2016 Section 5 Green Book

Stachler

by many inciting events, such as exercise, allergen or irritant

exposure, change in weather, or viral respiratory infection.

The symptoms and airflow limitation can resolve and re-

spond to medications, or may be very subtle and not be

noticed for some time. Episodic flare-ups can occur, which

can be life threatening. Asthma is associated with airway

hyperresponsiveness to direct or indirect stimuli. In some

cases, a complex process is initiated involving inflamma-

tory mediators, eosinophils, mast cells, T lymphocytes, neu-

trophils, and epithelial cells. Chronicity of the condition, if

it occurs, leads to advanced disease and airway remodeling.

This may lead to irreversible pulmonary mucosal changes.

These changes, inflammation with ensuing airway obstruc-

tion, can result in the classic symptoms of wheezing, chest

tightness, coughing, and breathlessness.

Clinicians need to

focus primarily on the inflammatory component of the dis-

ease to prevent the chronic changes that can occur, while

treating the reversible increased bronchial reactivity. Un-

controlled asthma or suboptimal management may result

in the chronic changes the clinician is trying to avoid.

Relationships between asthma and upper

airway disease

Asthma has been noted to be closely related to AR. Corren,

in 1997, reviewed this relationship and found that 78%

of asthmatics have nasal symptoms. Thirty-eight percent

(38%) of patients with rhinitis (AR and non-AR) will have

asthma. His data also suggests that rhinitis often precedes

the development of asthma. Other authors

10,11

have shown

a 3-fold increase in asthma over a 20-year period in allergic

patients when compared to nonallergic controls. Guerra

et al.’s study

also showed that patients with higher serum

immunoglobulin E (IgE) levels at the onset of the study

had a 5-fold increase in their risk of developing asthma.

Shaaban et al.,

in a longitudinal population-based study

noted that the presence of AR increases the relative risk

for asthma to 3.53 (95% confidence interval [CI], 2.11 to

5.91). The relative risk for asthma in patients with non-

AR was 2.71 (95% CI, 1.64 to 4.46). AR clearly is often

discovered concurrently with asthma, and predisposes one

to develop asthma over time.

Asthmatic Nordic children with AR had a higher risk of

hospital readmissions and more hospital days per year com-

pared to asthmatic patients without rhinitis.

Nasal symp-

toms have been associated with asthma. Patients with nasal

complaints (congestion, itching, and rhinorrhea), should be

carefully evaluated for asthma. Bronchial hyperactivity has

been demonstrated in patients with AR who were unaware

of their pulmonary condition.

14,15

Clinicians, otolaryngol-

ogists, pulmonologists, and primary care physicians need to

consider asthma on a more regular basis when evaluating

patients with severe nasal complaints.

AR has been shown to worsen the overall prognosis of

asthma.

Those who have asthma and AR have more se-

vere lower respiratory disease and account for more costs

TABLE 1.

Similar histopathologic findings in CRS and

asthma

Mucosal edema

Vasodilation

Cellular (eosinophil and lymphocyte) infiltration

Major basic protein deposition

Thickening of the basement membrane

Hyperplasia of the goblet cells

Mucous gland hypertrophy

Angiogenesis

Collagen deposition

Epithelial damage

Subepithelial fibrosis

CRS

chronic rhinosinusitis.

to the healthcare system. Tight control of the AR leads to

improved asthma control and vice versa.

16–18

Chronic rhinosinusitis, histopathologically, appears simi-

lar to asthma.

The nasal mucosa remodels and thickens in

a similar manner seen with chronic changes in the bronchial

mucosa. Under the microscope the findings are nearly indis-

tinguishable (Fig. 1). Remodeling is due to mucosal edema,

submucosal gland and bronchial smooth muscle hypertro-

phy, collagen deposition, basement membrane thickening,

and subepithelial fibrosis in the lamina reticularis (Table 1).

The only finding that is different is the mucosal thickening

is not as noted in the nose in rhinitis as it is in the bronchial

airway in asthma patients.

Nasal polyposis is associated with rhinitis and asthma.

It is one of the diagnostic criteria for allergic fungal

rhinosinusitis.

Aspirin-sensitive respiratory disease is an-

other condition with a strong association of polyps, rhinos-

inusitis, and asthma. It occurs when one has an allergy to

aspirin or other nonsteroidal anti-inflammatory agents. As-

pirin ingestion leads to an intense inflammatory response of

the upper and lower airways, exacerbations of rhinosinusi-

tis, and asthma (Samter’s triad).

Awad et al.

reported

that aspirin-intolerant asthmatics had statistically superior

asthma outcomes with endoscopic sinus surgery for chronic

rhinosinusitis compared to aspirin-tolerant sinus surgery

patients.

Chronic rhinosinusitis patients with asthma have a higher

rhinosinusitis severity score (Lund-Mackay score) than

nonasthmatic patients and more nasal polyps regardless

of atopic status, indicative of a strong relationship between

chronic rhinosinusitis severity and chronic airway inflam-

matory diseases, asthma, and nasal polyps.

Asthmatic pa-

tients with coexistent symptomatic chronic sinusitis have

greater asthmatic severities requiring more aggressive man-

agement to gain control of the condition.

24–31

Both medical

and surgical treatment of chronic rhinosinusitis has been

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