as an alternative to
maxillary sinus taps in those patients in whom culture is indi-
cated. This would reduce the morbidity to the patient and
would allow for screening and surveillance where necessary.18
TREATMENT
Because most cases of ARS are caused by viruses and are there-
fore self-limited, treatment is not needed, other than symp-
tomatic management. In addition, even in the case of ABRS,
most cases will be self-limited and will resolve even without
treatment. This, along with the recognition that URTIs will
typically not be bacterial until 7 to 14 days after onset, has led
to growing conservatism in antibiotic treatment. The recent
IDSA guidelines recommend a diagnosis and antibiotic treat-
ment if there is “onset with ‘persistent’ symptoms or signs
compatible with acute rhinosinusitis lasting for 10 days or
longer without any evidence of clinical improvement; onset
with ‘severe’ symptoms or signs of high fever 39°C or higher
and purulent nasal discharge or facial pain lasting for at least
3 to 4 days at the beginning of illness; or onset with ‘worsen-
ing’ symptoms or signs such as new onset of fever, headache,
or increase in nasal discharge following typical viral [upper
respiratory infection] symptoms that lasted 5 to 6 days and
were improving (i.e., ‘double sickening’).”30 The IDSA also
suggests that antibiotics should be begun once these criteria
are met.30
The shift in pathology, both in causative bacteria and in
antibiotic resistance patterns related to overuse of antibiotics,
along with the introduction of PCV into routine clinical use  third-generation cephalosporin (cefixime or cefpodoxime)
in 2000 have altered the traditional antibiotic treatment of  and clindamycin can be used in children with ABRS who have
ABRS. Several additional factors that have a significant impact
on the pathology of ABRS and selection of an appropriate
antibiotic are essential in formulating a comprehensive treat-
ment plan. Pharmacokinetics and pharmacodynamics are used
to assess the appropriateness of an antibiotic for the treatment
of respiratory tract infections and the mechanisms used to
overcome antibiotic resistance among common respiratory
tract pathogens.
The selection of an appropriate antibiotic for the treatment
of ABRS is based on a number of considerations that include
severity of disease, most likely pathogen, likelihood that the
infecting pathogen is resistant to one or more antibiotics, and
recent antibiotic use. These considerations combined with the
diagnostic uncertainty of ABRS present a very real challenge to
clinicians who treat patients with ABRS. The goals of treatment
are to 1) eradicate any causative pathogens from the paranasal
sinuses, 2) decrease the duration of symptoms, 3) prevent com-
plications and progression to CRS, and 4) bring the sinuses
back to normal health.29 It is important to achieve these goals
using appropriate antibiotics, in appropriate patients, for an
appropriate duration of time, the combination of which is
expected to preserve the clinical utility of available antibiotics
and to prevent the continuing spread of antibiotic resistance.
A number of treatment guidelines for the management of rhi-
nosinusitis, and an even greater number of reviews of these
guidelines, have been published to assist clinicians in the selec-
tion of an appropriate antibiotic. Over time, this antibiotic
resistance has led to changes in the appropriate recommenda-
tions for antibiotics. Amoxicillin, cephalosporins, and macro-
lides have traditionally been the first-line treatment for ABRS,
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although newer recommendations have suggested that this tra-
ditional approach should be modified.
The recent IDSA recommendations now state that
amoxicillin-clavulanate, rather than amoxicillin alone, is rec-
ommended as empiric antimicrobial therapy for ABRS in both
adults and children and that “high-dose” amoxicillin-clavulanate
is recommended for children and adults with ABRS who 1) are
from geographic regions with high endemic rates of penicillin-
nonsusceptible Streptococcus pneumoniae, 2) have severe infec-
tion, 3) were recently hospitalized or used antibiotics within the
past month, or 4) are immunocompromised.30 Macrolides
(clarithromycin and azithromycin) are not recommended
for empiric therapy because of high rates of resistance with 
S. pneumoniae (~30%), and trimethoprim-sulfamethoxazole is
not recommended for empiric therapy because of high rates of
resistance among both S. pneumoniae and H. influenzae (~30%
to 40%). A good alternative regimen to amoxicillin-clavulanate
for initial empiric antimicrobial therapy of ABRS is doxycy-
cline in adults (not recommended in children) because it
remains highly active against respiratory pathogens and has
excellent pharmacokinetic and pharmacodynamic properties.30
Because rates of resistance with S. pneumoniae vary, second- and
third-generation oral cephalosporins are not currently recom-
mended for empiric monotherapy of ABRS; however, for
patients from geographic regions with high endemic rates of
penicillin-nonsusceptible S. pneumoniae, combination therapy
that includes clindamycin and a third-generation cephalospo-
rin (cefixime or cefpodoxime) is recommended.30
In cases of type I hypersensitivity allergy to penicillin or
suspected allergy, doxycycline or a respiratory fluoroquinolone
(levofloxacin or moxifloxacin) may be recommended as alter-
native agents for empiric initial antimicrobial therapy in adults.
In children, levofloxacin is recommended when there is a
history of type I hypersensitivity to penicillin. Growing evidence
suggests that no cross allergenicity exists between penicillin and
the third-generation cephalosporins,32 so a combination of a
a history of non–type I hypersensitivity to penicillin.30 Although
Staphylococcus aureus—including MRSA—is a potential patho-
gen in ABRS, based on current data, routine antimicrobial
coverage for S. aureus or MRSA during initial empiric therapy
of ABRS is not recommended.30 This may be initiated with
failure of initial treatment or with culture-directed manage-
ment. Treatment should be for 5 to 7 days in adults and for 10
to 14 days in children based on current literature.30
A number of other treatment options may be considered for
ABRS. Probably the most significant is the recognition that the
use of intranasal steroid (INS) sprays may reduce both the
length of time the patient is symptomatic and the intensity of
the symptoms.18 Based on this information, it is not unreason-
able to begin an INS with ABRS, particularly in patients with
more significant symptoms.30,33 Saline irrigations or nasal
decongestants may help to improve symptoms, although they
probably play a minor role in the treatment of the infection.
Oral decongestants are not recommended given their poor
evidence of efficacy and side-effect profile.30 Although antihis-
tamines may be beneficial in allergic patients, they have little
to no efficacy in the nonallergic patient with ABRS. The drying
effects of the sedating antihistamines may even be counterpro-
ductive in disease management.
If symptoms worsen after 72 hours of initial empiric antimi-
crobial therapy, or they fail to improve despite 3 to 5 days of
initial empiric antimicrobial therapy, it is reasonable to con-
sider a change in medications. If the patient is already on high-
dose amoxicillin-clavulanate or a fluoroquinolone, and no
improvement has been seen after 72 hours, it is reasonable to
consider that the symptoms are not secondary to ABRS, and
728 PART IV  |  SINUS, RHINOLOGY, AND ALLERGY/IMMUNOLOGY
the physician must consider other etiologies such as allergy,
CRS, or facial pain disorder. If symptoms worsen, an evaluation
by an otolaryngologist is indicated.
COMPLICATIONS
Most episodes of ABRS respond to appropriate medical treat-
ment. However, ARS can become complicated by extension to
an adjacent structure. These infections can have devastating
outcomes, including blindness, neurologic morbidity, and
death. These complications are rare and are estimated to occur
once in every 95,000 pediatric hospital admissions.34 The loca-
tion and timing of complications directly relate to the develop-
ment of the paranasal sinuses and their proximity to the  This can be a complication of both acute and chronic rhinosi-
orbit and brain and are categorized as orbital, intracranial, and
those involving the bone of the sinus wall. Recognizing the
signs and symptoms early and initiating medical and/or surgi-
cal treatment is important to achieve good outcomes. However,
even with appropriate treatment death is a potential risk of
severe infections, particularly in the setting of cavernous sinus
thrombosis.35
The anatomy and development of the paranasal sinuses is
important in understanding the pathogenesis of this disease
process. Complications of ABRS primarily involve the orbit  congestion, rhinorrhea, facial pressure, sore throat, postnasal
and anterior cranial fossa because of their close proximity to
the ethmoid and frontal sinuses.36-39 They occur by one of two
mechanisms: either loss of an anatomic barrier or hematologic
spread. The lamina papyracea is the lateral border of the maxil-
lary, ethmoid, and frontal recess at the orbit. A dehiscence in
the lamina can be congenital or may result from osteitic bone
destruction, which can often be visualized radiologically. Hema-
tologic spread occurs through the valveless ophthalmic venous
system that connects the facial veins to the cavernous sinuses.
Spread can also occur through thrombophlebitis of the vessels
that transverse the bony boundaries.
The timing of the development of the paranasal sinuses is
also a factor in ABRS complications. Patients with orbital com-
plications tend to be younger than 7 years, whereas intracranial
complications are more frequently observed in adolescent  Many complicated ABS infections are polymicrobial.36,50,51
and teenage patients.40 The development of the ethmoid and
maxillary sinuses starts in utero. The maxillary sinuses have a
rapid phase of growth until age 4 years and continue to expand
into the teenage years. The ethmoid sinuses are the most devel-
oped sinuses at the time of birth, which contributes to the
propensity of orbital complications in younger children. The
ethmoid sinuses also gradually increase in volume into the
teenage years. The frontal sinuses first become visible radio-
graphically around age 5 years and increase in size through
puberty—hence the higher rate of intracranial complications
in adolescents. The sphenoid sinuses are the last to develop at
around age 6 years, but are rarely involved in any complications
of acute rhinosinusitis.
The orbital septum is an important anatomic structure to
understand in the pathogenesis of orbital complications of rhi-
nosinusitis. It is an extension of periosteum that is the anterior
border of the orbit. It extends from the orbital rim into the
upper and lower eyelids at the levator aponeurosis superiorly
and the tarsal plate inferiorly. When the eyes are closed, the
orbital septum and tarsal plates cover the entire orbital opening.
The orbital septum distinguishes a boundary between preseptal
and postseptal infections.
Orbital complications of rhinosinusitis were first classified
in the 1970s by Chandler and colleagues.41 This classification
remains the standard for describing orbital complications
today. Group I complications include patients with preseptal
cellulitis or inflammatory edema superficial to the tarsal plates
and orbital septum. Group II patients have orbital or postseptal
cellulitis in which there is edema of the orbital contents without
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a discrete abscess. Group III patients have a subperiosteal
abscess adjacent to the lamina papyracea and under the peri-
osteum of the medial orbit. Group IV patients have an orbital
abscess or a discrete collection within the orbital tissue. Lastly,
a group V complication is when a patient has a cavernous sinus
thrombosis.
Intracranial complications do not have a classification system
but include any infection involving the central nervous system,
particularly the anterior cranial fossa. This includes epidural or
subdural abscess or empyema, meningitis, intracerebral abscess,
and cavernous and/or sagittal sinus thrombosis.42-45
Potts’s puffy tumor is an osteomyelitis of the frontal bone with
an adjacent subperiosteal collection on the patient’s forehead.
nusitis or trauma to the anterior table of the frontal sinus. It is
often associated with other intracranial complications.
Patients with complications of ABRS are not likely to have a
history of nasal steroid use or seasonal allergies, and they often
do not have a predictable history of repeated infection. Inci-
dence is higher in males than in females, and the disease
process is more commonly seen in the pediatric population.46
Patients present with a history of symptoms similar to an upper
respiratory infection. Common symptoms include cough, nasal
drainage, anosmia, fever, otalgia, and fatigue. The diagnosis of
ABRS may have been made, and some patients present after
initiation of oral antibiotics. Patients with intraorbital complica-
tions present with periorbital edema or erythema, pain, and
possibly visual changes. Patients with intracranial complications
typically present with a history of upper respiratory infection,
fever, and headache. Altered mental status, seizures, meningis-
mus, and focal neurologic deficits are more concerning signs
of intracranial complications. The symptoms and physical exam
findings are detailed in Table 46-2.
The most frequent organisms in ABS predominantly include
S. pneumoniae, H. influenzae, and M. catarrhalis.14,47-49 Compli-
cated sinusitis isolates can include these three organisms but
commonly present with Streptococcus anginosis (formerly S. milleri).
Goytia and colleagues52 reported a 75% rate of polymicrobial
cultures. Olwoch51 reviewed the cultures of 163 patients with
complicated sinusitis and found that the most frequently iso-
lated organisms included S. anginosis (18.5%), S. aureus (12.4%),
β-hemolytic streptococci (10.3%), coagulase-negative staphylo-
cocci (8.6%) and H. influenzae (8.6%).51 MRSA is also a poten-
tial pathogen. Liao and colleagues53 found a rate of 5.9% in
orbital complications. The most common anaerobes are Pepto-
streptococcus (6.4%) and Prevotella (4.7%).51
A good clinical examination is crucial to obtain an appropri-
ate diagnosis and direct subsequent testing. Every patient
should have an examination with anterior rhinoscopy or nasal
endoscopy to evaluate for purulent drainage in the middle
meatus. An ophthalmologic examination assesses for visual
acuity, extraocular movements, and proptosis. When postseptal
involvement is suspected, an ophthalmology consultation
should be obtained immediately to help with surgical planning.
Symptoms that may indicate increased intracranial pressure
include frontal or retro-orbital headache, nausea and vomiting,
altered mental status, nuchal rigidity, and papilledema.
Laboratory testing should involve basic hematology to evalu-
ate for leukocytosis. Blood cultures should be drawn in patients
with intracranial complications and more severe orbital com-
plications. A lumbar puncture should be considered when
symptoms suggest intracranial involvement. Imaging should be
completed before lumbar puncture in the setting of focal neu-
rologic deficits to prevent herniation and neurologic compro-
mise. Contrast-enhanced CT is indicated when postseptal
involvement is suspected or with an intracranial complication.
 46  |  ACUTE RHINOSINUSITIS: PATHOGENESIS, TREATMENT, AND COMPLICATIONS 729

TABLE 46-2.  Signs and Symptoms of the Complications of Acute Rhinosinusitis

Complication Clinical Findings
Preseptal cellulitis Eyelid edema, erythema, and tenderness
Unrestricted extraocular movement
Normal visual acuity
Subperiosteal abscess Proptosis and impaired extraocular muscle movement
Orbital cellulitis Eyelid edema and erythema, proptosis, and chemosis
No limited impairment of extraocular movements
Normal visual acuity
Orbital abscess Significant exophthalmos, chemosis, ophthalmoplegia, and visual impairment
Cavernous sinus thrombosis Bilateral orbital pain, chemosis, proptosis, and ophthalmoplegia
Meningitis Headache, neck stiffness, and high fever
Epidural abscess Headache, fever, altered mental status, and local tenderness
Unenhanced CT reveals a hypodense or isodense crescent-shaped collection in the epidural space
Subdural abscess Headache, fever, meningismus, focal neurologic deficits, and lethargy with rapid deterioration
CT reveals a hypodense collection along a hemisphere or along the falx
MRI demonstrates low signal on T1 and high signal on T2 images with peripheral contrast enhancement
Intracerebral abscess Fever, headache, vomiting, lethargy, seizures, and focal neurologic deficits
Frontal deficits can include changes in mood and behavior
MRI demonstrates a cystic lesion with a distinct hypointense, strongly enhancing capsule on T2 images
Frontal bone osteomyelitis Fluctuant forehead swelling
(Pott’s puffy tumor)
CT, computed tomography; MRI, magnetic resonance imaging.

CT should also be considered when preseptal inflammation
progresses in 24 to 48 hours despite antibiotic treatment. When
intracranial complications are suspected based on physical
examination or CT findings, contrast-enhanced MRI is per-
formed and a neurosurgical consultation should be obtained.
Complications of pediatric ABRS are rare and can result
from delay in diagnosis. These patients often require multiple
surgical procedures and prolonged hospitalizations. Initiating
treatment promptly can potentially reduce morbidity. Medical
treatment should be started empirically based on the antimi-
crobial resistance patterns of the treating hospital. Orbital com-
plications are managed according to severity at the time of
presentation. Chandler group I infections may be successfully
treated with a course of oral antibiotics and close monitoring.
Broad-spectrum intravenous antimicrobial agents that cover
the most likely pathogens should be started at the time of
admission for all patients in Chandler groups II through V.
Antimicrobial treatment can then be modified based on subse-
quent microbiology results.
Medical treatment also includes nasal decongestants, saline
irrigations, and nasal and/or oral steroids. The use of antico-
agulants is controversial in the setting of venous thrombosis.
Surgical intervention is indicated in any patient with decreased
visual acuity, an afferent pupillary defect, or failure to improve
on medical treatment after 48 hours of antimicrobial treat-
ment. If neurosurgical intervention is planned, unilateral sinus
drainage should be coordinated. Surgical drainage is indicated
in most cases of abscess formation. However, a small subperios-
teal abscess can be treated medically for 48 hours if the patient
presents with normal vision.54 In the treatment of cavernous
sinus thrombosis all the involved sinuses must be drained,
including the sphenoid sinus.
SUMMARY
The pathogenesis of rhinosinusitis is dependent on its classifica-
tion. Certain environmental factors—such as allergy, smoke, or
chronic irritants—appear to predispose to an episode. Viruses
and aerobic bacteria are the major causes of ABRS, although
growing resistance and some shift in the distribution of
pathogens has altered the therapeutic approach. Complica-
tions of ABRS are rare, and suspicion of a potential or impend-
ing complication should warrant a thorough workup.
For a complete list of references, see expertconsult.com. 
SUGGESTED READINGS
Benninger MS, Brook I, Farrell DJ: Disease severity in acute bacterial
rhinosinusitis is greater in patients infected with Streptococcus pneu-
moniae than in those infected with Haemophilus influenzae. Otolaryngol
Head Neck Surg 135:523–528, 2006.
Benninger MS, Payne SC, Ferguson BJ, et al: Endoscopically directed
middle meatal cultures versus maxillary sinus taps in acute bacterial
maxillary rhinosinusitis: a meta-analysis. Otolaryngol Head Neck Surg
134:3–9, 2006.
Black S, Shinefield H, Baxter R, et al: Impact of the use of heptavalent
pneumococcal conjugate vaccine on disease epidemiology in chil-
deren and adults. Vaccine S2, 2006.
Black S, Shinefield H, Baxter R, et al: Postlicensure surveillance for
pneumococcal invasive disease after use of heptavalent pneumococ-
cal conjugate vaccine in northern California Kaiser Permanente.
Pediatr Infect Dis 23:485–489, 2004.
Brook I, Foote PA, Hausfeld JN: Frequency of recovery of patho-
gens causing acute maxillary sinusitis in adults before and after
introduction of vaccination of children with the 7-valent vaccine. 
J Med Microbiol 55:943–946, 2006.
Brook I, Gober AE: Frequency of recovery of pathogens from the naso-
pharynx of children with acute maxillary sinusitis before and after
the introduction of vaccination with the 7-valent pneumococcal
vaccine. Int J Pediatr Otorhinolaryngol 71:575–579, 2007.
Casey JR, Pichichero ME: Changes in frequency and pathogens causing
acute otitis media in 1995-2003. Pedatr Infect Dis 23:824–828, 2004.
Chow AW, Benninger MS, Brook I, et al: IDSA clinical practice guide-
line for acute bacterial rhinosinusitis in children and adults. Clin
Infect Dis 54:e72–e112, 2012.
DePestel DD, Benninger MS, Danziger L, et al: Cephalosporin use in
treatment of patients with penicillin allergies. J Am Pharm Assoc 48:
530–540, 2003.
Fokkens W, Lund V, Mullol J, et al: European Position Paper on Rhi-
nosinusitis and Nasal Polyps 2012. Rhinology (Suppl 23):1–298, 2012.
Hanage WP, Auranen K, Syrjanen R, et al: Ability of pneumococcal
serotypes and clones to cause acute otitis media: implications for the
prevention of otitis media by conjugate vaccines. Infect Immune 72:76–
81, 2004.

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Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2018. Elsevier Inc. Todos los derechos reservados.
730 PART IV  |  SINUS, RHINOLOGY, AND ALLERGY/IMMUNOLOGY

Meltzer EO, Bachert C, Staudinger H: Treating acute rhinosinusitis:
comparing efficacy and safety of mometasone furoate nasal spray,
amoxicillin, and placebo. J Allergy Clin Immunol 116:1285–1295, 2005.
Meltzer EO, Hamilos DL, Hadley JA, et al: Rhinosinusitis: establishing
definitions for clinical research and patient care. Otolaryngol Head
Neck Surg 131:S1–S62, 2004.
Payne SC, Benninger MS: Staphylococcus aureus is a major pathogen in
acute bacterial rhinosinusitis: a meta-analysis. Clin Infect Dis 45:e121–
e127, 2007.
Pichichero ME: Pathogen shifts and changing cure rates for otitis
media and tonsillopharyngitis. Clin Pediatr 45:493–502, 2006.
Pichichero ME, Brixner DI: A review of recommended antibiotic
therpay with impact on outcomes in acute otitis media and acute
bacterial sinusitis. Am J Managed Care 12:S292–S302, 2006.
Sinus and Allergy Health Partnership: Antimicrobial treatment guide-
lines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg
130(1 Suppl):1–45, 2004.

Descargado para Maria Manuela Chemas (mchemas@gmail.com) en PONTIFICIA UNIVERSIDAD JAVERIANA de ClinicalKey.es por Elsevier en agosto 24, 2018.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2018. Elsevier Inc. Todos los derechos reservados.
 46  |  ACUTE RHINOSINUSITIS: PATHOGENESIS, TREATMENT, AND COMPLICATIONS 730.e1
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Descargado para Maria Manuela Chemas (mchemas@gmail.com) en PONTIFICIA UNIVERSIDAD JAVERIANA de ClinicalKey.es por Elsevier en agosto 24, 2018.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2018. Elsevier Inc. Todos los derechos reservados.