Asthma

SUMMARY

Asthma is the most common chronic disease of childhood — a reversible airway obstruction caused by bronchial smooth-muscle spasm, airway mucosal edema, mucus impaction, airway inflammation, and airway hyperresponsiveness.

• Presentation: episodic wheeze, cough, chest tightness, and dyspnea, often triggered by viral infection, allergens, exercise, or cold air.
• Diagnosis: clinical picture plus spirometry showing reversible obstruction (≥ 10–12% rise in FEV₁ after a bronchodilator).
• Chronic management: a stepwise, control-based approach built on inhaled corticosteroids (ICS), stepping up or down roughly every 3 months.
• Acute exacerbation: oxygen + repeated SABA + early systemic corticosteroids, escalating to ipratropium and IV magnesium sulfate.
• Red flag: a silent chest, exhaustion, or a normalizing/rising pCO₂ signals impending respiratory failure (status asthmaticus).

Pathophysiology & Risk Factors

Asthma is a chronic inflammatory disorder producing reversible airway obstruction through four coexisting mechanisms: bronchial smooth-muscle spasm, airway mucosal edema, mucus impaction, and airway inflammation with hyperresponsiveness.

Etiology & contributing factors

• Genetic predisposition: family history of asthma or atopy (eczema, allergic rhinitis) is a major determinant of risk.
• Atopic sensitization: immune dysregulation with exaggerated IgE-mediated responses to inhaled or food allergens.
• Airway injury from infection: viral infections such as bronchiolitis in the first year of life are significant predisposing factors.
• Environmental triggers: allergens, pollutants, and tobacco smoke drive airway inflammation and hyperreactivity.

The pathophysiology is best appreciated by contrasting a normal airway with an asthmatic one:

Risk factors for childhood asthma

• Major: parental asthma, inhalant-allergen sensitization, eczema (atopic dermatitis).
• Minor: allergic rhinitis, wheezing apart from colds, peripheral blood eosinophilia ≥ 4%, food-allergen sensitization.

Top 4 precipitating factors for an attack

Clinical Presentation & Diagnosis

Clinical presentation

• Recurrent wheeze, respiratory distress, tachypnea, and accessory-muscle use during attacks.
• In school-age children, ~85% of exacerbations coincide with viral infection — the single biggest risk factor for hospitalization.
• ~15% of infants with recurrent wheeze continue to wheeze after age 6, and ~15% of children have their first wheezing episode after age 6.

Diagnosis

Diagnosis begins with a compatible history and physical examination — recurrent wheeze, shortness of breath, chest tightness, exercise intolerance, chronic cough, and occasionally mucoid vomiting.

Spirometry — the key test for confirming reversible obstruction: measure FEV₁ before and after a bronchodilator. A 10–12% increase in FEV₁ following the bronchodilator is consistent with reversible airway obstruction. An FEV₁/FVC ratio below 0.70 first establishes the obstructive pattern.

The obstructive versus normal spirometry pattern is shown here.

Reversibility also helps separate asthma from chronic obstructive pulmonary disease — open the reference for the FEV₁/FVC, bronchodilator-response, and DLCO patterns that distinguish them.

Classification & Control

Chronic asthma is graded along a severity spectrum from intermittent through severe persistent, with each step guiding the intensity of initial treatment. Once a patient is on therapy, reassess control every 3 months — control status (well controlled, not well controlled, very poorly controlled) guides whether to step up, step down, or maintain the current regimen.

Control assessment (in patients already on therapy):

• well controlled (minimal symptoms, no exacerbations, normal lung function) guides stepping down;
• not well controlled (some breakthrough symptoms or exacerbations)
• very poorly controlled (daily symptoms, multiple exacerbations) both prompt step-up to higher intensity therapy.

Chronic Management & Pharmacology

Goal: achieve and maintain good control

• Minimal/no daytime or nighttime symptoms and no exacerbations.
• No limitation of daily activity and no missed school or work.
• Minimal SABA use and minimal adverse effects from therapy.

Reassess every 3 months: if control is achieved, step down to a less-intense regimen; if symptoms remain uncontrolled, step up.

Stepwise controller therapy

• Intermittent asthma: no daily controller medication is recommended at any age.
• Mild persistent (symptoms > 2×/week but not daily): low-dose ICS is the preferred initial controller for all ages. In patients ≥ 12 years, concomitant ICS + SABA (without daily controller) is an option.
• If low-dose ICS fails to control, escalate by age:
  - ≤ 4 years → low-dose ICS + LABA (preferred alternatives: low-dose ICS + montelukast, or medium-dose ICS);
  - 5–11 years → low-dose ICS + inhaled LABA (e.g., formoterol).

The full escalation ladder from intermittent through severe persistent asthma is summarised here:

Drug classes at a glance

Corticosteroids are the most effective anti-inflammatory agents in asthma. For inhaled steroids, the highest-yield adverse effects are oral candidiasis (thrush), changes in growth velocity, and skin thinning/bruising; for systemic steroids, use the mnemonic below:

Three fixed ICS + LABA combination inhalers are in common use:

1. Fluticasone + salmeterol (Advair).
2. Budesonide + formoterol (Symbicort).
3. Mometasone + formoterol (Dulera).

LABAs provide up to 12 hours of bronchodilation, and formoterol has the faster onset — but they are used only in combination with ICS.

Theophylline is a methylxanthine with a narrow therapeutic range requiring serum-level monitoring; toxicity presents with tachycardia, GI symptoms, and behavioral effects. Levels rise with oral contraceptives, erythromycin, ciprofloxacin, and cimetidine, and fall with phenobarbital and phenytoin.

Acute Exacerbation & Status Asthmaticus

Immediate assessment & severity grading

Check vitals (HR, RR, SpO₂), accessory-muscle use, and ability to speak in full sentences. Grade acute severity as:

• Mild/moderate: SpO₂ > 92%, able to talk/feed, wheeze audible (may only with stethoscope).
• Severe: SpO₂ < 92%, PEFR 33–50%, too breathless to feed/talk, accessory-muscle use, tachycardia (HR > 125 for >5y; > 140 for <5y).
• Life-threatening: SpO₂ < 92%, PEFR < 33%, silent chest (no wheeze, minimal air entry), cyanosis, exhaustion, altered consciousness, poor respiratory effort.

Stepwise emergency management

• Step 1 — Oxygen: titrate to maintain SpO₂ 94–98%; high-flow O₂ may be needed for severe cases.
• Step 2 — SABA: nebulized salbutamol (albuterol) first-line, repeated every 20 minutes for the first hour.
• Step 3 — Systemic corticosteroids: oral or IV, given early to reduce inflammation and prevent relapse.
• Step 4 — Ipratropium bromide: add to SABA for moderate-to-severe attacks; shown to reduce hospitalizations.
• Step 5 — IV magnesium sulfate: a single infusion for severe attacks not responding to initial therapy.
• Step 6 — IV bronchodilators / adjuncts: aminophylline or IV salbutamol (rarely used due to side effects); heliox (helium–oxygen) may reduce work of breathing.

Monitoring & disposition

• Admit if: poor response after 1 hour of treatment, PEFR < 60–80% predicted, concerning vital signs, or an ongoing need for frequent bronchodilators.
• Discharge home if: good response, PEFR > 70–80% predicted, and minimal symptoms.

Status asthmaticus & respiratory failure

Acute severe asthma (status asthmaticus) is a severe attack in which the patient is at risk of developing respiratory failure. It typically occurs in patients with severe, poorly controlled asthma, or after massive exposure to allergens or sensitizing agents. A prior history of intubation for asthma is the single greatest predictor of death.

Clinical features of respiratory failure: extreme fatigue, inability to complete sentences, altered mental status (drowsiness, confusion), absent/minimal wheezing from poor air entry, cyanosis, and chest-wall retractions.

Laboratory findings: ↓ PaO₂ and ↓ pH with ↑ pCO₂ (respiratory acidosis). A rising or "normalizing" pCO₂ in a tiring asthmatic is an ominous sign — not improvement — because it reflects muscle fatigue and collapsing air entry rather than resolving bronchospasm.

Key Points for Exams

• Asthma = reversible obstructive airway disease; confirm with spirometry showing a ≥ 10–12% FEV₁ rise after a bronchodilator.
• Complete FEV₁/FVC reversibility favors asthma over COPD (which shows partial/no reversibility).
• ICS is the preferred controller for all persistent asthma; step therapy up or down based on control, reassessing roughly every 3 months.
• LABA is never used as monotherapy or as rescue — always combined with ICS (formoterol is the reliever component in SMART).
• Acute attack sequence: O₂ → SABA → systemic corticosteroids → ipratropium → IV magnesium sulfate.
• A silent chest, cyanosis, exhaustion, or a normalizing/rising pCO₂ signals impending respiratory failure.
• High-dose albuterol → hypokalemia (muscle weakness, hyporeflexia, tremor) — recheck electrolytes and obtain an ECG.
• Prior intubation for asthma is the strongest single predictor of death in status asthmaticus.
• Systemic corticosteroid side effects: remember "I COACH Growth–HPA" — immunosuppression, cataracts, osteoporosis, HPA-axis suppression, Cushing features, hyperglycemia, and growth retardation.
• Montelukast prevents exercise-induced asthma but can cause neuropsychiatric effects; theophylline has a narrow therapeutic index with dangerous drug interactions (e.g., macrolides).
• Beta-blockers are relatively contraindicated in asthma — they can precipitate bronchospasm.
• Top 4 precipitating triggers: CAVE — **C**igarette smoke, **A**llergen exposure, **V**iral infection, **E**xercise.