Asma Bronkiale Anak

01Pathophysiology

Pediatric asthma is a heterogeneous, chronic inflammatory disease of the airways that manifests as reversible airflow obstruction and bronchial hyperresponsiveness. Understanding the mechanism begins with the interplay between two foundational processes: chronic airway inflammation and autonomic nervous system imbalance.

The inflammatory cascade begins when a genetically predisposed child (carrying susceptibility genes such as ADAM33 or ORMDL3) encounters environmental inducers like ozone exposure or respiratory viral infections (rhinovirus, RSV, influenza), which sensitize the immune system toward a Th2-dominant response. Once sensitized, subsequent exposure to enhancers such as indoor allergens (house dust mites, mold) drives the immune system into a state of chronic bronchial inflammation. The key cytokines involved are IL-4, IL-5, and IL-13, produced by Th2 lymphocytes. This Th2 dominance is partly enabled by a reduction in regulatory T-cells (Treg) that normally suppress Th2 activity. The result is eosinophilic infiltration, mast cell degranulation releasing histamine, leukotrienes, and prostaglandins, and progressive mucosal edema with mucus hypersecretion.

The autonomic imbalance occurs simultaneously, though its exact mechanism remains incompletely mapped. The normal sympathetic nervous system promotes bronchodilation through beta-2 adrenergic receptor activation. In asthma, sympathetic tone is reduced while parasympathetic (cholinergic) tone is increased, causing smooth muscle spasm and bronchospasm. This concept is directly connected to why the two pillars of asthma therapy exist: anti-inflammatory agents (corticosteroids) to address chronic inflammation, and bronchodilators (beta-2 agonists, anticholinergics) to correct the autonomic imbalance.

Once the airway enters a state of hyperresponsiveness, it has two components: hypersensitivity (the threshold for triggering a response is lowered, so minimal stimuli can provoke symptoms) and hyperreactivity (the response is far more exaggerated than normal). In this primed state, when trigger factors such as cigarette smoke, dust, cold air, or exercise are encountered, a dual response emerges: acute inflammation flares on top of the chronic process, and parasympathetic tone surges further. The combined effect produces airway narrowing through mucosal edema, mucus plugging, and bronchospasm, explaining the triad of cough, wheezing, and dyspnea.

Over time, persistent inflammation leads to airway remodeling: proliferation of airway smooth muscle, subepithelial fibrosis, increased vascularity and angiogenesis, and mucous gland hyperplasia. In severe cases, remodeling causes irreversible airflow limitation. This is why early initiation of anti-inflammatory therapy (ICS) can improve respiratory function and why delayed treatment worsens long-term outcomes.

The hallmark clinical characteristics of asthma (best remembered by the mnemonic EVTAR or ENTAR: Episodicity, Variability/Nocturnal worsening, Trigger-dependence, Atopy/Allergy, Reversibility) are each a direct consequence of these pathophysiological processes. Episodicity reflects the fluctuating nature of the inflammation. Nocturnal worsening reflects circadian changes in autonomic tone and cortisol. Trigger-dependence reflects the hyperresponsive airway. Reversibility reflects that bronchospasm and acute inflammation can be resolved pharmacologically, at least before remodeling becomes fixed.

02Classification and Clinical Manifestation

By Frequency

By Severity of Exacerbation

Important rule: If even one criterion falls in a more severe category, the patient is classified and treated at that higher severity level.

By Degree of Control

The degree of asthma control is assessed retrospectively based on the child's condition over the previous four weeks. Four criteria are evaluated:

1. Daytime asthma symptoms occurring more than twice per week

2. Nighttime awakening due to asthma

3. Use of reliever medication more than twice per week

4. Activity limitation caused by asthma symptoms

The degree of control is classified as:

• Fully Controlled: The child meets none of the four criteria. In other words, over the past four weeks:

• Partly Controlled: The child meets one to two of the four criteria listed above. This indicates suboptimal control and should prompt the clinician to reassess adherence, inhaler technique, trigger exposure, and comorbidities before considering a step-up in therapy.

• Uncontrolled: The child meets three to four of the four criteria. This classification signals a clear need to step up the long-term management regimen after verifying modifiable factors such as incorrect inhaler technique, poor adherence, persistent allergen exposure, or untreated comorbidities.

03Diagnostic Workup

The diagnostic workup for pediatric asthma begins with a thorough clinical history, which remains the single most important diagnostic step because there is no gold standard test. The physician asks about the pattern of symptoms (cough, wheeze, dyspnea, chest tightness) and specifically screens for the EVTAR/ENTAR characteristics. Finding at least two of the five characteristics (episodicity, variability/nocturnal, trigger, atopy, reversibility) strongly supports the clinical diagnosis.

Physical examination is often normal between episodes. During an attack, findings include tachypnea, wheezing on auscultation, retractions, and decreased oxygen saturation. Signs of atopy (Dennie Morgan lines, allergic shiners, nasal crease, geographic tongue) add supportive evidence.

When available, spirometry is the recommended objective test. It measures $FE{V}_{1}FEV\_1$ and $FVCFVC$ to quantify airflow obstruction. A low $FE{V}_{1}FEV\_1$ (<80% predicted) or a reduced $FE{V}_1\mathrm{/}FVCFEV\_1/FVC$ ratio (<0.90) suggests obstruction. However, a normal result in an asymptomatic child with intermittent asthma does not rule out the diagnosis.

The bronchodilator reversibility test is performed by giving inhaled SABA and repeating spirometry. An increase in $FE{V}_{1}FEV\_1$ of more than 12% confirms reversible obstruction characteristic of asthma. Using a Peak Flow Meter (PFM), the threshold is a PEF increase of more than 20%.

If neither spirometer nor PFM is available, the guideline recommends an empiric therapeutic trial: give inhaled SABA for 3-5 days and observe clinical response. If symptoms improve, asthma is the working diagnosis. If there is no response to SABA, a short course of oral steroids (3-5 days) can be added. Persistent failure to respond should prompt investigation for alternative diagnoses.

Critically, tests for atopy (skin prick testing, serum IgE, blood eosinophils) are not recommended as routine diagnostic tools. Atopy increases the probability of asthma but is neither necessary nor sufficient for the diagnosis. Chest X-ray is similarly not routinely indicated and is reserved for cases where TB, foreign body aspiration, or congenital anomalies are suspected.

04Management and Treatment

Acute Attack Management

Long-Term Controller Therapy (Age 6-11 Years)

Long-Term Controller Therapy (Age 12-18 Years)

Acute Attack: The first priority in any asthma exacerbation is to assess the severity (using the classification table above) and to identify risk factors for asthma-related death (history of intubation/ventilator use, ER visit or hospitalization within the past year, current or recent systemic steroid use, SABA overuse equivalent to >1 canister/month, poor adherence, psychiatric or psychosocial comorbidity, food allergy, or comorbid pneumonia/diabetes/arrhythmia).

For a mild-moderate attack, the standard first step is inhaled SABA, either via nebulizer (salbutamol 2.5 mg/dose) or pMDI with spacer (2-4 puffs, each puff followed by 5-10 breaths through the spacer). This can be repeated every 20 minutes up to three times within one hour. If there is no adequate response to SABA alone, add ipratropium bromide. Systemic corticosteroid (prednisone or prednisolone 1-2 mg/kg/day, max 40 mg orally) is given for 3-5 days without tapering.

For a severe attack, the child should receive oxygen (target SpO2 >94%), combined SABA + ipratropium bromide via nebulizer, IV corticosteroid (methylprednisolone 1-2 mg/kg/day, max 60 mg/day), and high-dose inhaled corticosteroid via nebulizer (budesonide 0.5-1 mg per dose, repeatable up to a total of 1.5-3 mg). If there is no response, IV aminophylline (loading dose 6-8 mg/kg over 30 minutes, maintenance 0.5-1 mg/kg/hour; target serum level 10-20 mcg/mL) and/or IV MgSO4 (40-50 mg/kg over 60 minutes, max 1500 mg single dose) are considered.

For impending respiratory arrest (lethargy, inaudible breath sounds), the child is transferred to ICU and intubation is prepared. A child with dehydration and metabolic acidosis may develop tachyphylaxis to SABA; in that case, give SABA only once and prioritize correcting the dehydration and acidosis first.

Long-Term Controller Therapy: The approach is a personalized, control-based stepwise strategy. The initial step is determined by the frequency classification. Follow-up visits occur every 2-4 weeks initially, then every 1-2 months once stable.

Key principles:

• Step-up if asthma is not fully controlled after 6-8 weeks of treatment, but only after confirming correct inhaler technique, adequate adherence, allergen avoidance, and addressing comorbidities.

• Step-down if asthma has been fully controlled for at least 3 months and spirometry is stable. Reduce by only one step at a time. Overly rapid step-down increases the risk of severe exacerbation.

• A child with intermittent asthma who has one or more risk factors for exacerbation should be managed as mild persistent (step 2).

• After a severe or life-threatening attack, the long-term step should be raised one level higher than what the frequency classification alone would dictate.

MART (Maintenance and Reliever Therapy): ICS-formoterol is used as both the daily controller and the as-needed reliever. Formoterol is a LABA with rapid onset, making it suitable for both roles. MART has been shown to reduce exacerbation risk compared to separate ICS controller with SABA reliever, and is available for children 6-11 years (step 3-4) and 12-18 years (step 1-4). Maximum daily formoterol dose is 54 mcg/day.

Contraindications and cautions: Oral corticosteroids given long-term as a controller are not recommended due to side effects (hypertension, growth suppression, osteoporosis). LTRA (montelukast) is offered when families prefer oral medication, when ICS is unavailable, or when ICS is contraindicated. Parents must be educated about potential montelukast side effects including sleep disturbance and behavioral changes. For children aged <4 years, ICS-LABA combination does not yet have sufficient safety data and is not globally recommended.

Montelukast (LTRA) dose: 4 mg for ages 2-5, 5 mg for ages 6-14, 10 mg for ages 15 and above, given once daily at bedtime.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common trap on this topic is the assumption that "all that wheezes is asthma." The guideline dedicates an entire chapter to diagnostic errors, and test-writers love to exploit this. A vignette describing unilateral wheezing should immediately redirect you to foreign body aspiration, not asthma. A first-time wheezer under age 2 with a viral prodrome is bronchiolitis until proven otherwise.

Equally important is the reverse trap: underdiagnosis of cough variant asthma (CVA). A child who presents with chronic, episodic, nocturnal cough triggered by cold air or exercise but without audible wheezing can still have asthma. If the vignette describes cough with EVTAR characteristics but no wheeze, and the answer choices include "CVA" or "empiric bronchodilator trial," that is the intended answer. Asthma does not require spirometry for diagnosis, and the absence of a spirometry result in the vignette should not dissuade you from choosing asthma.

Another classic gotcha involves treatment errors. Test-writers will present a child with persistent asthma who is using SABA daily as the sole therapy. The correct next step is to add a controller (ICS), not to continue or increase SABA. Overreliance on SABA without controller therapy leads to tachyphylaxis, beta-2 receptor downregulation, increased inflammation, and higher risk of severe exacerbation. Similarly, using low-dose ICS to treat an acute attack is incorrect; during an exacerbation, ICS must be given at high doses if used at all, and systemic corticosteroids remain the standard.

Watch for vignettes that include antihistamine use during an acute asthma attack. First-generation antihistamines thicken mucus and worsen obstruction. This is a commonly tested management error.

The question of "silent chest" is a high-yield pearl: a child with severe asthma who suddenly has no audible wheezing is not improving. The absence of wheezing in the context of severe respiratory distress indicates such severe obstruction that airflow is insufficient to generate sound. This is an ominous sign indicating impending respiratory arrest.

Finally, remember the step-down rule: asthma must be fully controlled for at least 3 months before reducing therapy, and you can only step down one level at a time. Step-up, by contrast, can occur after 6-8 weeks of failed control, but only after verifying inhaler technique, adherence, trigger avoidance, and comorbidity management. The core competency being tested here is the ability to integrate classification, control assessment, and stepwise management into a logical, evidence-based sequence of decisions.