Bronchial Asthma in Children: A Clinical, Diagnostic and Management Primer Keya R Lahiri
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Definition, Pathophysiology and SeverityCHAPTER 1

 
As we stand at the threshold of the new millenium, it is time to take stock; evaluate our achievements, analyse past failures and mistakes and perform a medical audit. This is the appropriate time to look ahead, readapt our skills and put emerging technology to mass usage.
Hyperreactive airway disease would be affecting a large number of children in the coming decade. Hence protecting and salvaging the child's lung would be our major concern. It would be pertinent to delve into the diagnostic, management and preventive aspects of childhood asthma.
The NHLBI EPR-2, 1997 have prepared recommendations for use by clinicians, working in diverse health settings that address the practical decision making issues in the diagnosis and management. Early diagnosis, and effective management should reduce school and work absenteeism, hospitalisation and emergency department visits and deaths due to asthma.
 
How do We Define Childhood Asthma?
Asthma is a symptom complex to mean either a symptom, an exacerbation (attack) or underlying diseases of the airway. It is a reversible obstructive airway disease (ROAD) coupled with bronchial hyperresponsiveness (BHR) and airway inflammation.
Asthma = Road + BHR
Asthma, whatever the severity is a chronic inflammatory disorder of the airways. This has implications for the diagnosis, management and prevention of the disease.
 
Which are these Cells and Mediators Giving Rise to this Chronic Inflammatory and Hyperreactive State?
Airway inflammation leads to airflow limitation, hyperresponsiveness, recurrent episodes of cough, wheezing, breathlessness and chest tightness. Acute 2bronchoconstriction, oedema, mucous plug formation and airway wall remodelling lead to bronchial obstruction and disease chronicity. Inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli.
Histopathological features of asthma include:
  1. Denudation of airway epithelium.
  2. Mast cell activation.
  3. Inflammatory cell infiltration with eosinophils, lymphocytes (TH-2 like cells) and neutrophils (seen in sudden onset and fatal asthma exacerbations).
  4. Collagen deposits beneath basement membrane.
  5. Oedema.
Atopy, the genetic predisposition for the development of an IgE mediated response to common aeroallergens is the strongest identifiable predisposing factor for developing asthma. The episodes or attacks are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.
Viewing asthma as an immunological disorder, dendritic cell/macrophage and its communication with T-cells provides a mechanism for the induction of allergen related asthma probably through elaboration of cytokines which augment the IgE response (IL-4), encourages the proliferation, recruitment and priming of mast cells (IL-3, IL-5) and eosinophils (IL-3, IL-5, GM-CSF).
The various cellular and mediator components indicate a special form of inflammation involving a repertoire of cytokines that augment IgE, mast cell and eosinophilic responses in the airways. Thus, asthma results from complex interactions among inflammatory cells, mediators, and other cells and tissues in the airway. Research has substantiated that sub-basement membrane fibrosis contribute to persistent abnormalities in lung function.
The traditional view that mast cell was the most important cell no longer holds true. Antigens, allergens are taken up by macrophages, processed and presented to the lymphocytes which produce cytokines recruiting neutrophils and eosinophils. Eosinophil cationic protein damages epithelium, shedding occurs exposing nerve endings. Thus irritants via reflex pathways causes contraction. It is evident that inflammation occurs first. With the further advent of flexible scope, it was learnt that children with mild and newly detected, disease showed disrupted, damaged epithelium with few ciliated cells, 3indistinct membrane and oedema between cells. Below the basement membrane, infiltration of eosinophils, basophils and mast cell occurs. Due to inflammation and epithelial shedding, patients become hyperresponsive to variety of inhaled irritants. Hyperresponsiveness is a prerequisite for smooth muscle contraction, thus increasing the tendency of the airways to react to non-specific stimuli.
 
Assessing Severity and Patient Categorisation in Childhood Asthma
Since there is no universally accepted definition of asthma and the processes that result in symptoms unknown, it is not yet possible to determine the severity of the disease or how to measure it?
Asthma is loosely used to mean one of the following:
  1. A symptom
  2. An exacerbation/attack
  3. Underlying disease of the airways.
Hence severity could be applied to any one of the above.
 
Methods: Assessing Severity
 
The Underlying Disease
The level of airway hyperreactivity to histamine/methacholine is probably the best guide to the mechanical abnormality that allows airway to narrow too much and too easily to provoking stimuli.
Most authors assume that symptom score or the variability of PEF measurements indicate severity. Forced vital capacity (FVC) may be a better correlate of symptoms and perhaps the severity of an attack.
 
Good Parameters for Assessing Severity
Symptom scores, peak expiratory flow (PEF) on waking, bronchodilator use.
 
Scores
Table 1.1   Symptom score (Previous 3 months)
Symptom
Score
NIL for 3 months
0
< 1 per week
1
> 1 per week
2
Most days, waking at night
3
< 1 per week
Waking at night, > 1 per week
4
4
Table 1.2   Peak expiratory flow (PEF) (Previous 4 weeks)
Morning PEF%
Personal best (PB)
Score
> 93
0
85–93
1
78–85
2
70–78
3
< 70
4
Table 1.3   Bronchodilator score (Previous 3 months)
Bronchodilator use
Score
NIL for 3 months
0
< 1 per week
1
> 1 per week, not everyday
2
1–3 times a day
3
4 or more times a day
4
The above scores are calculated during a period when the child is free from exacerbations and it has been seen that a combined score correlates well with airway hyperreactivity. The most severe case would document a score of 12. There has been uniform consensus that there is no gold standard to measure the score.
 
Night Symptoms + PEF Variability Assess Severity Fairly Well
Measurement of severity of inflammation is not yet available. Nitrous oxide measurement and eosinophilic products in sputum may be the modalities for the future.
“Relationship between severity of inflammation and clinical manifestations of the disease has not yet been shown”.