Bronchial Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow obstruction. It is diagnosed based on a history of recurrent wheezing, chest tightness, and cough, especially at night or with triggers. Acute asthma can range from moderate to life-threatening and is treated with inhaled bronchodilators, steroids, magnesium, and oxygen to reverse hypoxia. Hospital treatment for severe acute asthma focuses on airway clearance, oxygenation, circulation support, and early use of steroids to improve outcomes. Distinguishing features, treatment response, and arterial blood gases are used to assess asthma severity.

1. Bronchial Asthma
By : D.Intesar Khalid

2. Definition
• Asthma is a chronic inflammatory disorder of the airways characterized by
bronchial hyperreactivity to a variety of stimuli, leading to a variable
degree of airway obstruction, some of which may become irreversible over
many years.
It is a clinical diagnosis based on:
• A history of recurrent episodes of wheeze, chest tightness,
breathlessness, and/or cough, particularly at night
• evidence of generalized and variable airflow obstruction, which may be
detected as intermittent wheeze on examination or via tests such as
peak expiratory flow (PEF) measurement.

3. • Airway obstruction occurs due to a combination of:
• Inflammatory cell infiltration
• Mucus hypersecretion with mucus plug formation
• Airway smooth muscle contraction.

4. Aetiology:
This is due to a combination of:
genetic/ environmental factors and Immunological mechanisms.

5. Classification
• Asthma is classified in to:
(1) Intermittent asthma
(2) Mild persistent asthma
(3) Moderate persistent asthma
(4) Sever persistent asthma

6. • Clinical features
• Cough
• shortness of breath (SOB)
• Wheeze
• Chest tightness.
Classically, these are variable, intermittent, worse at night, associated with
specific triggers, e.g. pollens, cat and dog dander, and non-specific triggers,
e.g. cold air, perfumes, and bleaches.

7. • Examination
• May be entirely normal
• Classically, expiratory wheeze is heard
• Chest deformity/hyperinflation in long-standing/poorly
controlled asthma
• severe life-threatening asthma may have no wheeze and a silent
chest.

8. • Baseline investigations
• Peak flow recording/simple spirometry looking for variability and
response to treatment. Airway obstruction leads to decreased in PEF and
forced expiratory volume in 1s (FEV1).
The diagnosis is highly likely if:
• 20% diurnal PEF variation on >3 days/week, in a week of peak flow
diary measures
• FEV1 ≥15% decrease after 6 min exercise
• FEV1 ≥15% (and 200 mL) increase after 2-week trial of oral steroid
(30 mg prednisolone od)

9. • Bronchodilator reversibility testing FEV1 ≥15% (and 200 mL) increase after
a single dose of a short-acting β2 agonist therapy (e.g. salbutamol 4 puff
(400 micrograms) by metred dose inhaler (MDI).

10. • Further investigations (if required)
Blood tests:
• Full blood count (FBC; eosinophilia is common in asthma, but, if
the total eosinophil count is unusually high, consider eosinophilic
granulomatosis with polyangiitis ( Churg– strauss syndrome).
• IgE (associated atopy, i.e. positive skin prick tests to common
allergens, often with associated allergic rhinitis and eczema).
•Specific IgEs if other environmental triggers suspected.

11. CXR if atypical symptoms may show hyperinflation or evidence of
localized abnormality simulating wheeze, e.g. adenoma (rare).
Skin prick tests to define atopic constitution or identify potential triggers.
Laryngoscopy/ENT examination Useful if concerns about nasal
symptoms or obstruction, e.g. from polyps, or to exclude upper airway
obstruction, or a vocal cord abnormality.
Bronchoscopy rarely needed. Its main use is to exclude an obstructing
airway tumour, e.g. carcinoid.

12. • Important differential diagnoses in asthma
Consider especially if unusual features in the history, or poor correlation
between objective measures and symptoms, or poor treatment response:
• Upper airway obstruction (breathlessness, noisy, stridous breathing,
• Foreign body aspiration
• tumour, especially tracheal
• Congestive cardiac failure (CCF) (young patient with a murmur)
• Vocal cord dysfunction (VCD)
• hyperventilation syndrome
• Bronchiolitis (see % p. 183)
• gastro-oesophageal reflex disease.

13. Acute Asthma
• Fatality in asthma is due to cardiac arrest 2° to hypoxia and acidosis—
reversal of hypoxia is paramount. Give high-flow O2
Initial assessment of acute asthma
• Clinical features e.g. tachypnoea, tachycardia, silent chest
• pulse oximetry
• Arterial blood gases are required in patients with a spO2 <92%.
In acute asthma the pCO2 is initially low due to hyperventilation. A normal CO2
may indicate fatigue
• CXR is not routinely recommended in the absence of suspected
pneumothorax or consolidation

14. Acute asthma either:
Moderate acute asthma.
Sever acute asthma
Life threatening asthma
Near fatal asthma

15. • Moderate acute asthma
• Increasing symptoms
• PEF ≥50–75% predicted or best
• No features of acute severe asthma
• 1 h following treatment in A&E, patients with PEF ≥75% predicted
or best may be discharged home with appropriate changes to their
asthma
medication.

16. • Acute severe asthma
Defied as any of:
• PEF 33–50% predicted or best
• respiratory rate (rr) ≥25
• heart rate (hr) ≥110
• Inability to complete sentence in one breath

17. • Life-threatening asthma
Any one of:
• peF ≤33% predicted or best
• saO2 ≤92% (needs arterial blood gases (ABg))
• PaO2 ≤8 kpa
• Normal CO2 (4.6–6 kpa)
• silent chest
• Cyanosis
• poor respiratory effrt
• Bradycardia/arrhythmia/hypotension
• exhaustion
• Altered conscious level.

18. • Near-fatal asthma
• raised paCO2, and/or
• Needing mechanical ventilation with raised infltion pressures.

19. • Hospital treatment of acute asthma
• Airway—ensure no upper airway obstruction
• Breathing—give high-flw O2
• Circulation—gain intravenous (IV) access.

20. • β2 agonist—inhaled or nebulized, e.g. nebulized salbutamol 2.5–5
mg, driven by O2
• give repeated doses or continuous, e.g. 5–10 mg/h
• Anticholinergic—nebulized ipratropium bromide (500 micrograms 4–
6hourly) added to β2 agonist therapy may improve bronchodilatation in
acute severe asthma.

21. • record O2 saturation, and maintain 94–98%
• ABG for ph and paCO2 (if saturation <92% or other severe features)
• record and document HR and RR
• Measure glucose and potassium.
• CXr to exclude infection/pneumothorax.

22. • Steroids—the earlier given in an attack, the better the outcome
• Oral is as effective as IV
• Dose 40–50 mg prednisolone, continuing for at least 5 days
or until recovery.
• Inhaled corticosteroids should be continued.
IV magnesium sulfate—immediately if acute severe and if poor
response to above therapies, 1.2–2 g IV infusion over 20 min.

23. Antibiotics—only give if definite infective element to the
exacerbation.
Most exacerbations are due to viruses, especially the
common cold.
• IV fluids—patients are often dehydrated
• Intramuscular (IM) adrenaline—may be useful if near
arrest, while
awaiting ICU support.

24. • ICU referral
When to discuss with ITU
• Worsening PEF despite treatment
• Worsening hypoxia
• hypercapnia
• Falling ph
• exhaustion/poor respiratory effort
• Drowsiness/confusion
• respiratory arrest.

25. THANKS