Acute Sinusitis

Back

Practice Essentials

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. Rhinosinusitis affects an estimated 35 million people per year in the United States and accounts for close to 16 million office visits per year.[1] See the image below.



View Image

Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.

Signs and symptoms

Clinical findings in acute sinusitis may include the following:

Symptoms of acute bacterial rhinosinusitis include the following:

The diagnosis of acute bacterial sinusitis should be entertained under either of the following circumstances:

The following signs may be noted on physical examination:

See Clinical Presentation for more detail.

Diagnosis

Acute sinusitis is a clinical diagnosis. However, the evaluation might include the following laboratory tests[2] :

Nasal cytology examinations may be useful to elucidate the following entities:

Tests for immunodeficiency are indicated if history findings indicate recurrent infection; they include the following:

Cultures are not routinely obtained in the evaluation of acute sinusitis but should be obtained in the following cases:

In adults, cultures are directed at the middle meatus. Aspiration of the sinus by direct antral puncture is the only accurate way to obtain a culture but is reserved for patients with any of the following:

Computed tomography scanning is the preferred imaging method for 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.

See Workup for more detail.

Management

Treatment of acute sinusitis consists of providing adequate drainage of the involved sinus and appropriate systemic treatment of the likely bacterial pathogens. Drainage can be achieved surgically with sinus puncture and irrigation techniques. Options for medical drainage are as follows:

Antibiotic treatment is usually given for 14 days. Usual first-line therapy is with one of the following:

Second-line antibiotic should be considered for patients with any of the following:

The most commonly used second-line therapies include the following:

Antibiotic selection with respect to previous antibiotic use and disease severity is as follows:

Symptomatic or adjunctive therapies may include the following:

See Treatment and Medication for more detail.

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.[4, 5]

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:

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.[6]

 

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.[5] 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).



View Image

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,[7] which is 5-100 μm 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 mm2 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.[8, 5]

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.[9] 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.[10] 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.[11] Jiang et al evaluated the bacteriology of maxillary sinuses with normal endoscopic findings.[12] 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.[13] 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

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.[14]

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.[2]

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.[15, 16]

Viral upper respiratory tract infections are the most important risk factor for the development of acute bacterial sinusitis.[17] 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.[18]

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.[19, 20] 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.[21] 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-lactamase–positive 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 also the mechanism of antimicrobial resistance for M catarrhalis. Of isolates from the paranasal sinus, 98% were found to be beta-lactamase–positive 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.[22] 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.[23]

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.[1]

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.[24]

In 1996, Americans spent approximately $3.39 billion treating rhinosinusitis.[25] The economic burden of acute sinusitis in children is $1.77 billion per year.[25]

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.[26, 27]

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.

Patient Education

For excellent patient education resources, visit eMedicineHealth’s Headache Center. Also, see eMedicineHealth'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:

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.[28]

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 2007 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.[29]

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.[2]

The 2007 guidelines[29] were updated in 2015[30] based on evidence from 42 new systematic reviews. They included a new algorithm to clarify action statement relationships and expanded opportunities for watchful waiting (without antibiotic therapy) as initial therapy for acute bacterial rhinosinusitis. They strongly recommended that clinicians (1) distinguish presumed acute bacterial rhinosinusitis from acute sinusitis caused by viral upper respiratory infections and noninfectious conditions and (2) confirm a clinical diagnosis of chronic sinusitis with objective documentation of sinonasal inflammation, which may be accomplished using anterior rhinoscopy, nasal endoscopy, or computed tomography.

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.[31]

Although diagnostic criteria for acute rhinosinusitis have been proposed,[4] no single sign or symptom has strong diagnostic value for bacterial rhinosinusitis.[32] 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:

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.[32]

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. Purulence can occur with and without any sinus bacterial infection, and is often present in those with nasopharyngitis.[55]

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:

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%).[33]

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.[28] 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[32] :

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%.

Approach Considerations

In June 2013, the American Academy of Pediatrics published updated guidelines on the diagnosis and management of acute bacterial sinusitis in children and adolescents. Changes include the following:

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.[34] 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.[2]

The 2007 guidelines by the American Academy of Otolaryngology--Head and Neck Surgery Foundation[29] were updated in 2015[30] and recommended that clinicians (1) reassess the patient to confirm acute bacterial rhinosinusitis, to exclude other causes of illness, and to detect complications if the patient worsens or fails to improve with the initial management option by 7 days after diagnosis or worsens during the initial management; (2) distinguish chronic sinusitis and recurrent acute sinusitis from isolated episodes of acute sinusitis and other causes of sinonasal symptoms; and (3) assess the patient with chronic sinusitis or recurrent acute sinusitis for multiple chronic conditions that would modify management, such as asthma, cystic fibrosis, immunocompromised state, and ciliary dyskinesia.

The 2015 guidelines[30] recommend that clinicians should not obtain radiographic imaging in patients who meet diagnostic criteria for acute sinusitis unless a complication or alternative diagnosis is suspected.

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.



View Image

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:

Nasal Cytology

Nasal cytology examinations may be useful to elucidate the following entities:

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 104 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.[35]

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.[2]

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.[2]

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.



View Image

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:

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.

Approach Considerations

In June 2013, the American Academy of Pediatrics published updated guidelines on the diagnosis and management of acute bacterial sinusitis in children and adolescents. Changes include the following:

The Canadian clinical practice guidelines for acute bacterial rhinosinusitis based the diagnosis of acute bacterial sinusitis on the presence of specific symptoms and their duration; imagining or cultures are not needed in uncomplicated cases.[36] The guidelines for treatment depend on symptom severity and recommend intranasal corticosteroids (INCSs) as monotherapy for mild and moderate cases, although the benefit might be modest. The use of INCSs plus antibiotics is reserved for patients who fail to respond to INCSs after 72 hours and for initial treatment of patients with severe symptoms. The guidelines recommended that antibiotic selection must account for the suspected pathogen, the risk of resistance, comorbid conditions, and local antimicrobial resistance trends. Adjunctive therapies such as nasal saline irrigation are recommended. Failure to respond to treatment, recurrent episodes, and signs of complications should prompt referral to an otolaryngologist.

The 2007 guidelines by the American Academy of Otolaryngology--Head and Neck Surgery Foundation[29] were updated in 2015[30] and recommended that clinicians (1) either offer watchful waiting (without antibiotics) or prescribe initial antibiotic therapy for adults with uncomplicated acute bacterial rhinosinusitis or (2) prescribe amoxicillin with or without clavulanate as first-line therapy for 5-10 days (if the decision is made to treat acute bacterial rhinosinusitis with an antibiotic).

The guidelines state that clinicians may (1) recommend analgesics, topical intranasal steroids, and/or nasal saline irrigation for symptomatic relief of viral rhinosinusitis; (2) recommend analgesics, topical intranasal steroids, and/or nasal saline irrigation for symptomatic relief of acute sinusitis; and (3) obtain testing for allergy and immune function in the evaluation of a patient with chronic or recurrent acute sinusitis.

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:

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.[37] However, a randomized, controlled trial of antibiotics and intranasal steroid showed no treatment benefit of intranasal steroids, either alone or with antibiotics.[38]

In a literature study, van Loon et al concluded that only limited evidence exists regarding the efficacy of intranasal corticosteroids in relieving the symptoms of recurrent acute rhinosinusitis. The best evidence, according to the investigators, came from a single study, which had a low bias risk but only moderate directness of evidence; according to that report, intranasal corticosteroids may shorten the time needed to achieve symptom relief.[39]

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.[40] However, another meta-analysis found no treatment effect of antibiotics, even in patients whose symptoms had persisted for more than 10 days.[41]

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-lactamase–mediated 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.[42]

The reduced efficacy of amoxicillin led the Infectious Diseases Society of America to generate new guidelines for the treatment of acute rhinosinusitis. These guidelines recommend amoxicillin-clavulanate over amoxicillin as empiric antimicrobial therapy in adults and children with acute bacterial rhinosinusitis.[43]

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 substantially magnified if more of the study patients actually had acute bacterial rhinosinusitis.

Sng and Wang evaluated 31 random control trials studying the clinical efficacy and side effects of cefuroxime axetil, telithromycin, amoxicillin/potassium clavulanate, levofloxacin, moxifloxacin and clarithromycin in the treatment of acute bacterial sinusitis. Among them, 9 studies were performed double-blinded with placebo controls. The results showed that, while antibiotics are more efficacious than placebo in the treatment of acute bacterial sinusitis, the risks of potential side effects need to be weighed against the potential benefits.[44]

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.[31]

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 5-10 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*



View Table

See Table

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*



View Table

See Table

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)*



View Table

See Table

Symptomatic Treatment

Symptomatic or adjunctive therapies may include the following:

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.[15, 45] Mometasone 200, 400, and 800 μg 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.[2]

In clinically diagnosed acute sinusitis, little evidence from randomized, controlled trials supports the use of antibiotics for the treatment of acute sinusitis.[15] Antibiotics have, however, been shown to have a role in the treatment of acute maxillary sinusitis that is diagnosed radiologically or bacteriologically.

Based on a literature review, Kaper et al concluded that no studies have adequately addressed whether the effects of antibiotic therapy in recurrent acute rhinosinusitis differ from those in primary or sporadic episodes of acute rhinosinusitis. The authors concluded, therefore, that the question of whether or not to use initial antibiotic therapy in patients with recurrent episodes of the condition should be decided by employing the same criteria used to weigh the need for antibiotic treatment in patients with primary or sporadic episodes of uncomplicated acute rhinosinusitis.[46]

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.[47] Penicillins, cephalosporins, and macrolides seem to be equally efficacious.[15] A 5- to 10-day regimen of amoxicillin 500 mg 3 times a day is recommended as first-line therapy.[30, 43, 48]

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.[49] 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.[50, 51]

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.[52] 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:

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.[28] 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[32] :

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.[53]

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%.

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:

Consider outpatient referral to an otolaryngologist for patients with subacute or chronic sinusitis. The following consultations are indicated:

Guidelines Summary

The 2015 updated guidelines by the American Academy of Otolaryngology--Head and Neck Surgery Foundation now recommends watchful waiting for initial management of all patients with uncomplicated acute bacterial rhinosinusitis, regardless of severity,[30] and not just for those with "mild" illness, as in the 2007 guideline.[29] In addition, the recommendation for the preferred agent when antibiotics are prescribed is now amoxicillin with or without clavulanate[30] , whereas the 2007 guideline called for amoxicillin alone.[29]

Other recommendations include the following:[30]

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[54] :

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:

Patients who remain symptomatic despite appropriate antibiotic therapy may be evaluated with sinus endoscopy, CT scanning, or sinus aspiration/culture.

Piperacillin and Tazobactam sodium (Zosyn)

Clinical Context:  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.

Ticarcillin and clavulanate potassium

Clinical Context:  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.

Penicillin VK

Clinical Context:  Penicillin V potassium 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.

Amoxicillin and clavulanate (Augmentin, Amoclan)

Clinical Context:  Amoxicillin-clavulanate is a second-line agent; this drug combination treats bacteria resistant to beta-lactam antibiotics.

Amoxicillin (Moxatag)

Clinical Context:  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.

Piperacillin

Clinical Context:  Piperacillin inhibits the biosynthesis of cell wall mucopeptides and the stage of active multiplication; it has antipseudomonal activity.

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.

Cefprozil

Clinical Context:  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.

Cefuroxime (Ceftin, Zinacef)

Clinical Context:  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.

Cefpodoxime

Clinical Context:  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.

Cefixime (Suprax)

Clinical Context:  Cefixime is a second-line agent. By binding to one or more penicillin-binding proteins, it arrests bacterial cell wall synthesis and inhibits bacterial growth.

Ceftriaxone (Rocephin)

Clinical Context:  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.

Cefdinir

Clinical Context:  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.

Cefaclor

Clinical Context:  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.

Cefotaxime (Claforan)

Clinical Context:  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.

Ceftazidime (Fortaz, Tazicef)

Clinical Context:  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.

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.

Erythromycin ethylsuccinate (E.E.S., Ery-Tab, PCE)

Clinical Context:  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.

Clarithromycin (Biaxin)

Clinical Context:  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.

Azithromycin (Zithromax, Zmax)

Clinical Context:  Azithromycin, an advanced-generation macrolide, works similarly to clarithromycin but with shorter dosage time.

Erythromycin base and sulfisoxazole (Pediazole)

Clinical Context:  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.

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.

Levofloxacin (Levaquin)

Clinical Context:  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%.

Ciprofloxacin (Cipro)

Clinical Context:  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.

Moxifloxacin (Avelox)

Clinical Context:  Moxifloxacin inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription.

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.

Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Sulfatrim Pediatric)

Clinical Context:  Trimethoprim-sulfamethoxazole is a first-line agent with more convenient dosing. It inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.

Vancomycin

Clinical Context:  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.

Metronidazole (Flagyl, Metro)

Clinical Context:  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).

Clindamycin (Cleocin)

Clinical Context:  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.

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.

Imipenem and cilastatin (Primaxin)

Clinical Context:  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.

Meropenem (Merrem)

Clinical Context:  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.

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.

Gentamicin

Clinical Context:  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.

Tobramycin

Clinical Context:  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.

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.

Doxycycline (Doryx, Adoxa, Monodox, Vibramycin)

Clinical Context:  Doxycycline 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.

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.

Phenylephrine nasal (Neo-Synephrine Cold & Sinus, Rhinall, Nasal Four)

Clinical Context:  Phenylephrine produces vasoconstriction. It is possibly helpful and is not harmful.

Oxymetazoline (Afrin 12 Hour, Afrin Sinus, QlearQuil)

Clinical Context:  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.

Tetrahydrozoline, ophthalmic (Tyzine)

Clinical Context:  The alpha-adrenergic effects of tetrahydrozoline on nasal mucosa produce vasoconstriction.

Pseudoephedrine (Sudafed, Nexafed, SudoGest, Genaphed)

Clinical Context:  Phenylephrine produces vasoconstriction. It is possibly helpful and is not harmful.

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.

Saline nasal spray (Ayr, Ocean Nasal Spray, Nasal Moist)

Clinical Context:  Saline nasal sprays loosen mucus secretions to help remove mucus from the nose and sinuses.

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.

Guaifenesin (Altarussin, Bidex, Geri-Tussin, Liquibid, Mucinex)

Clinical Context:  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.

Class Summary

Mucolytic agents such as guaifenesin have the theoretical benefit of thinning mucous secretions and improving drainage.

Beclomethasone, intranasal (Beconase AQ, QNASL)

Clinical Context:  Beclomethasone has potent vasoconstrictive and anti-inflammatory activity. It has a weak hypothalamic-pituitary-adrenocortical (HPA) axis inhibitory potency when applied topically.

Triamcinolone inhaled (Nasacort, Nasacort AQ)

Clinical Context:  Triamcinolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.

Flunisolide intranasal

Clinical Context:  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.

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).

Ipratropium (Atrovent)

Clinical Context:  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.

Class Summary

Anticholinergics block interactions between acetylcholine and muscarinic receptors on the smooth muscle preventing increases in cyclic GMP inhibiting bronchoconstriction and mucus secretion.

What are the symptoms of acute sinusitis (sinus infection)?What are the symptoms of acute bacterial rhinosinusitis (RS)?What is sinusitis (sinus infection)?When should acute bacterial sinusitis (sinus infection) be suspected?What are clinical signs of acute bacterial sinusitis (sinus infection)?How is acute sinusitis (sinus infection) diagnosed?What is the role of nasal cytology testing in the diagnosis of acute sinusitis (sinus infection)?When are immunodeficiency tests indicated in the diagnosis of acute sinusitis (sinus infection)?When are cultures indicated for the diagnosis of acute sinusitis?What is the role of imaging studies in the diagnosis of rhinosinusitis (RS)?How is acute sinusitis (sinus infection) treated?What are the options for medical drainage of acute sinusitis (sinus infection)?What are the options for first-line antibiotic therapy for acute sinusitis (sinus infection)?When are second-line antibiotics indicated for acute sinusitis (sinus infection)?What are the options for second-line antibiotic therapy for acute sinusitis (sinus infection)?Which antibiotics are recommended in the treatment of acute sinusitis (sinus infection) based on previous antibiotic use and disease severity?Which symptomatic or adjunctive therapies may be considered for acute sinusitis (sinus infection)?How is sinusitis (sinus infection) characterized?How is rhinosinusitis (RS) classified?How is acute sinusitis (sinus infection) diagnosed?What are the primary goals in the treatment of acute sinusitis (sinus infection)?When is evaluation by an otolaryngologist indicated for acute sinusitis (sinus infection)?What is the definition of acute rhinosinusitis (RS)?Over what timeframe do the paranasal sinuses develop?How do the paranasal sinuses develop during gestation?How are the paranasal sinuses structured?What is the composition of the anterior and posterior ethmoid sinuses?How is the blood supplied and lymphatic drainage accomplished in the paranasal sinuses?What is the drainage path of the sinuses?How is sinus drainage maintained?What is the function of the paranasal sinuses?How does infection develop in the sinuses?What causes sinusitis (sinus infection)?Can healthy sinuses be colonized with bacteria?Which factors are involved in the pathophysiology of rhinosinusitis (RS)?How does the ostia become blocked?What systemic diseases are predisposing risk factors for sinusitis (sinus infection)?Does immunodeficiency increase the risk for sinusitis (sinus infection)?Which mechanical obstructions may lead to ostial blockage and sinusitis (sinus infection)?How do obstructed sinuses lead to sinusitis (sinus infection)?What is the role of ciliary function in the pathogenesis of sinusitis (sinus infection)?What factors can lead to impaired ciliary function?What are the layers of the mucous blanket in the paranasal sinus?What is the role of mucus composition in the pathogenesis of sinusitis (sinus infection)?What is the pathophysiology of acute sinusitis (sinus infection) in the intensive care setting?What causes sinusitis (sinus infection)?Which pathogens cause acute viral rhinosinusitis (RS)?Which pathogens are responsible for acute nosocomial bacterial rhinosinusitis (sinus infection)?What is the role of S pneumoniae in the etiology of acute bacterial rhinosinusitis (sinus infection)?How often does H influenzae cause acute bacterial rhinosinusitis (sinus infection)?How often does M catarrhalis cause acute bacterial rhinosinusitis (sinus infection)?Does S aureus cause acute bacterial rhinosinusitis (sinus infection)?What is the incidence of sinusitis (sinus infection) in the US?What is the international prevalence of acute sinusitis (sinus infection)?Which conditions predispose to acute bacterial rhinosinusitis (RS)?How has pneumococcal vaccine changed the etiology of acute bacterial rhinosinusitis (sinus infection)?How often do sinus aspirates contain bacteria in acute bacterial rhinosinusitis (sinus infection), and what are the most common isolates?What are the most common pathogens isolated from maxillary sinus cultures in acute bacterial rhinosinusitis (RS)?How often are gram-negative organisms, gram-positive organisms, and polymicrobial invasion found on culture in acute bacterial rhinosinusitis (sinus infection)?What is the etiology of acute invasive fungal rhinosinusitis (RS)?What is the economic burden of rhinosinusitis (RS)?What is the prevalence of acute sinusitis (sinus infection) in children?Is acute sinusitis (sinus infection) more common in males or females?What is the prognosis of sinusitis (sinus infection)?Where can patients find information on sinusitis (sinus infection)?What are the symptoms of acute bacterial rhinosinusitis (RS)?How is acute sinusitis (sinus infection) diagnosed?What should be the focus of the medical history during evaluation for rhinosinusitis (RS)?Which medical history findings are relevant for suspected fungal sinusitis (sinus infection)?Which clinical findings suggest acute sinusitis (sinus infection)?What duration of respiratory tract infection suggests acute sinusitis (sinus infection)?When should acute bacterial sinusitis (sinus infection) be suspected during the course of a viral upper respiratory tract infection?Is it important to distinguish acute bacterial rhinosinusitis (sinus infection) from acute viral or noninfectious rhinosinusitis, and what are the clues for differentiation?How often is acute bacterial rhinosinusitis (RS) correctly diagnosed?What is the role of anterior rhinoscopic exam in the diagnosis of acute sinusitis (sinus infection)?What is the role of endoscopic exam in the diagnosis of acute sinusitis (sinus infection)?What are the common physical findings of acute sinusitis (sinus infection)?Is acute sinusitis (sinus infection) common in children?What physical findings suggest acute bacterial sinusitis (sinus infection) in children?How often is pediatric acute sinusitis (sinus infection) suspected and diagnosed, and what are the most commonly used treatments?What does nasal exam consist of in children younger than 6 years with acute sinusitis (sinus infection)?What are the symptoms of acute ethmoiditis in children?What are the AAP recommendations for the use of imaging studies in children with suspected acute bacterial sinusitis (sinus infection)?Which complications may result from sinusitis?What are mucoceles?How common is osteomyelitis as a complication of acute sinusitis?How does acute bacterial sinusitis (sinus infection) cause orbital complications?How is orbital inflammation due to sinusitis (sinus infection) diagnosed and classified?Can acute sinusitis (sinus infection) cause intracranial complications?What are systemic complications of sinusitis (sinus infection)?How is cystic fibrosis differentiated from acute sinusitis (sinus infection)?How is Kartagener syndrome differentiated from acute sinusitis (sinus infection)?How is Wegener granulomatosis differentiated from acute sinusitis (sinus infection)?How is ataxia-telangiectasia differentiated from acute sinusitis (sinus infection)?How is immotile cilia syndrome differentiated from acute sinusitis (sinus infection)?How are allergies and asthma differentiated from acute sinusitis (sinus infection)?How is Wiskott-Aldrich syndrome differentiated from acute sinusitis (sinus infection)?How is yellow-nail syndrome differentiated from acute sinusitis (sinus infection)?How is Young syndrome (Barry-Perkins-Young syndrome) (sinusitis-infertility syndrome) differentiated from acute sinusitis (sinus infection)?What are some of the less-common disorders that should be included in the differential diagnoses of acute sinusitis (sinus infection)?What are the differential diagnoses for Acute Sinusitis?What changes were made when the AAP updated its guidelines for the diagnosis and management of acute bacterial sinusitis (sinus infection) in children and adolescents?What lab tests are recommended by the AAAAI for the diagnosis of acute sinusitis (sinus infection)?What are the AAO-HNSF diagnostic guidelines for bacterial rhinosinusitis (RS)?What is the role of imaging studies in the diagnosis of sinusitis (sinus infection)?What is the role of blood studies in the diagnosis of acute sinusitis (sinus infection)?When are tests for immunodeficiency indicated in the diagnosis of acute sinusitis (sinus infection)?How is nasal cytology testing used in the diagnosis of acute sinusitis (sinus infection)?When is sweat chloride test screening indicated in acute sinusitis (sinus infection)?When should cultures of nasal secretions be obtained for acute sinusitis (sinus infection)?Is culture of nasal secretions useful in the diagnosis of acute sinusitis (sinus infection)?How should nasal cultures be obtained for acute sinusitis (sinus infection)?Which imaging study is preferred for the diagnosis of rhinosinusitis (RS)?What is the role of CT scanning in the diagnosis of acute sinusitis (sinus infection)?How often is CT evidence of sinusitis (sinus infection) associated with viral upper respiratory infections?What information can CT scanning provide in regard to the development of acute sinusitis (sinus infection)?When should CT scanning be performed for acute sinusitis (sinus infection)?Which projections should be included in basic radiographic exam of acute sinusitis (sinus infection)?Which radiographic findings suggest acute sinusitis (sinus infection)?What is the role of MRI in the diagnosis of acute sinusitis (sinus infection)?Is ultrasonography used in the diagnosis of acute sinusitis (sinus infection)?What is the role of paranasal biopsy in the diagnosis of acute sinusitis?What is the role of fiberoptic sinus endoscopy in the diagnosis of acute sinusitis?What are the AAP treatment guidelines for acute bacterial sinusitis (sinus infection) in children and adolescents?What are the Canadian clinical practice treatment guidelines for acute bacterial rhinosinusitis (RS)?What are the AAO-HNSF treatment guidelines for acute bacterial rhinosinusitis (RS) in adults?What are the AAO-HNSF guidelines for the symptomatic treatment of acute rhinosinusitis (RS) in adults?What are the primary goals of management of acute sinusitis (sinus infection)?How is drainage achieved in acute sinusitis (sinus infection)?When are sinus puncture and irrigation techniques indicated in the treatment of acute sinusitis (sinus infection)?When is evaluation by an otolaryngologist indicated for acute sinusitis (sinus infection)?How is acute sinusitis (sinus infection) treated in the emergency department (ED)?Are intranasal steroids effective for the treatment of acute sinusitis (sinus infection)?Are antihistamines effective in the treatment of acute sinusitis (sinus infection)?What is the role of oral alpha-adrenergic vasoconstrictors in the treatment of acute sinusitis (sinus infection)?Are topical vasoconstrictors effective in the treatment of acute sinusitis (sinus infection)?Are mucolytic agents effective for in the treatment of acute sinusitis (sinus infection)?Are antibiotics effective for the treatment of uncomplicated sinusitis (sinus infection)?What is the role of systemic antimicrobial therapy in the treatment of bacterial sinusitis (sinus infection)?Is amoxicillin effective in the treatment of acute sinusitis (sinus infection)?What is the efficacy of antimicrobial therapy for acute sinusitis (sinus infection)?What percentage of S pneumoniae strains are penicillin resistant in acute bacterial sinusitis (sinus infection)?How should antibiotic therapy for acute bacterial sinusitis (sinus infection) be selected?When is second-line antibiotic therapy indicated for the treatment of acute sinusitis (sinus infection)?When are IV antibiotics indicated in the treatment of acute sinusitis (sinus infection)?What adjunctive therapies may be considered for symptomatic treatment of acute sinusitis (sinus infection)?Are antihistamines an effective treatment for acute sinusitis (sinus infection)?Which medications are effective for symptomatic treatment of acute sinusitis?According to the AAAAI, what should be the basis for antibiotic selection in the treatment of acute sinusitis (sinus infection)?What are the effects of antibiotic therapy in recurrent acute rhinosinusitis (RS)?Which antibiotics are most effective for bacterial sinusitis (sinus infection)?What are the indications for surgical treatment of sinusitis (sinus infection)?What are the surgical options for treating sinusitis (sinus infection)?When is surgery indicated for acute frontal sinusitis (sinus infection)?What are the surgical options for treatment of acute maxillary sinusitis (sinus infection)?How is acute sphenoid sinusitis (sinus infection) treated?How is acute ethmoid sinusitis (sinus infection) treated?What are the possible complications of untreated acute sinusitis (sinus infection)?What are the local complications of sinusitis (sinus infection)?What are orbital complications of acute bacterial sinusitis (sinus infection)?How are orbital complications of acute bacterial sinusitis (sinus infection) diagnosed and classified?How are orbital complications of acute bacterial sinusitis (sinus infection) treated?What are the possible intracranial complications of acute sinusitis (sinus infection)?What are the possible systemic complications of acute sinusitis (sinus infection)?When is otolaryngology consultation for acute sinusitis (sinus infection) indicated?What are the AAO-HNSF treatment guidelines for acute sinusitis (sinus infection)?Which medications are used in the treatment of viral rhinosinusitis (RS)?Are antibiotics effective for the treatment of sinusitis (sinus infection)?What are the Sinus and Allergy Health Partnership treatment guidelines for acute bacterial rhinosinusitis (RS)?Which medications in the drug class Penicillins are used in the treatment of Acute Sinusitis?Which medications in the drug class Cephalosporins are used in the treatment of Acute Sinusitis?Which medications in the drug class Macrolides are used in the treatment of Acute Sinusitis?Which medications in the drug class Fluoroquinolones are used in the treatment of Acute Sinusitis?Which medications in the drug class Anti-Infectives are used in the treatment of Acute Sinusitis?Which medications in the drug class Carbapenems are used in the treatment of Acute Sinusitis?Which medications in the drug class Aminoglycosides are used in the treatment of Acute Sinusitis?Which medications in the drug class Tetracyclines are used in the treatment of Acute Sinusitis?Which medications in the drug class Decongestants are used in the treatment of Acute Sinusitis?Which medications in the drug class Nasal Sprays are used in the treatment of Acute Sinusitis?Which medications in the drug class Expectorants are used in the treatment of Acute Sinusitis?Which medications in the drug class Corticosteroids are used in the treatment of Acute Sinusitis?Which medications in the drug class Anticholinergics are used in the treatment of Acute Sinusitis?

Author

Itzhak Brook, MD, MSc, Professor, Department of Pediatrics, Georgetown University School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Brian E Benson, MD, FACS, Vice-Chair, Department of Otolaryngology/Head and Neck Surgery, Chief, Division of Laryngeal Surgery and Voice Disorders, Director, The Voice Center, Hackensack University Medical Center; Co-Chief, Division of Head and Neck Oncology, The John Theurer Cancer Center

Disclosure: Nothing to disclose.

Linas Riauba, MD, Assistant Professor of Clinical Medicine, Department of Medicine, Section of Infectious Disease, University Hospital, University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Disclosure: Nothing to disclose.

Acknowledgements

Michael Cunningham, DO Sr Clinical Instructor, Department of Emergency Medicine, University of Rochester School of Medicine and Dentistry

Michael Cunningham, DO is a member of the following medical societies: American College of Emergency Physicians, American Osteopathic Association, Medical Society of the State of New York, and National Association of EMS Physicians

Disclosure: Nothing to disclose.

Tracey Quail Davidoff, MD Senior Clinical Instructor, Department of Emergency Medicine, Rochester General Hospital

Tracey Quail Davidoff, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Forensic Examiners, American College of Physicians, and American Medical Association

Disclosure: Nothing to disclose.

Thomas E Herchline, MD Professor of Medicine, Wright State University Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of America, and Infectious Diseases Society of Ohio

Disclosure: Nothing to disclose.

Erhun Serbetci, MD Director, Department of Otolaryngology, Section of Nose and Sinus Surgery, Associate Professor, International Hospital of Istanbul, Turkey

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References

  1. Lucas JW, Schiller JS, Benson V. Summary health statistics for U.S. adults: National Health Interview Survey, 2001. Vital Health Stat 10. 2004 Jan. 1-134. [View Abstract]
  2. Slavin RG, Spector SL, Bernstein IL, Kaliner MA, Kennedy DW, Virant FS, et al. The diagnosis and management of sinusitis: a practice parameter update. J Allergy Clin Immunol. 2005 Dec. 116(6 Suppl):S13-47. [View Abstract]
  3. Lusk RP, Stankiewicz JA. Pediatric rhinosinusitis. Otolaryngol Head Neck Surg. 1997 Sep. 117(3 Pt 2):S53-7. [View Abstract]
  4. Lanza DC, Kennedy DW. Adult rhinosinusitis defined. Otolaryngol Head Neck Surg. 1997 Sep. 117(3 Pt 2):S1-7. [View Abstract]
  5. American Academy of Pediatrics - Subcommittee on Management of Sinusitis and Committee on Quality Management. Clinical practice guideline: management of sinusitis. Pediatrics. 2001 Sep. 108(3):798-808. [View Abstract]
  6. Meltzer EO, Hamilos DL, Hadley JA, et al. Rhinosinusitis: Establishing definitions for clinical research and patient care. Otolaryngol Head Neck Surg. 2004 Dec. 131(6 Suppl):S1-62. [View Abstract]
  7. Stark JM, Colasurdo GN. Lung Defense: intrinsic, innate and adaptive. Chernick V, Boat TF, Wilmott RW, Bush A, eds. Kendig's Disorders of the Respiratory Tract in Children. 7th Ed. Philadelphia, PA: Saunders Elsevier; 2006. Vol. 12: 206.
  8. Cherry JD, Shapiro NL, Deville JG. Sinusitis. Feigin RD, Cherry JD, Demmier GJ, Kaplan SL, eds. Textbook of pediatric infectious disease. 5th ed. Philadelphia, PA: WB Saunders; 2004. 201.
  9. Brook I. Aerobic and anaerobic bacterial flora of normal maxillary sinuses. Laryngoscope. 1981 Mar. 91(3):372-6. [View Abstract]
  10. Su WY, Liu C, Hung SY, Tsai WF. Bacteriological study in chronic maxillary sinusitis. Laryngoscope. 1983 Jul. 93(7):931-4. [View Abstract]
  11. Sobin J, Engquist S, Nord CE. Bacteriology of the maxillary sinus in healthy volunteers. Scand J Infect Dis. 1992. 24(5):633-5. [View Abstract]
  12. Jiang RS, Liang KL, Jang JW, Hsu CY. Bacteriology of endoscopically normal maxillary sinuses. J Laryngol Otol. 1999 Sep. 113(9):825-8. [View Abstract]
  13. Gordts F, Halewyck S, Pierard D, Kaufman L, Clement PA. Microbiology of the middle meatus: a comparison between normal adults and children. J Laryngol Otol. 2000 Mar. 114(3):184-8. [View Abstract]
  14. Hamilos DL. Clinical manifestations, pathophysiology, and diagnosis of chronic rhinosinusitis. UpToDate. Available at http://www.uptodate.com. Accessed: June 7th, 2009.
  15. Ah-See K. Sinusitis (acute). Clin Evid (Online). 2008 Mar 10. 2008:[View Abstract]
  16. Hwang PH, Getz A. Acute sinusitis and rhinosinusitis in adults. UpToDate. Available at http://www.uptodate.com. Accessed: June 7th, 2009.
  17. Revai K, Dobbs LA, Nair S, Patel JA, Grady JJ, Chonmaitree T. Incidence of acute otitis media and sinusitis complicating upper respiratory tract infection: the effect of age. Pediatrics. 2007 Jun. 119(6):e1408-12. [View Abstract]
  18. Gwaltney JM Jr. Acute community-acquired sinusitis. Clin Infect Dis. 1996 Dec. 23(6):1209-23; quiz 1224-5. [View Abstract]
  19. Brook I, Foote PA, Hausfeld JN. Frequency of recovery of pathogens causing acute maxillary sinusitis in adults before and after introduction of vaccination of children with the 7-valent pneumococcal vaccine. J Med Microbiol. 2006 Jul. 55:943-6. [View Abstract]
  20. Brook I, Gober AE. Frequency of recovery of pathogens from the nasopharynx of children with acute maxillary sinusitis before and after the introduction of vaccination with the 7-valent pneumococcal vaccine. Int J Pediatr Otorhinolaryngol. 2007 Apr. 71(4):575-9. [View Abstract]
  21. Jacobs MR, Bajaksouzian S, Windau A, Good CE, Lin G, Pankuch GA, et al. Susceptibility of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis to 17 oral antimicrobial agents based on pharmacodynamic parameters: 1998-2001 U S Surveillance Study. Clin Lab Med. 2004 Jun. 24(2):503-30. [View Abstract]
  22. Payne SC, Benninger MS. Staphylococcus aureus is a major pathogen in acute bacterial rhinosinusitis: a meta-analysis. Clin Infect Dis. 2007 Nov 15. 45(10):e121-7. [View Abstract]
  23. Brook I, Foote PA, Hausfeld JN. Increase in the frequency of recovery of meticillin-resistant Staphylococcus aureus in acute and chronic maxillary sinusitis. J Med Microbiol. 2008 Aug. 57:1015-7. [View Abstract]
  24. Bishai WR. Issues in the management of bacterial sinusitis. Otolaryngol Head Neck Surg. 2002 Dec. 127(6 Suppl):S3-9. [View Abstract]
  25. Ray NF, Baraniuk JN, Thamer M, Rinehart CS, Gergen PJ, Kaliner M, et al. Healthcare expenditures for sinusitis in 1996: contributions of asthma, rhinitis, and other airway disorders. J Allergy Clin Immunol. 1999 Mar. 103(3 Pt 1):408-14. [View Abstract]
  26. Fendrick AM, Saint S, Brook I, Jacobs MR, Pelton S, Sethi S. Diagnosis and treatment of upper respiratory tract infections in the primary care setting. Clin Ther. 2001 Oct. 23(10):1683-706. [View Abstract]
  27. Wald ER, Guerra N, Byers C. Upper respiratory tract infections in young children: duration of and frequency of complications. Pediatrics. 1991 Feb. 87(2):129-33. [View Abstract]
  28. Gwaltney JM Jr, Hendley JO, Simon G, Jordan WS Jr. Rhinovirus infections in an industrial population. II. Characteristics of illness and antibody response. JAMA. 1967 Nov 6. 202(6):494-500. [View Abstract]
  29. [Guideline] Rosenfeld RM, Andes D, Bhattacharyya N, Cheung D, Eisenberg S, Ganiats TG, et al. Clinical practice guideline: adult sinusitis. Otolaryngol Head Neck Surg. 2007 Sep. 137(3 Suppl):S1-31. [View Abstract]
  30. [Guideline] Rosenfeld RM, Piccirillo JF, Chandrasekhar SS, Brook I, Ashok Kumar K, Kramper M, et al. Clinical practice guideline (update): adult sinusitis. Otolaryngol Head Neck Surg. 2015 Apr. 152 (2 Suppl):S1-S39. [View Abstract]
  31. Hansen JG, Schmidt H, Rosborg J, Lund E. Predicting acute maxillary sinusitis in a general practice population. BMJ. 1995 Jul 22. 311(6999):233-6. [View Abstract]
  32. Hickner JM, Bartlett JG, Besser RE, Gonzales R, Hoffman JR, Sande MA. Principles of appropriate antibiotic use for acute rhinosinusitis in adults: background. Ann Intern Med. 2001 Mar 20. 134(6):498-505. [View Abstract]
  33. McQuillan L, Crane LA, Kempe A. Diagnosis and management of acute sinusitis by pediatricians. Pediatrics. 2009 Feb. 123(2):e193-8. [View Abstract]
  34. Savolainen S, Jousimies-Somer H, Karjalainen J, Ylikoski J. Do simple laboratory tests help in etiologic diagnosis in acute maxillary sinusitis?. Acta Otolaryngol Suppl. 1997. 529:144-7. [View Abstract]
  35. Gordts F, Abu Nasser I, Clement PA, Pierard D, Kaufman L. Bacteriology of the middle meatus in children. Int J Pediatr Otorhinolaryngol. 1999 May 5. 48(2):163-7. [View Abstract]
  36. [Guideline] Kaplan A. Canadian guidelines for acute bacterial rhinosinusitis: clinical summary. Can Fam Physician. 2014 Mar. 60 (3):227-34. [View Abstract]
  37. Zalmanovici A, Yaphe J. Steroids for acute sinusitis. Cochrane Database Syst Rev. 2007 Apr 18. CD005149. [View Abstract]
  38. Williamson IG, Rumsby K, Benge S, Moore M, Smith PW, Cross M, et al. Antibiotics and topical nasal steroid for treatment of acute maxillary sinusitis: a randomized controlled trial. JAMA. 2007 Dec 5. 298(21):2487-96. [View Abstract]
  39. van Loon JW, van Harn RP, Venekamp RP, et al. Limited evidence for effects of intranasal corticosteroids on symptom relief for recurrent acute rhinosinusitis. Otolaryngol Head Neck Surg. Nov 2013. 149(5):668-73. [View Abstract]
  40. Ahovuo-Saloranta A, Borisenko OV, Kovanen N, Varonen H, Rautakorpi UM, Williams JW Jr, et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev. 2008 Apr 16. CD000243. [View Abstract]
  41. Young J, De Sutter A, Merenstein D, van Essen GA, Kaiser L, Varonen H, et al. Antibiotics for adults with clinically diagnosed acute rhinosinusitis: a meta-analysis of individual patient data. Lancet. 2008 Mar 15. 371(9616):908-14. [View Abstract]
  42. Garbutt JM, Banister C, Spitznagel E, Piccirillo JF. Amoxicillin for acute rhinosinusitis: a randomized controlled trial. JAMA. 2012 Feb 15. 307(7):685-92. [View Abstract]
  43. Chow AW, Benninger MS, Brook I, Brozek JL, Goldstein EJ, Hicks LA, et al. IDSA Clinical Practice Guideline for Acute Bacterial Rhinosinusitis in Children and Adults. Clin Infect Dis. 2012 Apr. 54(8):e72-e112. [View Abstract]
  44. Sng WJ, Wang DY. Efficacy and side effects of antibiotics in the treatment of acute rhinosinusitis: a systematic review. Rhinology. 2015 Mar. 53 (1):3-9. [View Abstract]
  45. Zalmanovici A, Yaphe J. Intranasal steroids for acute sinusitis. Cochrane Database Syst Rev. 2009 Oct 7. CD005149. [View Abstract]
  46. Kaper NM, Breukel L, Venekamp RP, et al. Absence of evidence for enhanced benefit of antibiotic therapy on recurrent acute rhinosinusitis episodes: a systematic review of the evidence base. Otolaryngol Head Neck Surg. 2013 Nov. 149(5):664-7. [View Abstract]
  47. Falagas ME, Giannopoulou KP, Vardakas KZ, Dimopoulos G, Karageorgopoulos DE. Comparison of antibiotics with placebo for treatment of acute sinusitis: a meta-analysis of randomised controlled trials. Lancet Infect Dis. 2008 Sep. 8(9):543-52. [View Abstract]
  48. [Guideline] National Guidelines Clearinghouse. Clinical practice guideline: adult sinusitis. National Guidelines Clearinghouse. Available at http://guideline.gov/content.aspx?id=12385. Accessed: September 29, 2010.
  49. Marple BF, Roberts CS, Frytak JR, Schabert VF, Wegner JC, Bhattacharyya H, et al. Azithromycin extended release vs amoxicillin/clavulanate: symptom resolution in acute sinusitis. Am J Otolaryngol. 2010 Jan-Feb. 31(1):1-8. [View Abstract]
  50. Platt MP, Cunnane ME, Curtin HD, Metson R. Anatomical changes of the ethmoid cavity after endoscopic sinus surgery. Laryngoscope. 2008 Dec. 118(12):2240-4. [View Abstract]
  51. Huang BY, Lloyd KM, DelGaudio JM, Jablonowski E, Hudgins PA. Failed endoscopic sinus surgery: spectrum of CT findings in the frontal recess. Radiographics. 2009 Jan-Feb. 29(1):177-95. [View Abstract]
  52. Hnatuk LA, Macdonald RE, Papsin BC. Isolated sphenoid sinusitis: the Toronto Hospital for Sick Children experience and review of the literature. J Otolaryngol. 1994 Feb. 23(1):36-41. [View Abstract]
  53. DelGaudio JM, Evans SH, Sobol SE, Parikh SL. Intracranial complications of sinusitis: what is the role of endoscopic sinus surgery in the acute setting. Am J Otolaryngol. 2010 Jan-Feb. 31(1):25-8. [View Abstract]
  54. Anon JB, Jacobs MR, Poole MD, Ambrose PG, Benninger MS, Hadley JA, et al. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg. 2004 Jan. 130(1 Suppl):1-45. [View Abstract]
  55. Brook I, Gober AE. Dynamics of nasopharyngitis in children. Otolaryngol Head Neck Surg. 2000 May. 122 (5):696-700. [View Abstract]
  56. Barclay, L. Acute Bacterial Sinusitis Addressed in New AAP Guidelines. Medscape Medical News. Available at http://www.medscape.com/viewarticle/806791. Accessed: July 2, 2013.
  57. Wald ER, Applegate KE, Bordley C, Darrow DH, Glode MP, Marcy SM, et al. Clinical Practice Guideline for the Diagnosis and Management of Acute Bacterial Sinusitis in Children Aged 1 to 18 Years. Pediatrics. 2013 Jun 24. [View Abstract]
  58. Chan KH, Abzug MJ, Coffinet L, Simoes EA, Cool C, Liu AH. Chronic rhinosinusitis in young children differs from adults: a histopathology study. J Pediatr. 2004 Feb. 144(2):206-12. [View Abstract]
  59. Seo J, Kim HJ, Chung SK, Kim E, Lee H, Choi JW, et al. Cervicofacial tissue infarction in patients with acute invasive fungal sinusitis: prevalence and characteristic MR imaging findings. Neuroradiology. 2013 Feb 2. [View Abstract]

Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.

Sagittal section of the lateral nasal wall demonstrating openings of paranasal sinuses. Conchae have been cut to depict details of meatal structures.

Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.

CT cuts for a limited CT study.

Sagittal section of the lateral nasal wall demonstrating openings of paranasal sinuses. Conchae have been cut to depict details of meatal structures.

Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.

CT cuts for a limited CT study.

Antibiotic Dosage Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Anaerobic bacteria
Sensitive Intermediate Resistant
Amoxicillin500 mg PO tid++++++++++++



(except beta-lactamase producers)



Clarithromycin250-500 mg PO bid+++++++++++
Azithromycin500 mg PO first day, then



250 mg/d PO for 4 days



+++++++++++
*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism
Antibiotic Dosage Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Anaerobic bacteria
Sensitive Intermediate Resistant
Amoxicillin/



clavulanate



500 mg PO tid+++++++++++++++
Cefuroxime250-500 mg PO bid+++++++++++++
Cefpodoxime



+



cefixime



200 mg PO bid



400 mg/d PO



-



++



+++



-



++



-



+



+++



+++



+++



++



-



Ciprofloxacin500-750 mg PO bid++++++++++
Levofloxacin500 mg/d PO+++++++++++++++++
Trovafloxacin200 mg/d PO++++++++++++++++++
Clindamycin300 mg PO tid++++++++--+++
Metronidazole500 mg PO tid-----+++
*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism
Antibiotic Dosage Streptococcus pneumoniae † Haemophilus influenzae Moraxella catarrhalis Gram-negative Anaerobic bacteria
Piperacillin3-4 g IV q4-6h++++-++++++
Piperacillin/tazobactam3.375 g IV q6h++++++++++++++
Ticarcillin3 g IV q4h+++--+++++
Ticarcillin/clavulanate3.1 g IV q4h++++++-+++++
Imipenem500 mg IV q6h+++++++++++++++
Meropenem1 g IV q8h+++++++++++++++
Cefuroxime1 g IV q8h+++++++++++++
Ceftriaxone2 g IV bid++++++++++++++
Cefotaxime2 g IV q4-6h++++++++++++++
Ceftazidime2 g IV q8h++++++++++++++
Gentamicin1.7 mg/kg IV q8h-++++++++-
Tobramycin1.7 mg/kg IV q8h-++++++++-
Vancomycin1 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.