Asthma and status asthmaticus in children

Overview

Asthma is reversible narrowing of the large and small airways caused by hyperresponsiveness to many immune and non-immune triggers. It is a common chronic lung disease of childhood. It can start at any age; before puberty boys are affected about twice as often as girls, and the sexes are equal after puberty.

Young children have more severe attacks because they catch more viral colds and their narrow airways give higher resistance.

Triggers and risk factors

Pathophysiology

• Asthma is primarily an inflammatory disease; bronchospasm follows the inflammation.
• Allergen binds IgE on mast cells, which release histamine, leukotrienes (C4, D4, E4) and platelet-activating factor.
• Early phase (minutes): bronchoconstriction; relieved by beta-2 agonists, prevented by mast cell stabilisers (cromolyn, nedocromil).
• Late phase (6 to 8 hours later): eosinophil and neutrophil infiltration and continuing hyperresponsiveness; prevented and treated by steroids.
• Each attack has five components: bronchospasm, mucus plugging, mucosal oedema, inflammatory cell infiltration and shedding of epithelium.
• Narrowing is worst in expiration, so air is trapped and the chest hyperinflates. V/Q mismatch causes hypoxaemia; at first the child over-breathes and PaCO2 falls. A normal or rising PaCO2 means tiring and approaching respiratory failure.
• Hyperinflation raises intrathoracic pressure and cuts venous return, producing pulsus paradoxus.

Wheezing patterns

Clinical features

• Wheeze (the most characteristic sign), cough, breathlessness, chest tightness, exercise intolerance.
• Cough-variant asthma: persistent dry or night cough, cough after exercise or cold air, cough followed by vomiting.
• Symptoms are worse at night and early morning.
• Mild cases: prolonged expiration and wheeze only on forced expiry.
• Severe attack: flaring, intercostal and suprasternal recession, accessory muscle use, hyperresonant chest, central cyanosis, tachycardia, pulsus paradoxus; the child sits upright leaning on the arms (tripod position).
• Silent chest: wheeze disappears because little air moves.
• Chronic asthma: below-average height and weight, barrel chest, prominent sternum, Harrison's sulci.

Grading an acute attack

Diagnosis

The diagnosis is clinical: recurrent wheeze, cough or breathlessness that responds to bronchodilators, often with atopy.

Differential diagnosis of wheeze in children

• Acute bronchiolitis (infants), croup, pneumonia, pertussis.
• Inhaled foreign body.
• Endobronchial TB or enlarged TB lymph nodes pressing on a bronchus (important in Pakistan).
• Cystic fibrosis; congenital anomalies such as a vascular ring.
• Cardiac failure ("cardiac asthma").

Complications

• Pneumothorax and pneumomediastinum (rupture of over-distended alveoli).
• Respiratory failure and death (almost always from under-treatment).
• Slowed growth and delayed puberty in severe chronic disease; chest deformity.
• Steroid side effects with long oral use.

Acute attack: management

1. Oxygen by mask or prongs to keep saturation above 92%.
2. Nebulised salbutamol, driven by oxygen (about 6 L/min to avoid salbutamol-induced hypoxaemia), repeated every 20 to 30 minutes until the child responds. The dose is weight-based, using the 0.5% (5 mg/mL) nebuliser solution diluted with normal saline (Akbar). Hold or reduce it if the heart rate passes 180 per minute. Side effects: tachycardia, tremor, irritability, hypokalaemia.
3. Add nebulised ipratropium to salbutamol in moderate to severe attacks; it is weaker alone but helps in combination.
4. Systemic steroid early: IV hydrocortisone 5 to 10 mg/kg every 4 to 6 hours, then oral prednisolone 1 mg/kg daily over 5 days (or move to an inhaled steroid). Give it at once if the child is already on steroids.
5. Fluids: dehydration is common. Avoid overload; add potassium once the child passes urine because beta-agonists lower it.
6. Antibiotics only if bacterial infection is suspected.
7. Once controlled, continue inhaled salbutamol every 6 hours and review the preventer plan. Small airway narrowing may last 2 months or longer after a severe attack, so treatment continues for weeks or months.

Second-line drugs

• Aminophylline IV: 5 mg/kg diluted and given slowly over 5 to 15 minutes, no faster than 25 mg/min; omit the loading dose if the child had theophylline in the last few hours. It can be repeated 6 to 8 hourly, with a total of no more than 20 mg/kg per day. Too-rapid injection causes arrhythmias, hypotension and death.
• IV magnesium sulfate (Nelson): given in the emergency department if the child deteriorates despite beta-2 agonists, ipratropium and systemic steroids; typical dose 25-75 mg/kg (maximum 2 g) IV over 20 minutes.
• Subcutaneous adrenaline (1:1000) or terbutaline is not used routinely (Akbar); Nelson keeps it mainly for asthma with anaphylaxis or for a child not responding to continuous bronchodilators. Do not give adrenaline when the heart rate is above 180 (infants) or 160 (older children).

Status asthmaticus

• Definition: increasingly severe asthma that does not respond to drugs that usually work. It is a clinical diagnosis.
• Admit to intensive care and monitor blood count, electrolytes, blood gases and heart.
• Oxygen to keep PaO2 70 to 90 mmHg or SaO2 above 92%.
• Continue nebulised salbutamol with ipratropium, IV steroids, aminophylline infusion and careful hydration.
• IV magnesium (Nelson) if the child keeps deteriorating.
• Mechanical ventilation if respiratory failure develops despite all of this.

Long-term management

Four parts:

1. Education: inhaler technique with a spacer (metered-dose inhaler plus spacer for children), peak-flow monitoring, a written action plan, knowledge of drugs and side effects.
2. Regular assessment with objective lung function.
3. Avoidance of triggers: smoke, dust mite, pollution.
4. Drug plan for daily control and for attacks.

Drugs

Prognosis and prevention

• Generally good if treated early and properly. Death is rare and almost always due to under-treatment.
• About half of asthmatic children become largely symptom-less within 10 to 20 years; only about 5% have severe disease. Remission depends partly on airway growth.
• Children with severe, steroid-dependent asthma rarely outgrow it; most remain asthmatic as adults. Asthma can return in adult life.
• Prevention: breastfeeding for more than 4 months reduces wheezing; avoid tobacco smoke; reduce triggers; give all routine vaccines plus annual influenza vaccine.

Quick revision

• Reversible obstruction, hyperresponsive inflamed airways; boys 2:1 before puberty.
• Triggers: viral colds, exercise, cold air, dust mite, smoke, emotion, aspirin.
• Late phase at 6 to 8 hours, steroid-sensitive.
• Silent chest, drowsiness, bradycardia = imminent arrest; rising PaCO2 = tiring.
• PEF variation over 15 to 20%; reversibility with bronchodilator.
• Acute: oxygen, salbutamol every 20 to 30 min, ipratropium, hydrocortisone then prednisolone 1 mg/kg daily over 5 days.
• Aminophylline 5 mg/kg slowly (max 25 mg/min; up to 20 mg/kg/day).
• Status asthmaticus: unresponsive to usual drugs; ICU; SaO2 above 92%; IV magnesium 25-75 mg/kg (max 2 g); ventilate if failing.
• Persistent asthma: daily inhaled steroid; LABA never for attacks.

Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).

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