2016 Section 5 Green Book

allergy exacerbation could lead to mucosal swelling and

thus the cyclical sinusitis pattern (Fig. 9). In these

patients, they may respond to pharmacotherapy for the

allergy component of their CRS.

Asthmatic Sinusitis With Allergy

AScA represents the “unified airway” patients who

have been described in the literature.

The unified air-

way patients have sinusitis, allergic rhinitis, and

asthma but no aspirin sensitivity and is mediated via an

IgE Th2 inflammatory process. Upper respiratory tract

stimulation affects the lower respiratory tract and vice

versa in these patients.

The most plausible explanation

for the connection between the upper and lower airways

is circulation of activated eosinophils that are very high

in AScA CRS polyps. Eosinophils are activated in the

sinus mucosa due to exposure of stimulants in the nose.

The activated eosinophils are transported to the lung via

the circulatory system. These circulating eosinophils can

then bind to the adhesion molecules in the pulmonary

epithelial tissue. The activated eosinophils in the lower

respiratory tract can then create a local inflammatory

response in the lung.

The amount of eosinophils in the nasal polyp

appears to be a good histological marker or measure for

intrinsic mucosal inflammation. This type of inflamma-

tion should be called intrinsic mucosal inflammation

because the airway mucosa develops an abnormal

response to an irritant within the mucosa due to a

genetic predilection. Other intrinsic mucosal inflamma-

tory CRS subclasses are AFS and AERD. Intrinsic

inflammatory CRS has abundant eosinophils in tissue

samples. Hypercellularity of nasal polyps is also high in

intrinsic inflammatory CRS. However, hypercellularity,

which is also represented in CF, may not always be rep-

resentative of an intrinsic inflammation.

AScA patients commonly have a pediatric history of

allergy or asthma. On nasal endoscopy, they have exten-

sive nasal polyposis with little to no purulence. On CT

findings, they have pansinusitis with complete or near

complete opacification (Fig. 10). Because AScA had sig-

nificantly higher levels of CD4

cells than the control

group, AScA mucosal inflammation is driven by T helper

cells and most likely the Th2 process. Although Th2

mediated cytokines did not reach statistical difference in

our study, IL4 and IL13 have been implicated in these

IgE-associated atopic asthmatic patients.

12,13

The inflammation in AScA is usually not driven by

infection, and therefore AScA patients respond better to

oral steroids rather than antibiotics. The mucosal

inflammation in these patients is so severe that they are

likely to fail medical treatment and often require ESS to

debulk the nasal polyps. Removing the nasal polyps

decreases the local inflammation by eliminating the eo-

sinophils and associated inflammatory mediators to the

level where the mucosal inflammation can be controlled

with postoperative medications. Another reason for ESS

is to debulk the obstructive nasal polyps and open the

sinuses so that topical medications, such as topical bude-

sonide, can be delivered into the sinuses. Topical

budesonide has been shown to improve patient sinus

score and hyposmia in chronic eosinophilic sinusitis.

Another method to control the inflammation is immuno-

therapy (sublingual and subcutaneous immunotherapy)

that suppresses Th2-mediated response.

Immunomodu-

lators using anti–IL4, anti-IL5, and anti-IL13

monoclonal antibodies are certainly options to be consid-

ered and have been evaluated in the past.

12,16

Asthmatic Sinusitis Without Allergy

The phenotype and histology of ASsA is similar to

AScA and AERD, but ASsA is more comparable to

AERD than ASsA. An interesting thought is that ASsA

could be a precursor to AERD. Unlike AScA, ASsA

patients usually do not have a history of pediatric aller-

gic rhinitis or asthma. As stated earlier, AScA or unified

airway CRS commonly has a history of pediatric allergic

Fig. 9. Flow chart demonstrating the cyclical pattern of chronic

sinusitis.

Fig. 10. Coronal computed tomography of the sinus demonstrat-

ing pansinusitis with near-complete opacification of all the

sinuses.

Laryngoscope 123: March 2013

Han:

Subclassification

of Chronic

Sinusitis