Hubbry Logo
RhinosinusitisRhinosinusitisMain
Open search
Rhinosinusitis
Community hub
Rhinosinusitis
logo
7 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Rhinosinusitis
Rhinosinusitis
from Wikipedia

Rhinosinusitis is a simultaneous infection of the nasal mucosa (rhinitis) and an infection of the mucosa of the paranasal sinuses (sinusitis). A distinction is made between acute rhinosinusitis and chronic rhinosinusitis.

Background

[edit]

Because sinusitis typically is preceded by an infection of the nasal mucosa, some authors suggest generally replacing the term “sinusitis” with “rhinosinusitis”.[1] The functional unity of the two mucosa speaks in favor of this replacement. A distinction is made between acute and chronic rhinosinusitis. Acute sinusitis lasts a maximum of 12 weeks. The clinical symptoms of acute rhinosinusitis are purulent nasal secretion, nasal obstruction and/or tension headache or feeling of fullness in the facial area. Acute rhinosinusitis can be caused by a viral or bacterial infection – a distinction is not possible during the first days. If the clinical picture follows a two-stage development, it indicates a bacterial rhinosinusitis. Chronic rhinosinusitis lasts more than 12 weeks with no complete recovery. The symptoms of chronic rhinosinusitis are less prominent/pronounced than of acute rhinosinusitis. Chronic rhinosinusitis is characterized/shaped by an impaired nasal inspiration, feelings of pressure and swelling in the facial area, as well as a higher susceptibility to infection.[2]

Severe complications are rare, although orbital and intracranial inflammations can occur.

Therapy

[edit]

Inhalation therapy mechanically removes deposits and relieves the symptoms of allergic or inflammatory diseases like acute or chronic rhinosinusitis (CRS). In essence, inhalation therapy resolves the obstruction found to be bothersome, alleviates the irritation of the nasal mucosa and supports the self-cleaning mechanisms. Inhalation therapy is commonly mentioned in North American and international guidelines for treatment of CRS (Bachmann et al., 2000).[3] There are different therapeutic approaches for acute rhinosinusitis. Among other things, pain killers, decongestant nose drops or sprays to reduce the local swelling of the mucosa, topical steroids and phytotherapeutics can be used. In case of a bacterial rhinosinusitis, antibiotics are a typical therapeutic treatment.[4]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia
from Grokipedia
Rhinosinusitis, commonly referred to as , is a symptomatic of the mucosa of the and , typically characterized by two or more of the following: nasal blockage or congestion, anterior or posterior nasal discharge, facial or , and reduction or loss of smell. It is classified by duration into acute rhinosinusitis (lasting less than 4 weeks), subacute (4 to 12 weeks), chronic (more than 12 weeks), and recurrent acute (four or more episodes per year with complete resolution between). The condition arises from a complex interplay of infectious and noninfectious factors, with the most common being viral upper respiratory infections, though bacterial superinfections, allergies, anatomical abnormalities, and environmental irritants also play significant roles. The primary symptoms often include , discharge, facial pain or pressure, and . In chronic rhinosinusitis (CRS), symptoms persist for at least 12 weeks and may be subdivided into forms with or without nasal polyps (CRSwNP), the latter often involving eosinophilic inflammation. Epidemiologically, rhinosinusitis affects approximately 10-15% of the U.S. population annually, with CRS estimated at 4% to 12% globally and a pooled rate of 8.71% as of recent systematic reviews, while CRSwNP affects about 0.65%; higher rates are observed in adults over 65 and those with comorbidities like or . Diagnosis relies on clinical history and symptoms, supported by nasal or computed (CT) for confirmation in chronic or recurrent cases, while avoiding routine in uncomplicated acute rhinosinusitis. Management emphasizes symptomatic relief and antibiotic stewardship: most acute cases are viral and resolve spontaneously with supportive care and watchful waiting; for adults with uncomplicated acute bacterial rhinosinusitis (ABRS), the 2025 AAO-HNS guidelines recommend offering watchful waiting without antibiotics as the initial management, including in cases where symptoms persist without improvement for at least 10 days (which supports the diagnosis of ABRS), to promote antibiotic stewardship; antibiotics are indicated for severe symptoms, worsening after initial improvement, high-risk patients, or failure of watchful waiting, with first-line therapy being high-dose amoxicillin-clavulanate (preferred in areas with resistant S. pneumoniae or risk factors), alternatives including doxycycline or respiratory fluoroquinolones (reserved due to risks), and typical duration of 5-7 days (per 2025 AAO-HNS guidelines); chronic forms involve intranasal corticosteroids, extended antibiotics, or biologic therapies including recent approvals like tezepelumab for CRSwNP, with for refractory cases. Guidelines from EPOS 2020 and the updated 2025 AAO-HNS Clinical Practice Guideline stress a stepwise approach prioritizing medical therapy.

Overview

Definition

Rhinosinusitis is defined as the of the mucosa lining the and , often occurring simultaneously and resulting in symptoms such as and facial pain or pressure. This condition encompasses a spectrum of inflammatory processes affecting the contiguous nasal and sinus tissues, distinguishing it from isolated by highlighting the primary role of nasal involvement. The terminology shifted from "sinusitis" to "rhinosinusitis" in medical literature starting in the 1990s, as it better reflects that sinus inflammation is almost always accompanied by inflammation of the adjacent nasal mucosa. This change acknowledges the anatomical and pathophysiological continuum between the nasal passages and sinuses, where disease processes typically originate in the nose before extending to the sinuses. Anatomically, rhinosinusitis involves the —air-filled cavities within the frontal, ethmoidal, sphenoidal, and maxillary bones that drain into the —along with the . These structures are interconnected via ostia, allowing for the spread of between the and sinuses. Rhinosinusitis can manifest as acute or chronic forms, differentiated primarily by the duration of symptoms.

Classification

Rhinosinusitis is classified primarily based on duration of symptoms, with acute rhinosinusitis defined as lasting less than 4 weeks, subacute rhinosinusitis from 4 to 12 weeks, chronic rhinosinusitis exceeding 12 weeks, and recurrent acute rhinosinusitis involving four or more episodes per year with complete resolution between episodes. This temporal categorization facilitates initial management decisions, distinguishing self-limiting acute cases from persistent chronic forms requiring long-term intervention. Phenotypic subtypes of chronic rhinosinusitis (CRS) are delineated by the presence or absence of nasal polyps, resulting in CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP). CRSwNP typically involves bilateral polyps in the middle and is associated with higher rates of comorbidities such as . The EPOS 2020 guidelines further refine this by classifying CRS as primary (idiopathic onset) or secondary (due to underlying conditions like odontogenic sources), and as localized (unilateral or focal involvement) or diffuse (bilateral and widespread mucosal disease). Endotypic classification focuses on underlying inflammatory mechanisms, distinguishing eosinophilic (type 2-dominant) from non-eosinophilic (type 1 or 3) patterns. endotypes, characterized by elevated (≥10 per ) and type 2 cytokines like IL-5 and IL-13, predominate in CRSwNP and predict higher recurrence risk post-surgery. Non-eosinophilic endotypes often feature neutrophilic inflammation and are more common in CRSsNP. Severity is graded as mild, moderate, or severe based on symptom impact, commonly using the Sino-Nasal Outcome Test-22 (SNOT-22) score, with thresholds of 8-20 for mild, 21-50 for moderate, and >50 for severe disease. These gradings integrate clinical symptoms, endoscopic findings (e.g., modified Lund-Kennedy score ≥4), and radiographic evidence (e.g., Lund-Mackay CT score ≥4), as outlined in the EPOS 2020 guidelines to emphasize disease control via visual analogue scales for key symptoms like nasal obstruction and .

Epidemiology

Prevalence and Incidence

Rhinosinusitis, encompassing both acute and chronic forms, is a common condition worldwide. The global of chronic rhinosinusitis (CRS) is estimated at 8.71% (95% CI: 6.69–11.33), based on data from 20 studies involving over 237 million participants across 20 countries. A 2025 review of extended data through 2021 reports a pooled of approximately 9% among . Acute rhinosinusitis affects 6–15% of the annually, often linked to viral upper respiratory infections. In the United States, approximately 30 million experience acute rhinosinusitis each year, representing about 11.6% of the , while CRS impacts around 12% of . For children, the annual incidence of acute cases is higher, affecting 6–7% with respiratory symptoms, and chronic forms account for about 5.6 million outpatient visits annually among those aged 0–20 years. Prevalence varies by demographics and geography. CRS is more common in adults aged 18–65 years than in children or older adults, with global trends showing higher rates in this working-age group. In urban areas and regions with elevated , such as parts of where ranges from 2.1% to 28.4%, rhinosinusitis occurs more frequently due to environmental exposures; for instance, each 1 μg/m³ increase in PM10 levels is associated with a rise in CRS . Studies indicate urban residents face 1.5–2 times higher odds of chronic forms compared to rural populations, reflecting the impact of pollutants and allergens. Recent trends show an upward trajectory in both forms. Global CRS prevalence has risen from 4.72% in 1980–2000 to 19.40% in 2014–2020, partly attributed to increasing allergic burdens. Post-COVID-19, there has been a notable surge in acute bacterial rhinosinusitis cases, particularly complicated infections requiring hospitalization, with U.S. reports documenting elevated monthly incidences since 2020. This increase aligns with disruptions in respiratory pathogen patterns and reduced immunity from masking and .

Risk Factors

Rhinosinusitis risk factors encompass both non-modifiable and modifiable elements that predispose individuals to acute, recurrent, or chronic forms of the condition. Non-modifiable factors include , such as family history of or specific genetic variants like those in the CFTR gene ( [OR] 3.5, 95% CI not specified), HLA-DQ alleles (OR 4.25, p=0.001), and (higher prevalence of in recalcitrant cases, p=0.038). Age also plays a role, with peak incidence occurring between 45 and 54 years and prevalence peaking at 50 to 59 years for chronic rhinosinusitis. Sex differences show a slight predominance in females for chronic rhinosinusitis without nasal polyps (CRSsNP), while males are more prone to chronic rhinosinusitis with nasal polyps (CRSwNP). Modifiable risk factors primarily involve environmental exposures and lifestyle choices. significantly elevates risk, with current smokers facing an OR of 1.9 (95% CI 1.8–2.1) and exposure to carrying an OR of 2.2 (95% CI 1.5–3.2). and occupational irritants, such as , poisonous gases, or specific exposures like and processing (adjusted relative risk [aRR] 2.07, 95% CI 1.4–3.0), contribute to increased susceptibility, particularly in urban or industrial settings. High humidity environments can also exacerbate or increase the risk of chronic rhinosinusitis, as excess moisture promotes mold growth and thickens mucus, leading to impaired sinus drainage. is a strong modifiable risk, with an OR of 5.7 (95% CI 5.3–6.2) overall and up to 8.2 (95% CI 4.7–14.4) for persistent or moderate-severe cases. Anatomical abnormalities, including deviated , impair sinus drainage and are associated with higher incidence of acute and recurrent episodes. Comorbid conditions further heighten vulnerability. overlaps with rhinosinusitis in 20–30% of cases, conferring an OR of 3.1 (95% CI 2.8–3.4), which rises to 11.9 (95% CI 10.6–13.2) when combined with . Immunodeficiencies, such as , are linked to elevated prevalence due to impaired and recurrent infections. Recent viral upper respiratory infections (URIs) serve as a common trigger for acute rhinosinusitis, often progressing from viral to secondary bacterial involvement. Post-viral risks have been notably elevated following infections, with potentially including persistent sinonasal symptoms like sinus pressure, facial pain, and ; vaccination reduces the risk of developing sequelae.

Etiology and Pathophysiology

Causes

Rhinosinusitis is primarily triggered by infectious agents, with viral infections accounting for the majority of acute cases, estimated at 90 to 98 percent. Among these, is the most prevalent pathogen, responsible for approximately 30 to 50 percent of viral upper respiratory infections that commonly lead to rhinosinusitis, followed by influenza virus, parainfluenza virus, adenovirus, , and . Bacterial superinfections complicate about 0.5 to 2 percent of viral cases in adults and 5 to 13 percent in children, most commonly involving , which accounts for 20 to 43 percent of acute bacterial rhinosinusitis cases, and nontypeable , responsible for 22 to 35 percent. In chronic rhinosinusitis, anaerobes such as , , and species are frequently isolated, with isolation rates varying from 8 to 93 percent of cases, often alongside polymicrobial infections. Non-infectious causes play a significant role, particularly in chronic forms, through mechanisms like inflammation and mucosal disruption. Allergic rhinosinusitis arises from IgE-mediated hypersensitivity to environmental allergens, such as house dust mites (Dermatophagoides pteronyssinus), pollen, and animal dander, leading to eosinophilic inflammation and nasal obstruction. Irritant-induced rhinosinusitis results from exposure to chemical fumes, tobacco smoke, or dry air, which impair mucociliary clearance and provoke non-allergic inflammation. Structural abnormalities, such as a deviated nasal septum, nasal polyps, or adenoid hypertrophy in children, can obstruct sinus ostia and impair drainage, predisposing individuals to recurrent or chronic rhinosinusitis. In children, adenoid hypertrophy is a significant contributing factor, where enlarged adenoids obstruct the nasopharynx, impair sinus drainage, and act as a bacterial reservoir, facilitating secondary bacterial rhinosinusitis and progression to chronic forms. Fungal elements contribute in allergic fungal rhinosinusitis (AFRS), a subtype affecting 5 to 10 percent of chronic rhinosinusitis cases, characterized by type I hypersensitivity to dematiaceous fungi like Bipolaris and Curvularia species, with higher incidence in tropical and subtropical regions due to environmental fungal load. In contrast, invasive fungal rhinosinusitis is rare overall but occurs more frequently in immunocompromised patients, involving direct fungal invasion of sinonasal tissues and associated with high morbidity and mortality. In chronic rhinosinusitis, mixed etiologies often involve formation, where bacterial communities adhere to sinonasal mucosa, evading host defenses and antibiotics; is a common culprit, detected in up to 30 percent of biofilm-positive cases and associated with disease persistence. Recent studies also highlight the role of , with altered bacterial communities contributing to persistent inflammation in chronic forms. Recent updates indicate increasing antibiotic resistance among bacterial pathogens; for instance, methicillin-resistant Staphylococcus aureus (MRSA) has been noted in rising proportions of cases in chronic rhinosinusitis, with a 2025 study reporting involvement in 41 percent of S. aureus isolates and pronounced multidrug resistance patterns, often linked to prior antibiotic exposure.

Pathophysiological Mechanisms

Rhinosinusitis involves an inflammatory response in the sinonasal mucosa that disrupts normal sinus ventilation and drainage. In acute rhinosinusitis, viral infections typically initiate , leading to and impaired , which promotes secondary bacterial overgrowth and fluid accumulation within the sinuses. This process is exacerbated by obstruction of the sinus ostia, creating a hypoxic environment that further hinders ciliary function and . Mucosal inflammation in rhinosinusitis is characterized by edema, vascular permeability, and goblet cell hyperplasia, which collectively contribute to ostial obstruction and mucus hypersecretion. These changes impair the mucociliary clearance mechanism, a critical defense against pathogens, resulting in stasis and negative intrasinus pressure that draws fluid into the sinuses, fostering an environment conducive to infection persistence. In eosinophilic forms, particularly type 2 chronic rhinosinusitis with nasal polyps (CRSwNP), cytokines such as IL-5 and IL-13 play pivotal roles; IL-5 promotes eosinophil recruitment and activation, while IL-13 induces goblet cell hyperplasia and mucus production, amplifying obstruction. Chronic rhinosinusitis progresses through sustained leading to tissue remodeling, including subepithelial and formation in CRSwNP. This remodeling is driven by the Th2 pathway, where IL-4 and IL-13 upregulate transforming growth factor-beta (TGF-β), promoting deposition and epithelial-mesenchymal transition. Endotype-specific mechanisms further delineate pathophysiology; for instance, in non-eosinophilic chronic rhinosinusitis, enterotoxins function as superantigens, polyclonally activating T cells and skewing toward mixed Th1/Th2/Th17 responses, which exacerbate neutrophilic and polypoid changes independent of classic type 2 dominance. Recent 2024 analyses highlight how these superantigens elevate local IgE and cytokines like IL-4 and IL-5 in polyp tissue, linking bacterial factors to disease severity in non-eosinophilic subsets. Emerging research as of 2025 also points to viral persistence and alterations contributing to ongoing in chronic cases.

Clinical Presentation

Signs and Symptoms

Rhinosinusitis manifests primarily through symptoms involving the nasal and sinus regions, with variations depending on whether the condition is acute or chronic. The most frequently reported symptoms across cases include or obstruction (60-100%), which can lead to difficult breathing; mucopurulent nasal discharge (60-80%), often thick and yellow or green in bacterial infections; facial or pressure in approximately 50-60%, particularly in the cheeks, forehead, and around the eyes, which may worsen when bending the head forward; and or in 60-80%, reflecting a reduced sense of smell. These core symptoms reflect and obstruction in the and , often leading to discomfort and impaired daily functioning, as well as additional symptoms such as , fever, and weakness. In children, persistent nasal congestion accompanied by yellow-green (purulent) nasal discharge that persists beyond 10 days without improvement or worsens after initial improvement may suggest acute bacterial rhinosinusitis. Purulent discharge often indicates inflammation with possible bacterial contribution, though it is not exclusively diagnostic of bacterial etiology, as it can occur in viral infections. In chronic rhinosinusitis in children, adenoid hypertrophy is a common contributing factor, leading to nasal obstruction, mucus accumulation, and secondary bacterial infection. Lack of response to intranasal corticosteroids such as budesonide, which primarily reduce inflammatory or allergic swelling but are less effective against bacterial infections or structural issues such as enlarged adenoids, may differentiate from primarily allergic or inflammatory etiologies without infectious or structural components, potentially requiring further evaluation for bacterial superinfection or adenoid-related issues. Viral etiologies remain possible but are less likely in prolonged or unresponsive cases. In acute rhinosinusitis, defined by a duration of less than 4 weeks, symptoms tend to be more intense and may include fever and severe alongside the common nasal complaints. These features often arise from viral or bacterial infections and resolve relatively quickly with appropriate care. Chronic rhinosinusitis, persisting for more than 12 weeks, is characterized by additional systemic effects such as , persistent cough, and , which can exacerbate overall . These symptoms stem from ongoing and accumulation, distinguishing chronic cases from shorter-term episodes. Symptom severity in rhinosinusitis is commonly evaluated using the Sino-Nasal Outcome Test-22 (SNOT-22), a validated where total scores exceeding 20 typically indicate moderate disease impact.

Differential Diagnosis

Rhinosinusitis must be differentiated from several conditions that present with overlapping nasal, facial, or headache symptoms, as misdiagnosis can delay appropriate management. Common mimics include , which typically features prominent sneezing, itchy eyes, and watery without the purulent discharge or facial pressure characteristic of rhinosinusitis. In contrast, rhinosinusitis lacks the ocular pruritus and seasonal triggers often seen in , with aided by testing to confirm IgE-mediated responses. Migraine headaches can also imitate rhinosinusitis, particularly when presenting as unilateral facial pain or pressure, but they are distinguished by the absence of nasal discharge, congestion, or fever, and by accompanying features such as , , or . Up to 90% of self-reported "sinus headaches" are actually , emphasizing the need to assess for neurologic symptoms over infectious signs. Dental infections, especially odontogenic sources in the maxillary region, may cause localized pain mimicking maxillary rhinosinusitis, but they are identified by tooth-specific tenderness, swelling, or radiographic evidence of periapical rather than generalized nasal symptoms. More serious conditions warranting urgent evaluation include nasal tumors, such as , which often present with unilateral nasal obstruction, epistaxis, or foul-smelling discharge, unlike the bilateral involvement typical of rhinosinusitis. (GPA) can mimic chronic rhinosinusitis through persistent sinus inflammation and crusting, but it is differentiated by systemic manifestations like renal involvement, pulmonary symptoms, or positive ANCA , with nasal revealing granulomatous . Distinguishing features across these mimics include symptom duration (e.g., acute viral rhinosinusitis resolves in under 10 days, while chronic persists beyond 12 weeks), laterality (unilateral symptoms suggest or dental origin), and associated signs (e.g., absence of fever in non-infectious or ). According to 2025 clinical guidance, red flags such as vision changes, proptosis, , or severe unilateral pain indicate potential orbital or intracranial involvement, prompting immediate imaging and referral to exclude complications or alternative pathologies like tumors or GPA.

Diagnosis

History and Physical Examination

The history taking for rhinosinusitis begins with assessing the onset and duration of symptoms, which helps differentiate acute from chronic forms. Acute rhinosinusitis typically presents with symptoms lasting up to 4 weeks, often following an upper respiratory (URI) as a trigger, while chronic rhinosinusitis involves persistent symptoms for 12 weeks or longer. Clinicians should inquire about potential triggers such as recent viral illnesses, environmental exposures, or contact, as well as comorbidities like , which is present in up to 50% of chronic rhinosinusitis cases and may exacerbate symptoms. During the , are evaluated to identify fever or systemic involvement, followed by a head and assessment. Anterior rhinoscopy may reveal purulent nasal discharge, mucosal , or obstruction, while percussion or of the sinuses can elicit tenderness over the maxillary or frontal areas in acute cases. Nasal , when performed, provides detailed visualization of , including mucosal , polyps in chronic cases, or purulent secretions draining from sinus ostia. Symptom checklists align with AAO-HNS criteria, emphasizing major symptoms such as or obstruction, purulent anterior or posterior nasal discharge, and facial pain, pressure, or fullness to support . Minor symptoms like , , halitosis, dental pain, , or may accompany these but are not sufficient alone for . For acute bacterial rhinosinusitis, the checklist focuses on persistent symptoms for 10 days or longer without improvement, or worsening after initial amelioration. Red flags warranting urgent referral include unilateral symptoms, which may indicate complications or alternative such as or invasive fungal , as well as neurological deficits like severe , proptosis, visual changes, or altered mental status suggesting orbital or intracranial involvement.

Diagnostic Tests

Computed (CT) scanning is considered the gold standard imaging modality for confirming and characterizing chronic rhinosinusitis (CRS), particularly after of or prior to , as it delineates paranasal sinus opacification, mucosal thickening, and anatomical variations with high resolution. The Lund-Mackay scoring , applied to coronal CT images, quantifies severity across the bilateral maxillary, anterior ethmoid, posterior ethmoid, sphenoid, and frontal sinuses (10 sites) plus the bilateral ostiomeatal complexes (2 sites), for a total of 12 sites, assigning scores from 0 (no opacification) to 2 (complete opacification) per site for a total range of 0-24; scores ≥5 indicate clinically significant , while ≥12 suggest severe involvement. (MRI) is reserved for evaluating complications such as orbital or intracranial extension, invasive fungal , or allergic fungal rhinosinusitis, where it excels in differentiation (e.g., hypointense T1 and hyperintense T2 signals in fungal balls) and avoids . Routine plain radiographs (X-rays) are discouraged due to their low sensitivity (around 50-70%) and specificity for mucosal , offering minimal diagnostic value over clinical assessment. Nasal endoscopy, performed with flexible or rigid scopes under local anesthesia, provides direct visualization of the nasal cavity and middle meatus to identify polyps, purulent discharge, , and obstruction, serving as a key procedural test for CRS and endotyping with specificity up to 95%. It is particularly useful for staging nasal polyposis and postoperative monitoring, often employing the Lund-Kennedy scoring system, which evaluates polyp size, , discharge, crusting, and scarring on a 0-2 scale per feature per side (total maximum 20), correlating with symptom severity and treatment response. In pediatric cases or recurrent acute rhinosinusitis, confirms mucosal changes and guides targeted sampling, though it has lower sensitivity (30-73%) compared to CT. Laboratory tests support rhinosinusitis characterization by identifying infectious, allergic, or inflammatory contributors. Bacterial cultures, obtained via endoscopically directed middle meatal swabs or sinus aspirates, identify pathogens like Streptococcus pneumoniae or Staphylococcus aureus in acute bacterial or refractory cases, with >90% concordance to direct sinus sampling but limited routine use due to contamination risks (sensitivity 80.9%, specificity 90.5%). Allergy testing via skin prick or serum-specific IgE assesses atopy, revealing sensitization in up to 60% of CRS cases with type 2 inflammation, guiding management in comorbid allergic rhinitis. Biomarkers such as peripheral blood eosinophil counts exceeding 0.24 × 10⁹/L (or >10% of total leukocytes) indicate eosinophilic CRS with nasal polyps (CRSwNP), while tissue eosinophils >10 per high-power field on biopsy predict recurrence and type 2 endotype. Recent advancements in biologic therapy candidacy for severe CRSwNP, per 2023-2024 guidelines, incorporate biomarker testing to confirm eligibility. For , elevated (≥150 cells/μL) and clinical criteria like prior systemic use or , support initiation in uncontrolled cases. As of September 2024, is approved for patients aged 12 years and older. Monitoring includes evaluation of response at 6 months, including repeat counts, with thresholds adjusted for prior therapies.

Management

Acute Rhinosinusitis

Management of acute rhinosinusitis primarily focuses on symptomatic relief, as the majority of cases (approximately 90%) are viral and self-limiting within 7 to 10 days. Symptomatic treatments include analgesics such as ibuprofen at doses of 400-600 mg every 6-8 hours for and fever reduction, nasal saline irrigation to alleviate congestion and promote , and oral decongestants like (up to 60 mg every 4-6 hours) limited to less than 7 days to avoid rebound congestion. Intranasal corticosteroids may also be considered for moderate symptoms to reduce inflammation, though evidence is stronger for saline irrigation as an adjunctive . In children, intranasal corticosteroids such as budesonide may provide adjunctive benefits in reducing nasal discharge and cough when combined with antibiotics, but lack of response amid persistent nasal congestion and purulent (yellow-green) discharge suggests possible bacterial involvement requiring antibiotics or consideration of structural factors like adenoid hypertrophy. Antibiotics are reserved for suspected acute bacterial rhinosinusitis (ABRS) in adults and are indicated for severe symptoms (e.g., high fever >39°C or persistent purulent nasal discharge), worsening after initial improvement, or in high-risk patients (e.g., immunocompromised or those with comorbidities increasing complication risk). For uncomplicated ABRS, the 2025 American Academy of Otolaryngology–Head and Neck Surgery (AAO-HNS) Clinical Practice Guideline recommends offering watchful waiting without antibiotics as the initial management with assurance of follow-up, even when symptoms persist beyond 10 days without improvement (a criterion for diagnosing ABRS), to promote antibiotic stewardship. If a decision is made to initiate antibiotics, first-line therapy is amoxicillin-clavulanate, with high-dose preferred in areas with high prevalence of resistant Streptococcus pneumoniae or in patients with risk factors for resistance, at a typical duration of 5-7 days to minimize resistance risks while achieving efficacy comparable to longer regimens. Alternatives include doxycycline or respiratory fluoroquinolones (e.g., levofloxacin or moxifloxacin), though fluoroquinolones are reserved due to their serious adverse effect risks. Many cases are viral and can be managed with watchful waiting. The 2020 European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS) endorses a approach with delayed prescription for uncomplicated cases, allowing symptom monitoring for 7 to 10 days before initiating therapy if needed. In children, amoxicillin remains the first-line antibiotic at 45-90 mg/kg/day divided into two doses for 10-14 days when bacterial infection is suspected, such as persistent purulent nasal discharge beyond 10 days or severe symptoms despite adjunctive therapies like intranasal corticosteroids; corticosteroids primarily address inflammatory or allergic components and are adjunctive, whereas bacterial infections require targeted antibiotics and structural issues like adenoid hypertrophy may necessitate further evaluation or adenoidectomy if severe and persistent. Reflecting updated resistance patterns showing decreased prevalence of penicillin-resistant Streptococcus pneumoniae. Overall, this targeted strategy emphasizes avoiding unnecessary antibiotics to curb while addressing acute symptoms such as and facial pain. The 2025 American Academy of Otolaryngology–Head and Neck Surgery (AAO-HNS) Clinical Practice Guideline update reinforces avoiding routine antibiotics and imaging in uncomplicated acute rhinosinusitis.

Chronic Rhinosinusitis

Management of chronic rhinosinusitis (CRS) focuses on reducing inflammation, improving sinus drainage, and addressing persistent symptoms that last beyond 12 weeks, often involving a stepwise approach starting with therapies and escalating to biologics or for refractory cases. Intranasal corticosteroids, such as fluticasone administered daily, serve as the cornerstone of treatment by decreasing mucosal inflammation and polyp size in CRS with nasal polyps (CRSwNP). In pediatric patients, where CRS is often linked to adenoid hypertrophy rather than polyps, intranasal corticosteroids remain part of initial management alongside saline irrigation (and antibiotics if indicated), but failure to respond with persistent symptoms warrants consideration of adenoidectomy as the first-line surgical intervention in children. Short bursts of oral corticosteroids, typically at 0.5-1 mg/kg/day for 5-14 days, are recommended for severe exacerbations to rapidly control symptoms, though long-term use is avoided due to side effects. Saline nasal rinses, performed daily with isotonic or hypertonic solutions, aid in mucus clearance and reduce bacterial load, complementing . While nasal irrigation with saline is an effective supportive treatment recommended by ENT specialists to control symptoms in chronic rhinosinusitis, it does not completely cure the condition, especially in chronic cases. For patients with severe CRSwNP uncontrolled by standard medical therapy, biologic agents targeting offer targeted relief. , a against IL-4 and IL-13 receptors, is administered subcutaneously every two weeks and has demonstrated efficacy in reducing scores by over 50% and improving in clinical trials. , an anti-IgE antibody given subcutaneously every 2-4 weeks, similarly reduces polyp burden and nasal congestion in CRSwNP patients with comorbid or , with sustained benefits observed up to one year. These biologics are positioned in guidelines after failure of intranasal corticosteroids and short-course oral steroids. Surgical interventions are reserved for refractory CRS where medical management fails to achieve symptom control. (FESS) involves endoscopic removal of obstructing tissue and widening of sinus ostia to restore ventilation and drainage, with success rates exceeding 80% in reducing symptoms at one year post-procedure. , a less invasive alternative, uses inflatable catheters to dilate sinus openings without tissue removal, providing durable relief in select patients with mild to moderate obstruction. The European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS) 2020 outlines a stepwise , recommending initial trials of intranasal corticosteroids and saline , escalation to oral corticosteroids or , and biologics for persistent severe CRSwNP after failed medical and surgical interventions. An EPOS/EUFOREA 2023 update refines biologic indications, emphasizing blood counts ≥150 cells/μL and prior appropriate sinus for eligibility. This approach prioritizes minimizing while considering patient-specific factors like polyp recurrence risk. The 2025 AAO-HNS guideline update aligns with this stepwise approach, emphasizing evidence-based medical therapy before surgical options.

Prevention

Primary Prevention

Primary prevention of rhinosinusitis focuses on modifiable risk factors to reduce the initial onset, particularly in susceptible individuals such as those with atopic conditions or exposure to environmental irritants. Basic hygiene practices, such as regular handwashing and avoiding close contact with individuals showing respiratory symptoms, can help prevent viral upper respiratory infections that commonly precede rhinosinusitis. Lifestyle modifications play a central role, with being a key strategy. Active and passive tobacco smoke exposure contributes to chronic rhinosinusitis (CRS) by impairing and promoting in the sinonasal mucosa. Quitting smoking leads to progressive improvements in sinonasal symptoms, , and reduced need for corticosteroids and antibiotics, with benefits accumulating over years following cessation. Maintaining optimal indoor levels between 40% and 60% helps prevent mucosal , which can compromise the nasal barrier and increase susceptibility to infections. Low relative dries the nasal , reduces mucociliary function, and facilitates viral and bacterial , thereby elevating rhinosinusitis risk. Using humidifiers in dry environments, especially during winter, supports mucosal health and may lower incidence in at-risk populations. For individuals with , allergen avoidance measures are essential to mitigate , a common precursor to rhinosinusitis. High-efficiency particulate air () filters in homes or HVAC systems effectively reduce airborne allergens like dust mites and , alleviating nasal and preventing symptom escalation. , particularly subcutaneous or sublingual forms, modifies immune responses in atopic patients, reducing the frequency and severity of allergic triggers that contribute to rhinosinusitis onset. Vaccination against respiratory pathogens provides targeted protection. Annual vaccination reduces the risk of viral upper respiratory infections that often precede bacterial rhinosinusitis, as flu can lead to secondary sinus complications. Similarly, pneumococcal conjugate vaccines, such as PCV20 recommended by the CDC for adults aged 50 and older as of 2025, prevent invasive pneumococcal disease, including , by inhibiting bacterial colonization in the nasopharynx; studies show up to 66% reduction in hospitalizations post-vaccination in children, with analogous benefits in adults. In high-pollution areas, improving air quality through community-level interventions and personal measures curbs particulate matter exposure, a known exacerbator of sinonasal . Long-term exposure to fine particulate matter (PM2.5) is associated with increased CRS prevalence and severity, as it induces histologic changes and in the mucosa; reducing ambient via policy measures like emission controls has been linked to lower in urban settings.

Secondary Prevention

Secondary prevention of rhinosinusitis focuses on strategies to mitigate recurrences and disease progression in individuals with a history of the condition, emphasizing long-term maintenance and targeted interventions based on underlying factors. Maintenance therapy plays a central role in reducing symptom relapse and inflammation in chronic rhinosinusitis (CRS). Long-term use of intranasal corticosteroids (INCS), such as budesonide or fluticasone, is recommended to control sinonasal symptoms and decrease polyp size, with evidence from randomized controlled trials showing a standardized mean difference of -0.87 (95% CI -1.17 to -0.57) in polyp burden and a relative risk of 0.73 (95% CI 0.56-0.94) for polyp recurrence. These agents are safe for extended administration, with minimal systemic effects reported in long-term studies, though adherence remains low at approximately 20% among patients. Probiotics, aimed at restoring sinonasal microbiome balance, show emerging potential in preventing relapse; a systematic review of randomized trials indicated significantly lower symptom relapse rates across follow-up periods (p=0.045) and improvements in Sino-Nasal Outcome Test subscales for sleep, psychological function, and rhinology symptoms. However, meta-analyses note only modest, non-significant overall symptom benefits, underscoring the need for further high-quality trials. For patients undergoing for CRS, post-operative measures are essential to prevent recurrence, which occurs in 12-77% of cases depending on follow-up duration and polyp presence. Regular follow-up allows early detection of adhesions or polyp regrowth, while adherence to saline nasal irrigations—initiated 24-48 hours post-surgery—promotes mucosal healing, reduces symptoms, and supports postoperative recovery; nasal irrigation with saline serves as an effective supportive treatment recommended by ENT specialists to control the condition, though it does not completely cure rhinosinusitis, especially in chronic cases, with isotonic saline or Ringer's lactate solutions preferred to avoid from hypertonic variants. Managing comorbidities is critical to secondary prevention, as they exacerbate rhinosinusitis recurrences. In patients with coexisting asthma, which affects up to 57% of those with CRS with nasal polyps, optimizing control through inhaled corticosteroids reduces sinonasal symptom severity and emergency visits, with bidirectional improvements observed in both conditions following targeted asthma therapy. Allergy immunotherapy, including subcutaneous or sublingual administration, offers adjunctive benefits for allergy-driven CRS, particularly post-operatively, where weak but supportive evidence indicates reduced symptom persistence. In the (AERD) subtype of CRS, aspirin desensitization followed by daily low-dose therapy significantly curbs exacerbations. Recent analyses, including 2024 reviews of randomized trials, demonstrate symptom reductions (mean difference -3.51 on visual analog scales) and quality-of-life improvements (mean difference -0.54 on standardized scales), with up to 70% of patients experiencing fewer sinonasal episodes over 3-6 months, though adverse events like gastrointestinal upset occur in 30-50% of cases. This approach is recommended for compliant patients with confirmed AERD via nasal lysine-aspirin challenge.

Complications and Prognosis

Complications

Rhinosinusitis can lead to various local complications, primarily affecting the orbit and surrounding structures. is a notable complication of acute rhinosinusitis, occurring in approximately 3% of diagnosed cases, and is characterized by inflammation extending beyond the , often presenting with proptosis, restricted eye movements, and potential vision impairment due to optic nerve compression or ischemia. Vision loss complicates up to 11% of orbital cellulitis cases secondary to rhinosinusitis, underscoring the need for prompt intervention to prevent permanent damage. formation represents another local sequela, typically arising from chronic obstruction of sinus ostia due to persistent inflammation, leading to mucus accumulation and cystic expansion that may erode adjacent bone and cause proptosis or . Intracranial complications from rhinosinusitis are rare but severe, with an overall incidence below 0.5% in community settings, though rates rise to 3-4% among hospitalized patients with acute disease. These include , which develops via direct spread through valveless diploic veins, and brain es, often subdural or epidural, presenting with , fever, and neurological deficits. In diabetic patients, the risk escalates due to impaired immune responses and favoring bacterial proliferation, with studies showing higher rates of abscess formation and involvement in this population. In chronic rhinosinusitis, complications often involve structural changes that exacerbate symptoms. Nasal polyps, prevalent in up to 40% of chronic cases, contribute to significant nasal obstruction by prolapsing into the nasal cavity, impairing airflow and sinus drainage while promoting recurrent infections. , or bony inflammation and remodeling, affects 36-53% of patients with chronic rhinosinusitis, correlating with disease severity, prior , and poorer response to therapy due to persistent inflammatory nidi within affected . Recent reports as of 2025 highlight an increased incidence of invasive fungal rhinosinusitis as a complication following , particularly in immunocompromised individuals such as those with or on prolonged corticosteroids, where opportunistic pathogens like Mucorales invade sinonasal tissues, leading to rapid and high mortality rates exceeding 30%.

Prognosis

The for rhinosinusitis varies significantly between acute and chronic forms, with most cases of acute rhinosinusitis resolving spontaneously and favorable long-term outcomes achievable in chronic cases through appropriate management. For acute rhinosinusitis, the majority of cases, primarily viral in , resolve within 7 to 10 days with supportive care such as saline and symptom relief, without the need for antibiotics. Progression to bacterial occurs in less than 5% of cases, typically indicated by symptom worsening after initial improvement or persistence beyond 10 days, and even these often self-limit within 2 weeks. In chronic rhinosinusitis, symptom control is achieved in 50-70% of patients through a combination of medical therapies, including intranasal corticosteroids and saline irrigation, though recurrence remains common without ongoing treatment. Biologic therapies, such as or , further enhance outcomes in severe cases, improving in approximately 60% of patients by reducing polyp burden and enhancing olfaction. Factors influencing include the timing of intervention and presence of comorbidities; early treatment with supportive measures or targeted therapies leads to better symptom resolution and reduced of progression or complications. In contrast, comorbidities like are associated with worse disease control, more severe symptoms, and diminished . Recent data from a 2024 indicate that (FESS) yields sustained improvements in patient-reported outcomes, with significant benefits in and olfaction maintained at 5 years or longer in the majority of chronic rhinosinusitis with nasal polyps cases, though revision rates average around 27%.

References

Add your contribution
Related Hubs
User Avatar
No comments yet.