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☆

ASSESSMENT OF SEVERITY

 

MANAGEMENT–COMMUNITY SETTINGS

 

The severity of the exacerbationFigure (4.4-1 ) determines

Most patients with severe asthma exacerbations shoul

the treatment administered. Indices of severity,bepartreatedicularlyin an acute care facility (such as a hospital

PEF 187

 

(in patients older than 5 years), pulse rate,

 

emergency department) where monitoring, including

 

 

 

 

 

 

210

 

 

 

 

objective measurement of airflow obstruction, oxyge

respiratory rate, and pulse oximetry, should be

 

 

monitored during treatment.

 

 

 

 

saturation, and cardiac function, is possible. Milder

 

 

 

 

 

 

 

 

 

 

 

exacerbations, defined by a reduction in peak flow of

 

 

 

 

 

 

 

 

 

 

 

than 20%, nocturnal awakening, and increased use of

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Figure 4.4-1. Severity of Asthma Exacerbations*

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Mild

 

 

Moderate

 

 

 

 

 

Severe

 

Respiratory arrest

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

imminent

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Breathless

 

Walking

 

Talking

 

 

 

 

 

At rest

 

 

 

 

 

 

 

 

 

 

 

Infant—softer

 

 

 

Infant stops feeding

 

 

 

 

 

 

 

 

shorter cry;

 

 

 

 

 

OR

REPRODUCE!

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

difficulty feeding

 

 

 

 

 

 

 

 

Can lie down

 

Prefers sitting

 

 

 

 

 

 

 

 

 

 

 

 

 

Hunched forward

 

 

 

Talks in

 

Sentences

 

Phrases

 

 

 

 

 

Words

 

 

 

 

Alertness

 

May be agitated

 

Usually agitated

 

 

 

Usually agitated

Drowsy or confused

 

Respiratory rate

 

Increased

 

Increased

 

 

 

 

Often > 30/min

 

 

 

 

 

 

 

 

Normal rates of breathing in awake children:

ALTER

 

 

 

 

 

 

 

 

 

 

Age

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Normal rate

 

 

 

 

 

 

 

 

 

 

< 2 months

 

 

 

< 60/min

 

 

 

 

 

 

 

 

 

 

2-12 months

 

 

 

< 50/min

 

 

 

 

 

 

 

 

 

 

1-5 years

 

 

 

< 40/min

 

 

 

 

 

 

 

 

 

 

6-8 years

 

 

 

< 30/min

 

 

 

 

 

 

 

 

 

 

 

 

 

NOT

 

 

 

 

 

Accessory muscles

 

Usually not

 

Usually

DO

 

 

 

 

Usually

 

Paradoxical thoraco-

 

and suprasternal

 

 

 

 

 

 

 

 

 

 

 

abdominal movement

 

retractions

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Wheeze

 

Moderate, often only

 

-

 

 

 

 

Usually loud

 

Absence of wheeze

 

 

 

oud

 

 

 

 

 

 

 

 

 

 

 

end expiratory

 

 

 

 

 

 

 

 

 

 

 

 

Pulse/min.

 

< 100

 

 

100-120

 

 

 

 

 

>120

 

Bradycardia

 

 

 

 

 

Guide to limits of normal pulse rate in children:

 

 

 

 

 

 

 

 

Infants

2-12 months–Normal Rate

 

 

< 160/min

 

 

 

 

 

 

 

 

Preschool

1-2 years

 

 

 

 

 

< 120/min

 

 

 

 

 

 

 

 

School age

2-8 years

 

 

 

 

 

< 110/min

 

 

 

 

Pulsus paradoxus

 

Absent

 

May be present

 

 

 

 

Often present

 

Absence suggests

 

 

 

 

 

< 10 mm Hg

 

10-25 mm Hg

 

 

 

 

> 25 mm Hg (adult)

respiratory muscle

 

 

 

 

 

 

MATERIAL

 

 

 

 

 

20-40 mm Hg (child)

fatigue

 

PEF

 

 

 

Over 80%

 

 

Approx. 60-80%

 

 

 

 

< 60% predicted or

 

 

 

after initial

 

 

 

 

 

 

 

 

 

 

personal best

 

 

 

bronchodilator

 

 

 

 

 

 

 

 

 

 

(< 100 L/min adults)

 

 

 

% predicted or

 

 

 

 

 

 

 

 

 

 

or

 

 

 

 

% personal best

 

 

 

 

 

 

 

 

 

 

response lasts < 2 hrs

 

 

 

PaO

2 (on air)†

 

Normal

 

 

> 60 mm Hg

 

 

 

 

< 60 mm Hg

 

 

 

 

 

 

 

 

Test not usually

 

 

 

 

 

 

 

 

 

 

 

 

and/or

 

necessary

 

 

 

 

 

 

 

Possible cyanosis

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Pa

 

†

 

< 45 mm Hg

 

< 45 mm Hg

 

 

 

 

> 45 mm Hg;

 

 

 

 

 

2

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Possible respiratory

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

failure (see text)

 

 

 

SaO

2

% (on air) †

 

> 95%

 

91-95%

 

 

 

 

 

< 90%

 

 

 

 

COPYRIGHTED

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Hypercapnea (hypoventilation) develops more readily in young children than in

 

 

 

 

 

adults and adolescents.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

*Note: The presence of several parameters, but not necessarily all, indicates the general classification of the exac †Note: Kilopascals are also used internationally; conversion would be appropriate in this regard.

ASTHMA MANAGEMENT AND PREVENTION

65

short acting-agonists can usually be treated in a Assessment 2

community setting. If the patient responds to the increase

in inhaled bronchodilator treatment after the firstAbrieffew history and physical examination pertinent t doses, referral to an acute care facility is not required,exacerbationut should be conducted concurrently with t further management under the direction of a primarypromptcare initiation of therapy. The history should inc

physician may include the use of systemic glucocorticoseverity-

and duration of symptoms, including exerc

of -agonist required will depend on the severity of the

 

 

 

REPRODUCE!

steroids. Patient education and review of maintenancelimitation and sleep disturbance; all current medica

therapy should also be undertaken.

 

 

including dose (and device) prescribed, dose usually

 

 

 

taken, dose taken in response to the deterioration, and

Treatment

 

 

patientis response (or lack thereof) to this therapy; ti

 

 

 

onset and cause of the present exacerbation; and risk

Bronchodilators. For mild to moderate exacerbations,

factors for asthma-related death.

repeated administration of rapid-acting -inhaledagonists

 

 

 

 

 

 

 

2

 

The physical examination should assess exacerbation

(2 to 4 puffs every 20 minutes for the first hour) is usually

 

 

 

 

 

severity by evaluating the patientis ability to compl

the best and most cost-effective method of achieving rapid

 

 

 

 

 

 

sentence, pulse rate, respiratory rate, use of accessor

reversal of airflow limitation. After the first hour, the dose

OR

 

2

 

 

muscles, and other signs detailedFigurein4.4-2. Any

 

 

complicating factors should be identified (e.g., pneu

exacerbation. Mild exacerbations respond to 2 to 4 puffs

 

 

 

 

 

 

 

 

atelectasis, pneumothorax, or pneumomediastinum).

every 3 to 4 hours; moderate exacerbations will require 6

 

 

 

 

 

to 10 puffs every 1 or 2 hours. Treatment should also be

 

 

 

 

 

 

 

 

Functional assessments such as PEF1 orandFEVarterial

titrated depending upon the individual patientis response,

 

 

 

 

 

 

oxygen saturation measurements are strongly recommend

and if there is a lack of response or other concern about

 

 

 

 

 

 

 

 

as physical examination alone may not fully indicate t

how the patient is responding, the patient should be

 

 

 

 

 

referred to an acute care facility.

 

 

severity of the exacerbation, particularly the degree

 

 

hypoxemiaALTER. Without unduly delaying treatment, a

 

 

 

 

 

213,214

 

 

 

 

 

baseline PEF or FEV1 measurement should be made

Many patients will be able to monitor their PEF after the

 

 

 

 

 

initiation of increased bronchodilator therapy.

before treatment is initiated. Subsequent measure

should be made at intervals until a clear response to

 

 

 

Bronchodilator therapy delivered via a metered-dose NOT

 

 

 

 

 

 

 

 

treatment has occurred.

inhaler (MDI), ideally with a spacer, produces at least an

 

 

 

 

 

equivalent improvement in lung function as the same dose

 

 

 

164,211

DO

Oxygen saturation should be closely monitored, prefera

delivered via nebulizer. At the clinic level,-this route of

 

 

 

 

mg of prednisolone/kg or equivalentMATERIALduring a 24-hour

In adults a chest X-ray is not routinely required, but

delivery is the most cost212effective,provided patients are

by pulse oximetry. This is especially useful in ch

 

 

 

because objective measurements of lung function m

able to use an MDI. No additional medication is necessary

 

 

 

 

 

if the rapid-acting inhaled-agonist produces a complete

difficult. Oxygen saturation in children should no

2

 

 

greater than 95%, and oxygen saturation less than 92% is

response (PEF returns to greater than 80% of predicted or

 

 

 

 

210

 

 

 

a good predictor of the need for hospitalization

personal best) and the response lasts for 3 to 4 hours.(Evidence C

).

 

 

Glucocorticosteroids. Oral glucocorticosteroids (0.5 to 1

 

 

 

 

 

 

COPYRIGHTED

 

 

be carried out if a complicating cardiopulmonary proces

period) should be used to treat exacerbations, especially if

 

 

 

 

 

 

suspected, in patients requiring hospitalization, a

they develop after instituting the other short-term treatment

 

 

 

 

 

those not responding to treatment where a pneumothorax

options recommended for loss of control (see “Stepping up

 

 

 

215

 

 

 

may be difficult to diagnose clinically.Similarly, in children

treatment in response to loss of control” in Component 3).

 

 

 

 

 

 

 

 

routine chest X-rays are not recommended unless ther

If patients fail to respond to bronchodilator therapy, as

 

 

 

 

216

 

 

 

are physical signs suggestive of parenchymal. disea

indicated by persistent airflow obstruction, prompt transfer

 

 

to an acute care setting is recommended, especially if they

 

 

 

are in a high risk group.

 

 

Although arterial blood gas measurements are not

 

 

routinely required, they should be completed in patients

 

 

 

 

 

 

 

216

 

 

 

 

with a PEF of 30 to 50% predicted, those who do not

MANAGEMENT–ACUTE CARE SETTINGS

 

 

 

 

respond to initial treatment, or when there is concern

 

 

 

regarding deterioration. The patient should continue

Severe exacerbations of asthma are life-threatening medical

 

 

 

 

 

 

supplemental oxygen while the measurement is made.

emergencies, treatment of which is often most safely undertaken

 

 

in an emergency departmentFigure. 4.4-2

 

 

A PaO

2

< 60 mm Hg (8 kPa) and a normal or increased

illustrates the

2

(especially > 45 mm Hg, 6 kPa) indicates the

 

 

 

PaCO

approach to acute care-based management of exacerbations. presence of respiratory failure.

66 ASTHMA MANAGEMENT AND PREVENTION

Figure 4.4-2: Management of Asthma Exacerbations in Acute Care Setting

Initial Assessment (see Figure 4.4-1)

•History, physical examination (auscultation, use of accessory muscles, heart rate, respiratory1 , oxygenrate, PEF or FEV saturation, arterial blood gas if patient in extremis)

Initial Treatment

• Oxygen to achieve 2O saturation ≥ 90% (95% in children)

• Inhaled rapid-acting-agonist continuously for one hour. 2

• Systemic glucocorticosteroids if no immediate response, or if patient recently took oral glucocorticosteroid, or

• Sedation is contraindicated in the treatment of▼an exacerbation.

 

 

 

 

 

 

 

 

 

 

 

 

 

Reassess after 1 Hour

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Physical Examination, PEF,2O saturation and other tests as

needed

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

Criteria for Moderate Episode:

 

 

 

 

 

 

 

Criteria for Severe Episode:

 

 

 

 

 

 

 

 

 

 

•

 

 

 

 

 

 

 

 

 

 

 

 

 

REPRODUCE!

 

 

•

PEF 60-80% predicted/personal best

 

 

 

 

 

 

 

History of risk factors for near fatal asthma

 

 

 

 

 

 

 

 

 

•

PEF < 60% predicted/personal best

 

 

 

•

Physical exam: moderate symptoms, accessory muscle

 

 

 

 

 

 

use

Physical exam: severe symptoms at rest, chest retraction

 

Treatment:

 

 

 

 

 

 

 

 

 

 

 

•

 

 

 

 

 

 

 

 

 

 

 

 

•

 

 

 

 

 

 

 

 

 

 

OR

 

 

 

 

 

 

 

• Oxygen

 

 

 

 

 

 

 

 

 

 

 

No improvement after initial treatment

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Treatment:

 

 

 

 

 

 

 

 

 

 

 

 

 

•

Inhaled -agonist and inhaled anticholinergic every

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

60 min

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

2

 

 

 

 

 

 

 

 

 

 

 

 

 

 

•

Oxygen

 

 

 

 

 

 

 

 

 

 

 

 

 

• Oral glucocorticosteroids

 

 

 

 

 

 

 

 

 

 

 

• Inhaled -agonist and inhaled anticholinergic

 

• Continue treatment for 1-3 hours, provided there is

improvement

2

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Systemic glucocorticosteroids

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Intravenous magnesium

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ALTER

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Reassess after 1-2 Hours

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

NOT

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

Good Response within 1-2 Hours:

 

 

Incomplete Response within 1-2

 

 

 

Poor Response within 1-2 Hours:

 

 

 

 

Hours:

 

DO

 

 

 

 

 

 

 

 

 

 

 

• Risk factors for near fatal asthma

 

 

•

Response sustained 60 min after

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

last

 

-

 

 

 

 

 

 

 

 

 

 

 

 

• Physical exam: symptoms severe,

 

 

 

treatment

 

 

 

 

 

•

Risk factors for near fatal asthma

 

 

 

 

 

•

 

 

 

 

 

•

Physical exam: mild to moderate signs

drowsiness, confusion

 

 

Physical exam normal: No distress

 

 

 

 

 

 

•

PEF < 60%

 

 

 

 

 

 

 

 

 

 

 

 

 

 

•

PEF < 30%

 

 

 

•

PEF > 70%

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

•

O 2 saturation not improving

 

 

• PCO

2

> 45 mm Hg

 

 

 

•

O 2 saturation > 90% (95% children)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

•

P O

2

< 60mm Hg

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Admit to Acute Care Setting

 

 

 

 

 

 

 

 

Admit to Intensive Care

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Oxygen

 

 

 

 

 

 

 

 

 

 

 

 

 

• Oxygen

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Inhaled 2 -agonist + anticholinergic

 

 

 

 

 

 

 

 

 

 

 

 

• Inhaled -agonist ± anticholinergic

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Intravenous glucocorticosteroids

 

 

 

 

 

 

 

MATERIAL

2

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Consider intravenous-agonist

 

 

 

 

 

 

 

 

 

 

 

 

• Systemic glucocorticosteroid

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Intravenous magnesium

 

 

 

 

 

 

 

 

 

 

 

 

2

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Consider intravenous theophylline

 

 

 

 

 

 

 

 

 

 

 

 

• Monitor PEF, O 2 saturation, pulse

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Possible intubation and mechanical

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ventilation

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Reassess at intervals

 

▼

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

Improved: Criteria for Discharge Home

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Poor Response (see above):

 

 

• PEF > 60% predicted/personal best

 

 

 

 

 

 

 

 

 

 

 

 

 

 

•

Admit to Intensive Care

 

 

 

• Sustained on oral/inhaled medication

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Incomplete response in 6-12 hours

 

 

Home Treatment:

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

•

COPYRIGHTED

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

(see above)

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Continue inhaled-agonist

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

2

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

• Consider admission to Intensive

Care

 

• Consider, in most cases, oral glucocorticosteroids

 

 

 

 

 

 

 

 

 

• Consider adding a combination inhaler

 

 

 

 

 

 

 

 

 

 

 

 

 

if no improvement within 6-12 hours

 

• Patient education: Take medicine correctly

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Review action plan

 

 

 

 

 

 

 

 

 

 

 

▼

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Improved (see opposite)

 

 

 

 

 

 

Close medical follow-up

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ASTHMA MANAGEMENT AND PREVENTION

67

Treatment Additional bronchodilators.

The following treatments are usually administeredIpratropium bromideAcombination. of nebulized- 2

concurrently to achieve the most rapid resolution ofagonistthe with an anticholinergic (ipratropium bromide)

exacerbation:

may produce better bronchodilation than either drug

217

 

2

alone231 (Evidence B ) and should be administered before

REPRODUCE!

Oxygen. To achieve arterial oxygen saturation of ≥ 90%

methylxanthines are considered. Combination-

 

2

(≥ 95% in children), oxygen should be administered byagonist/anticholinergic therapy is associated with l

nasal cannulae, by mask, or rarely by head box in some

 

hospitalization rates(Evidence A ) and greater

 

 

 

 

 

 

 

 

212,232,233

 

infants. PaCO2 may worsen in some patients on 100

 

improvement in PEF and FEV1 233

(Evidence B ). Similar

percent oxygen, especially those with more severe airflow

 

212

 

 

 

 

 

 

data have been reported in the pediatric literature

obstruction. Oxygen therapy should be titrated against

 

 

 

 

218

 

 

 

 

 

(Evidence A ). However, once children with asthma are

 

 

 

 

 

 

pulse oximetry to maintain a satisfactory oxygen. saturat

on

 

 

 

 

 

 

219

 

hospitalized following intensive emergency departm

 

 

 

 

 

 

Rapid-acting inhaled ß2–agonists.

Rapid-acting inhaled

 

treatment, the addition of nebulized ipratropium brom

 

nebulized-agonist and systemic glucocorticosteroids

-agonists should be administered at regular220-222 intervals

2

 

234

2

 

 

 

 

 

appears to confer no extra benefit.

(Evidence A

). Although most rapid-acting- onists

 

 

 

 

OR

235

 

 

 

 

 

 

have a short duration of effect, the long-acting broncho-

 

 

 

 

 

 

 

 

 

TheophyllinIn.e view of the effectiveness and relati

dilator formoterol, which has both a rapid onset of action

 

 

 

 

 

 

 

 

 

safety of rapid-acting-agonists, theophylline has a

and a long duration of effect, has been shown to be

 

 

 

 

2

 

 

minimal role in the management of acute asthma.Its

equally effective without increasing side effects, though

 

 

it is considerably more expensive. The importance of

 

use is associated with severe and potentially fatal s

 

effects, particularly in those on long-term therapy w

 

 

148

 

 

 

 

 

 

 

 

this feature of formoterol is that it provides support and

 

 

reassurance regarding the use of a combination of

 

sustained-release theophylline, and their bronchodila

 

effect is less than-thatagonistsof . The benefit as

 

 

 

 

 

NOT

ALTER

2

 

formoterol and budesonide early in asthma exacerbations.

 

 

 

 

 

 

 

add-on treatment in adults with severe asthma exacer-

 

 

 

 

 

 

bations has not been demonstrated. However, in one

A modestly greater bronchodilator effect has been shown

 

 

 

 

 

 

 

 

 

study of children with near-fatal asthma, intravenou

with levabuterol compared to racemic albuterol in both

 

 

 

 

adults and children with an asthma exacerbation. In

 

theophylline provided additional benefit to patients

 

 

 

 

223-226

 

receiving an aggressive regimen of inhaled and

large study of acute asthma in children,and in adults not

intravenous-agonists, inhaled ipatropium bromide, and

 

 

227

 

 

 

 

 

 

 

 

previously treated with glucocorticosteroids, levabuterolDO

 

 

 

2

 

 

 

 

 

226

-

 

 

 

 

 

 

 

 

 

 

intravenous systemic glucocorticosteroids.

 

 

MATERIAL

 

 

 

 

 

236

treatment resulted in lower hospitalization rates compared

 

 

to racemic albuterol treatment, but in children the length of

 

Systemic

 

227

 

 

 

 

Systemic glucocorticosteroids.

hospital stay was no different.

 

 

 

glucocorticosteroids speed resolution of exacerbation

 

 

 

 

 

 

 

 

 

 

 

 

should be utilized in the all but the mildest

Studies of intermittent versus continuous nebulized short237,238-

 

 

 

 

 

 

 

 

exacerbations (Evidence A ), especially if:

acting -agonists in acute asthma provide conflicting

 

 

 

results. In a systematic review of,sixtherestudieswere

 

• The initial rapid-acting inhaled-agonist therapy fails

2

 

 

 

228

 

 

 

 

 

 

no significant differences in bronchodilator effect or

 

2

COPYRIGHTED

 

 

 

 

 

to achieve lasting improvement

hospital admissions between the two treatments. In

• The exacerbation develops even though the patient

 

 

 

 

229

 

 

patients who require hospitalization, onefoundstudy

 

 

was already taking oral glucocorticosteroids

that intermittent on-demand therapy led to a significantly

 

 

 

 

 

 

 

 

 

• Previous exacerbations required oral

shorter hospital stay, fewer nebulizations, and fewerglucocorticosteroids.

 

palpitations when compared with intermittent therapy given

 

 

every 4 hours. A reasonable approach to inhaled therapy

 

Oral glucocorticosteroids are usually as effective as

in exacerbations, therefore, would be the initial use of

 

 

 

 

 

 

 

 

 

administered intravenously and are preferred because

continuous therapy, followed by intermittent on-demand

 

 

239,240

 

 

 

 

 

 

route of delivery is less invasive and less. expensi

therapy for hospitalized patients. There is no evidence to

 

 

support the routine use of intrave-agonousits in

 

If vomiting has occurred shortly after administrati

 

glucocorticosteroids, then an equivalent dose should

 

 

2

230

 

 

patients with severe asthma exacerbations.

 

re-administered intravenously. In patients dischar

 

 

 

 

 

 

Epinephrine.

 

 

 

 

 

the emergency department, intramuscular administrat

A subcutaneous or intramuscular injection

241

 

 

 

 

 

 

 

 

may be helpful, especially if there are concerns about

of epinephrine (adrenaline) may be indicated for acute

 

 

 

 

treatment of anaphylaxis and angioedema, but is not

compliance with oral therapy. Oral glucocorticosteroids

require at least 4 hours to produce clinical improvemen

routinely indicated during asthma exacerbations.

 

Daily doses of systemic glucocorticosteroids equival

68 ASTHMA MANAGEMENT AND PREVENTION

60-80 mg methylprednisolone as a single dose, or 300-400

Leukotriene modifiers. There is little data to suggest a

mg hydrocortisone in divided doses, are adequate for role for leukotriene modifiers in acute. asthma

 

258

hospitalized patients, and 40 mg methylprednisolone or

200 mg hydrocortisone is probably adequate in most

Sedatives. Sedation should be strictly avoided during

cases238,242 (Evidence B ). An oral glucocorticosteroid dose exacerbations of asthma because of the respiratory

of 1 mg/kg daily is adequate for treatment of exacerbationsdepresant effect of anxiolytic and hypnotic drugs.

in children with mild persistent. A 7-dasthmaycourse

 

 

REPRODUCE!

association between the use of these drugs and avoida

 

 

243

 

has been demonstrated.

in adults has been found to be as effective as a 14-dayasthma deaths

 

 

 

209,259

 

course , and a 3- to 5-day course in children is usually

 

 

244

 

 

 

 

 

considered appropriateEvidence(

B ). Current evidence

Criteria for Discharge from the Emergency Department

suggests that there is no benefit to tapering thevsdose. Hospitalizationof

 

oral glucocorticosteroids, either in the shortover-term

 

 

 

several weeks(Evidence B

).

245

Criteria for determining whether a patient should be

246

 

 

 

 

 

 

 

 

discharged from the emergency department or admitted

Inhaled glucocorticosteroids.

Inhaled glucocortico-

the hospital have been succinctly reviewed and strat

steroids are effective as part of therapy for asthmabased on consensus260 . Patients with a pre-treatment exacerbations. In one study, the combination of highFEV-doseor PEF < 25% percent predicted or personal best, or inhaled glucocorticosteroids and salbutamol in acutethose1 with a post-ORtreatment1 orFEVPEF < 40% percent

asthma provided greater bronchodilation than salbutamolpredicted or personal best, usually require hospitali alone247 (Evidence B ), and conferred greater benefit thanPatients with post-treatment lung function of 40-60% the addition of systemic glucocorticosteroids acrosspredictedall may be discharged, provided that adequate parameters, including hospitalizations, especiallyfollowfor -up is available in the community and compliance

patients with more severe attacks.

 

 

 

assured. Patients with post-treatment lung functi

 

 

248

 

 

 

 

 

 

 

 

 

 

 

 

 

≥ 60% predicted can be discharged.

 

 

 

 

 

NOT

ALTER

Inhaled glucocorticosteroids can be as effective as oral

glucocorticosteroids at preventing relapses.Patients

 

Management of acute asthma in the intensive care uni

 

 

249,250

 

 

 

 

 

 

 

 

 

 

 

 

 

beyond the scope of this document and readers are

discharged from the emergency department on prednisone

 

 

 

 

 

 

 

referred to recent comprehensive261reviews.

and inhaled budesonide have a lower rate of relapse than

 

 

 

those on prednisone alone(Evidence B ). A high-dose

 

 

 

 

 

 

237

 

 

 

 

 

 

 

 

 

 

 

 

 

 

For patients discharged from the emergency departmen

of inhaled glucocorticosteroid (2.4 mg budesonide daily in

 

 

 

 

-

 

to 40

 

 

four divided doses) achieves a relapse rate similarDO

 

 

 

 

MATERIAL

 

 

 

• Ipratropium bromide is unlikely to provide addition

mg oral prednisone daily(Evidence ). Cost is a

 

 

 

• At a minimum, a 7-day course of oral glucoco-

 

251

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

rticosteroids for adults and a shorter course

significant factor in the use of such high-doses of inhaled

 

 

 

 

 

 

 

 

(3-5 days) for children should be prescribed, along wi

glucocorticosteroids, and further studies are required to

document their potential benefits, especially cost

 

continuation of bronchodilator therapy.

 

252

 

 

 

 

 

• The bronchodilator can be used on an as-needed

effectiveness, in acute. asthma

 

 

 

 

 

basis, based on both symptomatic and objective

 

 

 

 

 

 

 

 

Magnesium.

Intravenous magnesium sulphate (usually improvement, until the patient returns to his or

given as a single 2 g infusion over 20 minutes) is not

exacerbation use of rapid-acting inhaled-agonists.

 

2

COPYRIGHTED

 

 

 

 

 

 

 

 

recommended for routine use in asthma exacerbations,

 

benefit beyond the acute phase and may be quickly

but can help reduce hospital admission rates in certain

 

patients, including adults1 25with-30% predictedFEV

at

 

 

 

discontinued.

 

 

 

 

 

 

 

• Patients should initiate or continue inhaled gluc

presentation, adults and children who fail to respond to

 

initial treatment, and children whose1 failsFEVto improve

 

 

corticosteroids.

above 60% predicted after 1 hour of care (Evidence A ).

 

 

• The patientis inhaler technique and use of peak flo

 

 

253,254

 

 

 

 

 

meter to monitor therapy at home should be reviewed.

Nebulized salbutamol administered in isotonic magnesium

 

 

 

 

 

 

 

 

Patients discharged from the emergency departmen

sulfate provides greater benefit than if it is delivered in

 

255,256

 

 

 

 

 

 

with a peak flow meter and action plan have a better

normal saline (Evidence A ). Intravenous magnesium

 

 

response than patients discharged without these

sulphate has not been studied in young children.

 

 

 

 

 

 

 

8

 

 

 

 

 

 

 

 

resources.

 

 

 

 

 

 

 

• The factors that precipitated the exacerbation shou

Helium oxygen therapy. A systematic survey of studiesbe identified and strategies for their future a

that have evaluated the effect of a combination of helium

 

implemented.

and oxygen, compared to helium alone, suggests there is

 

• The patientis response to the exacerbation should be

no routine role for this intervention. It might be considered

for patients who do not respond to standard therapy.

evaluated. The action plan should be reviewed and

written guidance provided.

257

 

ASTHMA MANAGEMENT AND PREVENTION

69

•Use of controller therapy during the exacerbation shouldPregnancy be reviewed: whether this therapy was increased

promptly, by how much, and, if appropriate, why oral During pregnancy the severity of asthma often change

glucocorticosteroids were not added. Consider

and patients may require close follow-up and adjustme

providing a short course of oral glucocorticosteroidsofmedicationsto

. In approximately one-third of women

be on hand for subsequent exacerbations.

asthma becomes worse; in one-third asthma becomes

the emergency department for follow-up with specialistwomen without asthma. ForREPRODUCE!this reason, using

 

less severe; and in the remaining one-third it remain

• The patient or family should be instructed to contaunchangedt during pregnancy.

 

 

 

265-267

the primary health care professional or asthma

 

 

 

specialist within 24 hours of discharge. A followAlthough-up

there is a general concern about the use of any

appointment with the patient's usual primary caremedication in pregnancy, poorly controlled asthma can professional or asthma specialist should be madehave an adverse effect on the fetus, resulting in i within a few days of discharge to assure that treatmentperinatal mortality, increased prematurity, and low bir is continued until baseline control parameters,weight266,267 . The overall perinatal prognosis for children

including personal best lung function, are reachedborn. to women with asthma that is well-managed during

Prospective data indicate that patients dischargedpregnancyfrom is comparable to that for children born to

 

 

 

 

 

 

 

 

OR

care do better than patients returned to routine.

 

 

 

 

268

caremedications to obtain optimal control of asthma is jus

 

262

 

 

 

ALTER

 

 

 

 

 

even when their safety in pregnancy has not been

An exacerbation severe enough to require hospitalization

 

 

 

 

 

 

 

 

unequivocally proven. For most medications used to tr

may reflect a failure of the patientis self-management plan.

 

 

 

 

 

 

asthma there is little evidence to suggest an increa

Hospitalized patients may be particularly receptive to

 

 

 

 

 

 

 

 

to the fetus. Appropriately monitored use of theophyll

information and advice about their illness. Health care

 

 

 

351

 

 

 

 

inhaled glucocorticosteroids, -agonists, and

providers should take the opportunity to review patient

 

 

 

2

 

 

 

NOT

 

 

 

 

 

 

 

leukotriene modifiers (specifically montelukast) i

understanding of the causes of asthma exacerbation ,

 

 

 

 

avoidance of factors that may cause exacerbations

 

associated with an increased incidence of fetal

 

abnormalities. Inhaled glucocorticosteroids have been

 

 

 

 

 

 

 

369

 

(including, where relevant smoking cessation), theshown to prevent exacerbations of asthma during

purposes and correct uses of treatment, and the actions

 

269,270

(Evidence B ). As in other situations, the

to be taken to respond to worsening symptoms or peak

 

pregnancy

 

focus of asthma treatment must remain on control of

flow values(Evidence A ).

-

 

 

 

 

 

 

271

263

DO

 

symptoms and maintenance of normal lung function.

 

 

 

MATERIAL

 

Acute exacerbations should be treated aggressively in

Referral to an asthma specialist should be considered for

 

 

 

 

hospitalized patients. Following discharge from

 

order to avoid fetal hypoxia. Treatment should include

 

nebulized rapid-acting-agonists and

continuous supervision, the patient should be reviewed by

 

2

 

 

 

 

oxygen and systemic glucocorticosteroids should be

the family health care professional or asthma specialist

 

 

 

 

 

 

 

instituted when necessary.

regularly over the subsequent weeks until personal best

 

 

 

lung function is reached. Use of incentives improves

 

 

 

 

 

 

 

 

While all patients should have adequate opportunity to

primary care follow up but has shown no effect on long

 

 

 

 

COPYRIGHTED

 

 

 

discuss the safety of their medications, pregnant p

term outcomes. Patients who come to the emergency

 

 

 

 

 

 

264

 

 

 

with asthma should be advised that the greater risk t

department with an acute exacerbation should be

 

 

baby lies with poorly controlled asthma, and the safety

especially targeted for an asthma education program, if

 

 

 

 

one is available.

 

 

 

most modern asthma treatments should be stressed. Ev

 

 

 

with a good patient/health care professional relationsh

 

 

 

 

 

 

 

 

independent printed material, such as a statement fr

COMPONENT 5: SPECIAL

 

 

 

the US National Asthma Education and Prevention

 

 

 

 

Program on the treatment of asthma during pregnancy,

CONSIDERATIONS

 

 

 

 

 

 

 

272

 

 

 

 

 

 

 

265,273

 

 

 

 

will provide important additional reassurance.

 

 

 

 

Special considerations are required in managing asthma

Surgery in relation to pregnancy; surgery; rhinitis, sinusitis, and

nasal polyps; occupational asthma; respiratory infections;

Airway hyperresponsiveness, airflow limitation, and gastroesophageal reflux; aspirin-induced asthma; and

anaphylaxis.

mucus hypersecretion predispose patients with asth

intraoperative and postoperative respiratory complicati

70 ASTHMA MANAGEMENT AND PREVENTION

The likelihood of these complications depends on the

severity of asthma at the time of surgery, the typeTreatmentof of rhinitis may improve asthma286,287symptoms surgery (thoracic and upper abdominal surgeries pose(theEvidence A ). Anti-inflammatory agents including greatest risks), and type of anesthesia (general anesthesiaglucocorticosteroids and cromones as well as leukotrie with endotracheal intubation carries the greatest risk)modifiers. and anticholinergics can be effective in

These variables need to be assessed prior to surgeryconditionsand

. However, some medications are selectivel

be rapidly reduced 24 hours following surgery, as

Rhinitis and its ImpactREPRODUCE!on Asthma (ARIA) initiative can

pulmonary function should be measured. If possible,effectivethis

against rhinitis1 -antagonists)(e. ., H and others

evaluation should be undertaken several days before against asthma (e.g.2,-agonists)288 (Evidence A ). Use of surgery to allow time for additional treatment. In particular,intra-nasal glucocorticosteroids for concurrent rhin if the patientis1 isFEVless than 80% of personal best, a been found to have a limited benefit in improving as brief course of oral glucocorticosteroids should be and reducing asthma morbidity in some but not all

 

274,275

).

 

289-291

 

 

125,292

considered to reduce airflow limitation(Evide ce C

studies. Leukotriene modifiers, allergen-specific

Furthermore, patients who have received systemic

 

 

284,293

 

294,295

immunotherapy , and anti-IgE therapy are effective

 

 

 

in both conditionsEvidence(

A ).

glucocorticosteroids within the past 6 months should have

 

 

 

systemic coverage during the surgical period (100 mg

 

 

 

 

 

 

 

Additional information on this topic from the Allergi

hydrocortisone every 8 hours intravenously). This should

 

 

 

 

 

 

 

 

 

 

 

284

 

 

 

found at http://www.whiar..org

prolonged systemic glucocorticosteroid therapy may inhibit

 

OR

 

276

 

 

 

 

 

 

wound healing(Evidence C ).

 

 

 

 

 

 

 

 

 

Sinusitis. Sinusitis is a complication of upper respir

Rhinitis, Sinusitis, and Nasal Polyps

 

infections, allergic rhinitis, nasal polyps, and othe

 

 

 

nasal obstruction. Both acute and chronic sinusitis c

 

 

 

worsen asthma. Clinical features of sinusitis lack

Upper airway diseases can influence lower airway function

296

 

 

 

 

 

diagnostic precision, and CT Scan confirmation is

in some patients with asthma. Although the mechanisms

ALTER

 

 

 

 

 

recommended when available. In children with suspec

behind this relationship have not been established,

 

 

 

 

 

 

 

rhinosinusitis, antibiotic therapy for 10 days is

inflammation likely plays a similarly critical role in the

(Evidence B

 

 

 

 

recommended297

). Treatment should also

pathogenesis of rhinitis, sinusitis, and nasal polyps as

 

 

 

in asthma.

 

NOT

 

 

 

 

 

 

include medications to reduce nasal congestion, such

 

 

 

topical nasal decongestants or topical nasal or even

Rhinitis. The majority of patients with asthmaDOhave a systemic glucocorticosteroids. These agents remain

 

-

 

 

 

 

279,288

 

 

 

secondary to primary asthma therapies.

history or evidence of rhinitis and up to 30% of patients

 

 

 

 

 

277,278

 

 

 

 

 

 

with persistent rhinitis have or develop. asthma

Nasal polyps. Nasal polyps associated with asthma and

 

 

 

Rhinitis frequently precedes asthma, and is both a risk

 

 

 

298

factor for the development of279asthmaandis associated

 

 

 

 

rhinitis, and sometimes with aspirin hypersensit, are

 

 

 

seen primarily in patients over 40 years old. Between 36%

with increased severity and health resource use in

 

 

 

 

280

 

 

and 96% of aspirin-intolerant patients have polyps, and

asthma . Rhinitis and asthma share several risk factors:

 

 

 

 

 

 

 

29% to 70% of patients with nasal polyps may have

common indoor and outdoor allergens such as house dust

298,299

 

 

 

 

 

 

asthma . Children with nasal polyps should be

mites, animal dander, and, less commonly, pollen affecting

 

 

 

281,282

MATERIAL

283

assessed for cystic fibrosis and immotile cilia sy

both the nose and bronchi, occupational sensitizers,

 

 

 

 

 

and non-specific factors like aspirin. For these reasons,

 

 

 

the Allergic Rhinitis and its Impact on Asthma (ARIA)

Nasal polyps are quite responsive to topical

 

 

288

 

 

 

 

 

glucocorticosteroids. A limited number of patients with

initiative recommends that the presence of asthma must

 

 

 

 

 

 

glucocorticosteroid-refractory polyps may benefit from

be considered in all patients with rhinitis, and that in

 

 

 

 

 

284

 

 

 

 

 

planning treatment, both should be considered.together

 

 

 

 

 

 

 

Occupational Asthma

 

Both asthma and rhinitis are considered to be

 

Once a diagnosis of occupational asthma is established

 

 

 

inflammatory disorders of the airway, but there are some

 

 

 

 

 

 

 

complete avoidance of the relevant exposure is ideally

differences between the two conditions in mechanisms,

 

 

300-302

 

 

 

important component of management. Occupational

clinicalCOPYRIGHTEDfeatures, and treatment approach. Although the

 

 

 

 

 

 

 

asthma may persist even several years after removal f

inflammation of the nasal and bronchial mucosa may be

 

 

 

 

 

 

 

exposure to the causative agent, especially when the

similar, nasal obstruction is largely due to hyperemia in

 

 

 

 

 

 

patient has had symptoms for a long time before cessat

rhinitis, while airway smooth muscle contraction plays a

303,304

 

 

 

285

 

 

of exposure . Continued exposure may lead to increasingly

dominant role in asthma.

 

 

 

 

 

 

 

ASTHMA MANAGEMENT AND PREVENTION

71

can often persist for weeks after the infection isphysicalcleared,examination often reveals nasal polyps. Asth anti-inflammatory treatment should be continued forandthishypersensitivity to aspirin often develop subs

 

 

305

 

Gastroesophageal Reflux

 

 

severe and potentially fatal asthma exacerbations,

 

 

lower probability of subsequent remission, and, ultimately,

 

 

 

 

 

 

 

 

306

 

The relationship of increased asthma symptoms,

permanently impaired lung function. Pharmacologic

 

therapy for occupational asthma is identical to theraparticularlyfor

at night, to gastroesophageal reflux remai

other forms of asthma, but it is not a substitute uncertain,for

although this condition is nearly three t

 

 

 

 

prevalent in patients with asthma compared to the gene

adequate avoidance. Consultation with a specialist in

 

 

. Some of these patients also have a hiatal

 

 

 

 

 

 

318,319

 

 

 

 

population

asthma management or occupational medicine is advisable.

 

 

 

 

 

 

 

 

 

 

 

 

hernia; furthermore, theophylline 2and-agonistsoral

may

The British Occupational Health Research Foundation

increase the likelihood of symptoms by relaxing the l

 

 

 

 

esophageal ring.

 

 

 

 

Guidelines for the prevention, identification, and

 

 

 

 

 

 

 

 

management of occupational asthma are available at

A diagnosis of gastroesophageal reflux in patients wi

http://www.bohrf.org.uk/downloads/asthevre.pdf.

 

 

 

 

asthma can best be made by simultaneously monitoring

Respiratory Infections

 

 

 

esophageal pH and lung function. Medical management

 

 

 

 

should be given for the relief of reflux symptoms a

 

 

 

 

often effective. Patients may be advised to eat smal

Respiratory infections have an important relationship to

 

 

 

 

 

 

 

 

asthma as they provoke wheezing and increased

 

more frequent meals; avoid food or drink between meals

 

 

 

 

 

 

 

REPRODUCE!

 

307

 

 

 

and especially at bedtime; avoid fatty meals, alcohol,

symptoms in many patients. Epidemiological studies

theophylline, and oral-agonists; use proton pump

 

 

 

 

 

 

have found that infectious microorganisms associated

 

 

 

 

2

 

 

 

 

 

 

 

 

 

 

 

 

OR

 

and elevate the head of the

 

 

 

 

inhibitors -orantagonists;H

with increased asthma symptoms are often respiratory

 

 

2

 

 

 

 

 

308

309

 

 

bed. However, the role of anti-reflux treatment in as

viruses, but seldom bacteria. Respiratory syncytial

control is unclear, as it does not consistently improv

 

 

45

 

virus is the most common cause of wheezing ,in infancy

 

 

 

 

 

 

 

 

 

 

 

 

function, asthma symptoms, nocturnal asthma, or the u

while rhinoviruses (which cause the common cold), are the

 

 

 

 

 

 

 

 

 

 

 

 

of asthma medications in subjects with asthma but

principal triggers of wheezing and worsening of asthma in

 

 

 

 

 

 

310

 

 

 

 

ALTER

 

 

 

 

 

 

 

clear reflux-associated respiratory symptoms. Subgro

older children and adults. Other respiratory viruses,

of patients may benefit, but it appears difficult t

such as parainfluenza, influenza, adenovirus, and

 

 

 

 

 

 

 

320

 

 

 

 

 

which patients will respond to this. therapy

 

coronavirus, are also associated with increased wheezing

 

 

 

 

 

 

 

 

311

 

 

 

NOT

 

 

 

 

 

 

 

 

and asthma symptoms. Adults with asthma may be at

Surgery for gastroesophageal reflux is reserved for t

 

 

370

 

increased risk of serious pneumococcal disease.

severely symptomatic patient with well-documented

 

 

 

DO

 

 

 

esophagitis and failure of medical management. In pat

 

 

-

A number of mechanisms have been identified that explain

 

 

 

 

 

 

 

 

 

 

 

with asthma, it should be demonstrated that the refl

why respiratory infections trigger wheezing and increased

 

 

 

 

321,322

 

airway responsiveness, including damage to airway

causes asthma symptoms before surgery is advised.

epithelium, stimulation of virus-specific IgE antibody,

 

 

 

 

 

 

 

enhanced mediator release, and the appearance of a late

Aspirin-Induced Asthma (AIA)

 

 

 

 

312

 

 

 

 

 

 

 

 

 

 

asthmatic response to inhaled antigen. hus, there is

Up to 28% of adults with asthma, but rarely children wit

evidence that viral infections are an “adjuvant” to the

 

 

 

 

 

 

 

 

 

 

 

 

asthma, suffer from asthma exacerbations in respons

inflammatory response and promote the development of

 

 

 

 

 

 

 

 

 

 

MATERIAL

 

aspirin and other nonsteroidal anti-inflammatory drug

 

 

313

 

 

 

 

 

 

 

 

 

 

airway injury by enhancing airway inflammation.

(NSAIDs). This syndrome is more common in severe

 

 

 

 

 

 

 

 

 

323

 

 

 

 

 

 

 

 

 

 

 

asthma .

 

 

 

 

 

 

 

Treatment of an infectious exacerbation follows the same

 

 

 

 

 

 

 

principles as treatment of other asthma exacerbations—

 

 

 

 

 

 

 

 

that is, rapid-acting inhaled-agonists and early

 

The clinical picture and course of aspirin-induced as

 

 

 

 

 

 

324

 

 

 

2

 

 

 

(AIA) are characteristic. The majority of patients first

introduction of oral glucocorticosteroids or increases in

 

 

 

 

 

 

 

 

 

 

 

experience symptoms, which may include vasomotor

inhaled glucocorticosteroids by at least four-fold a e

 

 

 

 

 

 

 

 

recommended. Because increased asthma symptoms

rhinitis and profuse rhinorrhea, during the third to

decade of life. Chronic nasal congestion evolves, and

COPYRIGHTED

 

 

 

 

 

 

 

 

 

 

 

full period to ensure adequate control.

The hypersensitivity to aspirin presents a unique

 

within minutes to one or two hours following ingest

The role of chronic infectionChlamydiawithpneumoniae

aspirin, an acute, often severe, asthma attack develops,

and Mycoplasma pneumoniae in the pathogenesis or

and is usually accompanied by rhinorrhea, nasal

314

obstruction, conjunctival irritation, and scarlet fl

worsening of asthma is currently unc.Thertainbenefit

315-317

head and neck. This may be provoked by a single aspirin

from macrolide antibiotics remains unclear.

72 ASTHMA MANAGEMENT AND PREVENTION

or other cyclooxygnease-1 (COX-1) inhibitor and include Generally, asthma patients, especially those with adu violent bronchospasm, shock, loss of consciousness,onsetand asthma and associated upper airway disease (nasal

even respiratory arrest.

polyposis), should be counseled to avoid NSAIDs, taking

325,326

 

 

 

acetominophen/paracetemol instead.

Persistent marked eosinophilic inflammation, epithelial

 

disruption, cytokine production, and upregulation of

 

 

Anaphylaxis and Asthma

 

insect stings and bites,REPRODUCE!latex hypersensitivity,-

adhesion molecules are found in the airways of patients

 

with AIA . Airway expression of interleukin-5 (IL-5),Anaphylaxis is a potentially life-threatening condit

327,328

 

 

which is involved in recruitment and survival of eosinophils,

 

is also increased. AIA is further characterized by

can both mimic and complicate severe asthma. Effectiv

treatment of anaphylaxis demands early recognition of

328

 

 

increased activation of cysteinyl leukotriene pathways,

 

 

event. The possibility of anaphylaxis should be cons

which may be partly explained by a genetic polymorphism

 

 

in any setting where medication or biological substan

of the LTC4 synthase gene found in about 70% percent of

 

patients. However, the exact mechanism by which

are given, especially by injection. Examples of documen

329

causes of anaphylaxis include the administration of

 

aspirin triggers bronchoconstriction remains. unknown

 

330

allergenic extracts in immunotherapy, food intoleranc

 

 

(nuts, fish, shellfish, eggs, milk), avian-based vacc

The ability of a cyclooxygenase inhibitor to trigger reactions

OR

 

depends on the drug's cyclooxygenase inhibitory potency,

 

329

lactam antibiotics, aspirin and NSAIDs, and angiotensin

as well as on the individual sensitivity. of the patient

 

 

converting enzyme (ACE) inhibitors), and exercise.

A characteristic history of reaction is considered adequate

 

 

Symptoms of anaphylaxis include flushing, pruriti

for initiating avoidance strategies. However, the diagnosis

 

 

urticaria, and angioedema; upper and lower airway

can only be confirmed by aspirin challenge, as there are

 

 

involvement such as stridor, dyspnea, wheezing, or apn

no suitablein vitrotests for diagnosis. The aspirin challenge

 

 

dizziness or syncope with or without hypotension; and

test is not recommended for routine practice as it is associatedALTER

 

 

gastrointestinal symptoms such as nausea, vomiting

with a high risk of potentially fatal consequences and must

 

 

cramping, and diarrhea. Exercise-induced anaphylaxis,

only be conducted in a facility with cardiopulmonary

 

 

often associated with medication or food allergy, is a

resuscitation capabilities. Further safeguards are thatNOTunique physical allergy and should be differentiate

331

 

 

patients should only be challenged when their asthma is in

 

remission and their1 isFEVgreater than 70% of predicted exercise-induced bronchoconstriction.

or personal best. Bronchial (inhalational) and nasalDO

 

 

338

Airway anaphylaxis could account for the sudden onset o

 

 

-

challenges with lysine aspirin are safer than oral challenges

 

 

 

332,333

asthma attacks in severe asthma and the relative

and may be performed in specialized centers.

resistance of these attacks to increased -doses of

Once aspirin or NSAID hypersensitivity develops, it is

 

2

 

 

 

agonists. If there is a possibility that anaphylaxis

 

 

 

 

180

 

present for life. Patients with AIA should avoid aspirin,

 

 

 

 

involved in an asthma attack, epinephrine should be th

products containing it, other analgesics that inhibit COX-1,

 

 

 

334

bronchodilator of choice. Prompt treatment for

and often also hydrocortisone hemisuccinate. Avoid-

anaphylaxis is crucial and includes oxygen, intramus

ance does not prevent progression of the inflammatory

 

 

disease of the respiratory tract. Where an NSAID is

epinephrine, injectable antihistamine, intravenous

COPYRIGHTED

MATERIAL

hydrocortisone, oropharyngeal airway, and intravenous

indicated, a cyclooxygenase-2 (COX-2) inhibitor may be

fluid. Preventing a recurrence of anaphylaxis depend

352

 

 

consideredwith appropriate physician supervision and

 

 

 

 

335

identifying the cause and instructing the patient

observation for at least one hour after administration

 

 

(Evidence B

 

 

avoidance measures and self-administered emergency

). Glucocorticosteroids continue to be the

 

 

 

 

 

treatment with pre-loaded epinephrine339syringes.

mainstay of asthma therapy, but leukotriene modifiers may

 

also be useful for additional control of the underlying

 

disease

(Evidence B ). For NSAID-sensitive patients

 

 

 

332,336

 

 

 

 

 

with asthma who require NSAIDs for other medical

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74 ASTHMA MANAGEMENT AND PREVENTION

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