Childhood Asthma : Epidemiology & Determinants, Pathophysiology
• Asthma is the most common chronic condition of childhood.
• The prevalence and severity of childhood asthma have increased substantially in recent years.
• Despite continued research and the development of new pharmacological agents, it is one of the leading causes for emergency care requirements; one of the leading causes for missed school, and a cause for considerable morbidity, disability, and occasional mortality at all ages.

Asthma is a diffuse obstructive lung disease due to inflammation of the airways, increased mucus production, contraction of the bronchial smooth muscles, with hyperactivity of the airways to a variety of stimuli, a high degree of reversibility of the obstructive process which may occur either spontaneously or as a result of treatment. (Reversible obstructive airway disease).

Current thinking is that regardless of severity, asthma is a chronic inflammatory disorder of the airways.

Epidemiology and Determinants of Pediatric Asthma
• Despite the fact that pediatric asthma has become an important public health problem, the major determinants of childhood asthma are still unknown. Familial / genetic role for etiology is the most important factor.
• Atopy is the strongest predisposing factor for development of asthma.
• More than fifty percent of all children who wheeze with viral infection of the lungs during the first years of life have a transient condition that rapidly subsides sometime after the preschool years.
• Those who persist to have wheezing at 6 years, who have history or tests suggestive of asthma-related allergies or atopy or have a positive family history of asthma, are more likely to have persistent symptoms until late childhood or even adult life.
• Environmental factors are also important and the most preventable predisposing factors. The common environmental triggers are cigarette smoke, animal proteins, pet related biological matter and dust mite. Environmental agents work in synergy with viral infections to alter reactivity of the airways.
• The prevalence of asthma varies from 5 -20 %.
• Severe asthma leading to death is seen in about 1 %. Hypoxia or air leaks are the main cause of deaths.

Main reasons for increased mortality are:
1. Faulty assessment of severity of illness either by doctor or patient.
2. Late or sub optimal hospital treatment.
3. Lack of medical care.
4. Lack of knowledge of disease.
5. Delayed use of steroids
6. Over dependence on inhaled ?2 agents.

• Classical triad:
1) Eosinophilia of the mucosa i.e. inflammation and thickening of airway,
2) Increased mucus secretion and
3) Contraction of smooth muscle of airways.
• Hyperresponsiveness or hyperreactivity is the characteristic feature in asthma. This refers to the ease with which airways narrow in response to various nonallergic and nonsensitizing stimuli, including inhaled chemical mediators (e.g., histamine, methacholine) and natural physical stimuli (e.g. exercise, hyperventilation of cold air). It is likely that airway insult from chronic hyperresponsiveness early in life may lead to chronic changes in both lung structure and function.
• Airway inflammation is a major contributor to the pathology of asthma. The inflammatory process includes infiltration of airways by eosinophils, activation of T cells and production of cytokines as well as other mediators involved in inflammation, an increase in mast cell numbers, and desquamation of airway epithelium. Chronic inflammatory process causes remodeling of the airways with mucosal thickening and smooth muscle hypertrophy even in mild asthmatics. Inflammation causes an associated increase in the existing airway hyperresponsiveness to a variety of stimuli.
• Airway obstruction is due to narrowing of bronchioles and causes increased airway resistance, resulting in low forced expiratory volumes and flow rates. Obstruction causes premature closure of airways and air trapping. The blockage of airways from secretions and wall thickening causes atelectasis which leads V/ Q mismatch and the various changes in blood gases. Air trapping leads to hyperinflation and raised intrathoracic pressure, which in turn causes increase in work of breathing and may cause airleaks (pneumothorax, pneumomediastinum, subcutaneous emphysema). Increased intrathoracic pressure may cause hypotension by reducing venous return. Hypotension can cause hypoxia and decreased tissue perfusion and also affect the compliance.

• Precipitating factors:
1. Allergens – food, animal, mold, spores, pollens, insects, infective agents and drugs.
2. Irritants – paint odors, sprays, perfumes, chemicals, smoke, cold air, cold water and cough.
3. Weather changes
4. Infection – viral, fungal (aspergillosis), bacterial (B. Pertussis), and parasitic (Toxocara, ascariasis)
5. Exercise (70 % of all asthmatics)
6. Emotional factors
7. Gastroeosophageal reflux – (Nocturnal Symptoms)
8. Allergic rhinitis
9. Endocrine – menstrual cycles, oral contraceptive pills and hyperthyroidism.
10. Sinusitis (Nocturnal symptoms)

Steps at Cellular level:
- IgE antibodies are synthesized by plasma cells, which are present on surface of respiratory tract.
- These IgE antibodies become reversibly fixed to surface receptors of mast cells & basophils (sensitized)
- Antigen attaches to the specific IgE on sensitized mast cells resulting in activation of mast cells and a cascade of biochemical reactions.
- This results in degranulation and release of preformed mediators (early phase mediators - histamine, ECF, NCF, heparin, PAF) within 30 minutes.
- Arachidonic acid is formed through activation of phospholipase.
- From arachidonic acid Leukotrienes are formed via the lipooxygenase pathway and prostaglandins via the cyclooxygenase pathway.
- These late phase mediators are responsible for late reaction, which develops 6 – 8 hrs after exposure to allergen. (leukotrienes, C4, D4, E4 ,collectively called Slow releasing substance of anaphylaxis previously)


Contributor Information and Disclosures

C T Deshmukh
Department of Pediatrics, KEM Hospital, Mumbai, India

First Created : 12/21/2000
Last Updated : 8/1/2015


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