PE28.1-5 | Allergy and Asthma — Graded Quiz

Life-threatening or near-fatal asthma (silent chest, SpO₂ <90% despite maximal bronchodilator, unable to speak) unresponsive to first-line therapy requires IV MgSO₄ 25–75 mg/kg (max 2 g) over 20 minutes as per GINA/IAP guidelines, alongside ICU-level monitoring and preparation for mechanical ventilation if needed.

Life-threatening asthma with silent chest and failure of standard bronchodilators requires IV MgSO₄ 25–75 mg/kg (max 2 g) over 20 minutes plus IV corticosteroids and ICU transfer. Mechanical ventilation is a last resort but must be anticipated.

Ipratropium alone without additional escalation is insufficient for life-threatening asthma. High-dose salbutamol outpatient is not appropriate for silent chest. Oral prednisolone alone with 4-hour observation is dangerously inadequate in this severity class — IV corticosteroids and ICU transfer are needed.

Salbutamol use >2 days/week plus nocturnal symptoms >2×/month classifies this as at least mild persistent asthma, requiring a controller. GINA Step 2 = low-dose ICS (budesonide 100–200 mcg/day, or fluticasone propionate 100–200 mcg/day), which is the most effective and evidence-based first controller choice.

Mild persistent asthma in children is treated with Step 2: low-dose ICS (budesonide or fluticasone). ICS reduces airway inflammation, exacerbations, and steroid burst requirements. Step up if uncontrolled on low-dose ICS after 6–8 weeks.

Symptom frequency exceeds mild-intermittent threshold, so SABA-only management is inadequate. ICS+LABA is Step 3 and would be over-treatment at initial presentation without trialling ICS alone. Montelukast (leukotriene receptor antagonist) is an alternative second-line controller, not first-line in school-age children with persistent asthma.

Short-acting beta-2 agonist (SABA) — salbutamol 200 mcg by pMDI 15 minutes before exercise — is the most effective and widely recommended prophylaxis for EIB. It provides protection for 2–4 hours post-exercise. Optimising baseline ICS control also reduces EIB frequency.

Exercise-induced bronchoconstriction is managed with pre-exercise salbutamol 200 mcg 15 minutes before activity. Optimising baseline ICS controller reduces exercise triggers. EIB is not a contraindication to sport in children.

Exercise is encouraged — EIB is manageable, not a reason to ban sport. LABA monotherapy for EIB is contraindicated (no ICS = unsafe). Cromolyn sodium (mast-cell stabiliser) is an older, less effective alternative that requires inhalation 20–30 minutes before exercise — not 2 hours, and not first choice.

Allergen immunotherapy (subcutaneous or sublingual) is indicated for IgE-mediated allergic rhinitis with confirmed sensitisation when pharmacotherapy provides inadequate control. Uniquely, it modifies the underlying allergic immune response (reduces IgE, induces regulatory T cells and IgG4), offering benefit that persists for years after completing the 3–5 year course.

Allergen immunotherapy modifies the underlying allergic response, provides durable post-treatment benefit, may prevent asthma development in AR patients, and is indicated when pharmacotherapy is insufficient for IgE-mediated disease with confirmed sensitisation.

SCIT is used in children including those under 12 years in many centres (though some centres prefer sublingual for younger children due to anaphylaxis risk). Immunotherapy does provide durable post-treatment benefit — this is its key advantage over pharmacotherapy. Antihistamines provide symptomatic relief only, not disease modification.

PFT (spirometry) indications in paediatrics include: confirming and classifying obstructive, restrictive, or mixed lung disease; assessing severity of known asthma; monitoring response to therapy; detecting exercise-induced bronchoconstriction; and pre-operative pulmonary risk assessment. Monitoring an older child (≥5 years, cooperative) with known asthma is a clear indication. Spirometry requires cooperation and is reliable from approximately age 5–6 years.

Spirometry is reliable in cooperative children aged ≥5–6 years. Key indications: diagnosis and severity classification of asthma, reversibility testing, monitoring response to therapy, and evaluation of exercise-induced bronchoconstriction.

Spirometry requires active cooperation and reproducible manoeuvres — generally reliable from age 5–6 years, not age 4. Infants below 2 years cannot perform standard spirometry (infant lung function tests are specialised research tools). Routine spirometry in well children without symptoms is not a standard indication.

Effective jet nebulisation requires: a properly fitting mask (or mouthpiece in older children) to prevent drug loss; an upright position; and a driving gas flow of 6–8 L/min to generate particles in the 1–5 µm respirable range. Mask fit is critical — a 1-cm gap can waste 50% of the dose.

For paediatric nebulisation: use an upright position, a properly fitting face mask, 4–5 mL fill volume, and 6–8 L/min driving gas. A snug mask is the single most critical factor for drug delivery in young children.

Maximum fill volume does not improve efficiency — the optimal fill volume is 4–5 mL (drug + diluent); overfilling increases residual volume. Supine position is incorrect — nebulisation should be in an upright (sitting) position for comfort and optimal lung expansion. A 45-degree tilt reduces aerosol output significantly.

Before stepping up in a child who appears adherent and has good technique, repeating spirometry with bronchodilator reversibility quantifies current obstruction severity, confirms the diagnosis, detects fixed obstruction (alternative diagnoses like vocal cord dysfunction), and guides whether step-up, add-on therapy, or referral is needed.

Before stepping up asthma treatment in a seemingly adherent patient, spirometry with reversibility should be repeated to confirm the diagnosis, quantify severity, and exclude alternative diagnoses. Objective spirometric data guides the step-up decision.

CXR is useful for ruling out structural/infective causes but does not guide step-up directly. Serum IgE can support decision for omalizumab (Step 5+) but requires functional assessment first. FBC eosinophil count is relevant if biologic (anti-IL5) therapy is considered but should follow functional assessment.

The early phase (within 15–30 minutes) is driven by IgE-mediated mast-cell degranulation releasing histamine and early-release leukotrienes. The late phase (4–8 hours) is driven by eosinophil-mediated inflammation with cysteinyl leukotrienes (LTC4, LTD4, LTE4), IL-5, eosinophil cationic protein, and major basic protein causing sustained airway inflammation, oedema, and mucus hypersecretion.

Childhood asthma has a biphasic response: early phase (0–1 h, mast cells, histamine) and late phase (4–8 h, eosinophils, cysteinyl leukotrienes, IL-4/5/13). ICS target the late-phase inflammation; leukotriene antagonists (montelukast) target the leukotriene arm.

Histamine is a key early-phase mediator, not the primary late-phase driver. IgG/complement do not drive the classical allergic late-phase response. Bradykinin contributes to cough and airway oedema but is not the key late-phase mediator.

Mask aversion is common in toddlers. Evidence-based strategies include familiarising the child with the mask during play (between medication times), using reward charts, distraction with toys or songs, and having a parent hold the child. A proper airtight seal is critical — holding the mask off the face ('blow-by') reduces drug delivery by up to 80% and is not recommended.

For mask aversion in young children, use familiarisation and play-based introduction rather than switching to blow-by or discontinuing therapy. An airtight mask seal is mandatory — blow-by (mask off face) is ineffective and should never be recommended.

Home nebulisers are not preferred for routine controller therapy — pMDI+spacer is equally effective when used correctly and involves less drug waste. Holding the mask away from the face (blow-by) dramatically reduces drug delivery and is specifically discouraged. Stopping controller ICS and relying on rescue nebulisation alone leads to poor asthma control.

Second-generation antihistamines such as cetirizine or loratadine are preferred in children with AR and co-morbid asthma. They cause minimal sedation, lack significant anticholinergic effects (which can thicken bronchial secretions and impair mucociliary clearance in asthma), and are weight-dosed (cetirizine 0.25 mg/kg/dose once or twice daily, max 10 mg/day).

In children with allergic rhinitis and comorbid asthma, second-generation antihistamines (cetirizine, loratadine, fexofenadine) are preferred because they lack the anticholinergic effects of first-generation agents that can worsen asthma by thickening secretions and impairing mucociliary clearance.

First-generation antihistamines (promethazine, chlorpheniramine, diphenhydramine) have potent anticholinergic effects that can thicken airway secretions, impair mucociliary clearance, and worsen asthma control. They also cause sedation, impairing school performance.