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Sinusitis

Sinusitis, commonly referred to as a sinus infection, is the inflammation of the paranasal sinuses—the air-filled spaces within the bones of the face surrounding the nasal cavity—typically resulting from an infection, allergy, or other irritants that cause swelling and mucus buildup.^[1] It is classified into acute sinusitis, which lasts less than four weeks and often follows a viral upper respiratory infection like the common cold, and chronic sinusitis, which persists for 12 weeks or longer despite treatment.^[2]^[3] This condition affects approximately 30 million people annually in the United States, making it a leading cause of primary care visits and antibiotic prescriptions.^[1] Common symptoms of sinusitis include nasal congestion, thick yellow or greenish mucus drainage from the nose or down the back of the throat (postnasal drip), facial pain or pressure around the eyes, cheeks, nose, or forehead, and reduced sense of smell or taste.^[2]^[3] Additional signs may involve headache, cough, sore throat, bad breath, fatigue, and in acute cases, fever, though fever is rare in chronic forms.^[4] These symptoms arise from blocked sinus drainage pathways, leading to fluid accumulation and potential secondary infections.^[1] The primary causes of sinusitis are viral infections, such as those from rhinoviruses or influenza, which account for most acute cases and typically resolve without antibiotics.^[2]^[4] Bacterial infections, like those from Streptococcus pneumoniae or Haemophilus influenzae, can develop if sinuses remain obstructed, while fungal or allergic triggers are more common in chronic or immunocompromised individuals.^[1] Risk factors include allergies (e.g., hay fever), structural nasal issues like a deviated septum or polyps, exposure to cigarette smoke or pollutants, and underlying conditions such as cystic fibrosis or immune deficiencies.^[3]^[2] Treatment for sinusitis focuses on symptom relief and addressing the underlying cause; most viral cases improve with rest, hydration, saline nasal irrigation, and over-the-counter decongestants or pain relievers within 7-10 days.^[4] Antibiotics are reserved for confirmed bacterial infections, while chronic cases may require nasal corticosteroids, allergy management, or surgery for structural problems.^[3] Complications, though uncommon, can include the spread of infection to the eyes, brain, or bones, emphasizing the importance of prompt medical evaluation for severe or prolonged symptoms.^[2] Prevention strategies involve handwashing, vaccinations against flu and pneumococcus, avoiding smoke, and managing allergies.^[4]

Clinical Presentation

Symptoms by Location

Sinusitis symptoms often localize to the affected paranasal sinus due to their anatomical positions and shared innervation pathways, such as branches of the trigeminal nerve, which refer pain to specific facial regions.^[1] Inflammation in these air-filled cavities leads to pressure buildup, mucosal swelling, and impaired drainage, manifesting as site-specific pain, nasal congestion, and discharge.^[5] Frontal sinusitis, involving the sinuses located above the eyes in the frontal bone, typically causes pain or pressure in the forehead that worsens with leaning forward or Valsalva maneuver.^[1] This discomfort arises from the proximity to the supraorbital nerve branch of the trigeminal nerve, leading to referred pain across the brow.^[5] Associated nasal symptoms include anterior rhinorrhea or postnasal drip of purulent mucus, along with congestion that obstructs the frontal recess drainage pathway.^[6] Ethmoid sinusitis affects the ethmoid air cells between the eyes and behind the nasal bridge, resulting in periorbital pain or pressure that feels like a splitting headache between or behind the eyes.^[5] The thin lamina papyracea separating the ethmoid from the orbit contributes to this referral via ethmoidal branches of the trigeminal nerve, sometimes accompanied by tearing or eyelid swelling.^[1] Nasal manifestations feature purulent discharge from the middle meatus and significant postnasal drip, with congestion exacerbating obstruction at the osteomeatal complex.^[7] Due to its location adjacent to the cribriform plate and olfactory cleft, ethmoid involvement frequently causes hyposmia or anosmia by disrupting airflow to the olfactory receptors.^[1] Maxillary sinusitis, the most common form, inflames the largest paranasal sinuses beneath the cheeks and above the upper teeth, producing pain or tenderness over the cheeks, often radiating as a toothache in the upper molars.^[5] This pattern stems from innervation by the infraorbital nerve, a maxillary division of the trigeminal nerve, with palpable swelling sometimes noted on cheek percussion.^[1] Symptoms include unilateral or bilateral nasal congestion, anterior purulent rhinorrhea, and postnasal drip that may irritate the throat, due to blockage at the maxillary ostium in the middle meatus.^[7] Sphenoid sinusitis targets the deepest sinuses behind the sphenoid bone, near the pituitary and optic nerves, leading to vague, severe pain in the occipital region, vertex, or behind the eyes that lacks clear localization. The variable referral— to frontal, temporal, periorbital, or occipital areas—results from sensory innervation by the posterior ethmoidal nerve and branches of the maxillary nerve.^[1] Nasal symptoms encompass posterior purulent drainage and congestion, often without prominent anterior rhinorrhea, as the sphenoid ostium drains into the sphenoethmoidal recess.^[1]

Systemic and Associated Symptoms

Systemic symptoms of sinusitis extend beyond the nasal and facial regions, often manifesting as generalized signs of inflammation and infection. Fever, typically low-grade but potentially high (e.g., ≥102°F or 39°C in severe bacterial cases), is a common systemic indicator, particularly in acute cases, as part of the body's immune response to bacterial involvement.^[1] Malaise and fatigue frequently accompany these episodes, reflecting the overall energy drain from the inflammatory process, with tiredness being especially prominent in chronic presentations.^[8] Headaches in sinusitis can present diffusely across the head, differing from more localized facial pain, and may worsen with movement or position changes due to pressure buildup.^[9] Cough, often resulting from postnasal drip irritating the lower respiratory tract, further contributes to systemic discomfort by disrupting daily activities.^[10] Associated symptoms further illustrate the interconnected nature of sinus inflammation. Sore throat arises commonly from postnasal drip, where mucus drainage irritates the pharyngeal mucosa, leading to persistent discomfort.^[11] Ear fullness or pressure occurs due to eustachian tube dysfunction, as sinus swelling impedes proper drainage and equalization in the middle ear, sometimes mimicking ear infection symptoms.^[12] Halitosis, or bad breath, results from bacterial overgrowth in stagnant sinus secretions, exacerbating social and sensory issues for affected individuals.^[3] The presentation of these symptoms varies significantly between acute and chronic sinusitis, influencing their clinical management. In acute sinusitis, symptoms like fever and malaise often onset suddenly and intensely, lasting up to four weeks and resolving with targeted treatment, while cough and headache may peak early due to rapid inflammation.^[1] Chronic sinusitis, by contrast, features persistent low-grade fatigue and milder but enduring symptoms such as ongoing cough from chronic postnasal drip, with episodes lasting over 12 weeks and potentially leading to recurrent flares without underlying causes being addressed.^[3] These systemic and associated symptoms profoundly affect quality of life, often leading to sleep disruption from nasal congestion and postnasal drip, which impairs restorative rest and contributes to daytime somnolence.^[13] Studies indicate that 60-75% of individuals with chronic rhinosinusitis experience poor sleep quality, correlating with reduced cognitive function, mood disturbances, and overall functional impairment.^[13] This holistic burden underscores the need for comprehensive symptom evaluation in sinusitis care.

Causes and Risk Factors

Infectious Etiologies

Sinusitis often begins as a viral infection of the upper respiratory tract, with viruses accounting for the majority of acute cases. Approximately 90% to 98% of acute rhinosinusitis episodes are viral in origin, typically resolving within 7 to 10 days without bacterial involvement.^[1]^[14] Common viral pathogens include rhinoviruses, which cause 50% to 80% of cases, as well as influenza viruses, parainfluenza viruses, coronaviruses, adenoviruses, and respiratory syncytial virus.^[15]^[16] These viruses primarily affect the nasal mucosa, leading to inflammation and edema that obstructs sinus ostia.^[1] Bacterial superinfections complicate 0.5% to 2% of viral upper respiratory infections, transitioning acute viral rhinosinusitis to acute bacterial rhinosinusitis.^[14] The predominant bacterial pathogens in community-acquired cases are Streptococcus pneumoniae (20% to 45% prevalence), Haemophilus influenzae (non-typeable strains, 20% to 43%), and Moraxella catarrhalis (14% to 20%).^[17]^[16] Antibiotic resistance patterns vary geographically but include beta-lactamase production in 25% to 50% of H. influenzae and M. catarrhalis isolates, and penicillin non-susceptibility in 15% to 30% of S. pneumoniae strains, complicating empirical treatment.^[18]^[19] Fungal infections are less common and typically occur in specific populations, with invasive forms predominantly affecting immunocompromised individuals such as those with diabetes, HIV, or undergoing chemotherapy.^[20] Key pathogens include Aspergillus species in both invasive and noninvasive disease, and Mucor or Rhizopus (causing mucormycosis) in diabetics, leading to rapid tissue necrosis.^[20] Noninvasive variants, like allergic fungal rhinosinusitis, involve hypersensitivity to fungi such as Aspergillus, Bipolaris, or Curvularia in immunocompetent patients with chronic disease.^[20] Invasive fungal sinusitis carries a mortality rate of up to 50% due to potential orbital or intracranial extension.^[20] Transmission of sinusitis pathogens primarily occurs through viral upper respiratory infections, spread via respiratory droplets from coughing or sneezing, which cause mucosal swelling and blockage of sinus drainage pathways.^[21]^[1] Bacterial and fungal agents often arise opportunistically from this initial viral insult or endogenous flora, rather than direct person-to-person spread.^[22]

Non-Infectious Contributors

Allergic rhinitis serves as a significant non-infectious contributor to sinusitis by inducing IgE-mediated inflammation in the nasal mucosa, which leads to mucosal edema, impaired sinus drainage, and subsequent rhinosinusitis symptoms.^[23] This hypersensitivity reaction involves the release of inflammatory mediators such as histamine upon allergen exposure, causing nasal congestion and obstruction that predisposes the paranasal sinuses to stasis and secondary inflammation.^[24] There is substantial overlap in prevalence, with allergic rhinitis affecting up to 40% of individuals with chronic rhinosinusitis, highlighting its role as a common trigger for non-infectious sinus pathology.^[25] Anatomical abnormalities in the nasal cavity and paranasal sinuses can obstruct drainage pathways, fostering an environment conducive to sinusitis without primary infection. A deviated nasal septum, present in approximately 80% of patients with chronic sinusitis, narrows the nasal passages and impairs mucociliary clearance by altering airflow and secretion flow.^[26] Similarly, nasal polyps—benign mucosal growths—physically block sinus ostia, leading to mucus retention and chronic inflammation; they occur in about 20-30% of chronic rhinosinusitis cases and are particularly prevalent in eosinophilic subtypes.^[27] Concha bullosa, an pneumatized middle turbinate, contributes to obstruction in up to 35% of sinusitis patients by compressing adjacent structures and hindering ventilation in the osteomeatal complex.^[28] These structural variants often coexist, amplifying the risk of recurrent sinusitis through mechanical impedance of normal sinus physiology.^[29] Autoimmune and genetic conditions underlie certain non-infectious forms of sinusitis by disrupting mucociliary clearance and innate mucosal defenses. In cystic fibrosis, mutations in the CFTR gene result in viscous mucus accumulation and defective ion transport, impairing ciliary function and leading to chronic sinusitis in nearly all affected individuals; this manifests as opacified sinuses on imaging due to persistent inflammation and poor drainage. Primary ciliary dyskinesia (PCD), a ciliopathy caused by ultrastructural defects in motile cilia, similarly causes mucostasis and recurrent sinus infections starting in infancy, with sinonasal involvement in over 90% of cases and contributing to bronchiectasis through shared clearance impairments.^[30] These disorders highlight how inherent host defects in ciliary motility and mucus rheology perpetuate sinus pathology independently of microbial invasion.^[31] Aspirin-exacerbated respiratory disease (AERD), also known as Samter's triad, represents an immune-mediated syndrome that drives non-infectious sinusitis through dysregulated arachidonic acid metabolism and eosinophilic inflammation. Characterized by the triad of asthma, chronic rhinosinusitis with nasal polyps, and hypersensitivity to aspirin and other nonsteroidal anti-inflammatory drugs, AERD affects 7-10% of patients with severe asthma and leads to recurrent polypoid sinus disease via overproduction of cysteinyl leukotrienes.^[32] In this condition, aspirin triggers exacerbations by shunting prostaglandin synthesis toward leukotriene pathways, resulting in nasal congestion, anosmia, and progressive sinus obstruction that mimics infectious rhinosinusitis but stems from underlying hypersensitivity.^[33] Management focuses on leukotriene modifiers and aspirin desensitization to mitigate the inflammatory cascade and reduce polyp recurrence.^[27]

Environmental and Lifestyle Factors

Smoking, both active and passive, significantly contributes to the development and exacerbation of sinusitis by irritating the nasal mucosa and impairing ciliary function, which hinders mucociliary clearance and promotes chronic inflammation. Active smoking has been associated with an adjusted relative risk of 1.22 for chronic sinusitis, while odds ratios range from 1.91 (95% CI 1.77–2.05) in large surveys like GA²LEN, reflecting increased prevalence linked to mechanisms such as reduced ciliary beat frequency and suppression of innate immune responses like IL-8 production.^[34] Secondhand smoke exposure similarly elevates risk, with odds ratios of 2.20 (95% CI 1.51–3.20) for any exposure and 2.33 (95% CI 1.02–5.34) for childhood or current exposure, primarily through increased nasal airway resistance and delayed ciliary regeneration.^[34] Air pollution, particularly fine particulate matter (PM2.5) and ozone, exacerbates sinusitis by inducing chronic sinonasal inflammation, leading to mucosal swelling, congestion, and impaired sinus drainage. Long-term exposure to PM2.5 over 60 months is linked to a 1.5-fold increase in chronic rhinosinusitis risk and nearly five times greater odds of severe pansinusitis, as demonstrated in analyses of over 6,000 patients using EPA air quality data.^[35] Ozone and PM contribute to this by promoting oxidative stress and inflammatory cytokine release in sinonasal tissues. Urban areas, with higher pollution levels, show elevated sinusitis prevalence compared to rural settings; for instance, each 1 μg/m³ increase in PM10 correlates with higher chronic rhinosinusitis rates in urban cohorts, though some studies note variability.^[36] Occupational exposures to chemical irritants and physical stressors represent modifiable risks for sinusitis, often through direct mucosal damage or pressure-related injury. Irritants such as bleach, ammonia, paints, and pesticides are associated with odds ratios of 2.45 (95% CI 1.14–5.29) for chronic rhinosinusitis in patients undergoing sinus surgery, due to epithelial disruption and persistent inflammation. In woodworking-related activities, exposure to wood dust and fumes correlates with substantially elevated risk, exemplified by odds ratios of 30.6 (95% CI 6.9–135.6) for nasal polyps in woodstove users, a proxy for similar irritant environments. Diving poses a specific barotrauma risk, where pressure changes during descent or ascent cause sinus squeeze; divers with chronic sinusitis report higher dive counts (average 320 vs. 265 dives, p<0.05), affecting up to 48.9% of surveyed divers at some point.^[37]^[38] Climate and seasonal factors influence sinusitis incidence by altering air quality and allergen loads, particularly through dry conditions and fall/winter allergens that heighten acute episodes. Dry air exposure leads to squamous metaplasia of nasal mucosa, increasing irritation and susceptibility to inflammation, while low humidity in winter exacerbates this by drying nasal passages and promoting mucus stasis. Seasonal allergens, such as fungal spores in autumn and weed pollens in late summer transitioning to winter, trigger IgE-mediated responses that worsen sinus drainage, with global allergic rhinosinusitis affecting up to one-third of populations and correlating to pollen peaks. Radiologic evidence shows increased odds of sinus inflammation in winter and spring compared to summer, linking these factors to more frequent acute exacerbations.^[23]^[39] Allergic contributions from these seasonal elements can overlap with intrinsic sensitivities but primarily act through external environmental triggers.^[23]

Pathophysiology

Inflammatory Mechanisms

Sinusitis begins with inflammation of the sinonasal mucosa, leading to mucosal edema that causes swelling of the epithelial lining and impairs normal mucus drainage. This edema obstructs the ostiomeatal complex, a critical drainage pathway for the maxillary, frontal, and anterior ethmoid sinuses, resulting in mucus retention and stagnation that fosters further inflammatory responses.^[1] In the acute phase, proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) are upregulated in nasal secretions, promoting the recruitment of neutrophils to the site of inflammation. IL-6 acts as a chemoattractant and amplifies the inflammatory cascade, while TNF-α enhances endothelial activation and IL-6 expression in epithelial cells, facilitating neutrophil infiltration that characterizes the neutrophilic response in acute sinusitis.^[40] The transition to chronic sinusitis often involves a shift toward a Th2-skewed immune response, particularly in cases associated with allergy, where T helper 2 cells and innate lymphoid cells type 2 (ILC2s) drive the production of cytokines like IL-5 that promote eosinophil differentiation, survival, and tissue infiltration. Recent advances highlight the role of ILC2s, which are increased up to 100-fold in nasal polyps, and PD-1/PD-L1 dysregulation in amplifying these Th2 responses, contributing to persistent inflammation in type 2 chronic rhinosinusitis with nasal polyps (CRSwNP) as of 2025.^[41]^[42] This eosinophilic infiltration leads to persistent mucosal remodeling and hyperplasia, as seen in chronic hyperplastic eosinophilic sinusitis, exacerbating obstruction and inflammation.^[41] Resolution of sinus inflammation relies on the restoration of mucociliary clearance, where coordinated ciliary beating propels mucus and trapped pathogens out of the sinuses, supported by airway surface liquid dynamics. Epithelial repair mechanisms, including the regeneration of tight junction proteins such as occludin and zonula occludens-1, help reestablish the mucosal barrier integrity, reducing permeability and facilitating the clearance of inflammatory mediators to promote tissue homeostasis.^[43]

Structural and Microbial Factors

In chronic rhinosinusitis (CRS), biofilm formation represents a key structural factor contributing to disease persistence, where bacterial communities adhere to sinus mucosa and form protective matrices that resist both antibiotics and host immune responses. These biofilms, detected in over 65% of CRS cases, consist of structured communities encased in an extracellular polymeric substance (EPS) matrix comprising polysaccharides, proteins, and extracellular DNA, which shields bacteria from antimicrobial penetration and phagocytosis. Common pathogens include Pseudomonas aeruginosa, identified in approximately 22% of CRS biofilms, and Staphylococcus aureus in up to 50%, with P. aeruginosa particularly noted for its role in recalcitrant infections due to quorum sensing mechanisms that enhance matrix production and persister cell formation, leading to 10–1000-fold greater antibiotic resistance compared to planktonic bacteria. S. aureus further contributes through superantigens that enhance Th2 inflammation and disrupt epithelial barriers, detected in about two-thirds of CRSwNP cases.^[44]^[42] This resistance extends to host defenses, as biofilms impair ciliary function, reduce lactoferrin levels, and skew immune responses toward a Th2-dominant profile, perpetuating inflammation and increasing the risk of postoperative recurrence.^[44] Fungal elements further complicate microbial dynamics in CRS, particularly in allergic fungal rhinosinusitis (AFRS), a subtype characterized by noninvasive fungal hyphae embedded within eosinophilic mucin, triggering a hyperallergic response without tissue invasion. AFRS typically presents in atopic, immunocompetent individuals with nasal polyposis and thick, peanut butter-like eosinophil-rich mucin containing sparse fungal elements from dematiaceous fungi such as Bipolaris species, leading to type I and III hypersensitivity reactions that drive mucin hypersecretion and sinus expansion. Pathophysiologically, fungal antigens elicit IgE-mediated eosinophil recruitment and degranulation, resulting in characteristic CT findings of heterogeneous opacification and bony erosion in up to 56% of cases, distinguishing AFRS from other CRS variants through the presence of allergic mucin with fungal hyphae confirmed histologically.^[45] This eosinophilic mucin not only obstructs sinus drainage but also fosters a proinflammatory environment, exacerbating chronicity in affected patients.^[45] Structural alterations in chronic cases often manifest as osteitis, involving inflammation and remodeling of the paranasal sinus bony walls, which serves as a persistent reservoir for inflammatory mediators. Osteitis is histologically marked by neo-osteogenesis, increased osteoblastic-osteoclastic activity, immature woven bone formation, and periosteal thickening, driven by prolonged exposure to cytokines rather than direct bacterial invasion. Computed tomography (CT) imaging provides key evidence, revealing irregular sinus wall thickening and hyperostosis, quantified via the Global Osteitis Scoring Scale (GOSS) where scores above 20 correlate with severe involvement across maxillary (up to 100%), frontal (100%), and sphenoid (96.8%) sinuses, reflecting advanced remodeling that worsens disease severity and quality of life.^[46] These bony changes create a nidus for ongoing inflammation, as remodeled bone acts as a depot for proinflammatory signals, hindering resolution even after mucosal clearance.^[46] The one-airway theory underscores the interconnectedness of upper and lower respiratory tracts in sinusitis, positing a unified airway inflammation where sinus pathology influences and is influenced by lower airway diseases such as asthma. This hypothesis is supported by epidemiological data showing 60–90% comorbidity between CRS and asthma, with shared eosinophilic infiltration, Th2 cytokine profiles (e.g., IL-5), and systemic mediators like leukotrienes driving bidirectional effects—nasal inflammation exacerbates bronchial hyperreactivity, while lower airway challenges provoke upper airway responses. Experimental evidence from allergen provocation studies demonstrates that sinus stimulation induces distal airway eosinophilia, and treatments targeting sinusitis (e.g., surgery) improve asthma control, highlighting the respiratory tract as a continuum susceptible to common inflammatory cascades.^[47]

Diagnosis

Clinical Assessment

The clinical assessment of sinusitis begins with classifying the condition based on symptom duration to guide evaluation and management. Acute sinusitis is defined as symptoms lasting less than 4 weeks, subacute sinusitis as lasting 4 to 12 weeks, and chronic sinusitis as persisting for more than 12 weeks.^[48]^[49] These criteria help differentiate viral from bacterial etiologies in acute cases and identify the need for further investigation in prolonged presentations.^[50] History-taking focuses on key elements to characterize the episode and identify contributing factors. Clinicians inquire about the onset of symptoms, such as sudden versus gradual development of nasal congestion, discharge, or facial pain, along with potential triggers like recent upper respiratory infections, allergen exposure, or environmental irritants.^[51] Details on prior episodes, including frequency and response to treatments, are elicited to assess for recurrent patterns, while screening for comorbidities such as asthma, allergic rhinitis, or immunocompromising conditions provides context for disease severity and persistence.^[51] Patients are also asked about associated features like fever, headache, or olfactory changes to refine the differential diagnosis. The physical examination involves targeted inspection and palpation to detect signs of inflammation. Anterior rhinoscopy may reveal mucosal erythema, edema, or purulent secretions, while percussion or palpation over the maxillary or frontal sinuses can elicit tenderness indicative of localized involvement.^[1] In cases suggestive of chronic sinusitis, nasal endoscopy is performed to visualize mucosal edema, polypoid changes, or purulent discharge within the middle meatus, offering direct evidence of sinonasal pathology.^[51] To quantify symptom severity, particularly in chronic or recurrent cases, validated tools like the 22-item Sino-Nasal Outcome Test (SNOT-22) are employed. This questionnaire assesses domains including nasal obstruction, facial pain, sleep dysfunction, and emotional impact on a Likert scale, providing a reliable measure of health-related quality of life affected by rhinosinusitis.^[52] Higher scores correlate with greater disease burden and help track response to interventions.^[53]

Imaging and Endoscopy

Imaging modalities play a crucial role in visualizing sinus pathology, particularly when clinical symptoms persist or complications are suspected. Plain radiography, though largely obsolete, retains limited utility in acute sinusitis cases. Standard views, such as the Waters' or Caldwell projection, can reveal air-fluid levels indicative of acute infection, mucosal thickening, or complete opacification in the maxillary or frontal sinuses. However, these findings are nonspecific, with sensitivity around 76% for maxillary sinus involvement but only 14.6% for the frontal sinus, and poor visualization of ethmoid and sphenoid regions limits their diagnostic value.^[54]^[55] Computed tomography (CT) serves as the gold standard for evaluating chronic rhinosinusitis, providing detailed assessment of sinus anatomy and pathology. Noncontrast coronal CT scans demonstrate key features such as partial or complete opacification, mucosal thickening exceeding 4 mm, air-fluid levels, and sclerotic bone changes in chronic cases. These images excel in delineating the ostiomeatal complex, which is critical for understanding obstructive patterns in sinusitis. The Lund-Mackay scoring system quantifies disease severity on CT by assigning scores to each sinus group (maxillary, anterior/posterior ethmoid, frontal, sphenoid) and the ostiomeatal complex: 0 for no opacification, 1 for partial opacification, and 2 for total opacification (0 or 2 for the ostiomeatal complex), yielding a total score from 0 to 24. This validated tool correlates well with endoscopic findings and aids in staging disease extent for management decisions.^[56]^[57]^[58] Magnetic resonance imaging (MRI) complements CT in specific scenarios, offering superior soft tissue contrast for detecting fungal elements, neoplasms, or extensions into adjacent structures. T2-weighted MRI sequences highlight mucosal inflammation and fungal concretions as low-signal areas, while contrast-enhanced studies identify intracranial complications like abscesses in invasive fungal sinusitis. Unlike CT, MRI poorly resolves bony structures, making it less suitable for routine sinus evaluation but valuable when soft tissue or invasive pathology is suspected.^[56]^[58] Nasal endoscopy provides direct in-office visualization of the nasal cavity and sinus ostia, enhancing diagnostic precision beyond radiographic methods. Flexible fiberoptic or rigid Hopkins rod endoscopes (typically 0° or 30° angled, 4 mm diameter) allow assessment of the ostiomeatal complex for edema, mucopus, or obstruction, with a three-pass technique covering the nasal septum, middle meatus, and nasopharynx. It is particularly effective for detecting nasal polyps, which appear as pale, edematous masses in the middle meatus, and purulent discharge localizing infection sites. Endoscopy demonstrates high diagnostic accuracy, with substantial agreement to CT for polyp detection (kappa 0.833) and sensitivity of 80% for mucosal changes in acute cases.^[59]^[54]^[55]

Laboratory and Microbiological Tests

Laboratory and microbiological tests play a targeted role in confirming the etiology of sinusitis, particularly in complicated, recurrent, or refractory cases where clinical assessment alone is insufficient. These tests are not routinely recommended for uncomplicated acute sinusitis due to their invasiveness and limited yield in distinguishing viral from bacterial causes, but they guide antimicrobial therapy in severe or chronic presentations.^[1]^[54] Cultures from sinus aspirates or swabs represent the gold standard for identifying bacterial or fungal pathogens, though they are invasive and reserved for immunocompromised patients, treatment failures, or complications such as orbital or intracranial extension. Maxillary sinus puncture via trocar or needle provides direct aspirates with high specificity for pathogens like Streptococcus pneumoniae, Haemophilus influenzae, and anaerobes, but it is uncomfortable and requires specialized skills, limiting its use.^[54]^[60] Endoscopically directed middle meatal cultures offer a less invasive alternative in adults, achieving 87-94% concordance with aspirate results for aerobic and anaerobic bacteria, though nasal swabs alone have only 65% concordance due to contamination by normal flora.^[54] Fungal cultures, often combined with Gram stain and biopsy, are essential for suspected invasive fungal sinusitis, which can be life-threatening.^[61] Allergy testing, including skin prick tests or serum-specific IgE assays, helps identify atopy as a contributing factor in recurrent or chronic sinusitis, where allergic rhinitis coexists in up to 60% of refractory cases. Nasal cytology can further detect eosinophilia or markers of aspirin-exacerbated respiratory disease (Samter syndrome), supporting the distinction from non-allergic etiologies.^[1]^[61] Blood tests provide supportive evidence of inflammation or underlying conditions but lack specificity for routine diagnosis. Complete blood count (CBC) may reveal eosinophilia in allergic fungal sinusitis or chronic cases with atopy, while elevated C-reactive protein (CRP >10 mg/L) or erythrocyte sedimentation rate (ESR >20 mm/h in females or >10 mm/h in males) correlates with acute bacterial rhinosinusitis severity, though these markers are nonspecific and not cost-effective for initial evaluation.^[1]^[54] Immunoglobulin levels or HIV serology are indicated only if immunodeficiency is suspected.^[1] Emerging molecular techniques, such as polymerase chain reaction (PCR)-based nucleic acid amplification tests (NAATs), enable rapid detection of viral, bacterial, or atypical pathogens in acute sinusitis aspirates or swabs, offering higher sensitivity than traditional cultures for mixed infections. These methods are particularly useful in research or severe cases to differentiate etiologies and avoid unnecessary antibiotics, though they are not yet standard in guidelines.^[60]

Management

Initial and Supportive Therapies

Initial and supportive therapies for sinusitis primarily aim to alleviate symptoms, promote sinus drainage, and support the body's natural recovery processes, particularly in acute cases presumed to be viral in origin. These approaches are recommended as first-line management for most patients, given that the majority of acute sinusitis episodes resolve spontaneously within 7 to 10 days without specific antimicrobial intervention.^[62] Symptomatic relief focuses on non-pharmacological measures to enhance mucociliary clearance and reduce discomfort, with over-the-counter analgesics used judiciously for pain and fever control.^[1] Nasal irrigation with saline solution is a cornerstone of supportive care, facilitating the removal of mucus, allergens, and irritants to improve mucociliary clearance and reduce nasal congestion. Devices such as neti pots or squeeze bottles deliver isotonic or hypertonic saline, with high-volume irrigation (typically 240 mL per side) preferred for better efficacy in clearing the sinuses compared to low-volume sprays.^[63] Guidelines endorse its use as a safe, inexpensive adjunct, though patients must use distilled, sterile, or boiled water to prevent rare infections from contaminated sources.^[1] Evidence from randomized controlled trials supports modest symptom improvement, particularly in acute rhinosinusitis, without significant adverse effects beyond mild nasal irritation.^[63] Hydration and environmental humidification further aid in thinning mucus and maintaining optimal sinus function. Adequate fluid intake, aiming for at least 2-3 liters daily, helps liquefy secretions and supports overall recovery.^[1] Steam inhalation or use of cool-mist humidifiers can provide transient relief from congestion by adding moisture to the air, though high-quality evidence for shortening symptom duration is limited; humidifiers should be cleaned regularly to avoid mold growth.^[64] Maintaining indoor humidity between 40% and 60% is advised to prevent overly dry conditions that exacerbate irritation.^[1] For pain and fever management, nonnarcotic analgesics such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen are recommended at standard doses (e.g., acetaminophen 500-1000 mg every 6 hours as needed). These provide effective symptomatic relief without the risks associated with narcotics.^[62] Watchful waiting is appropriate for presumed viral cases, involving close monitoring for 7 to 10 days; approximately 70% of patients improve without escalation to antibiotics, which are reserved for persistent or worsening symptoms suggestive of bacterial involvement.^[62]

Pharmacological Interventions

Pharmacological interventions for sinusitis focus on addressing bacterial infections in acute cases and persistent inflammation in acute and chronic presentations, guided by clinical guidelines emphasizing evidence-based selections to optimize efficacy while minimizing resistance and adverse effects. In acute bacterial rhinosinusitis (ABRS), antibiotics are reserved for cases with persistent symptoms beyond 10 days, severe onset, or worsening after initial improvement, as most cases are viral and self-limiting. Amoxicillin-clavulanate is recommended as first-line empiric therapy in adults and children due to its broad coverage against common pathogens like Streptococcus pneumoniae and beta-lactamase-producing Haemophilus influenzae. High-dose formulations (e.g., 2 g orally twice daily for adults or 90 mg/kg/day divided twice daily for children) are preferred in regions with elevated resistance rates to standard amoxicillin, which can exceed 20-30% for H. influenzae in some populations. Alternative agents, such as doxycycline or levofloxacin, are considered for penicillin-allergic patients or treatment failures, with local antimicrobial susceptibility patterns informing choices to curb resistance development. Intranasal corticosteroids represent a cornerstone for managing inflammation in both acute and chronic sinusitis, particularly when allergic rhinitis overlaps or chronicity persists. Agents like fluticasone propionate (50 mcg per spray) or mometasone furoate (50 mcg per spray), administered twice daily, reduce mucosal edema by inhibiting inflammatory mediators such as cytokines and prostaglandins, thereby enhancing sinus ostia patency and drainage. Clinical trials demonstrate modest but significant symptom improvement, with up to 28% greater resolution rates compared to placebo after 15-21 days in acute cases, and sustained benefits in chronic rhinosinusitis when used long-term as maintenance therapy. For severe acute exacerbations or chronic sinusitis with marked inflammation or nasal polyps, short courses of oral corticosteroids may provide rapid symptom relief as adjunctive therapy. Prednisone at 40-60 mg daily for 5-14 days, tapered as needed, has shown superior short-term efficacy over intranasal agents alone in reducing polyp size and improving quality of life scores by 20-30% in responsive patients. Use is limited to brief durations due to risks of systemic effects like hyperglycemia and osteoporosis, with guidelines advising against routine application in mild cases. Biologic therapies are indicated for adults with chronic rhinosinusitis with nasal polyps (CRSwNP) refractory to intranasal corticosteroids and/or surgery, particularly in cases with type 2 inflammation. Dupilumab, a monoclonal antibody targeting interleukin-4 and -13 receptors (300 mg subcutaneously every two weeks after loading dose), omalizumab (anti-IgE, dosed by weight and IgE levels every 2-4 weeks), and mepolizumab (anti-IL-5, 100 mg subcutaneously every 4 weeks) have shown significant reductions in nasal polyp burden, symptom severity, and need for further interventions in randomized controlled trials. Guidelines as of 2025 endorse their use in severe, uncontrolled CRSwNP to improve quality of life and reduce oral corticosteroid dependence.^[65] Antihistamines and decongestants play a targeted role in sinusitis with allergic or vasomotor components, such as concurrent allergic rhinitis. Second-generation oral antihistamines (e.g., loratadine 10 mg daily or cetirizine 10 mg daily) alleviate histamine-driven symptoms like pruritus and rhinorrhea, achieving 10-30% symptom reduction over placebo in allergic rhinosinusitis. Oral or topical decongestants (e.g., pseudoephedrine 60 mg every 6 hours or oxymetazoline spray twice daily) offer vasoconstriction for congestion relief but are limited to 3-5 days to avoid rebound rhinitis medicamentosa, which can exacerbate obstruction.

Surgical Options

Surgical intervention is indicated for chronic rhinosinusitis (CRS) refractory to appropriate medical therapy, anatomical defects such as skull base anomalies, and complications arising from acute rhinosinusitis.^[66]^[67] These procedures aim to restore sinus drainage and ventilation when conservative measures fail. Functional endoscopic sinus surgery (FESS) is the cornerstone procedure for managing refractory CRS, utilizing nasal endoscopes to precisely widen obstructed sinus ostia, remove nasal polyps, and excise inflamed mucosal tissue while preserving sinus anatomy.^[67] This approach addresses underlying structural blockages in the ostiomeatal complex, promoting mucociliary clearance and reducing recurrent infections. Success rates for symptom improvement with FESS typically range from 80% to 90%, with sustained benefits observed in the majority of patients over long-term follow-up.^[68] Preoperative computed tomography imaging guides the surgical planning by identifying specific anatomical variations and disease extent.^[69] Balloon sinuplasty offers a less invasive alternative for patients with mild ostial obstruction, involving the insertion of a flexible balloon catheter into the sinus ostium under endoscopic guidance, followed by inflation to dilate the passageway without tissue removal.^[70] This technique is particularly suited for isolated sinus involvement in CRS that persists despite medical management, minimizing disruption to surrounding mucosa.^[71] Postoperative management is essential to optimize outcomes and includes routine sinus cavity debridement to remove crusts and promote healing, alongside daily nasal saline irrigations and ongoing topical corticosteroid therapy to control inflammation.^[72]^[73] These measures help maintain surgical patency and reduce the risk of adhesions or recurrent obstruction.^[74]

Prognosis and Complications

Short-Term and Long-Term Outcomes

For acute sinusitis, approximately 64% of uncomplicated cases resolve spontaneously within 2 weeks without specific intervention, primarily through supportive measures like hydration and nasal irrigation.^[75] The introduction of the 13-valent pneumococcal conjugate vaccine (PCV13) in 2010 has reduced the incidence of acute rhinosinusitis by 13-21% in adults and severe complications requiring hospitalization by 54%.^[75] This high resolution rate underscores the self-limiting nature of most viral or mild bacterial episodes, though persistence beyond 10 days or worsening symptoms may indicate a need for antibiotics to prevent progression.^[1] Untreated underlying risk factors, such as anatomical obstructions or environmental allergens, elevate the risk of recurrence, potentially leading to recurrent acute episodes defined as four or more per year.^[48] In chronic sinusitis, medical therapies including intranasal corticosteroids, saline irrigations, and antibiotics yield symptom improvement in 50-60% of patients after 8-12 weeks of treatment, with variations depending on disease severity and adherence.^[76] Quality-of-life assessments, such as the Sino-Nasal Outcome Test (SNOT-22), typically show significant reductions in total scores post-therapy, reflecting better control of nasal congestion, facial pain, and sleep disruption, though full resolution is uncommon without addressing persistent inflammation.^[77] Surgical interventions like functional endoscopic sinus surgery can further enhance these outcomes, achieving durable SNOT-22 improvements in a majority of refractory cases.^[78] Early intervention in acute cases markedly reduces the likelihood of progression to chronicity by targeting inflammation and infection promptly, thereby preserving sinus drainage pathways.^[79] Conversely, comorbidities such as asthma, allergies, or immunodeficiency adversely affect prognosis, correlating with higher symptom burden and lower response rates to standard therapies as measured by SNOT-22 scores.^[80] Overall mortality from sinusitis is extremely rare in the general population, almost exclusively linked to rare intracranial or orbital complications rather than the condition itself.

Specific Complication Types

Orbital complications represent a significant risk in acute sinusitis, particularly involving the ethmoid and maxillary sinuses, and can progress from superficial infections to vision-threatening conditions. Preseptal cellulitis, confined to the eyelid anterior to the orbital septum, typically presents with eyelid swelling and erythema without proptosis or ophthalmoplegia, distinguishing it from true orbital involvement.^[81] In contrast, orbital cellulitis involves post-septal spread, leading to proptosis, chemosis, decreased visual acuity, and restricted eye movements due to inflammation within the orbital cone.^[82] Chandler's classification system categorizes these into five stages: group I (preseptal cellulitis), group II (orbital cellulitis), group III (subperiosteal abscess), group IV (orbital abscess), and group V (cavernous sinus thrombosis with orbital involvement), guiding escalation from medical to surgical management.^[83] Subperiosteal or orbital abscesses can cause compressive optic neuropathy, resulting in permanent vision loss if untreated, with ethmoid sinusitis being the most common precursor.^[82] Intracranial complications arise from direct extension or hematogenous spread of sinus infection, often from frontal or sphenoid sinuses, and carry high morbidity and mortality rates. Meningitis manifests with fever, severe headache, nuchal rigidity, photophobia, and altered mental status, secondary to bacterial invasion of the meninges.^[84] Brain abscesses present with focal neurological deficits, seizures, and progressive headache, forming encapsulated collections in cerebral lobes adjacent to infected sinuses.^[85] Cavernous sinus thrombosis, a particularly devastating sequela, involves septic thrombosis of the cavernous sinus, leading to bilateral periorbital edema, cranial nerve palsies (III, IV, VI), proptosis, and severe headache; symptoms may include papilledema and rapid neurological deterioration.^[86] These intracranial events occur in approximately 3-4% of hospitalized sinusitis cases, predominantly affecting children and young adults, with Streptococcus species as common pathogens.^[87] Osseous complications involve bone erosion and infection, most notably in the frontal bone from protracted frontal sinusitis. Osteomyelitis of the frontal bone develops through contiguous spread, causing bone necrosis and potential intracranial extension, with symptoms including localized pain, swelling, and systemic fever.^[88] Pott's puffy tumor, a classic manifestation, refers to a subperiosteal abscess overlying frontal osteomyelitis, presenting as a fluctuant forehead swelling that may mimic a benign mass but harbors risk of epidural abscess or sagittal sinus thrombosis.^[89] This condition, historically linked to untreated sinusitis, now occurs rarely due to antibiotics but remains a marker of advanced disease with frontal bone involvement.^[90] Other severe sequelae include mucocele formation and airway obstruction associated with nasal polyps. Sinus mucoceles arise from obstructed drainage, leading to cystic expansion that erodes surrounding structures, causing headaches, proptosis, or diplopia depending on the affected sinus.^[91] In chronic rhinosinusitis with nasal polyps, large polypoid masses can cause significant nasal and nasopharyngeal obstruction, exacerbating airflow limitation and contributing to sleep-disordered breathing.^[92] Immunocompromised patients face heightened risk for these complications due to impaired host defenses against opportunistic pathogens.^[91]

Epidemiology

Global Prevalence and Incidence

Sinusitis, encompassing both acute and chronic forms, represents a significant global health burden, with acute rhinosinusitis (ARS) affecting approximately 6-15% of adults annually worldwide. This high prevalence is primarily driven by viral infections, which account for the majority of cases, often complicating upper respiratory tract infections such as the common cold. In the United States, for instance, about 11.6% of adults receive a diagnosis of sinusitis each year, underscoring its commonality in primary care settings.^[93]^[94]^[95] Chronic rhinosinusitis (CRS), defined as inflammation persisting for at least 12 weeks, has a global pooled prevalence of 8.71% based on recent meta-analyses, with estimates traditionally ranging from 5-12% across populations. The European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS 2020) supports this range, noting variations influenced by diagnostic criteria but confirming CRS as one of the most common chronic conditions. Incidence rates for CRS are lower, at approximately 0.73% per year globally, reflecting its persistent nature rather than frequent new onsets.^[96]^[97]^[98] Over recent decades, the prevalence of CRS has shown an upward trend, increasing from around 4.72% in studies from 1980-2000 to 19.40% in those from 2014-2020, potentially linked to rising environmental factors such as air pollution and allergies. This escalation highlights the need for ongoing surveillance, as noted in epidemiological reviews. In children, CRS is particularly underdiagnosed due to subtle symptoms overlapping with other respiratory conditions, leading to potential delays in management despite its commonality in pediatric populations. The estimated global prevalence of CRS in children is around 4%.^[96]^[99]^[100]^[101]

Demographic and Geographic Variations

Sinusitis exhibits notable variations across demographic groups, particularly in age distribution. Acute sinusitis is common in pediatric populations, often occurring as a complication following upper respiratory infections (URIs), with approximately 5-10% of viral URIs progressing to acute bacterial sinusitis in children.^[102]^[103] In adults, the incidence peaks between the ages of 45 and 64 years, reflecting cumulative exposure to environmental triggers and anatomical changes that predispose individuals to chronic forms.^[104] Chronic rhinosinusitis (CRS) prevalence increases with age, doubling in those over 60 compared to younger adults under 40.^[105] Sex-based differences are observed primarily in chronic sinusitis, where females show a predominance, with some studies reporting odds ratios indicating nearly twice the rate compared to males.^[106] This disparity is potentially linked to hormonal influences, such as estrogen fluctuations that affect nasal mucosa and mucus production, exacerbating inflammation during menstrual cycles, pregnancy, or menopause.^[106]^[107] Ethnic variations highlight disparities in CRS phenotypes. African Americans experience higher rates of CRS, with a reported diagnosis prevalence of 13.8% compared to 13.0% in whites, and they face an elevated risk of nasal polyposis and more severe disease manifestations, possibly influenced by genetic factors and socioeconomic determinants.^[108]^[109] Fungal sinusitis, including allergic fungal rhinosinusitis, is more prevalent in tropical regions, where hot and humid climates promote fungal growth, leading to higher incidences in areas like India and Sudan.^[110] Geographically, sinusitis rates are elevated in industrialized urban areas due to air pollution, with exposure to particulate matter (PM2.5) independently associated with increased CRS odds and disease severity.^[36]^[111] In temperate zones, the condition displays strong seasonality, with peak incidences during winter months attributed to dry air, lower humidity, and viral outbreaks that inflame sinuses.^[112]^[113]

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Cavernous Sinus Thrombosis - StatPearls - NCBI Bookshelf
Jun 16, 2025 · Assess for potential complications, including visual loss, stroke, and cranial nerve deficits, in a patient with cavernous sinus thrombosis.
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Frontal osteomyelitis (Pott's puffy tumour) associated with ...
Investigations revealed erosion of the anterior wall of the frontal sinus with subgaleal abscess formation, establishing a diagnosis of Pott's puffy tumour.Missing: osseous | Show results with:osseous
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Pott Puffy Tumor - StatPearls - NCBI Bookshelf - NIH
Feb 15, 2025 · Pott puffy tumor (PPT) is a subperiosteal abscess of the forehead associated with underlying frontal bone osteomyelitis.Missing: osseous | Show results with:osseous
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Pott's Puffy Tumor, a Forgotten Complication of Sinusitis - NIH
Jan 6, 2023 · It occurs as a sequela of frontal sinusitis or trauma, progressing as osteomyelitis of the frontal bone with associated subperiosteal abscess.Missing: osseous | Show results with:osseous
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Acute Bacterial Rhinosinusitis - PMC - PubMed Central - NIH
May 4, 2018 · In contrast to community-acquired sinusitis, nosocomial sinusitis is more likely to involve resistant bacteria, including Staphylococcus aureus ...
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Nasal Polyps - StatPearls - NCBI Bookshelf
May 5, 2025 · Nasal polyps are benign, inflammatory outgrowths of the sinonasal mucosa that can lead to chronic nasal obstruction, congestion, and diminished quality of life.Missing: airway | Show results with:airway
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FastStats - Sinus Conditions - CDC
Number of adults with diagnosed sinusitis: 28.9 million · Percent of adults with diagnosed sinusitis: 11.6%.
[95]
Acute rhinosinusitis in adults: an update on current management
The most common cause of acute rhinosinusitis is a viral upper respiratory infection. Approximately 9 out of 10 patients who have viral upper respiratory tract ...
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Global Incidence and Prevalence of Chronic Rhinosinusitis - PubMed
Nov 7, 2024 · Global pooled prevalence of CRS and CRS with nasal polyps (CRSwNP) was found to be 8.71% (95% CI, 6.69-11.33; number of studies, 20) and 0.65% ( ...
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Prevalence of chronic rhinosinusitis in the general population based ...
The prevalence of chronic rhinosinusitis (CRS) measured in epidemiologic studies is 5% to 12%. This might be an overestimation because of overlap with other ...
[98]
[PDF] European Position Paper on Rhinosinusitis and Nasal Polyps 2020
All available evidence for the management of acute rhinosinusitis and chronic rhinosinusitis with or without nasal polyps in adults and children is ...
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Global Incidence and Prevalence of Chronic Rhinosinusitis: A ...
Nov 7, 2024 · The global pooled prevalence of CRS was found to be 8.71% and the global pooled incidence of CRS was 0.73%. Among subgroups, adults were found ...ABSTRACT · Methods · Results · Discussion
[100]
National Trends in Allergic Rhinitis and Chronic Rhinosinusitis ... - NIH
Jan 5, 2024 · The prevalence of AR and CRS increased from 1998 to 2021, with AR prevalence rising from 5.84% (95% CI, 5.57–6.10) in 1998–2005 to 8.99 ...
[101]
May chronic rhinosinusitis in children be diagnosed by clinical ...
Abstract. Objectives: Chronic rhinosinusitis (CRS) is a common disease in childhood but is often underdiagnosed because the symptoms are subtle and similar to ...
[102]
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Jul 1, 2013 · Amoxicillin with or without clavulanate is the first-line treatment of acute bacterial sinusitis. Clinicians should reassess initial management ...
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Aug 14, 2025 · Treatment of acute sinusitis consists of providing adequate drainage of the involved sinus and appropriate systemic treatment of the likely bacterial pathogens.
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Chronic Rhinosinusitis in Elderly Patients is Associated with ... - NIH
Mar 1, 2020 · For example, a Korean study found that the prevalence of CRS in patients aged 60 or older was almost twice that of patients under the age of 40.
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Sinusitis: is it more common in men or women? - Nasodren
Apr 26, 2022 · Some studies have reported that women have almost twice the rate of chronic sinusitis as men, while other studies have found no difference.Missing: female | Show results with:female
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Commentary on gender differences in prevalence, treatment, and ...
... hormonal factors have been speculated to increase the overall susceptibility to rhinosinusitis in women. Women may be more susceptible to obstruction and ...
[108]
https://pmc.ncbi.nlm.nih.gov/articles/PMC3345896/
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Chronic rhinosinusitis, race, and ethnicity - PMC - NIH
A diagnosis of sinusitis was reported by 13.8% of African Americans and 13.0% of white respondents, with lower prevalence seen in Hispanics (8.8%) and Asians ( ...
[110]
African American Patients with Chronic Rhinosinusitis Have a ...
AAs with refractory CRS are at increased risk for nasal polyposis, smell loss, aspirin-exacerbated respiratory disease, and a greater severity of disease ...
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Chronic fungal sinusitis in Tamilnadu, India - ScienceDirect
The incidence of chronic fungal sinusitis is very high in tropical countries like India, Sudan, Pakistan, Saudi Arabia, etc., where the climate is hot and dry.
[112]
Air Pollution Exposure and the Development of Chronic ...
Jan 7, 2022 · This study showed that PM 2.5 exposure is a major independent contributor to the development of CRS.
[113]
Seasonality in the incidence of acute sinusitis, air pollutant levels ...
Specifically, individuals experience significantly higher incidence rates during winter compared to spring. These findings underscore winter as a period with ...
[114]
How Seasonal Weather Changes Can Affect Your Sinuses
The dip in humidity and temperatures during fall and winter months often contributes to dry air conditions, both indoors and out, ushering in a host of ...