History and exam
Key diagnostic factors
common
nasal obstruction
Occurs in 92% of patients with chronic rhinosinusitis.[2]
Most often obstruction is bilateral in patients with nasal polyps. Nasal obstruction may be valvular, with obstruction in either inspiration or expiration, depending on the size and location of the polyps.
Unilateral obstruction should be regarded as suspicious of a neoplasm until shown otherwise.[25][26]
nasal discharge
polyps visible on examination or imaging
Nasal polyps must be seen on anterior rhinoscopy or nasendoscopy, or indirectly on CT scan, for the diagnosis to be made.[2]
Other diagnostic factors
common
facial pain/pressure
Facial congestion-pressure-fullness occurs in 67% of patients with chronic rhinosinusitis.[2]
However, facial pain/pressure and nasal polyps are poorly correlated; facial pain/pressure is more common in patients with chronic rhinosinusitis without nasal polyps.
reduced sense of smell/anosmia
This occurs in 84% of patients with chronic rhinosinusitis.[2]
cough
Occurs secondary to tracheal and laryngeal irritation caused by postnasal drip, or as a result of associated asthma.
Risk factors
strong
asthma
eosinophilic granulomatous polyangiitis (EGPA, also known as Churg-Strauss syndrome)
This syndrome involves a combination of severe asthma, chronic rhinosinusitis (typically with nasal polyposis), eosinophilia, and eosinophilic vasculitis with granulomas.[23] Other features can include mononeuritis and cardiomyopathy.
allergic fungal rhinosinusitis (AFRS)
AFRS typically presents with nasal polyps and sinus opacification, which may be asymmetric and lead to sinus expansion and local tissue erosion. Allergic fungal rhinosinusitis is rare in the UK, but is more common in warm, humid climates such as the southern and southeastern US, India, and the Middle East.[24]
aspirin sensitivity
People with aspirin- and nonsteroidal anti-inflammatory drug-exacerbated respiratory disease have a higher incidence of nasal polyps (estimates range from 7% to 26%).[3]
weak
genetic predisposition
Genetic associations have been reported in some cases, but the evidence is limited.[8][9][10] Population studies have demonstrated a four- to fivefold increased risk of CRSwNP in people who have a first-degree relative with CRSwNP.[10][11] Specific risk genes are not yet well characterized.[12]
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