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Rhinosinusitis
Other namesSinus infection, sinusitis, chronic rhinosinusitis without nasal polyps, chronic rhinosinusitis with nasal polyps
An illustration showing the difference between healthy sinuses and diseased sinuses
SpecialtyOtorhinolaryngology
Symptomsnasal discharge, nasal blockage, facial pain, reduction or loss of smell, fever[1][2]
CausesInfection (bacterial, fungal, viral), allergies, air pollution, structural problems in the nose[3]
Risk factorsAsthma, cystic fibrosis, poor immune function[1]
Diagnostic methodUsually based on symptoms
Differential diagnosiscommon cold, rhinitis, upper respiratory infection, temporomandibular joint disorder, tension headache, vascular headache, dental infection
Preventionhandwashing, vaccinations, avoiding smoking[3]
TreatmentPain medications, nasal steroids, nasal irrigation, antibiotic[1][4]
Frequency10–30% each year (developed world)[1][5]

Sinusitis, also known as rhinosinusitis, is an inflammation of the mucous membranes that line the sinuses resulting in symptoms that may include production of thick nasal mucus, nasal congestion, facial congestion, facial pain, facial pressure, loss of smell, or fever.[6][2]

Sinusitis is a condition that affects both children and adults. It is caused by a combination of environmental factors and a person's health factors.[7] It can occur in individuals with allergies, exposure to environmental irritants, structural abnormalities of the nasal cavity and sinuses and poor immune function.[8] Most cases are caused by a viral infection.[3] Recurrent episodes are more likely in persons with asthma, cystic fibrosis, and immunodeficiency.[9]

The diagnosis of sinusitis is based on the symptoms and their duration along with signs of disease identified by endoscopic and/or radiologic criteria.[10] Sinusitis is classified into acute sinusitis, subacute sinusitis, and chronic sinusitis. In acute sinusitis, symptoms last for less than four weeks, and in subacute sinusitis, they last between 4 and 12 weeks. In chronic sinusitis, symptoms must be present for at least 12 weeks.[11] In the initial evaluation of sinusitis an otolaryngologist, also known as an ear, nose and throat (ENT) doctor, may confirm sinusitis using nasal endoscopy.[10] Diagnostic imaging is not usually needed in the acute stage unless complications are suspected.[12] In chronic cases, confirmatory testing is recommended by use of computed tomography.[12]

Prevention of sinusitis focuses on regular hand washing, staying up-to-date on vaccinations, and avoiding smoking.[13] Pain killers such as naproxen, nasal steroids, and nasal irrigation may be used to help with symptoms.[14][15] Recommended initial treatment for acute sinusitis is watchful waiting.[14] If symptoms do not improve in 7–10 days or worsen, then an antibiotic may be implemented or changed.[14] In those in whom antibiotics are indicated, either amoxicillin or amoxicillin/clavulanate is recommended first line, with amoxicillin/clavulanate being superior to amoxicillin alone but with more side effects.[16][14] Surgery may be recommended in those with chronic disease who have failed medical management.[17]

Sinusitis is a common condition.[18] It affects between about 10 and 30 percent of people each year in the United States and Europe.[18][5] The management of sinusitis in the United States results in more than US$11 billion in costs.[18]

Signs and symptoms

[edit]

Acute sinusitis can present as facial pain and tenderness that may worsen on standing up or bending over, headache, cough, bad breath, nasal congestion, ear pain, ear pressure or nasal discharge that is usually green in color, and may contain pus or blood.[19]Dental pain can also occur. A way to distinguish between toothache and sinusitis is that sinusitis-related pain is usually worsened by tilting the head forward or performing the Valsalva maneuver.[20][21]

Chronic sinusitis presents with more subtle symptoms of nasal obstruction, with less fever and pain.[22] Symptoms include facial pain, headache, night-time coughing, an increase in previously minor or controlled asthma symptoms, general malaise, thick green or yellow nasal discharge, feeling of facial fullness or tightness that may worsen when bending over, dizziness, aching teeth, and bad breath.[23] Often, chronic sinusitis can lead to anosmia, the loss of the sense of smell.[23]

A 2005 review suggested that most "sinus headaches" are migraines.[24] The confusion occurs in part because migraine involves activation of the trigeminal nerves, which innervate both the sinus region and the meninges surrounding the brain. As a result, accurately determining the site from which the pain originates is difficult. People with migraines do not typically have the thick nasal discharge that is a common symptom of a sinus infection.[25]

By location

[edit]

The four paired paranasal sinuses are the frontal, ethmoidal, maxillary, and sphenoidal sinuses. The ethmoidal sinuses are further subdivided into anterior and posterior ethmoid sinuses, the division of which is defined as the basal lamella of the middle nasal concha. In addition to the severity of disease, discussed below, sinusitis can be classified by the sinus cavity it affects:

  • Maxillary – may cause pain or pressure in the maxillary (cheek) region, often experienced as a toothache or headache.[26]
  • Frontal – may cause pain or pressure in the frontal sinus cavity (above the eyes), often experienced as a headache, particularly in the forehead area.
  • Ethmoidal – may cause pain or pressure pain between or behind the eyes, along the sides of the upper nose (medial canthi), and headaches.[27]
  • Sphenoidal – may cause pain or pressure behind the eyes, though it is often felt at top of the head, over the mastoid processes, or the back of the head.[27]

Complications

[edit]
Chandler Classification
Stage Description
I Preseptal cellulitis
II Orbital cellulitis
III Subperiosteal abscess
IV Orbital abscess
V Cavernous sinus septic thrombosis

Complications are thought to be rare (1 case per 10,000).[28] Infectious complications of acute bacterial sinusitis include eye, brain and bone complications.[29]

Orbital complications

[edit]

The Chandler Classification is used to group orbital complications into five stages based on their severity.[30] Stage I, known as preseptal cellulitis, occurs when an infection develops in front of the orbital septum.[31] It is thought to result from restricted venous drainage from the sinuses and affects the soft tissue of the eyelids and other superficial structures.[31] Stage II, known as orbital cellulitis, occurs when infection develops behind the orbital septum and affects the orbits.[31] This can result in impaired eye movement, protrusion of the eye, and eye swelling.[31] Stage III, known as subperiosteal abscess, occurs when pus collects between walls of the orbit and the surrounding periosteal structures.[31] This can result in impaired eye movement and acuity.[31] Stage IV, known as orbital abscess, occurs when an abscess forms within the orbital tissue.[31] This can result in severe vision impairment.[31] Stage V, known as cavernous sinus thrombosis, is considered an intracranial complication. It can occur as bacterial spread progresses, triggering blood clots that become trapped within the cavernous sinus.[32] This can result in previously described symptoms within the opposite eye and, in severe cases, meningitis.[31]

Intracranial complications

[edit]

The proximity of the sinuses to the brain makes brain infections one of the most dangerous complications of acute bacterial sinusitis, especially when the frontal and sphenoid sinuses are involved. These infections can result from invasion of anaerobic bacteria through the bones or blood vessels. Abscesses, meningitis, and other life-threatening conditions may occur. In rare cases, mild personality changes, headache, altered consciousness, visual problems, seizures, coma, and even death may occur.[33]

Osseous complications

[edit]

A rare complication of acute sinusitis is a bone infection, known as osteomyelitis, which affects the frontal and other facial bones.[34] Specifically, the combination of frontal sinusitis, osteomyelitis and subperiosteal abscess formation is referred to as Pott's puffy tumor.[35][34]

Other complications

When an infection originating from a tooth or dental procedure affects the maxillary sinus it can lead to odontogenic sinusitis (ODS).[36] Odontogenic sinusitis can often spread to nearby sinuses including the ethmoid, frontal, sphenoid sinuses, and the contralateral nasal cavity.[37] In rare instances, these infections may spread to the orbit, leading to orbital cellulitis.

Causes

[edit]

Acute

[edit]

Acute sinusitis is usually precipitated by an earlier upper respiratory tract infection, generally of viral origin, mostly caused by rhinoviruses (with RVA and RVC giving more severe infection than RVB), coronaviruses, and influenza viruses, others caused by adenoviruses, human parainfluenza viruses, human respiratory syncytial virus, enteroviruses other than rhinoviruses, and metapneumovirus. If the infection is of bacterial origin, the most common three causative agents are Streptococcus pneumoniae (38%), Haemophilus influenzae (36%), and Moraxella catarrhalis (16%).[38][39] Until recently, H. influenzae was the most common bacterial agent to cause sinus infections. However, introduction of the H. influenzae type B (Hib) vaccine has dramatically decreased these infections, and now non-typable H. influenzae (NTHI) is predominantly seen in clinics. Other sinusitis-causing bacterial pathogens include S. aureus and other streptococci species, anaerobic bacteria and, less commonly, Gram-negative bacteria. Viral sinusitis typically lasts for 7 to 10 days.[28]

Acute episodes of sinusitis can also result from fungal invasion. These infections are typically seen in people with diabetes or other immune deficiencies (such as AIDS or transplant on immunosuppressive antirejection medications) and can be life-threatening. In type I diabetics, ketoacidosis can be associated with sinusitis due to mucormycosis.[40]

Chronic

[edit]

Definition and nomenclature

[edit]

By definition, chronic sinusitis lasts longer than 12 weeks and can be caused by many different diseases that share chronic inflammation of the sinuses as a common symptom. It is subdivided into cases with and without polyps. When polyps are present, the condition is called chronic hyperplastic sinusitis; however, the causes are poorly understood.[28] It may develop with anatomic derangements, including deviation of the nasal septum and the presence of concha bullosa (pneumatization of the middle concha) that inhibit the outflow of mucus, or with allergic rhinitis, asthma, cystic fibrosis, and dental infections.[41]

Chronic rhinosinusitis represents a multifactorial inflammatory disorder, rather than simply a persistent bacterial infection.[28] The medical management of chronic rhinosinusitis is now focused upon controlling the inflammation that predisposes people to obstruction, reducing the incidence of infections.[42] Surgery may be needed if medications are not working.[42]

During nasal endoscopy, an accessory maxillary ostium can sometimes be observed in the middle meatus. While not all are functionally active, in certain cases, mucus exiting the natural maxillary ostium may re-enter the sinus through the accessory ostium. This mucus recirculation may be associated with chronic maxillary sinusitis.[43]

Attempts have been made to provide a more consistent nomenclature for subtypes of chronic sinusitis. The presence of eosinophils in the mucous lining of the nose and paranasal sinuses has been demonstrated in many people, and this has been termed eosinophilic mucin rhinosinusitis (EMRS). Cases of EMRS may be related to an allergic response, but allergy is not often documented, resulting in further subcategorization into allergic and nonallergic EMRS.[44]

Fungi

[edit]

A more recent, and still debated, development in chronic sinusitis is the role that fungi play in this disease.[45] Whether fungi are a definite factor in the development of chronic sinusitis remains unclear, and if they are, what is the difference between those who develop the disease and those who remain free of symptoms. Trials of antifungal treatments have had mixed results.[46]

One airway theory

[edit]

Recent theories of sinusitis indicate that it often occurs as part of a spectrum of diseases that affect the respiratory tract (i.e., the "one airway" theory) and is often linked to asthma.[47][48]

Smoking

[edit]

Both smoking and secondhand smoke are associated with chronic rhinosinusitis.[49]

Air pollution

[edit]

Exposure to fine particulate matter (PM2.5), which consists of particles with a diameter of less than 2.5 micrometers, has been associated with an increased risk of developing rhinosinusitis.[50][51] PM2.5 particles can penetrate deep into the respiratory tract, reaching the nasal and sinus mucosa, leading to inflammation and impaired mucociliary clearance.[52] Individuals living in areas with higher concentrations of PM2.5 experience increased symptoms and exacerbations of chronic rhinosinusitis.[53] The fine particles cause oxidative stress and inflammation, contributing to the pathogenesis of rhinosinusitis.[54]

While both PM10 (particles less than 10 micrometers) and PM2.5 can affect the respiratory system, PM2.5 particles are more closely associated with rhinosinusitis due to their ability to reach deeper into the sinus cavities.[55] These smaller particles bypass the nasal hair filtering mechanism and deposit in the mucous membranes of the sinuses, leading to greater inflammatory responses.[56]

The World Health Organization (WHO) recommends that annual mean concentrations of PM2.5 should not exceed 5 μg/m3, and 24-hour mean exposures should not exceed 15 μg/m3 to minimize health risks.[57] Exposure to concentrations above these thresholds has been linked to an increased incidence and severity of rhinosinusitis and other respiratory diseases.[58]

Other diseases

[edit]

Other diseases such as cystic fibrosis and granulomatosis with polyangiitis can also cause chronic sinusitis.[59]

Maxillary sinus

[edit]

Maxillary sinusitis may also develop from dental problems. These cases were calculated to be about 40% in one study and 50% in another.[60] The cause of this situation is usually a periapical or periodontal infection of a maxillary posterior tooth, where the inflammatory exudate has eroded through the bone superiorly to drain into the maxillary sinus.[60]

An estimated 0.5 to 2.0% of viral rhinosinusitis (VRS) cases in adults and 5 to 10% in children develop superimposed bacterial infections.[38]

Pathophysiology

[edit]

Chronic rhinosinusitis is a multifactorial process hypothesized to be caused by inflammatory processes driven by dysfunction between local host and environmental interactions.[61] It is divided into two phenotypes that depend on the presence or absence of nasal polyps.[62] Chronic rhinosinusitis with nasal polyps and chronic rhinosinusitis without nasal polyps are thought to have two different inflammatory pathways, with the latter form driven by a Th1 response and the former driven by a Th2 response.[63] Both pathways result in an increase in inflammatory molecules (cytokines). The Th1 response is characterized by secretion of interferon gamma.[62] The Th2 response is characterized by secretion of interleukin-4 receptor, interleukin 5, and interleukin 13.[62] Both forms of chronic rhinosinusitis are considered to be highly heterogeneous, each with the ability to demonstrate three inflammatory endotypes, the third being a Th17 response.[62]

Diagnosis

[edit]

Classification

[edit]
Illustration depicting sinusitis, note the fluid in the sini

Sinusitis (or rhinosinusitis) is defined as an inflammation of the mucous membrane that lines the paranasal sinuses and is classified chronologically into several categories:[64]

  • Acute sinusitis – A new infection that may last up to four weeks and can be subdivided symptomatically into severe and nonsevere. Some use definitions up to 12 weeks.[1]
  • Recurrent acute sinusitis – Four or more full episodes of acute sinusitis that occur within one year
  • Subacute sinusitis – An infection that lasts between four and 12 weeks, and represents a transition between acute and chronic infection.
  • Chronic sinusitis – When the signs and symptoms last for more than 12 weeks.[1]
  • Acute exacerbation of chronic sinusitis – When the signs and symptoms of chronic sinusitis exacerbate, but return to baseline after treatment.

Roughly 90% of adults have had sinusitis at some point in their lives.[65]

Acute

[edit]

Health care providers distinguish bacterial and viral sinusitis by watchful waiting.[1] If a person has had sinusitis for fewer than 10 days without the symptoms becoming worse, then the infection is presumed to be viral.[1] When symptoms last more than 10 days or get worse during that time, then the infection is considered bacterial sinusitis.[66] Pain in the teeth and bad breath are also more indicative of bacterial disease.[67]

Imaging by either X-ray, CT, or MRI is generally not recommended unless complications develop.[66] Pain caused by sinusitis is sometimes confused for pain caused by pulpitis (toothache) of the maxillary teeth, and vice versa. Classically, the increased pain when tilting the head forwards separates sinusitis from pulpitis.[68]

For cases of maxillary sinusitis, limited field CBCT imaging, as compared to periapical radiographs, improves the ability to detect the teeth as the sources for sinusitis. A coronal CT picture may also be useful.[60]

Chronic

[edit]

For sinusitis lasting more than 12 weeks, a CT scan is recommended.[66] On a CT scan, acute sinus secretions have a radiodensity of 10 to 25 Hounsfield units (HU). In a more chronic state, they become more viscous, with a radiodensity of 30 to 60 HU.[69]

Nasal endoscopy and clinical symptoms are also used to make a positive diagnosis.[28] A tissue sample for histology and cultures can also be collected and tested.[70] Nasal endoscopy involves inserting a flexible fiber-optic tube with a light and camera at its tip into the nose to examine the nasal passages and sinuses.

Sinus infections, if they result in tooth pain, usually present with pain involving more than one of the upper teeth, whereas a toothache usually involves a single tooth. Dental examination and appropriate radiography help rule out pain arising from a tooth.[71]

  • CT of chronic sinusitis
    CT of chronic sinusitis
  • CT scan of chronic sinusitis, showing a filled right maxillary sinus with sclerotic thickened bone
    CT scan of chronic sinusitis, showing a filled right maxillary sinus with sclerotic thickened bone
  • MRI image showing sinusitis. Edema and mucosal thickening appear in both maxillary sinuses.
    MRI image showing sinusitis. Edema and mucosal thickening appear in both maxillary sinuses.
  • Maxillary sinusitis caused by a dental infection associated with periorbital cellulitis
    Maxillary sinusitis caused by a dental infection associated with periorbital cellulitis
  • Frontal sinusitis
    Frontal sinusitis
  • X-ray of left-sided maxillary sinusitis marked by an arrow. There is a lack of air transparency, indicating fluid in contrast to the other side.
    X-ray of left-sided maxillary sinusitis marked by an arrow. There is a lack of air transparency, indicating fluid in contrast to the other side.

Treatment

[edit]
Treatments for sinusitis[72][73]
Treatment Indication Rationale
Time Viral and some bacterial sinusitis Sinusitis is usually caused by a virus, which is not affected by antibiotics.[72]
Antibiotics Bacterial sinusitis Cases accompanied by extreme pain, skin infection, or that last a long time may be caused by bacteria.[72]
Nasal irrigation Nasal congestion Can provide relief by helping decongest.[72]
Drink liquids Thick phlegm Remaining hydrated loosens mucus.[72]
Antihistamines Concern with allergies Antihistamines do not relieve typical sinusitis or cold symptoms much; this treatment is not needed in most cases.[72]
Nasal spray Desire for temporary relief Tentative evidence that it helps symptoms.[4] Does not treat cause. Not recommended for more than three days' use.[72]

Recommended treatments for most cases of sinusitis include rest and drinking enough water to thin the mucus.[74] Antibiotics are not recommended for most cases.[74][75]

Breathing high-temperature steam, such as from a hot shower or gargling, can relieve symptoms.[74][76] There is tentative evidence for nasal irrigation in acute sinusitis, for example during upper respiratory infections.[4] Decongestant nasal sprays containing oxymetazoline may provide relief, but these medications should not be used for more than the recommended period. Longer use may cause rebound sinusitis.[77] It is unclear if nasal irrigation, antihistamines, or decongestants work in children with acute sinusitis.[78] There is no clear evidence that plant extracts such as Cyclamen europaeum are effective as an intranasal wash to treat acute sinusitis.[79] Evidence is inconclusive on whether anti-fungal treatments improve symptoms or quality of life.[80]

Antibiotics

[edit]

Most cases of sinusitis are caused by viruses and resolve without antibiotics.[28] However, if symptoms do not resolve within 10 days, either amoxicillin or amoxicillin/clavulanate are reasonable antibiotics for first treatment with amoxicillin/clavulanate being slightly superior to amoxicillin alone but with more side effects.[81][28] A 2018 Cochrane review, however, found no evidence that people with symptoms lasting seven days or more before consulting their physician are more likely to have bacterial sinusitis as one study found that about 80% of patients have symptoms lasting more than 7 days and another about 70%.[82] Antibiotics are specifically not recommended in those with mild / moderate disease during the first week of infection due to risk of adverse effects, antibiotic resistance, and cost.[83]

Fluoroquinolones, and a newer macrolide antibiotic such as clarithromycin or a tetracycline like doxycycline, are used in those who have severe allergies to penicillins.[84] Because of increasing resistance to amoxicillin the 2012 guideline of the Infectious Diseases Society of America recommends amoxicillin-clavulanate as the initial treatment of choice for bacterial sinusitis.[85] The guidelines also recommend against other commonly used antibiotics, including azithromycin, clarithromycin, and trimethoprim/sulfamethoxazole, because of growing antibiotic resistance. The FDA recommends against the use of fluoroquinolones when other options are available due to higher risks of serious side effects.[86]

A short course (3–7 days) of antibiotics appears to be as effective as the typical longer course (10–14 days) of antibiotics for those with clinically diagnosed acute bacterial sinusitis without any other severe disease or complicating factors.[87] The IDSA guideline suggest five to seven days of antibiotics is long enough to treat a bacterial infection without encouraging resistance. The guidelines still recommend that children receive antibiotic treatment for ten days to two weeks.[85]

Corticosteroids

[edit]

For unconfirmed acute sinusitis, nasal sprays using corticosteroids are not better than a placebo either alone or in combination with antibiotics.[88] For cases confirmed by radiology or nasal endoscopy, treatment with intranasal corticosteroids alone or in combination with antibiotics is supported.[89] The benefit, however, is small.[90]

For confirmed chronic rhinosinusitis, there is limited evidence that intranasal steroids improve symptoms and insufficient evidence that one type of steroid is more effective.[91][92]

There is only limited evidence to support short treatment with corticosteroids by mouth for chronic rhinosinusitis with nasal polyps.[93][94][95] There is limited evidence to support corticosteroids by mouth in combination with antibiotics for acute sinusitis; it has only short-term effect improving the symptoms.[96][97]

Surgery

[edit]

For sinusitis of dental origin, treatment focuses on removing the infection and preventing reinfection by removing the microorganisms, their byproducts, and pulpal debris from the infected root canal.[60] Systemic antibiotics are ineffective as a definitive solution. They may afford temporary relief of symptoms by improving sinus clearing. They may be appropriate for rapidly spreading infections, but debridement and disinfection of the root canal system at the same time are necessary. Treatment options include non-surgical root canal treatment, periradicular surgery, tooth replantation, or extraction of the infected tooth.[60]

For chronic or recurring sinusitis, referral to an otolaryngologist may be indicated, and treatment options may include nasal surgery. Surgery should only be considered for those people who do not benefit with medication or have non-invasive fungal sinusitis[98][unreliable medical source?].[94][99] It is unclear how benefits of surgery compare to medical treatments in those with nasal polyps as this has been poorly studied.[100][101]

Several surgical approaches can be used to access the sinuses, and these have generally shifted from external/extranasal approaches to intranasal endoscopic ones. The benefit of functional endoscopic sinus surgery (FESS) is its ability to allow for a more targeted approach to the affected sinuses, reducing tissue disruption and minimizing post-operative complications.[102] However, if a traditional FESS with Messerklinger technique is followed the success rate will be as low as 30%, 70% of the patients tend to have recurrence within 3 years.[103][unreliable medical source?] On the other hand with use of TFSE technique along with navigation system, debriders and balloon sinuplasty or EBS can give a success rate of over 99.9%.[103][unreliable medical source?] The use of drug eluting stents such as propel mometasone furoate implant may help in recovery after surgery.[104]

Another recently developed treatment is balloon sinuplasty. This method, similar to balloon angioplasty used to "unclog" arteries of the heart, utilizes balloons in an attempt to expand the openings of the sinuses in a less invasive manner.[42] The effectiveness of the functional endoscopic balloon dilation approach compared to conventional FESS is not known.[42]

Histopathology of sinonasal contents removed from surgery can be diagnostically valuable:

Treatments directed to rhinovirus infection

[edit]

A study has shown that patients given a spray formulation of 0.73 mg of Tremacamra (a soluble intercellular adhesion molecule 1 [ICAM-1] receptor) reduced the severity of illness.[107][39]

Prognosis

[edit]

A 2018 review has found that without the use of antibiotics, about 46% were cured after one week and 64% after two weeks.[82]

Epidemiology

[edit]

Sinusitis is a common condition, with an estimated 24 to 31 million cases occurring annually in the United States.[108][109] Chronic sinusitis affects approximately 12.5% of people.[49]

Research

[edit]

Based on recent theories on the role that fungi may play in the development of chronic sinusitis, antifungal treatments have been used, on a trial basis. These trials have had mixed results.[28]

See also

[edit]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Sinusitis

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

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 , which refer to specific facial regions. in these air-filled cavities leads to buildup, mucosal swelling, and impaired drainage, manifesting as site-specific , , and discharge. Sinus headaches caused by allergic rhinitis commonly feature pain concentrated in the forehead, eye sockets, and bridge of the nose. Frontal sinusitis, involving the sinuses located above the eyes in the , typically causes pain or pressure in the forehead that worsens with leaning forward or . This discomfort arises from the proximity to the supraorbital nerve branch of the , leading to across the brow. Associated nasal symptoms include anterior or of purulent , along with congestion that obstructs the frontal recess drainage pathway. Ethmoid sinusitis affects the ethmoid air cells between the eyes and behind the , resulting in periorbital pain or pressure behind the eyes, often described as a dull ache or persistent heavy pressure feeling due to inflammation and mucus buildup, that feels like a splitting between or behind the eyes. The thin lamina papyracea separating the ethmoid from the orbit contributes to this referral via ethmoidal branches of the , sometimes accompanied by tearing or swelling. In children, this can present as prominent eye pain or pressure around the eyes due to inflammation in the ethmoid sinuses, and severe eye pain, swelling, redness, or vision changes may signal orbital cellulitis, a serious complication requiring immediate medical attention. Nasal manifestations feature purulent discharge from the middle meatus and significant , with congestion exacerbating obstruction at the osteomeatal complex. Due to its location adjacent to the and olfactory cleft, ethmoid involvement frequently causes or by disrupting airflow to the olfactory receptors. Maxillary sinusitis, the most common form, inflames the largest beneath the and above the upper teeth, producing or tenderness over the , often radiating as a in the upper molars. This pattern stems from innervation by the , a maxillary division of the , with palpable swelling sometimes noted on percussion. Symptoms include unilateral or bilateral , anterior purulent , and that may irritate the throat, due to blockage at the maxillary in the middle meatus. Sphenoid sinusitis targets the deepest sinuses behind the , near the pituitary and optic nerves, leading to vague, severe pain in the occipital region, vertex, or behind the eyes, often manifesting as a dull ache or constant heavy pressure behind the eyes due to inflammation and mucus buildup, 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 . Nasal symptoms encompass posterior purulent drainage and congestion, often without prominent anterior , as the sphenoid drains into the sphenoethmoidal recess.

Systemic and Associated Symptoms

Systemic symptoms of sinusitis extend beyond the nasal and facial regions, often manifesting as generalized signs of and . Fever is a common systemic indicator, especially prominent in children with acute cases, where it is often high (e.g., ≥102°F or 39°C in severe bacterial cases), as part of the body's to bacterial involvement. In children, typical symptoms also include nasal congestion, thick nasal discharge, cough, headache, and facial tenderness. and frequently accompany these episodes, reflecting the overall energy drain from the inflammatory process, with tiredness being especially prominent in chronic presentations. Headaches in sinusitis can present diffusely across the head, differing from more localized , and may worsen with movement or position changes due to buildup from mucus pooling in inflamed sinuses under the influence of gravity; pain often shifts with head orientation, increasing on the lower side where thicker mucus accumulates while allowing partial drainage on the higher side—such as worsening when bending forward or lying down as fluid directs downward, localizing to the downside when side-lying, and intensifying in the morning from overnight pooling. This gravity-dependent positional variation distinguishes sinus headaches from migraines, which are less affected by such changes. Cough, often resulting from involving excess mucus irritating the throat and triggering upper airway cough syndrome (UACS), can become chronic particularly in chronic sinusitis and positions sinusitis among the top three causes of chronic cough alongside asthma and gastroesophageal reflux disease; this further contributes to systemic discomfort by disrupting daily activities and may involve irritation extending to the lower respiratory tract. 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. 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. Halitosis, or bad breath, results from bacterial overgrowth in stagnant sinus secretions, exacerbating social and sensory issues for affected individuals. The presentation of these symptoms varies significantly between acute and chronic sinusitis, influencing their clinical management. In acute sinusitis, symptoms like fever and often onset suddenly and intensely, lasting up to four weeks and resolving with targeted treatment, while and may peak early due to rapid . Chronic sinusitis, by contrast, features persistent low-grade and milder but enduring symptoms such as ongoing from chronic , with episodes lasting over 12 weeks and potentially leading to recurrent flares without underlying causes being addressed. These systemic and associated symptoms profoundly affect , often leading to sleep disruption from and , which impairs restorative rest and contributes to daytime . Studies indicate that 60-75% of individuals with chronic experience poor , correlating with reduced cognitive function, mood disturbances, and overall functional impairment. This holistic burden underscores the need for comprehensive symptom in sinusitis care.

Causes and Risk Factors

Infectious Etiologies

Sinusitis often begins as a viral infection of the upper , with viruses accounting for the majority of acute cases. Approximately 90% to 98% of acute episodes are viral in origin, typically resolving within 7 to 10 days without bacterial involvement. Common viral pathogens include rhinoviruses, which cause 50% to 80% of cases, as well as viruses, parainfluenza viruses, coronaviruses, adenoviruses, and . These viruses primarily affect the , leading to and that obstructs sinus ostia. Bacterial superinfections complicate 0.5% to 2% of viral upper respiratory infections, transitioning acute viral to acute bacterial . The predominant bacterial pathogens in community-acquired cases are (20% to 45% prevalence), (non-typeable strains, 20% to 43%), and (14% to 20%). Antibiotic resistance patterns vary geographically but include 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. Fungal infections are less common and typically occur in specific populations, with invasive forms predominantly affecting immunocompromised individuals such as those with , , or undergoing . Key pathogens include species in both invasive and noninvasive disease, and Mucor or (causing ) in diabetics, leading to rapid tissue . Noninvasive variants, like allergic fungal rhinosinusitis, involve to fungi such as , Bipolaris, or in immunocompetent patients with chronic disease. Invasive fungal sinusitis carries a of up to 50% due to potential orbital or intracranial extension. 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. Bacterial and fungal agents often arise opportunistically from this initial viral insult or endogenous flora, rather than direct person-to-person spread.

Non-Infectious Contributors

serves as a significant non-infectious contributor to sinusitis by inducing IgE-mediated inflammation in the , which leads to mucosal , impaired sinus drainage, and subsequent symptoms. This reaction involves the release of inflammatory mediators such as upon exposure, causing and obstruction that predisposes the paranasal sinuses to stasis and secondary inflammation. There is substantial overlap in prevalence, with affecting up to 40% of individuals with chronic , highlighting its role as a common trigger for non-infectious sinus . Anatomical abnormalities in the and can obstruct drainage pathways, fostering an environment conducive to sinusitis without primary infection. A deviated , present in approximately 80% of patients with chronic sinusitis, narrows the nasal passages and impairs by altering airflow and secretion flow. Similarly, nasal polyps—benign mucosal growths—physically block sinus ostia, leading to retention and chronic ; they occur in about 20-30% of chronic cases and are particularly prevalent in subtypes. , 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. These structural variants often coexist, amplifying the risk of recurrent sinusitis through of normal sinus . Autoimmune and genetic conditions underlie certain non-infectious forms of sinusitis by disrupting and innate mucosal defenses. In , mutations in the CFTR gene result in viscous accumulation and defective ion transport, impairing ciliary function and leading to chronic sinusitis in nearly all affected individuals; this manifests as opacified sinuses on due to persistent and poor drainage. (PCD), a 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 through shared clearance impairments. These disorders highlight how inherent host defects in ciliary motility and rheology perpetuate sinus pathology independently of microbial invasion. Aspirin-exacerbated respiratory disease (AERD), also known as Samter's triad, represents an immune-mediated syndrome that drives non-infectious sinusitis through dysregulated metabolism and eosinophilic inflammation. Characterized by the triad of , chronic with nasal polyps, and to aspirin and other nonsteroidal anti-inflammatory drugs, AERD affects 7-10% of patients with severe and leads to recurrent polypoid sinus disease via overproduction of cysteinyl s. In this condition, aspirin triggers exacerbations by shunting synthesis toward pathways, resulting in , , and progressive sinus obstruction that mimics infectious but stems from underlying . Management focuses on modifiers and aspirin desensitization to mitigate the inflammatory cascade and reduce polyp recurrence.

Environmental and Lifestyle Factors

Smoking, both active and passive, significantly contributes to the development and exacerbation of sinusitis by irritating the and impairing ciliary function, which hinders and promotes chronic inflammation. Active has been associated with an adjusted of 1.22 for chronic sinusitis, while 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. exposure similarly elevates risk, with 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 and delayed ciliary regeneration. Air pollution, particularly fine particulate matter (PM2.5) and , exacerbates sinusitis by inducing chronic sinonasal , 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 risk and nearly five times greater odds of severe pansinusitis, as demonstrated in analyses of over 6,000 patients using EPA air quality data. and PM contribute to this by promoting and inflammatory cytokine release in sinonasal tissues. Urban areas, with higher levels, show elevated sinusitis prevalence compared to rural settings; for instance, each 1 μg/m³ increase in PM10 correlates with higher chronic rates in urban cohorts, though some studies note variability. 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 , , 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 . In woodworking-related activities, exposure to wood 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 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. 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. Allergic contributions from these seasonal elements can overlap with intrinsic sensitivities but primarily act through external environmental triggers.

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. 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. 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. This eosinophilic infiltration leads to persistent mucosal remodeling and hyperplasia, as seen in chronic hyperplastic eosinophilic sinusitis, exacerbating obstruction and inflammation. 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 and zonula occludens-1, help reestablish the mucosal barrier integrity, reducing permeability and facilitating the clearance of inflammatory mediators to promote tissue homeostasis.

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 , 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. 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. 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. This eosinophilic mucin not only obstructs sinus drainage but also fosters a proinflammatory environment, exacerbating chronicity in affected patients. 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. 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. 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.

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. These criteria help differentiate viral from bacterial etiologies in acute cases and identify the need for further investigation in prolonged presentations. 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. 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. 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. 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. 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. Higher scores correlate with greater disease burden and help track response to interventions.

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. 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. 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. 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.

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. 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. 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. Fungal cultures, often combined with Gram stain and biopsy, are essential for suspected invasive fungal sinusitis, which can be life-threatening. 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. 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. Immunoglobulin levels or HIV serology are indicated only if immunodeficiency is suspected. Emerging molecular techniques, such as (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 or severe cases to differentiate etiologies and avoid unnecessary antibiotics, though they are not yet standard in guidelines.

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 intervention. Symptomatic relief focuses on non-pharmacological measures to enhance and reduce discomfort, with over-the-counter analgesics used judiciously for pain and fever control. Nasal irrigation with saline solution is a cornerstone of supportive care, facilitating the removal of mucus, allergens, and irritants to improve and reduce and post-nasal drip. Devices such as or squeeze bottles deliver isotonic or hypertonic saline, with high-volume (typically 240 mL per side) preferred for better efficacy in clearing the sinuses compared to low-volume sprays. 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. Evidence from randomized controlled trials supports modest symptom improvement, particularly in acute , without significant adverse effects beyond mild nasal irritation. However, saline nasal irrigation does not completely cure sinusitis as it primarily cleans and drains mucus without addressing underlying causes such as allergies, bacterial or viral infections, nasal polyps, deviated septum, or immune factors. For acute sinusitis, it may help resolve symptoms faster when combined with rest and proper treatment; for chronic sinusitis, it reduces symptoms and recurrence but the disease may return without treating the root issues. Hydration and environmental humidification further aid in thinning mucus, reducing post-nasal drip, and maintaining optimal sinus function. Adequate fluid intake, aiming for at least 2-3 liters daily, helps liquefy secretions and supports overall recovery. inhalation or use of cool-mist humidifiers can provide transient relief from congestion by adding moisture to the air, though high-quality for shortening symptom duration is limited; humidifiers should be cleaned regularly to avoid mold growth. Maintaining indoor between 40% and 60% is advised to prevent overly dry conditions that exacerbate . For patients with recurrent sinus infections, avoiding exposure to smoke and irritants, along with stress reduction strategies such as meditation or exercise, can help manage exacerbations. 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. 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.

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 (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 in adults and children due to its broad coverage against common pathogens like and beta-lactamase-producing . 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 or levofloxacin, are considered for penicillin-allergic patients or treatment failures, with local antimicrobial susceptibility patterns informing choices to curb resistance development. Improvement typically starts within 2–3 days of starting antibiotics like amoxicillin-clavulanate, with symptoms continuing to improve over the next few days; some cases take up to 3–5 days for clear relief, and full resolution can take 7–10 days or more. Intranasal corticosteroids represent a cornerstone for managing in both acute and chronic sinusitis, particularly when overlaps or chronicity persists. Agents like fluticasone propionate (50 mcg per spray) or mometasone furoate (50 mcg per spray), administered twice daily, reduce mucosal 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 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 or nasal polyps, short courses of oral corticosteroids may provide rapid symptom relief as adjunctive therapy. 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 scores by 20-30% in responsive patients. Use is limited to brief durations due to risks of systemic effects like and , with guidelines advising against routine application in mild cases. Biologic therapies are indicated for adults with chronic rhinosinusitis with (CRSwNP) refractory to intranasal and/or surgery, particularly in cases with . , a targeting interleukin-4 and -13 receptors (300 mg subcutaneously every two weeks after ), (anti-IgE, dosed by weight and IgE levels every 2-4 weeks), and (anti-IL-5, 100 mg subcutaneously every 4 weeks) have shown significant reductions in 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 and reduce oral dependence. Antihistamines and decongestants play a targeted role in sinusitis with allergic or vasomotor components, such as concurrent . Second-generation oral antihistamines (e.g., loratadine 10 mg daily or 10 mg daily) alleviate histamine-driven symptoms like pruritus and , achieving 10-30% symptom reduction over in allergic . Oral or topical decongestants (e.g., 60 mg every 6 hours or spray twice daily) offer for congestion relief but are limited to 3-5 days to avoid rebound , 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. 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. 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. Preoperative computed tomography imaging guides the surgical planning by identifying specific anatomical variations and disease extent. Balloon sinuplasty offers a less invasive alternative for patients with mild ostial obstruction, involving the insertion of a flexible into the sinus under endoscopic guidance, followed by inflation to dilate the passageway without tissue removal. This technique is particularly suited for isolated sinus involvement in CRS that persists despite management, minimizing disruption to surrounding mucosa. 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 therapy to control . These measures help maintain surgical patency and reduce the risk of adhesions or recurrent obstruction.

Prognosis and Complications

Short-Term and Long-Term Outcomes

Patients should seek urgent medical attention for sinusitis if they develop a high fever above 38.5°C (particularly common in children), severe facial pain or eye pain, swelling around the eyes, symptoms persisting or worsening beyond 7–10 days, or signs of complications such as dizziness, nausea, or vision impairment. For acute sinusitis, approximately 64% of uncomplicated cases resolve spontaneously within 2 weeks without specific intervention, primarily through supportive measures like hydration and , while these measures aid in symptom relief and promote recovery in acute cases, they do not address underlying causes, which may lead to recurrence in chronic or predisposed individuals. The introduction of the 13-valent (PCV13) in 2010 has reduced the incidence of acute by 13-21% in adults and severe complications requiring hospitalization by 54%. 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. 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. 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. 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 , , and sleep disruption, though full resolution is uncommon without addressing persistent inflammation. Surgical interventions like can further enhance these outcomes, achieving durable SNOT-22 improvements in a majority of refractory cases. Early intervention in acute cases markedly reduces the likelihood of progression to chronicity by targeting and promptly, thereby preserving sinus drainage pathways. Conversely, comorbidities such as , allergies, or adversely affect prognosis, correlating with higher symptom burden and lower response rates to standard therapies as measured by SNOT-22 scores. 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 in children, involving the ethmoid and maxillary sinuses, and can progress from superficial infections to vision-threatening conditions. Preseptal , confined to the anterior to the , typically presents with swelling and without proptosis or ophthalmoplegia, distinguishing it from true orbital involvement. In contrast, involves post-septal spread, leading to severe eye pain, periorbital swelling, erythema, proptosis, chemosis, decreased visual acuity, restricted eye movements, and vision changes due to inflammation within the orbital cone. Severe eye pain, swelling, redness, or vision changes may signal orbital cellulitis, particularly in children, and require immediate medical attention to prevent permanent vision loss or other serious outcomes. Chandler's classification system categorizes these into five stages: group I (preseptal ), group II (), group III (subperiosteal abscess), group IV (orbital abscess), and group V ( with orbital involvement), guiding escalation from medical to surgical management. Subperiosteal or orbital abscesses can cause compressive , resulting in permanent vision loss if untreated, with ethmoid sinusitis being the most common precursor. 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. manifests with fever, severe headache, nuchal rigidity, , and altered mental status, secondary to bacterial invasion of the . abscesses present with focal neurological deficits, seizures, and progressive headache, forming encapsulated collections in cerebral lobes adjacent to infected sinuses. , a particularly devastating , involves septic of the , leading to bilateral periorbital edema, cranial nerve palsies (III, IV, VI), proptosis, and severe headache; symptoms may include and rapid neurological deterioration. These intracranial events occur in approximately 3-4% of hospitalized sinusitis cases, predominantly affecting children and young adults, with species as common pathogens. Osseous complications involve bone erosion and infection, most notably in the from protracted frontal sinusitis. Osteomyelitis of the develops through contiguous spread, causing bone necrosis and potential intracranial extension, with symptoms including localized pain, swelling, and systemic fever. , a classic manifestation, refers to a subperiosteal overlying frontal , presenting as a fluctuant swelling that may mimic a benign mass but harbors risk of epidural or sagittal sinus . This condition, historically linked to untreated sinusitis, now occurs rarely due to antibiotics but remains a marker of advanced disease with frontal bone involvement. Other severe sequelae include 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 depending on the affected sinus. In chronic with nasal polyps, large polypoid masses can cause significant nasal and nasopharyngeal obstruction, exacerbating limitation and contributing to sleep-disordered . Immunocompromised patients face heightened risk for these complications due to impaired host defenses against opportunistic pathogens.

Epidemiology

Global Prevalence and Incidence

Sinusitis, encompassing both acute and chronic forms, represents a significant burden, with acute (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 infections such as the . In the United States, for instance, about 11.6% of adults receive a of sinusitis each year, underscoring its commonality in settings. Chronic rhinosinusitis (CRS), defined as persisting for at least 12 weeks, has a global pooled 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. Over recent decades, the 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 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 of CRS in children is around 4%.

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. 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. Chronic (CRS) prevalence increases with age, doubling in those over 60 compared to younger adults under 40. 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. This disparity is potentially linked to hormonal influences, such as fluctuations that affect and production, exacerbating during menstrual cycles, , or . Ethnic variations highlight disparities in CRS phenotypes. African Americans experience higher rates of CRS, with a reported 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. , including allergic fungal , is more prevalent in tropical regions, where hot and humid climates promote fungal growth, leading to higher incidences in areas like and . Geographically, sinusitis rates are elevated in industrialized urban areas due to , with exposure to particulate matter (PM2.5) independently associated with increased CRS odds and disease severity. In temperate zones, the condition displays strong , with peak incidences during winter months attributed to dry air, lower , and viral outbreaks that inflame sinuses.

References

  1. https://www.ncbi.nlm.nih.gov/books/NBK547701/
  2. https://www.mayoclinic.org/diseases-conditions/acute-sinusitis/symptoms-causes/syc-20351671
  3. https://www.mayoclinic.org/diseases-conditions/chronic-sinusitis/symptoms-causes/syc-20351661
  4. https://my.clevelandclinic.org/health/diseases/9641-sinus-headaches
  5. https://www.cdc.gov/sinus-infection/about/index.html
  6. https://acaai.org/allergies/symptoms/headaches/
  7. https://www.merckmanuals.com/home/ear-nose-and-throat-disorders/nose-and-sinus-disorders/sinusitis
  8. https://www.ncbi.nlm.nih.gov/books/NBK279485/
  9. https://www.ncbi.nlm.nih.gov/books/NBK549820/
  10. https://www.mountsinai.org/health-library/diseases-conditions/sinusitis
  11. https://medlineplus.gov/sinusitis.html
  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC6737117/
  13. https://acaai.org/allergies/allergic-conditions/sinus-infection/
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC8604050/
  15. https://www.healthline.com/health/sore-throat-and-ears
  16. https://www.verywellhealth.com/sinus-infection-with-ear-pain-7562019
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC5967413/
  18. https://pmc.ncbi.nlm.nih.gov/articles/PMC4192102/
  19. https://www.ncbi.nlm.nih.gov/books/NBK532961/
  20. https://pubmed.ncbi.nlm.nih.gov/21364226/
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC9422375/
  22. https://pmc.ncbi.nlm.nih.gov/articles/PMC155833/
  23. https://pmc.ncbi.nlm.nih.gov/articles/PMC172002/
  24. https://www.ncbi.nlm.nih.gov/books/NBK551496/
  25. https://www.cdc.gov/common-cold/about/index.html
  26. https://pmc.ncbi.nlm.nih.gov/articles/PMC7123453/
  27. https://pmc.ncbi.nlm.nih.gov/articles/PMC7173501/
  28. https://www.worldallergy.org/component/content/article/rhinitis-in-depth-review-sullivan-a-kushnir-nm-updated-2020?catid=16&Itemid=101
  29. https://www.jacionline.org/article/s0091-6749%2809%2902881-4/fulltext
  30. https://www.scirp.org/journal/paperinformation?paperid=33854
  31. https://pmc.ncbi.nlm.nih.gov/articles/PMC5951071/
  32. https://pmc.ncbi.nlm.nih.gov/articles/PMC9431850/
  33. https://europepmc.org/article/pmc/pmc6033609
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC7483516/
  35. https://www.nhlbi.nih.gov/health/primary-ciliary-dyskinesia/symptoms
  36. https://www.aaaai.org/tools-for-the-public/conditions-library/asthma/aspirin-exacerbated-respiratory-disease-%28aerd%29
  37. https://www.mayoclinic.org/diseases-conditions/asthma/in-depth/aerd/art-20482797
  38. https://pmc.ncbi.nlm.nih.gov/articles/PMC3443524/
  39. https://www.hopkinsmedicine.org/news/newsroom/news-releases/2021/07/johns-hopkins-medicine-researchers-show-how-air-pollution-may-cause-chronic-sinusitis
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC9008184/
  41. https://pmc.ncbi.nlm.nih.gov/articles/PMC4681694/
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC8426117/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC12043346/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC7088912/
  45. https://pmc.ncbi.nlm.nih.gov/articles/PMC3781389/
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC12263562/
  47. https://pmc.ncbi.nlm.nih.gov/articles/PMC10614382/
  48. https://pmc.ncbi.nlm.nih.gov/articles/PMC5698538/
  49. https://pmc.ncbi.nlm.nih.gov/articles/PMC3179194/
  50. https://pmc.ncbi.nlm.nih.gov/articles/PMC10188844/
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC7121820/
  52. https://www.ncbi.nlm.nih.gov/books/NBK459372/
  53. https://www.merckmanuals.com/professional/ear-nose-and-throat-disorders/nose-and-paranasal-sinus-disorders/sinusitis
  54. https://www.entnet.org/wp-content/uploads/2021/04/adult-sinusitis-physicianresource-diagnostic-criteria-rhinosinusitis.pdf
  55. https://reference.medscape.com/viewarticle/adult-sinusitis-clinical-practice-guideline-update-aao-hns-2025a1000mm8
  56. https://pubmed.ncbi.nlm.nih.gov/19793277/
  57. https://onlinelibrary.wiley.com/doi/full/10.1002/lary.29766
  58. https://pmc.ncbi.nlm.nih.gov/articles/PMC7121979/
  59. https://www.aafp.org/pubs/afp/issues/2002/1115/p1882.html
  60. https://ajronline.org/doi/10.2214/AJR.07.7031
  61. https://www.sciencedirect.com/science/article/pii/S0194599897700056
  62. https://pubmed.ncbi.nlm.nih.gov/2125121/
  63. https://pmc.ncbi.nlm.nih.gov/articles/PMC4899354/
  64. https://pmc.ncbi.nlm.nih.gov/articles/PMC7108105/
  65. https://pmc.ncbi.nlm.nih.gov/articles/PMC3055847/
  66. https://www.aafp.org/pubs/afp/issues/2016/0715/p97.html
  67. https://www.aafp.org/pubs/afp/issues/2009/1115/p1117.html
  68. https://www.mayoclinic.org/diseases-conditions/chronic-sinusitis/diagnosis-treatment/drc-20351667
  69. https://www.uptodate.com/contents/uncomplicated-acute-sinusitis-and-rhinosinusitis-in-adults-treatment
  70. https://www.sinusdoctor.com/living-with-chronic-sinusitis/
  71. https://onlinelibrary.wiley.com/doi/abs/10.1002/lio2.70282
  72. https://www.ncbi.nlm.nih.gov/books/NBK563202/
  73. https://pmc.ncbi.nlm.nih.gov/articles/PMC3273939/
  74. https://pmc.ncbi.nlm.nih.gov/articles/PMC11375676/
  75. https://pmc.ncbi.nlm.nih.gov/articles/PMC3198264/
  76. https://www.ncbi.nlm.nih.gov/books/NBK546671/
  77. https://pubmed.ncbi.nlm.nih.gov/30507684/
  78. https://pubmed.ncbi.nlm.nih.gov/22144050/
  79. https://pmc.ncbi.nlm.nih.gov/articles/PMC6517168/
  80. https://pubmed.ncbi.nlm.nih.gov/30407624/
  81. https://my.clevelandclinic.org/health/diseases/15285-acute-sinusitis
  82. https://aao-hnsfjournals.onlinelibrary.wiley.com/doi/10.1002/ohn.1344
  83. https://pmc.ncbi.nlm.nih.gov/articles/PMC3404479/
  84. https://pmc.ncbi.nlm.nih.gov/articles/PMC10646061/
  85. https://pmc.ncbi.nlm.nih.gov/articles/PMC4352106/
  86. https://pmc.ncbi.nlm.nih.gov/articles/PMC3283797/
  87. https://pubmed.ncbi.nlm.nih.gov/33906469/
  88. https://pmc.ncbi.nlm.nih.gov/articles/PMC9052236/
  89. https://pmc.ncbi.nlm.nih.gov/articles/PMC4110986/
  90. https://my.clevelandclinic.org/health/diseases/24499-orbital-cellulitis
  91. https://pmc.ncbi.nlm.nih.gov/articles/PMC4569601/
  92. https://pmc.ncbi.nlm.nih.gov/articles/PMC7917423/
  93. https://pmc.ncbi.nlm.nih.gov/articles/PMC4757916/
  94. https://www.ncbi.nlm.nih.gov/books/NBK448177/
  95. https://pubmed.ncbi.nlm.nih.gov/2000009/
  96. https://pmc.ncbi.nlm.nih.gov/articles/PMC3307540/
  97. https://www.ncbi.nlm.nih.gov/books/NBK560789/
  98. https://pmc.ncbi.nlm.nih.gov/articles/PMC9899488/
  99. https://pmc.ncbi.nlm.nih.gov/articles/PMC7122468/
  100. https://www.ncbi.nlm.nih.gov/books/NBK560746/
  101. https://www.bmj.com/content/346/bmj.f2687
  102. https://www.cdc.gov/nchs/fastats/sinuses.htm
  103. https://pmc.ncbi.nlm.nih.gov/articles/PMC2600057/
  104. https://pubmed.ncbi.nlm.nih.gov/39506931/
  105. https://www.jacionline.org/article/S0091-6749%2818%2932786-6/fulltext
  106. https://www.rhinologyjournal.com/Documents/Supplements/supplement_29.pdf
  107. https://pmc.ncbi.nlm.nih.gov/articles/PMC11126196/
  108. https://pubmed.ncbi.nlm.nih.gov/25847466/
  109. https://www.dynamed.com/condition/chronic-rhinosinusitis
  110. https://publications.aap.org/pediatrics/article/132/1/e262/31288/Clinical-Practice-Guideline-for-the-Diagnosis-and
  111. https://journals.healio.com/doi/10.3928/19382359-20180919-01
  112. https://emedicine.medscape.com/article/232670-overview
  113. https://pmc.ncbi.nlm.nih.gov/articles/PMC6408962/
  114. https://pmc.ncbi.nlm.nih.gov/articles/PMC4541639/
  115. https://www.ophthalmologyadvisor.com/news/women-have-higher-odds-of-chronic-rhinosinusitis-without-nasal-polyps/
  116. https://pmc.ncbi.nlm.nih.gov/articles/PMC3345896/
  117. https://pubmed.ncbi.nlm.nih.gov/26868728/
  118. https://www.sciencedirect.com/science/article/abs/pii/S1156523308000930
  119. https://academic.oup.com/milmed/article/188/7-8/e1965/6499880
  120. https://pubmed.ncbi.nlm.nih.gov/40587220/
  121. https://entcet.com/patient-resources/nose-sinus/how-seasonal-weather-changes-can-affect-your-sinuses/
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