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Nasal congestion

Nasal congestion, also known as a stuffy nose, is a common condition characterized by the blockage of nasal passages due to and swelling of the tissues lining the , leading to a sensation of fullness in the or face. This swelling often arises from inflamed vessels and increased production, which can obstruct airflow and may be accompanied by (runny nose) or . Typically a symptom of an underlying issue rather than a itself, nasal congestion affects people of all ages and can range from mild and temporary to chronic and disruptive. The primary causes of nasal congestion include infections such as the , , or acute , which trigger viral inflammation in the . Allergies, particularly affecting 10-30% of adults, lead to an immune response involving and other mediators that cause mucosal swelling. Non-infectious factors encompass structural abnormalities like a deviated or nasal polyps, environmental irritants such as dry air, tobacco smoke, or pollutants, and hormonal changes during pregnancy. Other contributors include , overuse of nasal sprays (known as rebound congestion), (), and certain medications like those for high . Symptoms of nasal congestion extend beyond nasal blockage and may include sinus pressure or pain, reduced , , and in severe cases, or sleep disturbances. In conditions like chronic rhinosinusitis, persistent inflammation can lead to ongoing obstruction lasting 12 weeks or more, while acute episodes from colds usually resolve within 1-2 weeks. Associated issues such as can cause throat irritation, , or . Treatment for nasal congestion focuses on addressing the underlying cause and alleviating symptoms through home remedies like saline nasal sprays, humidifiers, steam inhalation, and elevating the head during sleep. Over-the-counter options include decongestants, antihistamines for allergic cases, and short-term use of nasal sprays (limited to 3 days to avoid effects). For chronic or severe cases, prescription medications such as nasal corticosteroids, or surgical interventions for structural issues like polyps or deviated septum, may be necessary. attention is advised if symptoms persist beyond 10-14 days, accompany high fever, severe pain, or bloody discharge, or occur in infants under 3 months.

Overview

Definition

Nasal congestion refers to the partial or complete blockage of the nasal passages caused by swelling of the , resulting in reduced airflow and a sensation of stuffiness. This swelling occurs when the tissues lining the inside of the nose become inflamed, often leading to impaired and difficulty in clearing . The condition is a frequent symptom in various respiratory disorders, characterized by the engorgement of blood vessels in the nasal lining that narrows the airway. Unlike nasal obstruction, which involves a physical or structural blockage—such as a deviated , nasal polyps, or foreign bodies—nasal congestion is primarily functional, arising from reversible and rather than fixed anatomical issues. This distinction is important for , as congestion typically responds to treatments targeting , whereas obstruction may require surgical intervention. In clinical contexts, the terms are sometimes used interchangeably by patients, but medically, congestion emphasizes the dynamic swelling process over permanent barriers. Nasal congestion commonly arises from irritants like or , though detailed etiologies are explored elsewhere.

Epidemiology

Nasal congestion is a widespread , serving as a primary symptom in various forms of and affecting 10% to 30% of the global adult population, with prevalence rates climbing to 40% or higher among children. This equates to over 400 million individuals worldwide experiencing symptoms annually, particularly in regions with high exposure. Prevalence varies geographically, tending to be elevated in settings where environmental triggers are more concentrated. Demographic patterns reveal distinct risk factors influencing susceptibility. Age plays a key role, with incidence peaking among children and adolescents aged 5 to 15 years due to developing immune systems and greater exposure to school-based allergens. Gender differences show a slight predominance in females, attributed in part to hormonal fluctuations that exacerbate vascular responses in the , especially post-puberty. Comorbidities significantly amplify risk; for instance, individuals with face a 2- to 3-fold higher likelihood of nasal congestion, as up to 80% to 90% of asthma patients also experience symptoms.44364-2/fulltext) Epidemiological trends indicate a rising burden since the , driven by rapid , increased , and climate-related changes in distribution. These factors have contributed to a global uptick in cases, underscoring the need for interventions in densely populated areas. Nasal congestion frequently co-occurs with , sharing similar demographic and environmental risk profiles.

Causes

Infectious Causes

Infectious causes of nasal congestion are predominantly , accounting for the majority of acute episodes through direct and subsequent inflammatory response in the . The , the most frequent culprit, is primarily caused by rhinoviruses, which are responsible for 30-50% of cases and lead to symptoms such as nasal stuffiness and due to mucosal and increased secretions. viruses also commonly induce nasal congestion as part of upper respiratory involvement, often accompanied by systemic symptoms like fever and , while (RSV) frequently causes significant nasal obstruction, particularly in infants and young children. These infections exhibit seasonal patterns, with peaks typically occurring in winter months when transmission rates rise due to indoor crowding and lower humidity. Bacterial etiologies are less common and usually arise as secondary complications following viral upper respiratory infections, progressing to acute bacterial in a small subset of cases. Pathogens such as and are the primary agents, colonizing obstructed sinuses and exacerbating congestion through purulent discharge and prolonged inflammation; such bacterial superinfections develop in approximately 0.5-2% of viral upper respiratory infections. Fungal infections represent a rarer cause of nasal congestion, primarily affecting immunocompromised individuals where impaired immunity allows opportunistic pathogens to invade the sinuses. species, such as A. fumigatus, are commonly implicated in invasive forms, contributing to persistent obstruction and tissue damage rarely, in a small subset of cases among at-risk patients.

Non-Infectious Causes

Nasal congestion frequently arises from , an IgE-mediated inflammatory response triggered by environmental allergens such as , dust mites, mold, or pet dander. This condition affects 10% to 30% of adults worldwide, with higher rates in children up to 40%, leading to nasal mucosal swelling and obstruction due to release and production. Seasonal allergens like exacerbate symptoms during specific times of the year, while perennial triggers such as dust mites cause year-round congestion in sensitized individuals. Nonallergic forms of rhinitis, particularly vasomotor rhinitis, result from exposure to irritants and environmental factors rather than allergens, causing non-immune-mediated nasal hyperreactivity. Common triggers include , , strong odors, chemical fumes, and changes in or , which provoke parasympathetic nerve stimulation and subsequent in the nasal vasculature. This subtype accounts for 10% to 15% of chronic rhinitis cases in adults, often presenting with intermittent congestion worsened by dry air or occupational exposures. Structural abnormalities in the nasal anatomy also contribute to persistent nasal congestion by mechanically obstructing airflow. A deviated , where the and dividing the nostrils is misaligned, affects up to 80% of the population to some degree but causes symptomatic obstruction in approximately 5% to 10% of cases, frequently requiring surgical correction like . Nasal polyps, benign inflammatory growths arising from the sinus mucosa, occur in 1% to 4% of the general population and up to 20% to 30% of those with chronic rhinosinusitis, leading to bilateral blockage and impaired drainage. These structural issues often necessitate imaging, such as computed tomography, for confirmation and management planning. In all these non-infectious scenarios, congestion stems primarily from vascular engorgement and mucosal edema in the nasal passages. Other non-infectious causes include hormonal changes, such as pregnancy rhinitis, which affects approximately 20-30% of pregnant individuals due to increased blood volume and levels leading to nasal mucosal swelling. Certain medications, including (ACE) inhibitors, beta-blockers, and alpha-adrenergic antagonists, can induce rhinitis through effects on nasal vasculature or mucus production, contributing to in a subset of users. (GERD) may cause or exacerbate nasal symptoms via postnasal drip from acid irritation, with higher prevalence of chronic observed in GERD patients. Rebound , or , results from prolonged overuse of sprays, affecting 1-9% of otolaryngology clinic visits and leading to worsened obstruction upon withdrawal.

Pathophysiology

Vascular Mechanisms

Nasal congestion arises primarily from vascular changes in the , where increased blood flow leads to swelling that obstructs airflow. The nasal passages contain rich in venous sinusoids, which function as vessels capable of rapid engorgement to regulate nasal patency. Parasympathetic stimulation plays a key role in this process by promoting of arteriovenous anastomoses and venous sinusoids, resulting in engorgement and mucosal swelling that narrows the nasal airway. This engorgement is particularly pronounced in the of the nasal turbinates, where blood pooling increases and contributes to the sensation of blockage. The nasal turbinates serve as vascular reservoirs, with their capacitance vessels expanding in response to autonomic signals or external triggers such as , thereby substantially reducing nasal airflow resistance. In physiological states, this vascular mechanism underlies the normal , a reciprocal alternation of and decongestion between the two nasal sides, occurring every 4-6 hours and mediated by sympathetic tone that induces via noradrenaline release. This cycle maintains overall nasal function without discomfort, as total airflow remains constant despite unilateral changes. In pathological conditions, however, the vascular response becomes dysregulated, leading to persistent bilateral engorgement rather than the alternating pattern of the . Reduced sympathetic activity exacerbates venous pooling in the turbinates, causing prolonged mucosal swelling that impairs airflow beyond physiological levels. Such persistent congestion distinguishes disease states like from the adaptive nasal cycle, where vascular adjustments are transient and balanced.

Inflammatory Processes

In allergic responses contributing to nasal congestion, triggered by allergen-IgE cross-linking leads to the rapid release of preformed mediators such as , resulting in immediate mucosal swelling and increased within minutes. This early-phase reaction is followed by a late-phase inflammatory response, where s and other immune cells produce cytokines such as interleukin-4 (IL-4), interleukin-5 (IL-5), and interleukin-13 (IL-13), which promote recruitment (via IL-5) and with increased production (via IL-13), exacerbating congestion over hours to days. Leukocyte recruitment plays a central role in amplifying inflammation in the , with and neutrophils migrating from the bloodstream in response to chemotactic signals from cytokines and released during the allergic cascade. In cases, such as persistent , this infiltration leads to prolonged through the release of toxic granule proteins and by , while neutrophils contribute to tissue damage and excessive production via enzymes like . These processes collectively heighten nasal obstruction by increasing mucosal thickness and secretory activity. Neurogenic inflammation further intensifies congestion in non-allergic through the release of neuropeptides like from sensory nerve endings in the , which stimulate local and plasma extravasation without involving IgE-mediated mechanisms. and related tachykinins activate mast cells and endothelial cells, promoting and hypersecretion that mimic allergic symptoms but stem from neural reflexes triggered by irritants. This pathway underscores the sensory nervous system's role in perpetuating inflammatory cycles independent of adaptive immunity.

Clinical Presentation

Primary Symptoms

Nasal congestion, often described as a sensation of stuffiness or blockage in the nasal passages, results from and swelling of the , leading to reduced airflow through the . This obstruction forces individuals to breathe through the , which can cause dryness in the and , and is frequently accompanied by difficulty in smelling, known as . In cases of , affects a notable portion of patients, with studies reporting prevalence rates around 20-40% due to the mechanical blockage and inflammatory effects on . The duration of nasal congestion helps distinguish between acute and chronic forms. Acute nasal congestion typically lasts less than 4 weeks and is commonly triggered by viral infections such as the . In contrast, chronic nasal congestion persists for more than 12 weeks and is often linked to or structural issues like deviated septum. Nasal congestion significantly impairs by disrupting and contributing to daytime . The reduced nasal , which can decrease by approximately 50% due to increased resistance from mucosal swelling, leads to sleep-disordered , fragmented , and subsequent . This limitation often results in during , exacerbating and reducing overall well-being. Associated symptoms such as may occur alongside congestion but are addressed separately.

Secondary Symptoms

Secondary symptoms of nasal congestion encompass a range of manifestations stemming from mucus production, sinus pressure, and associated inflammatory responses, often exacerbating the primary sensation of nasal blockage. These include excessive nasal , facial discomfort, and systemic complaints that typically accompany acute or episodes. , characterized by the overproduction of nasal , frequently occurs alongside nasal congestion and can vary in consistency from clear and watery to thicker and purulent. This often drains posteriorly into the nasopharynx, resulting in , which irritates the pharyngeal mucosa and leads to sensations of throat clearing, , or discomfort. In upper respiratory infections, affects approximately 81% of cases, while associated from contributes to symptoms in 80-84% of affected individuals. Facial pain and headache arise primarily from the engorgement and pressure within the secondary to mucosal inflammation and fluid accumulation. These symptoms are more pronounced in infectious , where involvement intensifies the pressure, often localizing to the cheeks, , or periorbital regions. Approximately 30% of patients with infectious cases experience significant pain or pressure, with headaches reported in up to 32% of presentations. In acute viral etiologies of nasal congestion, such as the , systemic effects including , , and low-grade fever may emerge due to the spread of to adjacent airways and the body's . often results from stimulating the , while stems from direct viral invasion or secondary irritation; fever, when present, is typically mild. These symptoms generally resolve within 7-10 days as the viral infection subsides.

Diagnosis

Clinical Evaluation

The clinical evaluation of nasal congestion begins with a detailed to determine the onset, triggers, and duration of symptoms, which aids in classifying the condition. Patients are queried about the age of symptom onset, frequency, severity, and patterns such as seasonal (e.g., pollen-related) versus perennial triggers, which may suggest , or nonallergic irritants like temperature changes or odors indicating . Duration helps classify as acute (symptoms <4 weeks, often infectious) or chronic (symptoms >12 weeks, per rhinosinusitis guidelines). For , intermittent symptoms are defined as occurring <4 days per week and for <4 consecutive weeks per year, while persistent symptoms occur ≥4 days per week and for ≥4 consecutive weeks per year. Physical examination primarily involves anterior rhinoscopy, performed using a nasal speculum and headlight or an , to visualize the and structures. This allows assessment of mucosal , turbinate , and the presence, color, and consistency of discharge—such as clear in allergic cases or mucopurulent in infectious ones—while distinguishing unilateral from bilateral involvement. If significant congestion obscures visualization, may be applied to facilitate the exam. Red flags during evaluation include unilateral nasal congestion, which may indicate rare conditions such as sinonasal tumors (incidence approximately 1 per 100,000), foreign bodies, or structural abnormalities warranting urgent referral. Persistent symptoms despite initial management or associated features like bloody discharge also signal the need for specialist evaluation to rule out underlying .

Diagnostic Tests

Diagnostic tests for nasal congestion aim to identify underlying causes such as allergies, infections, or structural issues by employing laboratory assays, imaging modalities, and specialized evaluations. These tests are typically selected based on clinical suspicion derived from patient symptoms like persistent blockage or discharge. Imaging such as CT is reserved for complicated or persistent cases, particularly in children, to minimize radiation exposure. Allergy testing is a cornerstone for evaluating allergic rhinitis as a contributor to nasal congestion, particularly in chronic presentations. Skin prick tests involve applying small amounts of common aeroallergens to the skin and observing for wheal-and-flare reactions, while serum-specific immunoglobulin E (IgE) measurements quantify antibody levels against suspected allergens via blood sampling. These methods confirm sensitization in a substantial proportion of chronic rhinitis cases, guiding targeted management. Imaging techniques provide detailed visualization of nasal and sinus structures to detect inflammation, obstructions, or anomalies. Computed tomography () scans are the preferred modality for assessing , revealing mucosal thickening, air-fluid levels, or opacification in affected sinuses; scans may reveal pansinus opacification in cases suggestive of bacterial sinusitis. , an in-office procedure using a flexible fiberoptic scope, allows direct inspection of the to identify polyps or other lesions, often confirming findings from history and physical exam. Other specialized tests include nasal cytology, which involves scraping or swabbing the to examine cellular composition under , highlighting in or neutrophils in non-allergic forms. This non-invasive technique aids in differentiating inflammatory phenotypes. Additionally, pH testing, such as nasal pH-impedance monitoring, assesses for acid exposure and as triggers in non-allergic rhinitis, showing correlations with elevated acid exposure times in neutrophilic cases.

Management

Non-Pharmacological Approaches

Non-pharmacological approaches to managing nasal congestion emphasize simple, accessible strategies that promote clearance, reduce , and minimize exposure to irritants. These methods are particularly useful for acute and chronic cases, often providing without side effects associated with medications. Humidification techniques, such as saline using devices like a neti pot, involve flushing the nasal passages with a saltwater solution to remove excess and allergens. This process enhances by mechanically clearing debris and hydrating the , leading to symptom improvement. A of clinical indicates that regular saline improves nasal symptomatology in approximately 35% of cases and quality of life by 30% in patients with . In a , large-volume saline was more effective than saline spray, reducing symptom severity scores by up to 8.2 points on the SNOT-20 scale and lowering the odds of frequent nasal symptoms by 50% after eight weeks. For acute cases, such as those from upper respiratory infections, can provide rapid by thinning , with studies suggesting potential benefits in symptom , though is limited. A 2024 study of over 11,000 people further confirmed the efficacy of nasal saline , initiated at the first sign of a , in reducing symptom duration and severity. Steam inhalation and positional adjustments offer additional home-based relief. Inhaling steam from a hot or bowl of warm water moistens the nasal passages, loosens thickened , and improves . A double-blind demonstrated that steam inhalation significantly increased nasal patency and alleviated symptoms in a higher of treated patients compared to . Sleeping with the head elevated, such as by raising the bed head by 4-6 inches or using extra pillows, reduces venous pooling in the and promotes sinus drainage, thereby decreasing positional congestion. This approach is recommended for nighttime relief, as it counters gravity-dependent accumulation and has been shown to ease stuffiness in conditions like . Avoidance techniques focus on eliminating environmental triggers that exacerbate . Removing exposure to irritants like is crucial, as it impairs and worsens nasal inflammation. Quitting smoking or avoiding can improve nasal by 63% within one month, leading to reduced in environmental cases. Other measures include steering clear of dry air, strong odors, and pollutants, which collectively alleviate symptoms by minimizing irritation to the nasal lining.

Pharmacological Interventions

Pharmacological interventions for nasal congestion target the , , and allergic responses that contribute to nasal obstruction, offering symptomatic through various classes of medications. These treatments are selected based on the , such as acute versus chronic , and are guided by clinical guidelines emphasizing , safety, and duration of use to minimize adverse effects. As of 2025, the AAO-HNSF Adult Guidelines recommend and intranasal corticosteroids as first-line options for symptom in chronic , consistent with prior updates. Decongestants provide rapid of the to alleviate swelling and improve . Oral , a sympathomimetic , is administered in doses of 30 to 60 mg every 4 to 6 hours for adults, effectively reducing nasal congestion by stimulating alpha-adrenergic receptors and decreasing mucosal edema. Note that oral , once common in OTC products, was proposed for removal by the FDA in November 2024 due to lack of demonstrated effectiveness as a nasal decongestant. , such as nasal spray, similarly act via alpha-adrenergic agonism for quicker onset but are recommended for short-term use limited to 3 days to avoid , a rebound congestion resulting from prolonged vasoconstrictor dependence. Antihistamines are indicated primarily for congestion linked to , where release exacerbates symptoms. Second-generation options like loratadine, which block peripheral H1 receptors to inhibit allergic mediator effects, provide effective relief for mild to moderate cases by reducing nasal itching, sneezing, and congestion without significant sedation. Intranasal corticosteroids are the cornerstone for managing persistent or chronic nasal congestion, particularly in allergic and non-allergic rhinitis, as endorsed by the 2020 Rhinitis Practice Parameter Update from the on Practice Parameters and reaffirmed in 2025 guidelines. Agents such as fluticasone propionate decrease by suppressing production and activity, with initial improvements in congestion observable within 12 hours but optimal effects requiring 1 to 2 weeks of daily use. For severe chronic with nasal s unresponsive to standard therapies, biologic agents such as (approved 2019) or tezepelumab (Tezspire, showing reduced congestion and polyp size in 2025 trials) may be considered, offering targeted anti-inflammatory effects via IL-4/IL-13 or TSLP inhibition.

Surgical Treatments

Surgical treatments for nasal congestion are typically considered for persistent cases refractory to non-pharmacological and pharmacological approaches, particularly when structural abnormalities such as hypertrophic turbinates, septal deviation, or polypoid disease impair . These interventions focus on correcting anatomical obstructions to improve nasal patency and , with procedures performed under general or in outpatient settings. Success depends on accurate via or , and long-term outcomes often exceed 80% symptom relief in appropriately selected patients, as per the 2025 AAO-HNSF Clinical Practice Guideline for Surgical Management of Chronic . Turbinate reduction addresses hypertrophic inferior turbinates, a common cause of chronic nasal obstruction, through minimally invasive techniques like or surgical resection. Radiofrequency turbinoplasty uses controlled thermal energy to shrink turbinate tissue while preserving the overlying mucosa, resulting in improved in approximately 85% of chronic cases with minimal complications such as or crusting. Surgical resection, including partial turbinectomy or microdebrider-assisted methods, removes excess tissue and for more substantial volume reduction, achieving up to 94.7% improvement in nasal obstruction scores in refractory patients. Both approaches demonstrate sustained benefits, with significant reductions in nasal resistance persisting for at least three years postoperatively. Septoplasty corrects a deviated , a structural contributing to nasal congestion in a notable subset of patients, typically after conservative therapies fail. This procedure straightens the septum to restore symmetric , with studies reporting rates of approximately 80-90% in alleviating obstruction symptoms, as evidenced by validated tools like the NOSE scale. Indications include moderate to severe blockage unresponsive to medications, and outcomes show high patient satisfaction, though long-term follow-up reveals slight declines in over years due to formation. Functional endoscopic sinus surgery (FESS) targets polypoid congestion from chronic rhinosinusitis with nasal polyps, where inflammatory growths block sinus ostia and exacerbate obstruction. Introduced by Heinz Stammberger in the 1980s, FESS employs rigid endoscopes and microinstruments for precise, minimally invasive removal of polyps and mucosal obstructions, preserving surrounding structures to promote drainage and ventilation. Clinical data indicate over 89% of patients achieve normalized symptom scores postoperatively, with low complication rates including minor bleeding in less than 1% of cases. This technique has become the gold standard for refractory polypoid disease, offering durable relief from congestion and associated symptoms like facial pressure. For pediatric cases, drug-free options like the FDA-approved Sonu Band (2025) may provide adjunctive relief for allergic or nonallergic rhinitis-related congestion.

Prevention

Environmental Controls

Environmental controls play a crucial role in mitigating nasal congestion by reducing exposure to irritants and s in living spaces. One key strategy involves mitigation through the use of high-efficiency particulate air () filters and allergen-proof encasements for bedding. filters capture at least 99.97% of particles 0.3 microns in size, including dust mite allergens, which are often carried on larger fecal pellets that become during activities like bed-making. Allergen-proof encasements create a barrier on mattresses, pillows, and box springs, trapping existing dust mites and preventing new infestations, with studies showing reductions in dust mite levels exceeding 70% and up to 90% when combined with regular . According to guidelines from the U.S. Environmental Protection Agency (EPA), integrating these measures with low-humidity environments and frequent vacuuming can significantly lower overall exposure to dust mites, a common trigger for and associated congestion. Humidity management is another essential environmental control to prevent nasal passages from drying out, which can exacerbate congestion through irritation and increased mucus production. Maintaining indoor relative humidity between 40% and 60% helps keep nasal mucosa moist without promoting mold or dust mite growth, as levels above 60% favor mite proliferation while below 30% lead to dryness. In dry climates, humidifiers can raise humidity to this optimal range, whereas in humid areas, dehumidifiers are recommended to lower excess moisture and reduce irritant buildup, thereby alleviating symptoms of non-allergic rhinitis. Regular monitoring with hygrometers ensures consistent levels, supporting overall respiratory comfort. Avoiding environmental pollutants, particularly in settings with high levels, involves deploying air purifiers equipped with or filters to target (PM2.5) and volatile organic compounds from traffic and industry. These devices can reduce indoor pollutant concentrations by 30-60%, depending on room size and filter efficiency, thereby decreasing exposure to irritants that inflame nasal tissues. Clinical observations indicate that such interventions lead to symptom improvement in approximately 50% of cases involving irritant-induced nasal congestion, including reduced stuffiness and runny , as evidenced by decreases in nasal symptom scores of up to 55%. The EPA emphasizes sealing windows during high-pollution days and maintaining clean HVAC systems to complement purifier use, enhancing protection against air quality challenges.

Vaccination and Hygiene

Vaccination plays a key role in preventing infectious causes of nasal congestion, particularly those stemming from upper respiratory infections. The annual is estimated to reduce the risk of influenza illness by 40% to 60% among the overall population during seasons when the vaccine viruses match circulating strains well, thereby lowering the incidence of associated nasal congestion. For at-risk groups, such as older adults, children, and individuals with chronic conditions, the (PCV13 or PCV20) is recommended to prevent bacterial complications like ; studies show it leads to a 66% lower risk of hospitalization for in children following its introduction. Hygiene practices further mitigate the spread of viruses that cause nasal congestion. Regular handwashing with and can prevent approximately 20% of respiratory infections, including those leading to congestion, a finding reinforced by post-2020 data emphasizing its role in reducing viral transmission in community settings. Masking, particularly in indoor public spaces, has been associated with lower odds of infection and overall respiratory virus spread, with consistent use reducing transmission risks based on epidemiologic evidence from the era. Nasal hygiene through regular saline rinses is an effective preventive strategy for individuals prone to , where it helps remove and to reduce bacterial colonization and prevent overgrowth. Daily or hypertonic saline improves symptoms, decreases the need for antibiotics, and lowers the bacterial load in the nasal passages, as supported by clinical studies on its role in managing cases.