4. Pathophysiology
Trigger factors cause bronchial hyperactivity leading
to bronchoconstriction, mucosal edema and increased
mucus secretion.
Results in airway obstruction, decrease in lung
compliance, alveolar hypoventilation, pulmonary
vasoconstriction and decreased production of
surfactant.
Hypercapnea, acidosis, respiratory failure may occur if
it persists
5.
6. Trigger Factors in
Asthma
Viral Infections
Dusts and pollutants incl. cigarette smoke
Allergens – house dust
mite, pollens, moulds, spores, animal dander and
feathers, certain foods, etc
Exercise
Changes in weather patterns and cold air
Psychological factors eg. Stress and emotion
7. Classification –based on
risk factors and prognosis
Transient Infant Wheezers- wheeze early in life but
no subseq. increased risk of developing persistent
asthma. Risk factor is low lung function in early life
that persists until adolescence
Atopic Asthma – Sx appear early in life but persist
into childhood and adolescence. More likely to have
+ve skin test to allergens, bronchial hyper-
responsiveness to trigger factors and increased daily
peak flow variability. Sxx are severe and deficits in
lung function, tho absent immediately after birth, are
present by the age of 6yrs
8. Non-atopic asthma – May have early or late onset of
Sxx but are usually not skin test +ve to allergens by
age 6.
Other atopic dxx are common eg. Eczema, vernal
conjunctivitis and allergic rhinitis(Samter’s triad).
Strong ass. with total serum IgE and Increased daily
peak flow variability.
9. Clinical Classification
Mild, Infrecquent Asthma(75% of pts) –attacks occurring
less than once a month
Frequent episodic asthma(20%) – more than one episode
every week with symptom free intervals
Chronic Asthma(4%) – low grade wheeze present most
days; wheeze with exertion, nocturnal cough and some
limitation of physical activity
Severe Chronic Asthma(1%) – Sxx present everyday with
stunting of growth and barrel chest deformity, and marked
limitation of activity
10. ER Management
Brief Hx:
time of onset of current exacerbation
current medications and allergies
recent frequent use of beta2-agonists
risk factors for severe, uncontrolled disease (e.g. ER visits, admissions to
the hospital and ICU, and prior intubations)
Age of onset – poorer prognosis with earlier onset
Frequency of attacks
Prev or current atopic dermatitis/allergic rhinitis
Persistent nocturnal cough(cough-variant asthma)
Exposure to asthma triggers
Use of peak flow with home management respiratory score
11. PE
Level of Consciousness, Ability to speak in full
sentences, color, pulse, blood pressure, shape of
chest, FAN, Use of accessory muscles of
resp, RR, AE, PN, BS, Rhonchi, Creps, etc
PEFR
Pulse oximetry
STOP THE PE AND PROCEED TO RESUSCITATE IF
THERE IS: SILENT CHEST(imminent resp failure) or
CEREBRAL HYPOXEMIA(Mental
agitation, drowsiness and confusion)
12. Classification of Asthma Severity
Clinical Features Mild Moderate Severe Life-threatening
asthma
Mental Status Normal Might look agitated Usually Agitated Drowsy of Confused
Activity Normal Activity,
Exertional dyspnea
Decreased Activity
or feeding(infant)
Decreased activity,
infant stops feeding
Unable to eat
Speech Normal Speaks in phrases Speaks in words Unable to speak
Work of breathing Minimal intercostal
retractions
Intercostal and
substernal
retractions
Signif. resp distress.
FAN+, ICR+, SCR+
and paradoxical
thoraco-abdominal
movement
Marked resp distress
at rest. FAN+, ICR+,
SCR+ and
paradoxical thoraco-
abdominal
movement
Chest Auscultation Moderate wheeze Loud pan-expiratory
and inspiratory
wheeze
Wheezes might be
audible without
stethoscope
The chest is silent
(absence of wheeze)
SpO2 on room Air >94% 91–94% 91–94% <90%
Peak flow vs
Personal Best
>80% 60–80% best <60% Unable to perform
the task or <33%
13. Life-threatening Asthma –
Silent chest, Cyanosis, Poor respiratory
effort, Hypotension, bradycardia, Exhaustion, Confusion or
drowsiness
•Acute Severe Asthma –
Unable to complete sentences in one breath; too breathless to talk
or feed, Agitation, Accessory muscle use
• Pulse rate >140/min in children 2-5 years old; >125/min in children
>5 years old
• Respiration >40 breaths/min in children 2-5 years old; >30
breaths/min in children >5 years old
15. Principles of Treatment
Treat hypoxemia,
Give short-acting ß2-agonists,
Prescribe corticosteroids,
Assess treatment response, and
Consider other modalities of treatment.
16. Immediate Treatment
High flow O2 via face mask at 6-8L/min
Nebulize with 5mg Salbutamol(2.5mg in very young
children) in 4mls of saline for 5-10min
Prednisolone 1-2mg/kg PO(max. 40mg)
If life-threatening – IV Aminophylline 1mg/kg/hr, IV
Hydrocortisone 100mg(4mg/kg/dose) 6hrly, Add
Ipratropium bromide 0.25mg(0.125 in younger
children) to Neb Salbutamol
Rehydration – o/a excessive sweating, fluid loss and
poor/lack of intake during acute episode. 3000mls/m2
17. Subsequent mngt
IF THE PT IS IMPROVING, CONTINUE:
High flow O2,
Prednisolone 1-2mg/kg dly(max. 40mg)
Nebulised Salbutamol 4hrly
18. IF PT IS NOT IMPROVING AFTER 30MIN:
Continue O2 and steroids
Give Nebulised Salbutamol more frequently up to
30min
Add ipratropium to nebulizer and repeat 6hrly until
improvement starts
IF PT STILL NOT IMPROVING, GIVE:
Aminophylline infusion(1mg/kg/hr)
20. Discharge
Before discharging from hospital the pt:
Shd have been on discharge medications for 24hrs and have had
inhaler technique checked recorded
If recorded PEF>75% predicted or best and PEF variability <25%
Treatment with soluble steroid tablets and inhaled
steroid(Seretide/Symbicort) in addition to
bronchodilators(Ventolin). MDIs are difficult to use in young
children so include a spacer.
Nedocromil Sodium or Zafirlukast(Accolate) as prophylaxis
Educate mother on trigger factors and first aid before getting to
hospital
Review within 4wks, and then every 3 to 6mnths