4/6/2016 Acute Sinusitis: Practice Essentials, Background, Anatomy

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Acute SinusitisAuthor: Itzhak Brook, MD, MSc; Chief Editor: Michael Stuart Bronze, MD more...

Updated: Mar 22, 2016

Practice EssentialsSinusitis is characterized by inflammation of the lining of the paranasal sinuses.Because the nasal mucosa is simultaneously involved and because sinusitis rarelyoccurs without concurrent rhinitis, rhinosinusitis is now the preferred term for thiscondition. Rhinosinusitis affects an estimated 35 million people per year in theUnited States and accounts for close to 16 million office visits per year.[1] See theimage below.

Airfluid level (arrow) in the maxillary sinus suggests sinusitis.

Signs and symptoms

Clinical findings in acute sinusitis may include the following:

Pain over cheek and radiating to frontal region or teeth, increasing withstraining or bending downRedness of nose, cheeks, or eyelidsTenderness to pressure over the floor of the frontal sinus immediately abovethe inner canthusReferred pain to the vertex, temple, or occiputPostnasal dischargeA blocked nosePersistent coughing or pharyngeal irritationFacial painHyposmia

Symptoms of acute bacterial rhinosinusitis include the following:

Facial pain or pressure (especially unilateral)Hyposmia/anosmiaNasal congestionNasal drainagePostnasal dripFeverCoughFatigueMaxillary dental painEar fullness/pressure

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

Presence of symptoms or signs of acute rhinosinusitis 10 days or morebeyond the onset of upper respiratory symptomsWorsening of symptoms or signs of acute rhinosinusitis within 10 days afteran initial improvement

The following signs may be noted on physical examination:

Purulent nasal secretionsPurulent posterior pharyngeal secretionsMucosal erythemaPeriorbital edemaTenderness overlying sinusesAirfluid levels on transillumination of the sinuses (60% reproducibility rate forassessing maxillary sinus disease)

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Facial erythema

See Clinical Presentation for more detail.

Diagnosis

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

Nasal cytologyNasalsinus biopsyTests for immunodeficiency, cystic fibrosis, or ciliary dysfunction

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

Allergic rhinitis [3]EosinophiliaNasal polyposisAspirin sensitivity

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

Immunoglobulin studiesHIV serology

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

Patients in intensive care or with immunocompromiseChildren not responding to appropriate medical managementPatients with complications of sinusitis

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

Lifethreatening illnessImmunocompromiseDisease unresponsive to therapy

Computed tomography scanning is the preferred imaging method for rhinosinusitis.A complete sinus CT scan with frontal and coronal planes is used if an alternativediagnosis (eg, tumors) must be excluded. CT scanning is characteristic in allergicfungal 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 involvedsinus and appropriate systemic treatment of the likely bacterial pathogens. Drainagecan be achieved surgically with sinus puncture and irrigation techniques. Options formedical drainage are as follows:

Oral alphaadrenergic vasoconstrictors (eg, pseudoephedrine, andphenylephrine) for 1014 daysTopical vasoconstrictors (eg, oxymetazoline hydrochloride) for a maximum of35 days

Antibiotic treatment is usually given for 14 days. Usual firstline therapy is with one ofthe following:

Amoxicillin, at double the usual dose (8090 mg/kg/d), especially in areaswith known Streptococcus pneumoniae resistanceClarithromycinAzithromycin

Secondline antibiotic should be considered for patients with any of the following:

Residence in communities with a high incidence of resistant organismsFailure to respond within 4872 hours of commencement of therapyPersistence of symptoms beyond 1014 days

The most commonly used secondline therapies include the following:

AmoxicillinclavulanateSecond or thirdgeneration cephalosporins (eg, cefuroxime, cefpodoxime,cefdinir)Macrolides (ie, clarithromycin)Fluoroquinolones (eg, ciprofloxacin, levofloxacin, moxifloxacin)Clindamycin

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

Adults with mild disease who have not received antibiotics:Amoxicillin/clavulanate, amoxicillin (1.53.5 g/day), cefpodoxime proxetil, orcefuroxime is recommended as initial therapy.Adults with mild disease who have had antibiotics in the previous 46 weeksand adults with moderate disease: Amoxicillin/clavulanate, amoxicillin (33.5g), cefpodoxime proxetil, or cefixime is recommended.Adults with moderate disease who have received antibiotics in the previous46 weeks: Amoxicillin/clavulanate, levofloxacin, moxifloxacin, or doxycyclineis recommended.

Symptomatic or adjunctive therapies may include the following:

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Humidification/vaporizerWarm compressesAdequate hydrationSmoking cessationBalanced nutritionNonnarcotic analgesia

See Treatment and Medication for more detail.

BackgroundSinusitis is characterized by inflammation of the lining of the paranasal sinuses.Because the nasal mucosa is simultaneously involved and because sinusitis rarelyoccurs without concurrent rhinitis, rhinosinusitis is now the preferred term for thiscondition.[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 (nasalpolyposis, immunosuppression, anatomic variants). (See Anatomy, Pathophysiology,and Etiology.)

Acute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is ofparamount importance in differentiating this entity from allergic or vasomotor rhinitisand common upper respiratory infections. No specific clinical symptom or sign issensitive or specific for acute sinusitis, so the overall clinical impression should beused 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. (SeeTreatment and Management.) Most patients with acute sinusitis are treated in theprimary care setting. Further evaluation by an otolaryngologist is recommended inany of the following cases:

When continued deterioration occurs with appropriate antibiotic therapyWhen episodes of sinusitis recurWhen symptoms persist after 2 courses of antibiotic therapyWhen comorbid immunodeficiency, nosocomial infection, or complications ofsinusitis are present

Definition of acute rhinosinusitis

Many classifications, both clinical and radiological, have been proposed in theliterature to define acute sinusitis. Although no consensus on the precise definitioncurrently exists subacute sinusitis represents a temporal progression of symptomsfor 412 weeks. Recurrent acute sinusitis is diagnosed when 24 episodes ofinfection occur per year with at least 8 weeks between episodes and, as in acutesinusitis, the sinus mucosa completely normalizes between attacks. Chronic sinusitisis the persistence of insidious symptomatology beyond 12 weeks, with or withoutacute exacerbations.[6]

AnatomyTo properly diagnose and treat infectious disorders of the paranasal sinuses, theclinician should have knowledge of the developmental milestones. The developmentof the paranasal sinuses begins in the third week of gestation and continues untilearly adulthood.

Development of paranasal sinuses

During the third week of embryonic development, proliferation and medial migrationof ectodermal cells form the notochord. After the heart tube and pericardium haverotated from the cranial position to lie anteriorly, the notochord, which is initially inthe caudal region of the embryonic disc, rotates to lie posterior to the primitiveforegut. The paraxial layer of mesenchyme, which lies adjacent to the notochord,differentiates into the somite ridges, intermediate cell mass, and lateral platemesoderm. From these mesodermal structures, the branchial arches develop, thefirst of which gives rise to internal nasal structures.

The paranasal sinuses develop in conjunction with the palate from changes in thelateral wall of the nasal cavity. At 40 weeks' gestation, 2 horizontal grooves developin the mesenchyme of the lateral wall of the nasal cavity. Proliferation ofmaxilloturbinate mesenchyme between these grooves results in an outpouching oftissue medially into the nasal lumen. This outpouching is the precursor of the middleand inferior meatus as well as the inferior turbinate. Ethmoidoturbinate folds developsuperiorly to give rise to the middle and superior turbinates. Once the turbinatestructures are established, sinus development begins and continues until early adultlife.

The sinuses open into the nose via small openings called ostia.[5] The maxillary andethmoid sinuses form at 34 months' gestation. Thus, an infant is born with 34ethmoid cells and tiny teardropshaped maxillary sinuses. By the teenage years,each maxillary sinus progressively enlarges to an adult capacity of 15 mL. In healthyindividuals, the ethmoid sinuses increase in number to 1820, and each drains by anindividual ostium that is 12 mm in diameter.

The frontal sinus develops from an anterior ethmoid cell and moves to itssupraorbital position when the individual is aged 67 years. Frontal sinuses maybegin to develop at this age but usually do not appear radiologically until theindividual is aged approximately 12 years. The maxillary, anterior ethmoid, andfrontal sinuses drain into the middle meatus; the posterior ethmoid and sphenoidsinuses drain into the superior meatus (see the image below).

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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 airfilled bony cavities that extend from the skull base tothe alveolar process and laterally from the nasal cavity to the inferomedial aspect ofthe 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 mucusproducing goblet cells. These gobletcells in the epithelium and the submucosal seromucous glands contribute to theairway surface liquid,[7] which is 5100 μm thick and covers the epithelium.

Anterior and posterior ethmoid sinuses are composed of multiple air cells separatedby thin bony partitions. Each cell is drained by an independent ostium that measuresonly 12 mm in diameter. These small openings are readily clogged by secretions orare occluded by swelling of the nasal mucosa. The sphenoid sinuses sit immediatelyanterior to the pituitary fossa and just behind the posterior ethmoid.

The arterial supply of the paranasal sinuses is from branches of the internal andexternal carotid arteries, while the venous and lymphatic drainage path is throughthe sinus ostia into the nasal cavity plexus. In addition, venous drainage occursthrough valveless vessels corresponding to the arterial supply.

All sinus ostia drain into the nares at locations beneath the middle and superiorturbinates. The posterior ethmoid and sphenoid sinuses drain into the superiormeatus below the superior turbinate. The ostia of the maxillary, anterior ethmoid,and frontal sinuses share a common site of drainage within the middle meatus. Thisregion is called the ostiomeatal complex and can be visualized by coronal CT scan.The common drainage pathway of the frontal, maxillary, and anterior ethmoidsinuses within the middle meatus allows relatively localized mucosal infectionprocesses to promote infection in all these sinuses.

The successful maintenance of sinus drainage represents a complicated interactionbetween ciliary action, mucus viscosity, size of sinus ostia, and orientation of bodystructures. Ciliary beat at the rate of 815 Hz is continuously moved by the cilia at aspeed of 6 mm/min. The ciliary action can be affected due to local factors, such asinfection and local hypoxia that is associated with complete occlusion of sinus ostia.The sinus mucosa has less secretory and vasomotor function than the nasal cavitydoes. Cilia are concentrated near and beat toward the natural sinus ostia. Blockageof the ostium results in stasis of mucous flow, which can lead to development ofdisease.

The exact function of the paranasal sinuses is not well understood. The possibleroles of the sinuses may include reducing the weight of the skull; dampeningpressure; humidifying and warming inspired air; absorbing heat and insulating thebrain; aiding in sound resonance; providing mechanical rigidity; and increasing theolfactory surface area.

PathophysiologyThe sinuses are normally sterile under physiologic conditions. Secretions producedin 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, towardthe ostia), which prevents back contamination of the sinuses. In most individuals, themaxillary sinus has a single ostium (2.5 mm in diameter, 5 mm2 in crosssectionalarea) serving as the only outflow tract for drainage. This slender conduit sits high onthe medial wall of the sinus cavity in a nondependent position. Most likely, theedema of the mucosa at these 1 to 3mm openings becomes congested by somemeans (eg, allergy, viruses, chemical irritation) that causes obstruction of the outflowtract stasis of secretions with negative pressure, leading to infection by bacteria.

Retained mucus, when infected, leads to sinusitis. Another mechanism hypothesizesthat because the sinuses are continuous with the nasal cavity, colonized bacteria inthe nasopharynx may contaminate the otherwise sterile sinuses. These bacteria areusually 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. Thebacterial flora of noninflamed sinuses were studied for aerobic and anaerobicbacteria in 12 adults who underwent corrective surgery for septal deviation.[9]Organisms were recovered from all aspirates, with an average of 4 isolates per sinusaspirate. The predominant anaerobic isolates were Prevotella, Porphyromonas,Fusobacterium and Peptostreptococcus species. The most common aerobicbacteria were S pyogenes, S aureus, S pneumonia, and H influenzae. In anotherstudy, specimens were processed for aerobic bacteria only, and Staphylococcusspecies and alphahemolytic streptococci were isolated.[10] Organisms wererecovered in 20% of maxillary sinuses of patients who underwent surgicalrepositioning of the maxilla.

In contrast, another report of aspirates of 12 volunteers with no sinus diseaseshowed no bacterial growth.[11] Jiang et al evaluated the bacteriology of maxillary

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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 alreported the microbiology of the middle meatus in normal adults and children.[13]This study noted in 52 patients that 75% had bacterial isolates present, mostcommonly coagulasenegative staphylococci (CNS) (35%), Corynebacteriumspecies (23%), and S aureus (8%) in adults. Low numbers of these species werepresent. In children, the most common organisms were H influenzae (40%), Mcatarrhalis (34%), and S pneumoniae (50%), a marked difference from findings inadults. Nonhemolytic streptococci and Moraxella species were absent in adults.

The pathophysiology of rhinosinusitis is related to 3 factors:

Obstruction of sinus drainage pathways (sinus ostia)Ciliary impairmentAltered mucus quantity and quality

Obstruction of sinus drainage

Obstruction of the natural sinus ostia prevents normal mucus drainage. The ostiacan be blocked by mucosal swelling or local causes (eg, trauma, rhinitis), as well asby certain inflammationassociated systemic disorders and immune disorders.Systemic diseases that result in decreased mucociliary clearance, including cysticfibrosis, respiratory allergies, and primary ciliary dyskinesia (Kartagener syndrome),can be predisposing factors for acute sinusitis in rare cases. Patients withimmunodeficiencies (eg, agammaglobulinemia, combined variableimmunodeficiency, and immunodeficiency with reduced immunoglobulin G [IgG]–and immunoglobulin A [IgA]–bearing cells) are also at increased risk of developingacute sinusitis.

Mechanical obstruction because of nasal polyps, foreign bodies, deviated septa, ortumors can also lead to ostial blockage. In particular, anatomical variations thatnarrow the ostiomeatal complex, including septal deviation, paradoxical middleturbinates, and Haller cells, make this area more sensitive to obstruction frommucosal inflammation. Usually, the margins of the edematous mucosa have ascalloped 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 nasalturbinates are swollen. Airfluid levels and bone erosion are not features ofuncomplicated allergic sinusitis; however, swollen mucosa in a poorly draining sinusis more susceptible to secondary bacterial infection.

Hypoxia within the obstructed sinus is thought to cause ciliary dysfunction andalterations in mucus production, further impairing the normal mechanism for mucusclearance.

Impaired ciliary function

Contrary to earlier models of sinus physiology, the drainage patterns of theparanasal sinuses depend not on gravity but on the mucociliary transportmechanism. The metachronous coordination of the ciliated columnar epithelial cellspropels the sinus contents toward the natural sinus ostia. Any disruption of the ciliaryfunction results in fluid accumulation within the sinus. Poor ciliary function can resultfrom the loss of ciliated epithelial cells; high airflow; viral, bacterial, or environmentalciliotoxins; inflammatory mediators; contact between 2 mucosal surfaces; scars; andKartagener 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 ofsecretions and predisposition to sinus infection. Ciliary function is also reduced inthe presence of low pH, anoxia, cigarette smoke, chemical toxins, dehydration, anddrugs (eg, anticholinergic medications and antihistamines).

Exposure to bacterial toxins can also reduce ciliary function. Approximately 10% ofcases of acute sinusitis result from direct inoculation of the sinus with a largeamount of bacteria. Dental abscesses or procedures that result in communicationbetween 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 theciliary epithelium, leading to impaired ciliary movement and retention of secretions inthe sinus cavities. On the contrary, inhaling dry air desiccates the sinus mucouscoat, leading to reduced secretions. Any mass lesion with the nasal air passagesand sinuses, such as polyps, foreign bodies, tumors, and mucosal swelling fromrhinitis, may block the ostia and predispose to retained secretions and subsequentinfection. Facial trauma or large inoculations from swimming can produce sinusitisas well. Drinking alcohol can also cause nasal and sinus mucosa to swell and causeimpairment 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 serouslayer (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. Properbalance between the inner sol phase and outer gel phase is of critical importance fornormal 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 gellayer becomes demonstrably thicker. This results in a collection of thick mucus thatis retained in the sinus for varying periods. In the presence of a lack of secretions ora loss of humidity at the surface that cannot be compensated for by mucous glandsor goblet cells, the mucus becomes increasingly viscous, and the sol phase maybecome extremely thin, thus allowing the gel phase to have intense contact with the

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cilia and impede their action. Overproduction of mucus can overwhelm themucociliary 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 1832% of patients with prolonged periods of intubation, and is usually diagnosedduring the evaluation of unexplained fever. Cases in which the cause is obstructionare usually evident and can include the presence of prolonged nasogastric ornasotracheal intubation. Moreover, patients in an intensive care setting are generallydebilitated, predisposing them to septic complications, including sinusitis. Finally,sinusitis in intensive care settings is associated with nasal catheter placement.

EtiologyPurulent sinusitis can occur when ciliary clearance of sinus secretions decreases orwhen the sinus ostium becomes obstructed, which leads to retention of secretions,negative sinus pressure, and reduction of oxygen partial pressure. This environmentis then suitable for growth of pathogenic organisms. Factors that predispose thesinuses to obstruction and decreased ciliary function are allergic, nonallergic, or viralinsults, which produce inflammation of the nasal and sinus mucosa and result inciliary dysmotility and sinus obstruction.

In individuals with recurrent or persistent sinusitis, suspect other predisposingconditions such as cystic fibrosis, ciliary dyskinesia, allergic inflammation,immunodeficiency, or an anatomic problem. These predisposing factors are alsocited by the 2005 practice parameter for diagnosis and management of sinusitisissued by the American Academy of Allergy, Asthma and Immunology (AAAAI), asare 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 viralupper respiratory tract infections are caused by rhinovirus, but coronavirus, influenzaA and B, parainfluenza, respiratory syncytial virus, adenovirus, and enterovirus arealso causative agents. Rhinovirus, influenza, and parainfluenza viruses are theprimary pathogens in 315% of patients with acute sinusitis. In about 0.52% ofcases, viral sinusitis can progress to acute bacterial sinusitis.[15, 16]

Viral upper respiratory tract infections are the most important risk factor for thedevelopment of acute bacterial sinusitis.[17] Approximately 90% of patients who haveviral upper respiratory tract infections have sinus involvement, but only 510% ofthese patients have bacterial superinfection requiring antimicrobial treatment.[18]

Acute bacterial rhinosinusitis

Acute bacterial rhinosinusitis is very frequently associated with viral upperrespiratory tract infection, although allergy, trauma, neoplasms, granulomatous andinflammatory diseases, midline destructive disease, environmental factors, dentalinfection, 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 childrenwith the 7valent pneumococcal vaccine introduced in 2000 in the United Statesbrought about the decline in the recovery rate of S pneumoniae and an increase in Hinfluenza.[19, 20] In addition, the rate of recovery of S pneumoniae penicillinresistantstrains was different after vaccination.

P aeruginosa and other gramnegative rods have been recovered in acute sinusitisof nosocomial origin (especially in patients who have nasal tubes or catheters),immunocompromised persons, patients with HIV infection, and those with cysticfibrosis.

Sixtysix percent of patients with acute sinusitis grow at least 1 pathogenic bacterialspecies on sinus aspirates, while 2630% percent of patients have multiplepredominant bacterial species. The bacteria most commonly involved in acutesinusitis are part of the normal nasal flora. These bacteria can become sinuspathogens when they are deposited into the sinuses by sneezing, coughing, ordirect invasion under conditions that optimize their growth.

The most common pathogens isolated from maxillary sinus cultures in patients withacute bacterial rhinosinusitis include Streptococcus pneumoniae, Haemophilusinfluenzae, and Moraxella catarrhalis.Streptococcus pyogenes, Staphylococcusaureus,and anaerobes are less commonly associated with acute bacterialrhinosinusitis; they have been found in fewer than 10% of patients with acutebacterial sinusitis, despite the ample environment available for their growth. Theexceptions are in sinusitis resulting from a dental source and in patients with chronicsinus disease, in whom anaerobic organisms are usually isolated.

S pneumoniae are grampositive, catalasenegative, facultatively anaerobic coccithat account for 2043% of acute bacterial rhinosinusitis cases in adults. The rise ofantimicrobial resistance in S pneumoniae is a major concern.

A 1998 surveillance study of respiratory tract isolates estimated that 12.3% of Spneumoniae isolates obtained from the paranasal sinuses had intermediateresistance to penicillin; 37.4% were penicillinresistant. The paranasal sinusesrepresented the anatomic location with the highest resistance rate.[21] Resistance tomacrolide, clindamycin, trimethoprimsulfamethoxazole, and doxycycline was morecommon in isolates with intermediate penicillin resistance and those that werepenicillinresistant.

H influenzae are gramnegative, facultatively anaerobic bacilli. H influenza type Bwas a leading cause of meningitis until the widespread use of the vaccine.Nontypeable strains of H influenzae are responsible for 2235% of acute bacterial

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rhinosinusitis cases in adults. Betalactamase production is the mechanism ofantimicrobial resistance for this organism . Of isolates from the paranasal sinus,32.7% were found to be betalactamase–positive for H influenza; other reportssuggest a rate of 44%.

M catarrhalis are gramnegative, oxidasepositive, aerobic diplococci. M catarrhalisis the responsible pathogen in 210% of acute bacterial rhinosinusitis cases inadults. Betalactamase production is the mechanism of antimicrobial resistance forM catarrhalis as well . Of isolates from the paranasal sinus, 98% were found to bebetalactamase–positive for M catarrhalis.

S aureus, though accounting for 10% of episodes of acute bacterial rhinosinusitis, isnow recognized as an increasingly common pathogen in acute bacterialrhinosinusitis.[22] While methicillinresistant S aureus (MRSA) still represents aminority of episodes of S aureus rhinosinusitis, increasing trends of drugresistant Saureus may alter future treatment recommendations.[23]

Gramnegative organisms, including Pseudomonas aeruginosa (15.9%), Escherichiacoli (7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae, and Enterobacterspecies, predominate in nosocomial sinusitis, accounting for 60% of cases.Polymicrobial invasion is seen in 25100% of cultures. The other pathogenicorganisms found in nosocomial patients are grampositive organisms (31%) andfungi (8.5%).

Acute invasive fungal rhinosinusitis

Rarely, sinusitis is caused by fungi. Fungal sinusitis (eg, allergic fungal sinusitis) mayappear similar to lower airway disorder and allergic bronchopulmonary aspergillosis.

Fungal agents associated with this condition include Aspergillus and Alternariaspecies. Bipolaris and Curvularia species are the most common fungi recovered inallergic fungal sinusitis, accounting for 60% and 20%, respectively, in most studies.Curvularia species is occasionally reported as the most common causative organismin the deep southern United States.

Please go to the main article Fungal Sinusitis for more information.

EpidemiologySinusitis affects 1 out of every 7 adults in the United States, with more than 30million individuals diagnosed each year. Sinusitis is more common from early fall toearly spring. Rhinosinusitis affects an estimated 35 million people per year in theUnited States and accounts for close to 16 million office visits per year.[1]

According to the National Ambulatory Medical Care Survey (NAMCS), approximately14% of adults report having an episode of rhinosinusitis each year, and it is the fifthmost common diagnosis for which antibiotics are prescribed, accounting for 0.4% ofambulatory diagnoses.[24]

In 1996, Americans spent approximately $3.39 billion treating rhinosinusitis.[25] Theeconomic 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 sinusitisaffects 1 in 1000 people. Sinusitis is more common in winter than in summer.Rhinoviral infections are prevalent in autumn and spring. Coronaviral infectionoccurs mostly from December to March.

Acute sinusitis in children

An average child is likely to have 68 colds (ie, upper respiratory tract infections) peryear, and approximately 0.52% of upper respiratory tract infections in adults and 613% of viral upper respiratory tract infections in children are complicated by thedevelopment of acute bacterial sinusitis.[26, 27]

Sex distribution for acute sinusitis

Women have more episodes of infective sinusitis than men because they tend tohave more close contact with young children. The rate in women is 20.3%,compared with 11.5% in men.

PrognosisSinusitis does not cause any significant mortality by itself. However, complicatedsinusitis may lead to morbidity and, in rare cases, mortality.

Approximately 40% of acute sinusitis cases resolve spontaneously withoutantibiotics. The spontaneous cure for viral sinusitis is 98%. Patients with acutesinusitis, when treated with appropriate antibiotics, usually show promptimprovement. The relapse rate after successful treatment is less than 5%.

In the absence of response within 48 hours or worsening of symptoms, reevaluatethe patient. Untreated or inadequately treated rhinosinusitis may lead tocomplications such as meningitis, cavernous sinus thrombophlebitis, orbital cellulitisor abscess, and brain abscess.

In patients with allergic rhinitis, aggressive treatment of nasal symptoms and signs ofmucosal edema, which can cause obstruction of the sinus outflow tracts, maydecrease secondary sinusitis. If the adenoids are chronically infected, removingthem eliminates a nidus of infection and can decrease sinus infection.

Patient Education

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

Clinical Presentation

Contributor Information and DisclosuresAuthorItzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for theAdvancement of Science, American College of PhysiciansAmerican Society of Internal Medicine, AmericanMedical Association, American Society for Microbiology, Association of Military Surgeons of the US, InfectiousDiseases Society of America, International Immunocompromised Host Society, International Society for InfectiousDiseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric InfectiousDiseases Society, Society for Experimental Biology and Medicine, Society for Pediatric Research, SouthernMedical Association, Society for Ear, Nose and Throat Advances in Children, American Federation for ClinicalResearch, Surgical Infection Society, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.

Coauthor(s)Linas Riauba, MD Assistant Professor of Clinical Medicine, Department of Medicine, Section of InfectiousDisease, University Hospital, University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Linas Riauba, MD is a member of the following medical societies: American Medical Association, InfectiousDiseases Society of America

Disclosure: Nothing to disclose.

Brian E Benson, MD Chief, Division of Laryngeal Surgery and Voice Disorders; Director, The Voice Center atHackensack University Medical Center; Clinical Assistant Professor, Department of Otolaryngology/Head & NeckSurgery, UMDNJ, New Jersey Medical School

Brian E Benson, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy ofOtolaryngic Allergy, American Academy of OtolaryngologyHead and Neck Surgery, Sigma Xi

Disclosure: Nothing to disclose.

Chief EditorMichael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G WolfEndowed 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

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, AmericanMedical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Associationof Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

AcknowledgementsMichael Cunningham, DO Sr Clinical Instructor, Department of Emergency Medicine, University of RochesterSchool of Medicine and Dentistry

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

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

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, InfectiousDiseases 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, AssociateProfessor, International Hospital of Istanbul, Turkey

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center Collegeof Pharmacy; EditorinChief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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