Asthma

C T Deshmukh
Department of Pediatrics, KEM Hospital, Mumbai, India
First Created: 12/21/2000  Last Updated: 12/21/2000

Introduction

  • 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.

Definition: 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. The familial/genetic role in etiology is the most important factor.

  • Atopy is the strongest predisposing factor for the development of asthma.

  • More than fifty percent of all children who wheeze with a 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 a 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 the 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 death.

Main reasons for increased mortality are:

  • Faulty assessment of the severity of illness either by doctor or patient.

  • Late or sub-optimal hospital treatment.

  • Lack of medical care.

  • Lack of knowledge of the disease.

  • Delayed use of steroids

  • Over-dependence on inhaled ß2 agents.

Pathophysiology

  • Classical triad:
    • Eosinophilia of the mucosa i.e. inflammation and thickening of the airway,

    • Increased mucus secretion and

    • Contraction of the smooth muscle of airways.

  • Hyperresponsiveness or hyperreactivity is the characteristic feature of asthma. This refers to the ease with which airways narrow in response to various nonallergic and non-sensitizing 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. The 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 the narrowing of bronchioles and causes increased airway resistance, resulting in low forced expiratory volumes and flow rates. The obstruction causes premature closure of airways and air trapping. The blockage of airways from secretions and wall thickening causes atelectasis which leads to V/Q mismatch and the various changes in blood gases. Air trapping leads to hyperinflation and raised intrathoracic pressure, which in turn causes an increase in work of breathing and may cause air leaks (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 compliance.
  • Precipitating factors:
    • Allergens - food, animal, mold, spores, pollens, insects, infective agents, and drugs.

    • Irritants - paint odors, sprays, perfumes, chemicals, smoke, cold air, cold water, and cough.

    • Weather changes

    • Infection - viral, fungal (aspergillosis), bacterial (B. Pertussis), and parasitic (Toxocara, ascariasis)

    • Exercise (70% of all asthmatics)

    • Emotional factors

    • Gastroesophageal reflux - (Nocturnal Symptoms)

    • Allergic rhinitis

    • Endocrine - menstrual cycles, oral contraceptive pills, and hyperthyroidism.

    • Sinusitis (Nocturnal symptoms)

    Steps at the Cellular level:

    • IgE antibodies are synthesized by plasma cells, which are present on the surface of the respiratory tract.

    • These IgE antibodies become reversibly fixed to surface receptors of mast cells & basophils (sensitized)

    • The 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 the 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 the late reaction, which develops 6-8 hrs after exposure to the allergen. (leukotrienes, C4, D4, E4, collectively called Slow releasing substance of anaphylaxis previously)

Clinical Features

Classical presentation of recurrent prolonged cough, often with breathlessness or wheeze, suggests asthma. Demonstration of a favorable clinical response to bronchodilators and, when measurable, bronchodilation by Pulmonary function test confirms the diagnosis. Positive family history for allergic diseases or asthma, although not essential, tends to support a suspected diagnosis of asthma.

The main symptoms and signs in asthma are cough, wheeze, tachypnea, dyspnea, and prolonged expiration. Other findings include anxiety, use of accessory muscles, monosyllabic speech, diaphoresis, fatigue, pulsus paradoxicus, cyanosis, hyperinflation, tachycardia, abdominal pain, and vomiting. The symptoms may come up acutely (exposure to aero-allergen) or insidiously (following viral infections).

Asthma is mainly diagnosed by history and physical examination but may be difficult in infants and young children. The diagnosis and estimation of asthma severity in smaller children depend on the history and response to therapy as assessed by inconstant third-party observations. In older children direct history and as well as the more objective assessment is possible.

Asthma management strategies require the identification of the clinical pattern of disease in the patient.

Clinical Patterns

  • Intermittent: Patients have episodic illness, with extended symptom-free periods. Episodes are most commonly triggered by viral respiratory infections or exposure to an environmental allergen or irritant.
  • Chronic: Patients experience virtually daily symptoms and, in the absence of continuous therapy, do not have extended symptom-free periods.
  • Seasonal allergic: Patients experience virtually daily symptoms during an inhalant allergy season. Allergens and seasonal patterns will vary with the geographic region. Seasonal symptoms may be in reaction to molds, pollens, or a combination of both.

There is a potential overlap among these clinical patterns. For example, patients with chronic diseases often have intermittent exacerbations from viral respiratory illness and may have seasonal allergic exacerbations. Nonetheless, the identification of the clinical pattern contributes to the determination of a therapeutic strategy.

Severity, as assessed by the degree of morbidity, is independent of the clinical pattern. Both intermittent and chronic disease may range from relatively benign to life-threatening. Severity should be judged by the frequency and intensity of urgent care requirements, missed school or work, and interference with activity or sleep.

The most important cause of death in an asthmatic is the failure to identify severe exacerbation of the disease. There are various scores to diagnose the severity of asthma. Following features are seen in a patient who has Severe acute symptoms:

Sensorium - Irritable or drowsy

Speech - Unable to talk more than a few words at a time.

Posture - Sit up leaning forward with the support of back with hands (tripod) or Limp.

Color - Cyanosis, pale, sweating

Use of accessory muscles of respiration

Respiratory rate - Tachypnoea or decreasing respiratory rate.

Pulse - pulsus paradoxux, tachycardia hypotension.

Chest findings - Loud wheeze, absence of wheeze, reduced air entry

O2 Saturation - less than 90-92% in room air

PEFR - less than 30-50% of normal

Wheeze need not be present for the diagnosis of asthma. If there is not a firmly established alternative diagnosis asthma should be considered when patients present with the following symptoms:

  • Recurrent/chronic lower respiratory tract wheezing

  • Recurrent/chronic cough
  • Repeated diagnosis of bronchitis
  • Repeated diagnosis of pneumonia not consistent with pyogenic infections

The diagnosis may be confirmed by demonstrating the complete response of symptoms, or spirometric measurement of airway obstruction, to an inhaled ß2 agonists and/or 5 to 10-day course of oral steroids.


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