Background

Sinusitis is characterized by inflammation of the lining of the paranasal sinuses. Because the
nasal mucosa is simultaneously involved and because sinusitis rarely occurs without
concurrent rhinitis, rhinosinusitis is now the preferred term for this condition.
[1, 2]

Rhinosinusitis may be further classified according to the anatomic site (maxillary, ethmoidal,
frontal, sphenoidal), pathogenic organism (viral, bacterial, fungal), presence of complication
(orbital, intracranial), and associated factors (nasal polyposis, immunosuppression, anatomic
variants). (See Anatomy, Pathophysiology, and Etiology.)
Acute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is of
paramount importance in differentiating this entity from allergic or vasomotor rhinitis and
common upper respiratory infections. No specific clinical symptom or sign is sensitive or
specific for acute sinusitis, so the overall clinical impression should be used to guide
management. (See Clinical Presentation.)
The primary goals of management of acute sinusitis are to eradicate the infection, decrease
the severity and duration of symptoms, and prevent complications. (See Treatment and
Management.) Most patients with acute sinusitis are treated in the primary care setting.
Further evaluation by an otolaryngologist is recommended in any of the following cases:
When continued deterioration occurs with appropriate antibiotic therapy
When episodes of sinusitis recur
When symptoms persist after 2 courses of antibiotic therapy
When comorbid immunodeficiency, nosocomial infection, or complications of
sinusitis are present
Definition of acute rhinosinusitis
Many classifications, both clinical and radiological, have been proposed in the literature to
define acute sinusitis. Although no consensus on the precise definition currently exists
subacute sinusitis represents a temporal progression of symptoms for 4-12 weeks. Recurrent
acute sinusitis is diagnosed when 2-4 episodes of infection occur per year with at least 8
weeks between episodes and, as in acute sinusitis, the sinus mucosa completely normalizes
between attacks. Chronic sinusitis is the persistence of insidious symptomatology beyond 12
weeks, with or without acute exacerbations.
[3]

Anatomy
To properly diagnose and treat infectious disorders of the paranasal sinuses, the clinician
should have knowledge of the developmental milestones. The development of the paranasal
sinuses begins in the third week of gestation and continues until early adulthood.
Development of paranasal sinuses
During the third week of embryonic development, proliferation and medial migration of
ectodermal cells form the notochord. After the heart tube and pericardium have rotated from
the cranial position to lie anteriorly, the notochord, which is initially in the caudal region of
the embryonic disc, rotates to lie posterior to the primitive foregut. The paraxial layer of
mesenchyme, which lies adjacent to the notochord, differentiates into the somite ridges,
intermediate cell mass, and lateral plate mesoderm. From these mesodermal structures, the
branchial arches develop, the first of which gives rise to internal nasal structures.
The paranasal sinuses develop in conjunction with the palate from changes in the lateral wall
of the nasal cavity. At 40 weeks' gestation, 2 horizontal grooves develop in the mesenchyme
of the lateral wall of the nasal cavity. Proliferation of maxilloturbinate mesenchyme between
these grooves results in an outpouching of tissue medially into the nasal lumen. This
outpouching is the precursor of the middle and inferior meatus as well as the inferior
turbinate. Ethmoidoturbinate folds develop superiorly to give rise to the middle and superior
turbinates. Once the turbinate structures are established, sinus development begins and
continues until early adult life.
The sinuses open into the nose via small openings called ostia.
[2]
The maxillary and ethmoid
sinuses form at 3-4 months' gestation. Thus, an infant is born with 3-4 ethmoid cells and tiny
teardrop-shaped maxillary sinuses. By the teenage years, each maxillary sinus progressively
enlarges to an adult capacity of 15 mL. In healthy individuals, the ethmoid sinuses increase in
number to 18-20, and each drains by an individual ostium that is 1-2 mm in diameter.
The frontal sinus develops from an anterior ethmoid cell and moves to its supraorbital
position when the individual is aged 6-7 years. Frontal sinuses may begin to develop at this
age but usually do not appear radiologically until the individual is aged approximately 12
years. The maxillary, anterior ethmoid, and frontal sinuses drain into the middle meatus; the
posterior ethmoid and sphenoid sinuses drain into the superior meatus (see the image below).
Sagittal section of the lateral nasal wall demonstrating
openings of paranasal sinuses. Conchae have been cut to depict details of meatal structures.
Structure and function of paranasal sinuses
The paranasal sinuses are air-filled bony cavities that extend from the skull base to the
alveolar process and laterally from the nasal cavity to the inferomedial aspect of the orbit and
the zygoma. The sinus cavities are lined with pseudostratified, ciliated, columnar epithelium
that is contiguous, via ostia, with the lining of the nasal cavity. This epithelium contains a
number of mucus-producing goblet cells. These goblet cells in the epithelium and the
submucosal seromucous glands contribute to the airway surface liquid,
[4]
which is 5-100 m
thick and covers the epithelium.
Anterior and posterior ethmoid sinuses are composed of multiple air cells separated by thin
bony partitions. Each cell is drained by an independent ostium that measures only 1-2 mm in
diameter. These small openings are readily clogged by secretions or are occluded by swelling
of the nasal mucosa. The sphenoid sinuses sit immediately anterior to the pituitary fossa and
just behind the posterior ethmoid.
The arterial supply of the paranasal sinuses is from branches of the internal and external
carotid arteries, while the venous and lymphatic drainage path is through the sinus ostia into
the nasal cavity plexus. In addition, venous drainage occurs through valveless vessels
corresponding to the arterial supply.
All sinus ostia drain into the nares at locations beneath the middle and superior turbinates.
The posterior ethmoid and sphenoid sinuses drain into the superior meatus below the superior
turbinate. The ostia of the maxillary, anterior ethmoid, and frontal sinuses share a common
site of drainage within the middle meatus. This region is called the ostiomeatal complex and
can be visualized by coronal CT scan. The common drainage pathway of the frontal,
maxillary, and anterior ethmoid sinuses within the middle meatus allows relatively localized
mucosal infection processes to promote infection in all these sinuses.
The successful maintenance of sinus drainage represents a complicated interaction between
ciliary action, mucus viscosity, size of sinus ostia, and orientation of body structures. Ciliary
beat at the rate of 8-15 Hz is continuously moved by the cilia at a speed of 6 mm/min. The
ciliary action can be affected due to local factors, such as infection and local hypoxia that is
associated with complete occlusion of sinus ostia. The sinus mucosa has less secretory and
vasomotor function than the nasal cavity does. Cilia are concentrated near and beat toward
the natural sinus ostia. Blockage of the ostium results in stasis of mucous flow, which can
lead to development of disease.
The exact function of the paranasal sinuses is not well understood. The possible roles of the
sinuses may include reducing the weight of the skull; dampening pressure; humidifying and
warming inspired air; absorbing heat and insulating the brain; aiding in sound resonance;
providing mechanical rigidity; and increasing the olfactory surface area.
Pathophysiology
The sinuses are normally sterile under physiologic conditions. Secretions produced in the
sinuses flow by ciliary action through the ostia and drain into the nasal cavity. In the healthy
individual, flow of sinus secretions is always unidirectional (ie, toward the ostia), which
prevents back contamination of the sinuses. In most individuals, the maxillary sinus has a
single ostium (2.5 mm in diameter, 5 mm
2
in cross-sectional area) serving as the only outflow
tract for drainage. This slender conduit sits high on the medial wall of the sinus cavity in a
nondependent position. Most likely, the edema of the mucosa at these 1- to 3-mm openings
becomes congested by some means (eg, allergy, viruses, chemical irritation) that causes
obstruction of the outflow tract stasis of secretions with negative pressure, leading to
infection by bacteria.
Retained mucus, when infected, leads to sinusitis. Another mechanism hypothesizes that
because the sinuses are continuous with the nasal cavity, colonized bacteria in the
nasopharynx may contaminate the otherwise sterile sinuses. These bacteria are usually
removed by mucociliary clearance; thus, if mucociliary clearance is altered, bacteria may be
inoculated and infection may occur, leading to sinusitis.
[5, 2]

Data are available that support the fact that healthy sinuses are colonized. The bacterial flora
of noninflamed sinuses were studied for aerobic and anaerobic bacteria in 12 adults who
underwent corrective surgery for septal deviation.
[6]
Organisms were recovered from all
aspirates, with an average of 4 isolates per sinus aspirate. The predominant anaerobic isolates
were Prevotella, Porphyromonas, Fusobacterium and Peptostreptococcus species. The most
common aerobic bacteria were S pyogenes, S aureus, S pneumonia, and H influenzae. In
another study, specimens were processed for aerobic bacteria only, and Staphylococcus
species and alpha-hemolytic streptococci were isolated.
[7]
Organisms were recovered in 20%
of maxillary sinuses of patients who underwent surgical repositioning of the maxilla.
In contrast, another report of aspirates of 12 volunteers with no sinus disease showed no
bacterial growth.
[8]
Jiang et al evaluated the bacteriology of maxillary sinuses with normal
endoscopic findings.
[9]
Organisms were recovered from 14 (47%) of 30 swab specimens and
7 (41%) of 17 of mucosal specimens. Gordts et al reported the microbiology of the middle
meatus in normal adults and children.
[10]
This study noted in 52 patients that 75% had
bacterial isolates present, most commonly coagulase-negative staphylococci (CNS) (35%),
Corynebacterium species (23%), and S aureus (8%) in adults. Low numbers of these species
were present. In children, the most common organisms were H influenzae (40%), M
catarrhalis (34%), and S pneumoniae (50%), a marked difference from findings in adults.
Nonhemolytic streptococci and Moraxella species were absent in adults.
The pathophysiology of rhinosinusitis is related to 3 factors:
Obstruction of sinus drainage pathways (sinus ostia)
Ciliary impairment
Altered mucus quantity and quality
Obstruction of sinus drainage
Obstruction of the natural sinus ostia prevents normal mucus drainage. The ostia can be
blocked by mucosal swelling or local causes (eg, trauma, rhinitis), as well as by certain
inflammation-associated systemic disorders and immune disorders. Systemic diseases that
result in decreased mucociliary clearance, including cystic fibrosis, respiratory allergies, and
primary ciliary dyskinesia (Kartagener syndrome), can be predisposing factors for acute
sinusitis in rare cases. Patients with immunodeficiencies (eg, agammaglobulinemia,
combined variable immunodeficiency, and immunodeficiency with reduced immunoglobulin
G [IgG] and immunoglobulin A [IgA]bearing cells) are also at increased risk of developing
acute sinusitis.
Mechanical obstruction because of nasal polyps, foreign bodies, deviated septa, or tumors can
also lead to ostial blockage. In particular, anatomical variations that narrow the ostiomeatal
complex, including septal deviation, paradoxical middle turbinates, and Haller cells, make
this area more sensitive to obstruction from mucosal inflammation. Usually, the margins of
the edematous mucosa have a scalloped appearance, but in severe cases, mucus may
completely fill a sinus, making it difficult to distinguish an allergic process from infectious
sinusitis. Characteristically, all of the paranasal sinuses are affected and the adjacent nasal
turbinates are swollen. Air-fluid levels and bone erosion are not features of uncomplicated
allergic sinusitis; however, swollen mucosa in a poorly draining sinus is more susceptible to
secondary bacterial infection.
Hypoxia within the obstructed sinus is thought to cause ciliary dysfunction and alterations in
mucus production, further impairing the normal mechanism for mucus clearance.
Impaired ciliary function
Contrary to earlier models of sinus physiology, the drainage patterns of the paranasal sinuses
depend not on gravity but on the mucociliary transport mechanism. The metachronous
coordination of the ciliated columnar epithelial cells propels the sinus contents toward the
natural sinus ostia. Any disruption of the ciliary function results in fluid accumulation within
the sinus. Poor ciliary function can result from the loss of ciliated epithelial cells; high
airflow; viral, bacterial, or environmental ciliotoxins; inflammatory mediators; contact
between 2 mucosal surfaces; scars; and Kartagener syndrome.
[11]

Ciliary action can be affected by genetic factors, such as Kartagener syndrome. Kartagener
syndrome is associated with immobile cilia and hence the retention of secretions and
predisposition to sinus infection. Ciliary function is also reduced in the presence of low pH,
anoxia, cigarette smoke, chemical toxins, dehydration, and drugs (eg, anticholinergic
medications and antihistamines).
Exposure to bacterial toxins can also reduce ciliary function. Approximately 10% of cases of
acute sinusitis result from direct inoculation of the sinus with a large amount of bacteria.
Dental abscesses or procedures that result in communication between the oral cavity and
sinus can produce sinusitis by this mechanism. Additionally, ciliary action can be affected
after certain viral infections.
Several other factors can lead to impaired ciliary function. Cold air is said to stun the ciliary
epithelium, leading to impaired ciliary movement and retention of secretions in the sinus
cavities. On the contrary, inhaling dry air desiccates the sinus mucous coat, leading to
reduced secretions. Any mass lesion with the nasal air passages and sinuses, such as polyps,
foreign bodies, tumors, and mucosal swelling from rhinitis, may block the ostia and
predispose to retained secretions and subsequent infection. Facial trauma or large
inoculations from swimming can produce sinusitis as well. Drinking alcohol can also cause
nasal and sinus mucosa to swell and cause impairment of mucous drainage.
Altered quality and quantity of mucus
Sinonasal secretions play an important role in the pathophysiology of rhinosinusitis. The
mucous blanket that lines the paranasal sinuses contains mucoglycoproteins,
immunoglobulins, and inflammatory cells. It consists of 2 layers: (1) an inner serous layer (ie,
sol phase) in which cilia recover from their active beat and (2) an outer, more viscous layer
(ie, gel phase), which is transported by the ciliary beat. Proper balance between the inner sol
phase and outer gel phase is of critical importance for normal mucociliary clearance.
If the composition of mucus is changed, so that the mucus produced is more viscous (eg, as in
cystic fibrosis), transport toward the ostia considerably slows, and the gel layer becomes
demonstrably thicker. This results in a collection of thick mucus that is retained in the sinus
for varying periods. In the presence of a lack of secretions or a loss of humidity at the surface
that cannot be compensated for by mucous glands or goblet cells, the mucus becomes
increasingly viscous, and the sol phase may become extremely thin, thus allowing the gel
phase to have intense contact with the cilia and impede their action. Overproduction of mucus
can overwhelm the mucociliary clearance system, resulting in retained secretions within the
sinuses.
Acute sinusitis in the intensive care setting
Acute sinusitis in the intensive care population is a distinct entity, occurring in 18-32% of
patients with prolonged periods of intubation, and is usually diagnosed during the evaluation
of unexplained fever. Cases in which the cause is obstruction are usually evident and can
include the presence of prolonged nasogastric or nasotracheal intubation. Moreover, patients
in an intensive care setting are generally debilitated, predisposing them to septic
complications, including sinusitis. Finally, sinusitis in intensive care settings is associated
with nasal catheter placement.
Etiology
Purulent sinusitis can occur when ciliary clearance of sinus secretions decreases or when the
sinus ostium becomes obstructed, which leads to retention of secretions, negative sinus
pressure, and reduction of oxygen partial pressure. This environment is then suitable for
growth of pathogenic organisms. Factors that predispose the sinuses to obstruction and
decreased ciliary function are allergic, nonallergic, or viral insults, which produce
inflammation of the nasal and sinus mucosa and result in ciliary dysmotility and sinus
obstruction.
In individuals with recurrent or persistent sinusitis, suspect other predisposing conditions
such as cystic fibrosis, ciliary dyskinesia, allergic inflammation, immunodeficiency, or an
anatomic problem. These predisposing factors are also cited by the 2005 practice parameter
for diagnosis and management of sinusitis issued by the American Academy of Allergy,
Asthma and Immunology (AAAAI), as are cocaine addiction and nasal polyps and other
causes of ostiomeatal obstruction.
[12]

Acute viral rhinosinusitis
The vast majority of rhinosinusitis episodes are caused by viral infection. Most viral upper
respiratory tract infections are caused by rhinovirus, but coronavirus, influenza A and B,
parainfluenza, respiratory syncytial virus, adenovirus, and enterovirus are also causative
agents. Rhinovirus, influenza, and parainfluenza viruses are the primary pathogens in 3-15%
of patients with acute sinusitis. In about 0.5-2% of cases, viral sinusitis can progress to acute
bacterial sinusitis.
[13, 14]

Viral upper respiratory tract infections are the most important risk factor for the development
of acute bacterial sinusitis.
[15]
Approximately 90% of patients who have viral upper
respiratory tract infections have sinus involvement, but only 5-10% of these patients have
bacterial superinfection requiring antimicrobial treatment.
[16]

Acute bacterial rhinosinusitis
Acute bacterial rhinosinusitis is very frequently associated with viral upper respiratory tract
infection, although allergy, trauma, neoplasms, granulomatous and inflammatory diseases,
midline destructive disease, environmental factors, dental infection, and anatomic variation,
which may impair normal mucociliary clearance, may also predispose to bacterial infection.
S aureus is a common pathogen in sphenoid sinusitis. The vaccination of children with the 7-
valent pneumococcal vaccine introduced in 2000 in the United States brought about the
decline in the recovery rate of S pneumoniae and an increase in H influenza.
[17, 18]
In addition,
the rate of recovery of S pneumoniae penicillin-resistant strains was different after
vaccination.
P aeruginosa and other gram-negative rods have been recovered in acute sinusitis of
nosocomial origin (especially in patients who have nasal tubes or catheters),
immunocompromised persons, patients with HIV infection, and those with cystic fibrosis.
Sixty-six percent of patients with acute sinusitis grow at least 1 pathogenic bacterial species
on sinus aspirates, while 26-30% percent of patients have multiple predominant bacterial
species. The bacteria most commonly involved in acute sinusitis are part of the normal nasal
flora. These bacteria can become sinus pathogens when they are deposited into the sinuses by
sneezing, coughing, or direct invasion under conditions that optimize their growth.
The most common pathogens isolated from maxillary sinus cultures in patients with acute
bacterial rhinosinusitis include Streptococcus pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis.Streptococcus pyogenes, Staphylococcus aureus,and anaerobes are less
commonly associated with acute bacterial rhinosinusitis; they have been found in fewer than
10% of patients with acute bacterial sinusitis, despite the ample environment available for
their growth. The exceptions are in sinusitis resulting from a dental source and in patients
with chronic sinus disease, in whom anaerobic organisms are usually isolated.
S pneumoniae are gram-positive, catalase-negative, facultatively anaerobic cocci that account
for 20-43% of acute bacterial rhinosinusitis cases in adults. The rise of antimicrobial
resistance in S pneumoniae is a major concern.
A 1998 surveillance study of respiratory tract isolates estimated that 12.3% of S pneumoniae
isolates obtained from the paranasal sinuses had intermediate resistance to penicillin; 37.4%
were penicillin-resistant. The paranasal sinuses represented the anatomic location with the
highest resistance rate.
[19]
Resistance to macrolide, clindamycin, trimethoprim-
sulfamethoxazole, and doxycycline was more common in isolates with intermediate penicillin
resistance and those that were penicillin-resistant.
H influenzae are gram-negative, facultatively anaerobic bacilli. H influenza type B was a
leading cause of meningitis until the widespread use of the vaccine. Nontypeable strains of H
influenzae are responsible for 22-35% of acute bacterial rhinosinusitis cases in adults. Beta-
lactamase production is the mechanism of antimicrobial resistance for this organism . Of
isolates from the paranasal sinus, 32.7% were found to be beta-lactamasepositive for H
influenza; other reports suggest a rate of 44%.
M catarrhalis are gram-negative, oxidase-positive, aerobic diplococci. M catarrhalis is the
responsible pathogen in 2-10% of acute bacterial rhinosinusitis cases in adults. Beta-
lactamase production is the mechanism of antimicrobial resistance for M catarrhalis as well .
Of isolates from the paranasal sinus, 98% were found to be beta-lactamasepositive for M
catarrhalis.
S aureus, though accounting for 10% of episodes of acute bacterial rhinosinusitis, is now
recognized as an increasingly common pathogen in acute bacterial rhinosinusitis.
[20]
While
methicillin-resistant S aureus (MRSA) still represents a minority of episodes of S aureus
rhinosinusitis, increasing trends of drug-resistant S aureus may alter future treatment
recommendations.
[21]

Gram-negative organisms, including Pseudomonas aeruginosa (15.9%), Escherichia coli
(7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae, and Enterobacter species,
predominate in nosocomial sinusitis, accounting for 60% of cases. Polymicrobial invasion is
seen in 25-100% of cultures. The other pathogenic organisms found in nosocomial patients
are gram-positive organisms (31%) and fungi (8.5%).
Acute invasive fungal rhinosinusitis
Rarely, sinusitis is caused by fungi. Fungal sinusitis (eg, allergic fungal sinusitis) may appear
similar to lower airway disorder and allergic bronchopulmonary aspergillosis.
Fungal agents associated with this condition include Aspergillus and Alternaria species.
Bipolaris and Curvularia species are the most common fungi recovered in allergic fungal
sinusitis, accounting for 60% and 20%, respectively, in most studies. Curvularia species is
occasionally reported as the most common causative organism in the deep southern United
States.
Please go to the main article Fungal Sinusitis for more information.
Epidemiology
Sinusitis affects 1 out of every 7 adults in the United States, with more than 30 million
individuals diagnosed each year. Sinusitis is more common from early fall to early spring.
Rhinosinusitis affects an estimated 35 million people per year in the United States and
accounts for close to 16 million office visits per year.
[22]

According to the National Ambulatory Medical Care Survey (NAMCS), approximately 14%
of adults report having an episode of rhinosinusitis each year, and it is the fifth most common
diagnosis for which antibiotics are prescribed, accounting for 0.4% of ambulatory
diagnoses.
[23]

In 1996, Americans spent approximately $3.39 billion treating rhinosinusitis.
[24]
The
economic burden of acute sinusitis in children is $1.77 billion per year.
[24]

International prevalence
Acute sinusitis affects 3 in 1000 people in the United Kingdom. Chronic sinusitis affects 1 in
1000 people. Sinusitis is more common in winter than in summer. Rhinoviral infections are
prevalent in autumn and spring. Coronaviral infection occurs mostly from December to
March.
Acute sinusitis in children
An average child is likely to have 6-8 colds (ie, upper respiratory tract infections) per year,
and approximately 0.5-2% of upper respiratory tract infections in adults and 6-13% of viral
upper respiratory tract infections in children are complicated by the development of acute
bacterial sinusitis.
[25, 26]

Sex distribution for acute sinusitis
Women have more episodes of infective sinusitis than men because they tend to have more
close contact with young children. The rate in women is 20.3%, compared with 11.5% in
men.
Prognosis
Sinusitis does not cause any significant mortality by itself. However, complicated sinusitis
may lead to morbidity and, in rare cases, mortality.
Approximately 40% of acute sinusitis cases resolve spontaneously without antibiotics. The
spontaneous cure for viral sinusitis is 98%. Patients with acute sinusitis, when treated with
appropriate antibiotics, usually show prompt improvement. The relapse rate after successful
treatment is less than 5%.
In the absence of response within 48 hours or worsening of symptoms, reevaluate the patient.
Untreated or inadequately treated rhinosinusitis may lead to complications such as
meningitis, cavernous sinus thrombophlebitis, orbital cellulitis or abscess, and brain abscess.
In patients with allergic rhinitis, aggressive treatment of nasal symptoms and signs of
mucosal edema, which can cause obstruction of the sinus outflow tracts, may decrease
secondary sinusitis. If the adenoids are chronically infected, removing them eliminates a
nidus of infection and can decrease sinus infection.
Complications
Complications of sinusitis include acute and chronic sequelae. Acute distant effects include
toxic shock syndrome. Acute local effects can also occur. Acute orbital complications include
the following: cellulitis, proptosis, chemosis, ophthalmoplegia, orbital cellulitis, subperiosteal
abscess, and orbital abscess.
Other acute complications include intracranial sequelae such as meningitis; encephalitis;
cavernous or sagittal sinus thrombosis; or extradural, subdural, or intracerebral abscesses.
The incidence of intracranial complications in all patients hospitalized with sinusitis has been
reported as 3.7%. Sinusitis is implicated as a source of subdural abscess in 35-65% of cases.
Bony complications include dental involvement and osteitis or osteomyelitis. Potts puffy
tumor refers to swelling of the scalp, caused by an underlying osteitis of the skull or
extradural abscess. A classical cause of such a swelling is complicated frontal sinusitis. Toxic
shock syndrome is an unusual complication of acute sinusitis. It occurs after surgery for
foreign body removal and is associated with S aureus.
Patient Education
For excellent patient education resources, visit eMedicines Headache Center. Also, see
eMedicine's patient education article Sinus Infection.
History
Acute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is of
paramount importance in differentiating this entity from allergic or vasomotor rhinitis and
common upper respiratory infections. No specific clinical symptom or sign is sensitive or
specific for acute sinusitis, so the overall clinical impression should be used to guide
management.
A history of occupational or allergic rhinitis, vasomotor rhinitis, nasal polyps, rhinitis
medicamentosa, or immunodeficiency should be sought in an evaluation for rhinosinusitis.
Rhinosinusitis is more common in individuals with congenital defects that affect humoral
immunity and ciliary motility, in those with cystic fibrosis, and in persons with AIDS.
Obtain a history of diabetes or organ transplant if invasive fungal sinusitis is being
considered. Fungal infections are more common in people with diabetes and those who are
immunocompromised. Clinicians should maintain a high index of suspicion for acute
invasive fungal sinusitis in immunocompromised patients with orbital or CNS complications
of rhinosinusitis.
Clinical findings may include the following:
Pain over cheek and radiating to frontal region or teeth, increasing with straining or
bending down
Redness of nose, cheeks, or eyelids
Tenderness to pressure over the floor of the frontal sinus immediately above the inner
canthus
Referred pain to the vertex, temple, or occiput
Postnasal discharge
A blocked nose
Persistent coughing or pharyngeal irritation
Facial pain
Hyposmia
The duration of the condition should be determined. Suspect acute sinusitis in any patient
with an upper respiratory tract infection that persists beyond 7-10 days, particularly if the
infection is severe and is accompanied by high fever, purulent nasal discharge, or periorbital
edema (ethmoid sinusitis).
The condition may start as an upper respiratory tract infection, and the patient may seem to
be recovering; however, the condition becomes acutely worse around the seventh day of
illness. This should be considered a red flag because most upper respiratory tract infections
last 5-7 days. The natural history of rhinovirus infection, as described by Gwaltney et al, lasts
from 1-33 days. One fourth of patients have symptoms that last longer than 14 days.
[27]

Bacterial and viral sinusitis
During the course of a viral upper respiratory tract infection, 3 three common clinical
presentations should prompt the clinician to consider that the patient is experiencing an
episode of acute bacterial sinusitis. These presentations are described as onset with persistent
symptoms, onset with severe symptoms, or onset with worsening symptoms. What is meant
by persistent symptoms, in the context of acute bacterial sinusitis, is respiratory symptoms
that last more than 10 days but less than 30 days and which have not begun to improve. Such
symptoms include nasal discharge (of any quality, eg, thick or thin, serous, mucoid or
purulent) or daytime cough (which may be worse at night) or both.
A consensus statement published in Otolaryngology-Head and Neck Surgery made strong
recommendations that clinicians should distinguish between acute rhinosinusitis caused by
bacterial causes and those episodes caused by viral upper respiratory infections and
noninfectious conditions.
[28]

The panel suggests that the diagnosis of acute bacterial sinusitis be entertained when (1)
symptoms or signs of acute rhinosinusitis are present 10 days or more beyond the onset of
upper respiratory symptoms, or (2) symptoms or signs of acute rhinosinusitis worsen within
10 days after an initial improvement. A history of purulent secretions and facial or dental pain
are specific symptoms that may point to a bacterial etiology. In a patient in intensive care,
acute sinusitis should be suspected in the presence of sepsis of unknown origin.
The consensus statement is in accordance with the AAAAI 2005 practice parameter for
diagnosis and management of sinusitis, which states that upper respiratory tract infections
persisting after 10-14 days are suspicious for acute bacterial sinusitis. The likelihood of
bacterial disease increases if the infection history includes persistent purulent rhinorrhea,
postnasal drainage, and facial pain.
[12]

Acute bacterial rhinosinusitis is commonly overdiagnosed. In fact, acute bacterial
rhinosinusitis is the correct diagnosis in only 40-50% of cases in which a primary care
physician initially classifies a patient as likely having the condition.
[29]

Although diagnostic criteria for acute rhinosinusitis have been proposed,
[1]
no single sign or
symptom has strong diagnostic value for bacterial rhinosinusitis.
[30]
As noted, however, acute
bacterial rhinosinusitis should be suspected in patients who exhibit symptoms of viral upper
respiratory tract infection that do not improve after 10 days or that worsen after 5-7 days.
Symptoms of acute bacterial rhinosinusitis include the following:
Facial pain or pressure (especially unilateral)
Hyposmia/anosmia
Nasal congestion
Nasal drainage
Postnasal drip
Fever
Cough
Fatigue
Maxillary dental pain
Ear fullness/pressure
A change in the color or characteristic of the nasal discharge is not a specific sign of bacterial
rhinosinusitis. A previous diagnosis of rhinosinusitis is not a predictor of acute bacterial
rhinosinusitis.
[30]

Physical Examination
Anterior rhinoscopic examination, with or without a topical decongestant, is important to
assess the status of the nasal mucosa and the presence and color of nasal discharge.
Predisposing anatomical variations can also be noted during anterior rhinoscopy.
Endoscopic examination may reveal the origin of the purulent discharge from the middle
meatus and may provide information about the nature of ostiomeatal obstruction. The use of
endoscopy may also aid in the etiologic diagnosis of acute sinusitis by allowing the careful
attainment of purulent secretions from the sinus ostia for culture. Purulent secretions in the
middle meatus (highly predictive of maxillary sinusitis) may be seen using a nasal speculum
and a directed light.
Fever is seen in fewer than 2% of individuals with sinusitis. Sinus transillumination and
palpation are of little predictive value. Facial tenderness to palpation is present. Complete
opacification of maxillary or frontal sinuses may be seen on transillumination; partial
opacification is a nonspecific finding, and it is not as reliable. A basic evaluation of ocular
and neurological function is also necessary to rule out potential complications.
The following may be noted:
Purulent nasal secretions
Purulent posterior pharyngeal secretions
Mucosal erythema
Periorbital edema
Tenderness overlying sinuses
Air-fluid levels on transillumination of the sinuses (60% reproducibility rate for
assessing maxillary sinus disease)
Facial erythema
Evaluation of the pediatric patient
Sinusitis and upper respiratory tract infections are common pediatric problems. As many as
10% of upper respiratory tract infections can be complicated by acute sinusitis. Untreated
chronic sinusitis can lead to life-threatening complications.
Physical examination findings may not be helpful in making a diagnosis of acute bacterial
sinusitis in a child because the findings are almost identical to those of a child with viral
rhinosinusitis. The presence of pus in the middle meatus suggests involvement of maxillary,
frontal, or ethmoid sinuses; pus in the superior meatus suggests involvement of sphenoid or
posterior ethmoid cells.
According to a study by Mcquillan et al in which pediatricians were asked how they diagnose
and manage nonsevere acute sinusitis in children, on the basis of age group, pediatricians
reported first considering acute sinusitis at the following rates: ages 0-5 (6%), 6-11 (17%),
12-23 (36%), 24-35 (21%), and 36 months or older (20%).
[31]

In the Mcquillan study, symptoms thought to be very important included prolonged symptom
duration (93%), purulent rhinorrhea (55%), and nasal congestion (43%); 60% reported that
symptom duration is more important than symptom combination. Symptom duration before
considering the diagnosis were 1-6 days (3%), 7-9 days (17%), 10-13 days (37%), 14-16 days
(38%), and 17 or more days (6%).
Mcquillan et al reported that CT scanning was used by 58% in making the diagnosis of acute
sinusitis. Antibiotics were used frequently or always by 96% of the respondents. Adjuvants
used frequently or always included saline washes (44%), systemic decongestants (28%),
nasal corticosteroids (20%), and systemic antihistamines (13%).
In children younger than 6 years, the nasal examination usually consists of evaluating the
anterior nasal cavity and middle meatus with anterior rhinoscopy using an otoscope and ear
speculum. The superior meatus can never be observed with this technique and is difficult to
observe with nasal endoscopy, rigid rhinoscopy, or both. Purulence running into the posterior
nasal cavity and nasopharynx, observed only by rigid rhinoscopy, can indicate probable
drainage from the sphenoethmoid recess, which drains the posterior ethmoids and sphenoid
sinuses.
In persons with acute ethmoiditis, especially in infants and younger children, periorbital
cellulitis with edema of the soft tissues and erythema of the overlying skin is not uncommon.
American Academy of Pediatrics (AAP) recommendations do not require imaging in the
diagnosis of children aged 6 years or younger to make the diagnosis of uncomplicated acute
bacterial sinusitis if they meet the criteria for the diagnosis.
Complications of Disease
Approximately 75% of orbital or periorbital infections are the result of extending sinusitis.
Untreated, inadequately treated, or partially treated rhinosinusitis may lead to chronic
rhinosinusitis, meningitis, brain abscess, or other extra-sinus complications. (See Treatment
and Management.)
Local complications
Mucoceles are chronic epithelial cysts that develop in sinuses in the presence of either an
obstructed sinus ostium or minor salivary gland duct. They have the potential for progressive
concentric expansion that can lead to bony erosion and extension beyond the sinus.
Maxillary sinus mucoceles are usually found incidentally on sinus radiographs and are of
little significance in the absence of symptomatology or infection. Frontoethmoidal and
sphenoethmoidal mucoceles, on the other hand, tend to be symptomatic and have a high
potential for bony erosion.
Osteomyelitis is a potential local complication most commonly occurring with frontal
sinusitis. Osteomyelitis of the frontal bone is called a Pott puffy tumor and represents a
subperiosteal abscess with local edema anterior to the frontal sinus. This can advance to form
a fistula to the upper lid with sequestration of necrotic bone.
Orbital complications
Orbital complications are the most common complications encountered with acute bacterial
sinusitis. Infection can spread directly through the thin bone separating the ethmoid or frontal
sinuses from the orbit or by thrombophlebitis of the ethmoid veins.
Diagnosis should be based on an accurate physical examination, including ophthalmological
evaluation and appropriate radiological studies. CT scanning is the most sensitive means of
diagnosing an orbital abscess, although ultrasound has been found to be 90% effective for
diagnosing anterior abscesses.
[27]
The classification by Chandler, which is based on physical
examination findings, provides a reasonable framework to guide management. This
classification consists of 5 groups of orbital inflammation
[30]
:
Group 1 - Inflammatory edema (preseptal cellulitis) with normal visual acuity and
extraocular movement
Group 2 - Orbital cellulitis with diffuse orbital edema but no discrete abscess
Group 3 - Subperiosteal abscess beneath the periosteum of the lamina papyracea
resulting in downward and lateral globe displacement
Group 4 - Orbital abscess with chemosis, ophthalmoplegia, and decreased visual
acuity
Group 5 - Cavernous sinus thrombosis with rapidly progressive bilateral chemosis,
ophthalmoplegia, retinal engorgement, and loss of visual acuity; possible meningeal
signs and high fever
Intracranial complications
Intracranial complications may occur as a result of direct extension through the posterior
frontal sinus wall or through retrograde thrombophlebitis of the ophthalmic veins. Subdural
abscess is the most common intracranial complication, although cerebral abscesses and
infarction that result in seizures, focal neurological deficits, and coma may occur.
Systemic complications
Sinusitis can result in sepsis and multisystem organ failure caused by seeding of the blood
and various organ systems. Reports of bacteremia, thoracic empyema, and nosocomial
pneumonia have been documented in the intensive-care population with acute sinusitis, and
the mortality rate in this group can be as high as 11%.
Diagnostic Considerations
Wegener granulomatosis involves angiitis associated with focal necrosis and granulomatous
reaction, which initially affects the respiratory tract but which may progress to involve other
organs.
Ataxia-telangiectasia is an autosomal recessive disorder associated with recurrent sinusitis,
pulmonary infections, bronchiectasis, pulmonary fibrosis, tracheomegaly, diminished
lymphoid tissue, and cerebral and cerebellar atrophy.
Cystic fibrosis is an autosomal recessive disorder associated with respiratory, GI,
cardiovascular and sinus abnormalities, among others.
Immotile cilia syndrome is an autosomal recessive disorder associated with recurrent chest
infections and/or pulmonary consolidation, sinusitis, bronchiectasis, and Kartagener
syndrome.
Kartagener syndrome is an autosomal recessive disease associated with sinusitis, situs
inversus, recurrent respiratory infections, and bronchiectasis, among other abnormalities.
Hyperallergic patients may have innumerable polyps filling the nasal cavity and obstructing
the paranasal sinuses, giving a characteristic imaging appearance. This disease is closely
associated with asthma. To see complete information on Asthma and Sinusitis, please go to
the main article by clicking here.
Wiskott-Aldrich syndrome is an X-linked, recessive, immune deficiency disease associated
with recurrent respiratory tract infections and/or pneumonia, sinusitis, and mastoiditis.
Yellow-nail syndrome is associated with recurrent pleural effusions, pericardial effusions,
chylothorax, bronchiectasis, and sinusitis.
Young syndrome is associated with azoospermia secondary to epididymal obstruction and
recurrent respiratory infections and sinusitis.
Other problems to consider include the following:
Gastroesophageal reflux
Cystic fibrosis
Immotile cilia syndrome
Dental abscess
Periapical abscess
Migraine headache
Sinonasal polyposis
Chemical rhinitis
Nasal foreign body
Chronic invasive fungal sinusitis
Sinonasal neoplasm
Upper respiratory tract infection
Primary ciliary dyskinesia
Unilateral choanal atresia
Adenoidal hypertrophy
Foreign body
Immune deficiency (immunoglobulin [Ig]A, IgG subclass)
Differential Diagnoses
Allergic and Environmental Asthma
Asthma
Bronchitis
Haemophilus Influenzae Infections
Headache, Cluster
Headache, Tension
Influenza
Migraine Headache
Moraxella Catarrhalis Infections
Mucormycosis
Otitis Media
Parainfluenza Virus
Rhinitis, Allergic
Rhinocerebral Mucormycosis
Rhinoviruses
Sinusitis, Chronic
Staphylococcal Infections
Approach Considerations
Some authors have reported on the use of laboratory tests, including sedimentation rate, white
blood cell counts, and C-reactive protein levels, to help diagnose acute sinusitis.
[32]
These
tests appear to add little to the predictive value of clinical findings in the diagnosis.
According to the AAAAI 2005 practice parameter, evaluation of acute, chronic, or recurrent
sinusitis might include the following laboratory tests: nasal cytology, nasal-sinus biopsy, or
tests for immunodeficiency, cystic fibrosis, or ciliary dysfunction.
[12]

Imaging studies are not necessary when the probability of sinusitis is either high or low but
may be useful when the diagnosis is in doubt, based upon a thorough history and physical
examination. Plain sinus radiographs may demonstrate mucosal thickening, air-fluid levels
(see the image below), and sinus opacification.
Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.
Limitations of plain films include interobserver variability, inability to distinguish infection
from a polyp or tumor disease, and poor depiction of the ethmoid and sphenoid sinuses.
Blood Studies
The erythrocyte sedimentation rate and C-reactive protein level may be elevated in
rhinosinusitis, but these findings are nonspecific.
The findings of complete blood cell (CBC) count with differential may be within reference
ranges.
Tests for Immunodeficiency
Tests for immunodeficiency are indicated if history findings indicate recurrent infection, to
include the following:
Immunoglobulin studies
HIV serology
Nasal Cytology
Nasal cytology examinations may be useful to elucidate the following entities:
Allergic rhinitis
[33]

Eosinophilia
Nasal polyposis
Aspirin sensitivity
Sweat Chloride Test
Sweat chloride test screening should be performed if cystic fibrosis is suggested.
Cultures of Nasal Secretions
Cultures of nasal secretions are of limited value because they are usually contaminated by
normal flora. Consequently, cultures are not routinely obtained in the evaluation of acute
sinusitis; however, they should be obtained in a patient in intensive care or with
immunocompromise, in children not responding to appropriate medical management, and in
patients with complications of sinusitis.
Because the nose is colonized with multiple nonpathogenic species of bacteria, care must be
taken when evaluating culture results. A specific organism is considered pathogenic when
more than 10
4
colony-forming units of the species are grown on culture or when polymorph
counts are greater than 5000 cells/mL. Important to note is that this sample must be taken
from the cavity of a paranasal sinus, not nasal secretions, cultures from which are considered
useless. Obtaining cultures endoscopically is useful.
Aspiration of the sinus by direct antral puncture is the only accurate way to obtain a culture;
however, this is reserved for those with life-threatening illness or an immunocompromised
status or those who have disease that is unresponsive to therapy. However, in adults, if
attainable, cultures directed at the middle meatus more accurately reflect the contents of the
sinuses themselves, according to most studies. This may not be useful in children because the
meatus is usually colonized.
[34]

Computed Tomography
CT scanning is the preferred imaging method for rhinosinusitis. A screening sinus CT scan is
adequate for diagnosis and less expensive than other methods but is necessary only in cases
of treatment failure or chronic rhinosinusitis. A complete sinus CT scan with frontal and
coronal planes is used if an alternative diagnosis (eg, tumors) must be excluded. CT scanning
is characteristic in allergic fungal sinusitis and is one of the major criteria for diagnosis.
The 2005 AAAAI practice parameter states that the optimal technique for evaluating the
ethmoid sinuses and for preoperative evaluation of the nose and paranasal sinuses, including
assessment of the ostiomeatal complex areas, is CT.
[12]

CT scanning has poor specificity for the diagnosis of acute sinusitis, demonstrating sinus air-
fluid levels in 87% of individuals with simple upper respiratory tract infections and 40% of
asymptomatic individuals. CT scanning is the modality of choice, however, in specific
circumstances such as in the evaluation of a patient in intensive care, when complications are
suspected, or in the preoperative evaluation of surgical candidates.
According to the 2005 AAAAI practice parameter, CT evidence of sinusitis is associated with
viral upper respiratory infections 40%-90% of the time. Symptoms of viral upper respiratory
tract infections do not differ between patients with CT abnormalities and patients with no CT
evidence of sinusitis, and both groups appear to self-resolve without antibiotics within 21
days. It is inappropriate to prescribe antibiotic treatment for uncomplicated viral upper
respiratory tract infection. Doing so is strongly discouraged.
[12]

CT scanning can provide valuable information regarding the anatomical and mechanical
contributions in the development of acute sinusitis. Coronal views with bone windows are the
preferred sinus study for evaluating each of the sinuses as well as the ostiomeatal complex.
CT scan findings may be used to differentiate orbital cellulitis from periorbital cellulitis as a
complication or to evaluate extension into intracranial space.
Delay CT scanning until antibiotics control acute exacerbation; this practice allows correct
diagnosis of chronic inflammation, mucoperiosteal thickening, soft tissue swelling, and
ethmoid osteitis.
Because of concerns of radiation exposure, use of limited sinus CT scanning (see the image
below) is gaining wide acceptance as an alternative to a single Waters view for evaluation of
pediatric chronic sinusitis.
CT cuts for a limited CT study.
See the main article Imaging in Sinusitis for more information.
Radiography
Basic radiographic examination includes 3 projections as follows:
Waters view (occipitofrontal) - Primarily useful for evaluation of maxillary and
frontal sinuses
Caldwell view (angled posteroanterior) - Only view that visualizes the ethmoid air
cells
Lateral view - Primarily for adenoid and/or nasopharyngeal size and sphenoid disease
Radiographic findings in patients with acute sinusitis include diffuse opacification, mucosal
thickening (>4 mm), or an air fluid level. These findings, in conjunction with clinical features
of acute sinusitis, are helpful in confirming the diagnosis.
When plain film radiographs are compared with the criterion standard (CT scans), however, a
75-80% disagreement occurs. This means that plain film radiography reveals disease in 40%
of cases in which no disease is demonstrated on CT scanning and that plain film radiographs
appear normal in 35-40% of cases in which disease is found on CT scanning.
See the main article Imaging in Sinusitis for more information.
Magnetic Resonance Imaging
MRI is useful only if fungal infection or a tumor is suggested. MRI is excellent for evaluating
soft tissue disease within the sinuses, but it is of little value in the diagnostic workup for acute
sinusitis.
This type of imaging may be too sensitive to define soft tissue structures. MRI is not useful
for detecting bone pathology. MRI is mainly used to evaluate intracranial extension and can
be used as an adjunct to CT scanning in defining allergic fungal sinusitis.
To see complete information on Imaging in Sinusitis, please go to the main article by clicking
here.
Ultrasonography
Ultrasonography is of limited use. A-mode ultrasonography may be useful in screening for
fluid in the maxillary sinus. B-mode (gray scale) ultrasonography may be useful in detecting
fluid in the cavity, mucosal thickening, or soft tissue mass in the maxillary sinus.
See the main article Imaging in Sinusitis for more information.
Paranasal Biopsy
Paranasal biopsy is used to help exclude neoplasia, fungal disease, and granulomatous
disease.
Fiberoptic Sinus Endoscopy
Fiberoptic sinus endoscopy is used to visualize posterior sinonasal structures. This test is
useful to help exclude structural lesions, fungal disease, and granulomatous diseases.
Proceed to Treatment & Management

Approach Considerations
The primary goals of management of acute sinusitis are to eradicate the infection, decrease
the severity and duration of symptoms, and prevent complications. These goals are achieved
through the provision of adequate drainage and appropriate systemic treatment of the likely
bacterial pathogens.
Drainage of the involved sinus can be achieved both medically and surgically. Aggressively
treat patients in intensive care who develop acute sinusitis in order to avoid septic
complications. Consider removal of nasotracheal and nasogastric tubes and promote drainage
either medically or surgically.
Sinus puncture and irrigation techniques allow for a surgical means of removal of thick
purulent sinus secretions. The purpose of surgical drainage is to enhance mucociliary flow
and provide material for culture and sensitivity. A surgical means of sinus drainage should be
used when appropriate medical therapy has failed to control the infection and prolonged or
slowly resolving symptoms result or when complications of sinusitis occur.
Another indication for sinus puncture is to obtain culture material to guide antibiotic selection
if empiric therapy has failed or antibiotic choice is limited. This is particularly important in
patients who are immunocompromised or in intensive care. Sinusitis can be a prominent
source of sepsis in these patients. In adults, sinus puncture can usually be achieved using
local anesthesia; however, in children, a general anesthetic is usually necessary.
Most patients with acute sinusitis are treated in the primary care setting. Further evaluation
by an otolaryngologist is recommended when any of the following exist:
When continued deterioration occurs with appropriate antibiotic therapy
When episodes of sinusitis recur
When symptoms persist after 2 courses of antibiotic therapy
When comorbid immunodeficiency, nosocomial infection, or complications of
sinusitis are present
While in the emergency department and upon discharge, patients may obtain significant
immediate relief with the administration of first-generation antihistamines, decongestants,
and nonsteroidal anti-inflammatory drugs (NSAIDs).
Recommendations for nonantimicrobial therapy
Intranasal steroids have not been conclusively shown to be of benefit in cases of acute
sinusitis. One meta-analysis of 4 double-blind, placebo-controlled trials of intranasal
corticosteroid treatment in acute rhinosinusitis supports its use as monotherapy or as an
adjuvant therapy to antibiotics.
[35]
However, a recent randomized, controlled trial of
antibiotics and intranasal steroid showed no treatment benefit of intranasal steroids, either
alone or with antibiotics.
[36]

No available data suggest that antihistamines are beneficial in acute sinusitis. In fact,
antihistamines may cause harm by drying mucous membranes and decreasing clearance of
secretions. Antihistamines are beneficial for reducing ostiomeatal obstruction in patients with
allergies and acute sinusitis; however, they are not recommended for routine use for patients
with acute sinusitis. Antihistamines may complicate drainage by thickening and pooling
sinonasal secretions.
Medical drainage is achieved with topical and systemic vasoconstrictors. Oral alpha-
adrenergic vasoconstrictors, including pseudoephedrine and phenylephrine, can be used for
10-14 days to allow for restoration of normal mucociliary function and drainage.
Because oral alpha-adrenergic vasoconstrictors may cause hypertension and tachycardia, they
may be contraindicated in patients with cardiovascular disease. Oral alpha-adrenergic
vasoconstrictors may also be contraindicated in competitive athletes because of rules of
competition.
Topical vasoconstrictors (eg, oxymetazoline hydrochloride) provide good drainage, but they
should be used only for a maximum of 3-5 days, given the increased risk of rebound
congestion, vasodilatation, and rhinitis medicamentosa when used for longer periods.
Mucolytic agents (eg, guaifenesin, saline lavage) have the theoretical benefit of thinning
mucous secretions and improving drainage. They are not, however, commonly used in
clinical practice in the treatment of acute sinusitis.
Recommendations for antimicrobial therapy
Ahovuo-Saloranta et al, in a 2008 Cochrane Review meta-analysis of 57 studies, concluded
that antibiotics yield a small treatment effect in a primary care setting in patients with
uncomplicated sinusitis whose symptoms have lasted more than 7 days.
[37]
However, another
meta-analysis found no treatment effect of antibiotics, even in patients whose symptoms had
persisted for more than 10 days.
[38]

In cases of suspected or documented bacterial sinusitis, the second principle of treatment is to
provide adequate systemic treatment of the likely bacterial pathogens (ie, Streptococcus
pneumoniae, Haemophilus influenzae, Moraxella catarrhalis). The physician should be
aware of the probability of bacterial resistance within their community. Reports range from
approximately 33-44% of H influenzae and almost all of M catarrhalis strains have beta-
lactamasemediated resistance to penicillin-based antimicrobials in children.
A study by Garbutt et al evaluated the effect of amoxicillin treatment over symptomatic
treatments for adults with clinically diagnosed acute sinusitis. In a randomized, placebo-
controlled trial of 166 adults with uncomplicated, acute sinusitis patients received a 10-day
course of either amoxicillin (85 patients) or placebo (81 patients). On day 3 of treatment,
there was no difference in improvement between placebo-takers and those prescribed
antibiotics. On day 7, the antibiotic group reported a slight improvement, but that edge
disappeared by day 10, when 80% of patients in both groups reported they felt better or
cured.
[39]

The reduced efficacy of amoxicillin led the Infectious Diseases Society of America to
generate new guidelines for the treatment of acute rhinosinusits. These guidelines recommend
amoxicillin-clavulanate over amoxicillin as empiric antimicrobial therapy in adults and
children with acute bacterial rhinosinusitis.
[40]

Several systematic reviews have also been published on antimicrobial therapy versus placebo,
with at least 5 since 2005. Pediatric studies have also examined antimicrobial treatment.
Evaluating the results of meta-analyses is essential to determine the quality of the studies
included in the meta-analyses. A review of many of these studies indicates 2 common
methodologic flaws: (1) many patients were declared eligible for study with only 7 days of
symptoms (without a qualifier regarding whether these symptoms have begun to improve)
and (2) images (plain radiographs, CT scans, ultrasounds, MRIs) were often used as
diagnostic entry criteria. Accordingly, good logic exists to believe that many patients enrolled
in these studies had uncomplicated viral upper respiratory tract infections rather than acute
bacterial rhinosinusitis, thereby diluting the results. Nonetheless, most studies do show a
modest benefit with the use of antimicrobials. This benefit may possibly be
substantiallymagnifiedifmoreofthestudypatients actually had acute bacterial rhinosinusitis.
As many as 64% of S pneumoniae strains are penicillin resistant because of altered penicillin-
binding proteins. Multidrug-resistant S pneumoniae strains are also found in substantial
numbers of children in daycare settings.
[29]

Initial selection of the appropriate antibiotic therapy (see Table 1, below) should be based on
the likely causative organisms given the clinical scenario and the probability of resistant
strains within a community. The course of treatment is usually 14 days.
First-line therapy at most centers is usually amoxicillin or a macrolide antibiotic in patients
allergic to penicillin because of the low cost, ease of administration, and low toxicity of these
agents. Amoxicillin should be given at double the usual dose (80-90 mg/kg/d), especially in
areas with known S pneumoniae resistance.
Table 1. Dosage, Route, and Spectrum of Activity of Commonly Used First-Line
Antibiotics* (Open Table in a new window)
Antibiotic
Dosag
e
Streptococcus pneumoniae
Haemophilu
s influenzae
Moraxella
catarrhali
s
Anaerobi
c bacteria
Sensitiv
e
Intermediat
e
Resistan
t
Amoxicillin 500
mg PO
tid
+++ ++ + ++ + +++

(except
beta-
lactamase
producers)
Clarithromyci
n
250-
500
++ ++ + ++ +++ +
mg PO
bid
Azithromycin 500
mg PO
first
day,
then

250
mg/d
PO for
4 days
++ ++ + ++ +++ +
*+, low activity against microorganism; ++, moderate activity against microorganism;
+++, good activity against microorganism
Patients who live in communities with a high incidence of resistant organisms, those who fail
to respond within 48-72 hours of commencement of therapy, and those with persistence of
symptoms beyond 10-14 days should be considered for second-line antibiotic therapy (see
Table 2, below).
The most commonly used second-line therapies include amoxicillin-clavulanate, second- or
third-generation cephalosporins (eg, cefuroxime, cefpodoxime, cefdinir), macrolides (ie,
clarithromycin), fluoroquinolones (eg, ciprofloxacin, levofloxacin, moxifloxacin), and
clindamycin.
In patients with dental causes of sinusitis or those with foul-smelling discharge, anaerobic
coverage using clindamycin or amoxicillin with metronidazole is necessary.
Table 2. Dosage, Route, and Spectrum of Activity of Commonly Used Second-Line
Antibiotics* (Open Table in a new window)
Antibiotic
Dosag
e
Streptococcus pneumoniae
Haemophilu
s influenzae
Moraxella
catarrhali
s
Anaerobi
c bacteria
Sensitiv
e
Intermediat
e
Resistan
t
Amoxicillin/

clavulanate
500
mg PO
tid
+++ ++ + +++ +++ +++
Cefuroxime 250-
500
mg PO
bid
+++ ++ + +++ ++ ++
Cefpodoxime

+

cefixime
200
mg PO
bid

400
-

++
+++

-
++

-
+

+++
+++

+++
++

-
mg/d
PO
Ciprofloxacin 500-
750
mg PO
bid
++ + + ++ +++ +
Levofloxacin 500
mg/d
PO
+++ +++ +++ +++ +++ ++
Trovafloxacin 200
mg/d
PO
+++ +++ +++ +++ +++ +++
Clindamycin 300
mg PO
tid
+++ +++ ++ - - +++
Metronidazol
e
500
mg PO
tid
- - - - - +++
*+, low activity against microorganism; ++, moderate activity against microorganism;
+++, good activity against microorganism; -, no activity against microorganism
Patients with nosocomial acute sinusitis require adequate intravenous coverage of gram-
negative organisms (see Table 3, below). Aminoglycoside antibiotics are usually the drugs of
choice for the treatment of such patients because of their excellent gram-negative coverage
and sinus penetration. Selection of an antibiotic is usually based on the culture results of
attained maxillary secretion.
In addition to surgical management, complications of acute sinusitis should be managed with
a course of intravenous antibiotics. Third-generation cephalosporins (eg, cefotaxime,
ceftriaxone) in combination with vancomycin provide adequate intracranial penetration,
making them a good first-line choice.
Table 3. Dosage, Route, and Spectrum of Activity of Commonly Used Intravenous
Antibiotics (Second-Line)* (Open Table in a new window)
Antibiotic
Dosag
e
Streptococcu
s
pneumoniae

Haemophilu
s influenzae
Moraxella
catarrhali
s
Gram-
negativ
e
Anaerobi
c bacteria
Piperacillin 3-4 g
IV q4-
6h
+++ + - +++ +++
Piperacillin/tazobacta
m
3.375 g
IV q6h
+++ +++ +++ +++ ++
Ticarcillin 3 g IV
q4h
+++ - - +++ ++
Ticarcillin/clavulanate 3.1 g
IV q4h
+++ +++ - +++ ++
Imipenem 500 mg
IV q6h
+++ +++ +++ +++ +++
Meropenem 1 g IV
q8h
+++ +++ +++ +++ +++
Cefuroxime 1 g IV
q8h
+++ +++ +++ ++ ++
Ceftriaxone 2 g IV
bid
+++ +++ +++ +++ ++
Cefotaxime 2 g IV
q4-6h
+++ +++ +++ +++ ++
Ceftazidime 2 g IV
q8h
+++ +++ +++ +++ ++
Gentamicin 1.7
mg/kg
IV q8h
- +++ +++ ++ -
Tobramycin 1.7
mg/kg
IV q8h
- +++ +++ ++ -
Vancomycin 1 g IV
q6-12h
+++ - - - ++
*+, low activity against microorganism; ++, moderate activity against microorganism;
+++, good activity against microorganism; -, no activity against microorganism Does not
take into account penicillin-resistant types.
Symptomatic Treatment
Symptomatic or adjunctive therapies may include the following:
Humidification/vaporizer
Warm compresses
Adequate hydration
Smoking cessation
Balanced nutrition
Nonnarcotic analgesia
Antihistamines are not recommended and have not been proven beneficial. Topical
decongestants such as oxymetazoline can be used to decrease mucosal edema. To prevent
rebound congestion, they should not be used for more than 3 days.
A 15- to 21-day course of intranasal corticosteroids may reduce symptom duration when
compared to placebo.
[13, 41]
Mometasone 200, 400, and 800 g twice daily for 15 days is the
usual regimen given, with minimal adverse effects. Systemic steroids have no proven benefit
in sinusitis.
Topical ipratropium bromide 0.06% can be used to decrease rhinorrhea. Antihistamines have
not been shown to be of benefit in decreasing nasal congestion; in fact, they may cause
overdrying of the nasal mucosa. Mucolytics such as guaifenesin can be used to thin
secretions, though they have not been definitively shown to be of benefit.
Antimicrobial Therapy
Antimicrobial therapy is the mainstay of medical treatment in sinusitis. Choice of antibiotic
depends on whether the sinusitis is acute, chronic, or recurrent. The AAAAI 2005 practice
parameter states that choice of antibiotic should be based on predicted effectiveness, cost, and
side effects.
[12]

In clinically diagnosed acute sinusitis, little evidence from randomized, controlled trials
supports the use of antibiotics for the treatment of acute sinusitis.
[13]
Antibiotics have,
however, been shown to have a role in the treatment of acute maxillary sinusitis that is
diagnosed radiologically or bacteriologically.
Antibiotics are indicated for sinusitis that is thought to be bacterial, including sinusitis that is
severe or involves the frontal, ethmoid, or sphenoid sinuses, since this type of sinusitis is
more prone to complications.
[42]
Penicillins, cephalosporins, and macrolides seem to be
equally efficacious.
[13]
A 10- to 14-day regimen of amoxicillin 500 mg 3 times a day is
recommended by many as first-line therapy.
[43]

One study suggests that a single dose of 2 g of extended-release azithromycin may be more
effective than a 10-day course of amoxicillin/clavulanate.
[44]
However, azithromycin is not
likely a good choice in sinusitis because symptoms may improve only because of the anti-
inflammatory efficacy of the agent and because it has poor efficacy against S pneumoniae and
H influenzae. The risk of adverse effects should be weighed against the severity of disease
and patient comorbidities prior to initiating antibiotic treatment.
Patterns of bacterial resistance should also be taken into account in the choice of antibiotic.
(See Etiology.)
Overview of Surgical Therapy
Recurrent or persistent sinusitis and presence of complications may require surgical therapy.
Failure to respond to appropriate antibiotic therapy, especially in chronic and persistent
sinusitis (eg, cystic fibrosis), is an indication for surgical intervention.
Functional endoscopic sinus surgery (FESS) has revolutionized the treatment of sinusitis in
recent years. The therapeutic benefits of FESS have helped a large number of patients with
chronic sinus disease.
[45, 46]

See the article on Functional Endoscopic Sinus Surgery for more information.
Acute Frontal Sinusitis
Surgical treatment for acute frontal sinusitis is undertaken when the infection fails to respond
to conservative therapy (defined as the use of intravenous antibiotics and mucolytic agents
along with topical and systemic decongestants for 3-5 days) or when dangerous
complications arise. An additional indication is recurrent acute sinusitis, defined as 3-4
infections per year.
Acute Maxillary Sinusitis
Several techniques have been described for drainage of the maxillary sinus. The inferior
meatus and canine fossae are optimal drainage sites because of their ease of accessibility and
relatively thin well-vascularized bone.
Preoperative imaging is necessary to document the presence of acute sinusitis and to guide
surgical planning. Place conscious patients in the sitting position to allow for drainage of the
sinus contents into a provided basin. Protect the airway and suction the oropharynx during
sinus puncture performed on unconscious patients. In patients in the intensive care unit,
catheterization of the sinus may be undertaken with puncture to ensure continued adequate
drainage.
See the article on Acute Maxillary Sinusitis for more information.
Acute Sphenoid Sinusitis
In general, start medical treatment of acute sphenoid sinusitis once the diagnosis is made.
Institute antibiotics and decongestants for 24 hours, and if the patient does not improve over
this time course, schedule surgical therapy. If the patient has evidence of complications,
undertake urgent surgical decompression.
Some individuals advocate early and aggressive surgical and medical treatment for acute
sphenoid sinusitis. Hnatuk comments on the aggressive nature of the disease and concludes
that nonoperative medical management is not indicated.
[47]
These conclusions are based on a
small number of patients, all in their teenage years.
See the article on Acute Sphenoid Sinusitis for more information.
Acute Ethmoid Sinusitis
The typical case of acute ethmoidal sinusitis is treated with medical therapy. Medical
treatment can reduce the inflammation and edema of the mucosa, alleviate the pain, combat
the infection, open the ostia of the sinuses, and restore normal mucociliary secretions.
However, surgery is indicated in the following instances:
Sinusitis not responsive to medical management
Rapidly progressing sinusitis
Sinusitis that creates an abscess either in the sinus or adjacent areas such as the orbit
or brain
Sinusitis that compromises the survival of the patient
See the article on Acute Ethmoid Sinusitis for more information.
Complications
Treatment fails in 10-25% of patients. If this occurs, consider taking a repeat history and
perform an additional physical examination; consider an imaging study. Start second-line
antibiotics. Approximately 75% of orbital or periorbital infections are the result of extending
sinusitis. Untreated, inadequately treated, or partially treated rhinosinusitis may lead to
chronic rhinosinusitis, meningitis, brain abscess, or other extra-sinus complications.
Local complications
Mucoceles are chronic epithelial cysts that develop in sinuses in the presence of either an
obstructed sinus ostium or minor salivary gland duct. They have the potential for progressive
concentric expansion that can lead to bony erosion and extension beyond the sinus.
Maxillary sinus mucoceles are usually found incidentally on sinus radiographs and are of
little significance in the absence of symptomatology or infection. Surgical treatment is not
usually necessary, and these lesions often regress spontaneously over time.
Frontoethmoidal and sphenoethmoidal mucoceles, on the other hand, tend to be symptomatic
and have a high potential for bony erosion. Frontoethmoidal mucoceles should be completely
removed and the sinus obliterated. Sphenoethmoid mucoceles should be widely opened into
the nasal cavity.
Osteomyelitis is a potential local complication most commonly occurring with frontal
sinusitis. Osteomyelitis of the frontal bone is called a Pott puffy tumor and represents a
subperiosteal abscess with local edema anterior to the frontal sinus. This can advance to form
a fistula to the upper lid with sequestration of necrotic bone. This rare complication should be
managed with a combination of systemic antibiotics, surgical drainage of affected sinuses,
and debridement of necrotic bone.
Orbital complications
Orbital complications are the most common complications encountered with acute bacterial
sinusitis. Infection can spread directly through the thin bone separating the ethmoid or frontal
sinuses from the orbit or by thrombophlebitis of the ethmoid veins.
Diagnosis should be based on an accurate physical examination, including ophthalmological
evaluation and appropriate radiological studies. CT scanning is the most sensitive means of
diagnosing an orbital abscess, although ultrasound has been found to be 90% effective for
diagnosing anterior abscesses.
[27]
The classification by Chandler, which is based on physical
examination findings, provides a reasonable framework to guide management. This
classification consists of 5 groups of orbital inflammation
[30]
:
Group 1 - Inflammatory edema (preseptal cellulitis) with normal visual acuity and
extraocular movement
Group 2 - Orbital cellulitis with diffuse orbital edema but no discrete abscess
Group 3 - Subperiosteal abscess beneath the periosteum of the lamina papyracea
resulting in downward and lateral globe displacement
Group 4 - Orbital abscess with chemosis, ophthalmoplegia, and decreased visual
acuity
Group 5 - Cavernous sinus thrombosis with rapidly progressive bilateral chemosis,
ophthalmoplegia, retinal engorgement, and loss of visual acuity; possible meningeal
signs and high fever
Medical management, including sinus drainage and intravenous antibiotics, is advocated for
any degree of orbital complication. Among the classifications by Chandler, surgical drainage
of both the infected sinuses and the orbit are advocated for groups 3-5 if inadequate
improvement or progression of orbital cellulitis occurs despite medical therapy or if the
patient has loss of visual acuity.
Intracranial complications
Intracranial complications may occur as a result of direct extension through the posterior
frontal sinus wall or through retrograde thrombophlebitis of the ophthalmic veins. Subdural
abscess is the most common intracranial complication, although cerebral abscesses and
infarction that result in seizures, focal neurological deficits, and coma may occur. Intracranial
complications of sinusitis should be managed surgically with drainage of both the affected
sinus and the cranial abscess.
In a retrospective review of 23 cases (8 epidural, 10 subdural, 2 intracerebral abscess, and 3
meningitis) of intracranial complications of sinusitis (ICS) to identify the role and
effectiveness of endoscopic sinus surgery (ESS) in the acute setting of ICS, DelGuadio et al
concluded that ESS did not alter the need for neurosurgical intervention, which was
ultimately necessary in most patients, even those with lesions less than 1 cm.
[48]

In the study by DelGuadio et al, of the 23 patients, 22 (96%) had radiologic evidence of
frontal sinusitis with prefrontal or frontal lobe ICS at presentation. Medical therapy alone was
successful in avoiding craniotomy in only 3 of 8 cases, and treatment with endoscopic sinus
surgery and intravenous antibiotics was successful in avoiding craniotomy in only 1 of 6
patients. Of 23 patients, 18 required neurosurgical procedures (9 emergent procedures for
abscesses more than 1 cm and 9 delayed procedures for persistent disease despite ICS less
than 1 cm).
Systemic complications
Sinusitis can result in sepsis and multisystem organ failure caused by seeding of the blood
and various organ systems. Reports of bacteremia, thoracic empyema, and nosocomial
pneumonia have been documented in the intensive-care population with acute sinusitis, and
the mortality rate in this group can be as high as 11%.[#TreatmentConsultations]
Consultations
Emergent otolaryngology consultation for admission and definitive care should be obtained
in all patients with suspected CNS or orbital invasion or fungal infections. These patients
may present with the following symptoms:
Abnormal vision
Mental status changes
Periorbital edema
Consider outpatient referral to an otolaryngologist for patients with subacute or chronic
sinusitis. The following consultations are indicated:
Ear, nose, and throat specialist for complications or when routine management
techniques fail
Infectious disease specialist in complicated cases
Ophthalmological or neurosurgical consultation when either orbital or intracranial
complications develop
Surgical consultation when chronic sinusitis is refractory to maximal medical therapy
or a complication such as formation of mucopyocele with orbital or intracranial
extension is suspected
Medication Summary
Viral rhinosinusitis does not require antimicrobial treatment. Standard nonantimicrobial
treatment options include topical steroids, topical and/or oral decongestants, mucolytics, and
intranasal saline spray.
Antimicrobial therapy is the mainstay of medical treatment in sinusitis. The choice of
antibiotics depends on whether the sinusitis is acute, chronic, or recurrent.
Antibiotic efficacy rates are as follows
[49]
:
Levofloxacin, moxifloxacin, and amoxicillin/clavulanate - Greater than 90%
High-dose amoxicillin, cefpodoxime proxetil, cefixime, cefuroxime axetil, and
trimethoprim-sulfamethoxazole - 80-90%
Clindamycin, doxycycline, cefprozil, azithromycin, clarithromycin, and erythromycin
- 70-80%
Cefaclor - 50-60%
On the basis of the 2000 Sinus and Allergy Health Partnership treatment guidelines for acute
bacterial rhinosinusitis, patients are divided into 3 groups, as follows:
Adults with mild disease who have not received antibiotics: Amoxicillin/clavulanate,
amoxicillin (1.5-3.5 g/d), cefpodoxime proxetil, or cefuroxime is recommended as
initial therapy.
Adults with mild disease who have had antibiotics in the previous 4-6 weeks and
adults with moderate disease: Amoxicillin/clavulanate, amoxicillin (3-3.5 g),
cefpodoxime proxetil, or cefixime is recommended.
Adults with moderate disease who have received antibiotics in the previous 4-6
weeks: Amoxicillin/clavulanate, levofloxacin, moxifloxacin, or doxycycline is
recommended.
Patients who remain symptomatic despite appropriate antibiotic therapy may be evaluated
with sinus endoscopy, CT scanning, or sinus aspiration/culture.
Penicillins
Class Summary
The penicillins are bactericidal antibiotics that work against sensitive organisms at adequate
concentrations and inhibit the biosynthesis of cell wall mucopeptide. The penicillins are also
available in combination with agents that inactivate beta-lactamase enzymes, extending their
antibiotic spectrum.
View full drug information
Piperacillin and Tazobactam sodium (Zosyn)

The piperacillin-tazobactam combination includes an antipseudomonal penicillin plus beta-
lactamase inhibitor. It inhibits biosynthesis of cell wall mucopeptide and is effective during
the stage of active multiplication.
View full drug information
Ticarcillin and clavulanate potassium (Ticar)

The ticarcillin-clavulanate combination inhibits the biosynthesis of cell wall mucopeptide and
is effective during the stage of active growth. It has antipseudomonal penicillin plus a beta-
lactamase inhibitor that provides coverage against most gram-positive, gram-negative, and
anaerobic organisms.
View full drug information
Penicillin VK (Beepen-VK, Pen-Vee K)

Penicillin V is a first-line antibiotic choice. It inhibits biosynthesis of cell wall mucopeptide.
It is bactericidal against sensitive organisms when adequate concentrations are reached and
most effective during the stage of active multiplication. Inadequate concentrations may
produce only bacteriostatic effects.
View full drug information
Amoxicillin and clavulanate (Augmentin)

Amoxicillin-clavulanate is a second-line agent; this drug combination treats bacteria resistant
to beta-lactam antibiotics.
View full drug information
Amoxicillin (Amoxil, Trimox)

Amoxicillin is a first-line antibiotic choice. It interferes with synthesis of cell wall
mucopeptides during active multiplication, resulting in bactericidal activity against
susceptible bacteria.
View full drug information
Piperacillin

Piperacillin inhibits the biosynthesis of cell wall mucopeptides and the stage of active
multiplication; it has antipseudomonal activity.
Cephalosporins
Class Summary
Cephalosporins are structurally and pharmacologically related to penicillins. They inhibit
bacterial cell wall synthesis, resulting in bactericidal activity. Cephalosporins are divided into
first, second, third and fourth generation. First-generation cephalosporins have greater
activity against gram-positive bacteria, and succeeding generations have increased activity
against gram-negative bacteria and decreased activity against gram-positive bacteria.
View full drug information
Cefprozil (Cefzil)

Cefprozil is a second-line agent. It binds to one or more of the penicillin-binding proteins,
which, in turn, inhibits cell wall synthesis and results in bactericidal activity.
View full drug information
Cefuroxime (Ceftin)

Cefuroxime is a second-line agent. It is a second-generation cephalosporin that maintains the
gram-positive activity of first-generation cephalosporins, adding activity against Proteus
mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and M catarrhalis.
View full drug information
Cefpodoxime (Vantin)

Cefpodoxime is a second-line agent. It binds to one or more penicillin-binding proteins,
which, in turn, inhibits cell wall synthesis and results in bactericidal activity.
View full drug information
Cefixime (Suprax)

Cefprozil is a second-line agent. By binding to one or more penicillin-binding proteins, it
arrests bacterial cell wall synthesis and inhibits bacterial growth.
View full drug information
Ceftriaxone (Rocephin)

Ceftriaxone is a third-generation cephalosporin with broad-spectrum, gram-negative activity;
it has lower efficacy against gram-positive organisms and higher efficacy against resistant
organisms. It arrests bacterial growth by binding to one or more penicillin binding proteins. It
has good penetration.
View full drug information
Cefdinir (Omnicef)

Classified as a third-generation cephalosporin, cefdinir inhibits mucopeptide synthesis in the
bacterial cell wall. It is typically bactericidal, depending on organism susceptibility, dose, and
serum or tissue concentrations.
View full drug information
Cefaclor (Ceclor, Ceclor CD)

Cefaclor is used for treatment of infections caused by susceptible organisms including H
influenzae and for treatment of otitis media, sinusitis, and infections involving the respiratory
tract. It may not be appropriate in acute sinusitis, owing to less activity and the potential for
severe allergic reactions.
View full drug information
Cefotaxime (Claforan)

Cefotaxime is a third-generation cephalosporin with broad gram-negative spectrum, lower
efficacy against gram-positive organisms, and higher efficacy against resistant organisms. It
arrests bacterial cell wall synthesis by binding to one or more of the penicillin-binding
proteins, which, in turn, inhibits bacterial growth.
View full drug information
Ceftazidime (Fortaz, Tazicef)

Ceftazidime is a third-generation cephalosporin with broad-spectrum, gram-negative activity,
including pseudomonas; lower efficacy against gram-positive organisms; and higher efficacy
against resistant organisms. It arrests bacterial growth by binding to one or more penicillin-
binding proteins, which, in turn, inhibits the final transpeptidation step of peptidoglycan
synthesis in bacterial cell wall synthesis, thus inhibiting cell wall biosynthesis.
Macrolides
Class Summary
Macrolide antibiotics have bacteriostatic activity and exert their antibacterial action by
binding to the 50S ribosomal subunit of susceptible organisms, resulting in inhibition of
protein synthesis. Macrolide antibiotics are often used in patients allergic to penicillins.
View full drug information
Erythromycin (E.E.S., E-Mycin, Eryc)

Erythromycin is a first-line treatment in patients allergic to penicillin. It inhibits bacterial
growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-
dependent protein synthesis to arrest.
View full drug information
Clarithromycin (Biaxin)

Clarithromycin is a second-line agent. It inhibits bacterial growth, possibly by blocking
dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to
arrest.
View full drug information
Azithromycin (Zithromax, Zmax)

Azithromycin, an advanced-generation macrolide, works similarly to clarithromycin but with
shorter dosage time.
View full drug information
Erythromycin and sulfisoxazole (Eryzole, Pediazole)

This agent is used for treatment of susceptible bacterial infections of upper and lower
respiratory tract: in children, it is used for otitis media caused by susceptible strains of H
influenzae; it is used for many other infections in patients allergic to penicillin.
Fluoroquinolones
Class Summary
Fluoroquinolones have broad-spectrum activity against gram-positive and gram-negative
aerobic organisms. They inhibit DNA synthesis and growth by inhibiting DNA gyrase and
topoisomerase, which is required for replication, transcription, and translation of genetic
material.
View full drug information
Levofloxacin (Levaquin)

Levofloxacin is used to treat acute maxillary sinusitis caused by S pneumoniae, H influenzae,
or M catarrhalis. Fluoroquinolones should be used empirically in patients likely to develop
exacerbation due to resistant organisms to other antibiotics. This is the L stereoisomer of the
D/L parent compound ofloxacin, the D form being inactive. It provides good monotherapy
with extended coverage against Pseudomonas species, as well as excellent activity against
pneumococcus. The agent acts by inhibition of DNA gyrase activity. The oral form has
bioavailability that is reportedly 99%.
View full drug information
Ciprofloxacin (Cipro)

Ciprofloxacin is a broad spectrum antibiotic with activity against gram-positive and gram-
negative aerobic organisms. It inhibits bacterial DNA synthesis and, consequently, growth,
by inhibiting DNA gyrase and topoisomerase, which are required for replication,
transcription, and translation of genetic material.
View full drug information
Moxifloxacin (Avelox)

Moxifloxacin inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA
replication and transcription.
Anti-Infectives
Class Summary
Anti-infectives such as vancomycin, clindamycin, metronidazole, and sulfamethoxazole-
trimethoprim are effective against some types of bacteria that have become resistant to other
antibiotics.
View full drug information
Trimethoprim and sulfamethoxazole (Bactrim DS, Septra)

Trimethoprim-sulfamethoxazole is a first-line agent with more convenient dosing. It inhibits
bacterial growth by inhibiting synthesis of dihydrofolic acid.
View full drug information
Vancomycin (Vancocin, Lyphocin, Vancoled)

Vancomycin is a potent antibiotic directed against gram-positive organisms and active
against Enterococcus species (useful in septicemia and skin structure infections;
Enterococcus is very rare in sinusitis). Vancomycin is indicated for patients who cannot
receive or have failed to respond to penicillins and cephalosporins or who have infections
with resistant staphylococci.
View full drug information
Metronidazole

Metronidazole is an imidazole ring-based antibiotic that is active against various anaerobic
bacteria and protozoa. It is used in combination with other antimicrobial agents (except C
difficile enterocolitis).
View full drug information
Clindamycin

Clindamycin is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-
hydroxyl group of parent compound lincomycin. It inhibits bacterial growth, possibly by
blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein
synthesis to arrest. Clindamycin widely distributes in the body without penetration of the
CNS. It is protein bound and is excreted by the liver and kidneys.
Carbapenems
Class Summary
Carbapenems are structurally related to penicillins and have broad-spectrum bactericidal
activity. The carbapenems exert their effect by inhibiting cell wall synthesis, which leads to
cell death. They are active against gram-negative, gram-positive, and anaerobic organisms.
View full drug information
Imipenem and cilastatin (Primaxin)

The imipenem-cilastin combination is used for the treatment of multiple-organism infections
in which other agents do not have wide-spectrum coverage or are contraindicated because of
the potential for toxicity.
View full drug information
Meropenem (Merrem IV)

A bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis,
meropenem is effective against most gram-positive and gram-negative bacteria. Compared
with imipenem, meropenem has slightly increased activity against gram-negative organisms
and slightly decreased activity against staphylococci and streptococci.
Aminoglycosides
Class Summary
Aminoglycosides are bactericidal antibiotics used to primarily treat gram-negative infections.
They interfere with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.
View full drug information
Gentamicin (Gentacidin, Garamycin)

Gentamicin is an aminoglycoside antibiotic effective against Pseudomonas aeruginosa; E
coli; and Proteus, Klebsiella, and Staphylococcus species. Gentamicin is also variably
effective against some strains of certain gram-positive organisms, including S aureus,
enterococci, and L monocytogenes. Dosing regimens are numerous; adjust the dose based on
creatinine clearance and changes in volume of distribution.
View full drug information
Tobramycin (Nebcin)

Tobramycin is used in skin, bone, and skin structure infections caused by S aureus, P
aeruginosa, Proteus species, E coli, Klebsiella species, and Enterobacter species. It is
indicated in the treatment of staphylococcal infections when penicillin or potentially less-
toxic drugs are contraindicated and when bacterial susceptibility and clinical judgment justify
its use. Like other aminoglycosides, tobramycin is associated with nephrotoxicity and
ototoxicity.
Tetracyclines
Class Summary
Tetracyclines inhibit protein synthesis and, thus, bacterial growth by binding to 30S and
possibly 50S ribosomal subunits of susceptible bacteria. They may block dissociation of
peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
View full drug information
Doxycycline (Periostat, Doryx, Bio-Tab, Vibramycin Vibra-tabs)

Doxycycline is has broad-spectrum activity and is a synthetically derived bacteriostatic
antibiotic in the tetracycline class. Doxycycline inhibits protein synthesis, and thus bacterial
growth, by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
Decongestants
Class Summary
These agents cause vasoconstriction, which reduces nasal congestion. Topical agents are
locally active vasoconstrictor agents such as phenylephrine and oxymetazoline, which
provide immediate symptomatic relief by shrinking the inflamed and swollen nasal mucosa.
Oral decongestants such as pseudoephedrine can be used for 10-14 days to allow for
restoration of normal mucociliary function and drainage.
View full drug information
Phenylephrine nasal (Neo-Synephrine)

Phenylephrine produces vasoconstriction. It is possibly helpful and is not harmful.
View full drug information
Oxymetazoline (Afrin)

Oxymetazoline is applied directly to mucous membranes. It stimulates alpha-adrenergic
receptors and causes vasoconstriction. Decongestion occurs without drastic changes in blood
pressure, vascular redistribution, or cardiac stimulation.
View full drug information
Tetrahydrozoline, ophthalmic (Tyzine, Visine)

The alpha-adrenergic effects of tetrahydrozoline on nasal mucosa produce vasoconstriction.
View full drug information
Pseudoephedrine (Sudafed)

Phenylephrine produces vasoconstriction. It is possibly helpful and is not harmful.
Nasal Sprays
Class Summary
Nasal saline spray and steam inhalation help by moistening dry secretions, reducing mucosal
edema, and reducing mucus viscosity. The symptomatic relief gained in some patients can be
substantial; moreover, these are benign modalities of therapy.
Saline nasal spray (Ayr, Ocean)

Saline nasal sprays loosen mucus secretions to help remove mucus from the nose and sinuses.
Expectorants
Class Summary
Mucolytic agents such as guaifenesin have the theoretical benefit of thinning mucous
secretions and improving drainage.
View full drug information
Guaifenesin (Anti-Tuss, Humibid LA, Robitussin)

Guaifenesin increases respiratory tract fluid secretions and helps to loosen phlegm and
bronchial secretions. It is indicated for patients with bronchiectasis complicated by tenacious
mucous and/or mucous plugs.
Corticosteroids
Class Summary
Intranasal steroids have not been conclusively shown to be of benefit in cases of acute
sinusitis. Study results conflict, with some reporting benefit as monotherapy or in
combination with antibiotics and others reporting no benefit (combination or monotherapy).
Beclomethasone (Beconase, Vancenase)

Beclomethasone has potent vasoconstrictive and anti-inflammatory activity. It has a weak
hypothalamic-pituitary-adrenocortical (HPA) axis inhibitory potency when applied topically.
View full drug information
Triamcinolone inhaled (Nasacort, Nasacort AQ)

Triamcinolone decreases inflammation by suppressing migration of polymorphonuclear
leukocytes and reversing capillary permeability.
View full drug information
Flunisolide (AeroBid, Nasalide)

Flunisolide inhibits bronchoconstriction mechanisms, producing direct smooth muscle
relaxation. It may decrease the number and activity of inflammatory cells, in turn decreasing
airway hyperresponsiveness. Flunisolide decreases inflammation by suppressing migration of
polymorphonuclear leukocytes and reversing capillary permeability. It does not depress the
hypothalamus.
Anticholinergics
Class Summary
Anticholinergics block interactions between acetylcholine and muscarinic receptors on the
smooth muscle preventing increases in cyclic GMP inhibiting bronchoconstriction and mucus
secretion.
View full drug information
Ipratropium (Atrovent, Atrovent HFA)

Topical ipratropium bromide can be used to decrease rhinorrhea. Anticholinergics such as
ipratropium have anti-secretory properties, and when applied locally, inhibit secretions from
serous, and seromucous glands lining the nasal mucosa.