Asthma in Childhood PDF

ASTHMA DR ODOCHI EWURUM DEPARTMENT OF PAEDIATRICS GREGORY UNIVERSITY, UTURU  INTRODUCTION Asthma is characterized by episodic wheezing and /or coughing with recognizable variable airways obstruction but responsive either spontaneously or to an effective bronchodilator ther...

ASTHMA DR ODOCHI EWURUM DEPARTMENT OF PAEDIATRICS GREGORY UNIVERSITY, UTURU  INTRODUCTION Asthma is characterized by episodic wheezing and /or coughing with recognizable variable airways obstruction but responsive either spontaneously or to an effective bronchodilator therapy. Asthma is a heterogenous condition where hereditary/genetic and environmental factors may interact.  INTRODUCTION Asthma characteristically affects the small and medium sized bronchi usually 2 to 5mm in diammeter. The airflow limitation in asthma results from bronchial spasm, mucosal oedema, excessive tenacious secretions. Asthma manifests with variety of symptoms, none of which is specific for asthma.  DEFINITION OF ASTHMA Asthma is a chronic inflammatory condition of the lung airways resulting in episodic airflow obstruction. ASTHMA is a syndrome characterised by ❖ Airway inflammation and remodelling ❖ Airway hyper-responsiveness and ❖ Variable but reversible airway/airflow obstruction.  BURDEN OF ASTHMA Asthma is a major non-communicable disease affecting both children and adults. In Nigeria, asthma is second only to pulmonary tuberculosis as a common chronic disease of children. Asthma is often under diagnosed and under treated particularly in low and middle income countries.  BURDEN OF ASTHMA Approximately 13 million people have clinical asthma in Nigeria. Asthma is commoner in industrialized nations, urban areas and affluent people. M:F is 1.3:1  AETIOLOGY OF ASTHMA Environmental exposures and inherent biological and genetic vulnerabilities have been implicated as causes of asthma. Respiratory exposures in this causal environment include inhaled allergens, respiratory viral infections, chemical and biological air pollutants such as environmental tobacco smoke.  AETIOLOGY OF ASTHMA Immune responses to these common exposures in the predisposed host can be a stimulus for prolonged, pathogenic inflammation and aberrant repair of injured airways tissues. Lung dysfunction (i.e., AHR and reduced airflow) therefore develops. Once asthma has developed, ongoing exposures appear to worsen it, leading to persistence of the symptoms and increasing the risk of severe exacerbations.  AETIOLOGY OF ASTHMA Certain factors lead to increased risk of developing asthma. They include; (1) History of asthma in close relatives such as parents and siblings. (2) Other allergic conditions such as eczema, rhinitis etc. (3) Urbanization. (4) Low birth weight  AETIOLOGY OF ASTHMA (4) Prematurity (5) Viral respiratory tract infections (6) Overweight or Obesity (7) Environmental allergens and irritants; indoor and outdoor pollution, house dust mite, moulds, exposure to chemicals, fumes, dust etc.  GENETIC BASIS Various studies have produced variable results; -More than 22 loci on 15 autosomal chromosomes have been linked to asthma -Asthma has been consistently linked with the interleukin(IL) 4 gene cluster on chromosome 5 -other genes include ADAM-33, genes for the postanoid receptor, genes on chromosome 5q31  GENETIC BASIS Some studies suggest dominant inheritance. Others believe that the gene locus is linked at the B sub unit of high- affinity IgE receptors. Major gene locus for expression of asthma are probably located on chromosome 11q13. Expression of genetic component of asthma probably linked the 11q13 locus to increased IgE concentration.  GENETIC BASIS CONTD. Linkage occurs in maternal alleles only. Binding of IgE to the high–affinity IgE receptor on the surface of mast cells lead to increased production of IgE. Suggestion is that atopy is transmitted through the mother more often than the father.  ENVIRONMENTAL BASIS The hygiene hypothesis. -There is observed increase in asthma prevalence in industrialized societies (assumed to be clean society) -The abundance of microbial fauna at birth protects against hyperactivity disorders  ENVIRONMENTAL BASIS -Exposure to microorganism during early developmental stages drive immune responses towards Th1 responses. -The Th1 type of responses is protective against atopic asthma. This is the immunological basis for hygiene hypothesis.  PATHOGENESIS OF ASTHMA Chronic inflammation is now accepted as the major disorder in asthma. The inflammatory process starts with a deviation in the maturation of helper T lymphocytes to a sub-type designated Th2 Th2 secretes soluble cytokines eg interleukin-3, GM-CSF, etc which lead to recruitment of Ig E, mast cells, basophils and eosinophils.  PATHOGENESIS OF ASTHMA In the presence of antigen, various toxic substances are released. Eg leukotrienes major proteins, eosinophil cationic protein, etc The toxic substances lead to denudation of bronchial epithelium leaving the sub-epithelial nerves exposed to external factors. The Th2 response, once established is difficult to reverse hence the toxic substances continually damage the epithelium. PATHOGENESIS OF ASTHMA contd. Other inflammatory mediators (via the arachidonic acid cascade) like cysteinyl leukotrienes open epithelial tight junctions, lead to epithelial shedding, plasma exudation and thickening of the basement membrane. Consequently the architecture of the bronchial epithelium is left in a state of anarchy (Jeffery P. Asthma, Academic press. 1998). Other substances (activation of protein kinase C and neuropeptide) lead to bronchoconstriction and increased mucus secretion.  PATHOPHYSIOLOGY OF ASTHMA The hallmark of asthma is airflow obstruction particularly involving the small and medium sized (2-5mm) bronchi. The obstruction is brought about when the resting bronchial hyper-reactivity(BHR) is exposed to trigger factors. Following the exposure to trigger factors, bronchoconstriction, mucosal edema and increased mucous secretion occur.  PATHOPHYSIOLOGY OF ASTHMA The resulting airway obstruction deprives the asthmatic of oxygen supply hence decreased oxygen saturation during asthma episode. Other effects include atelectasis and varying degree of abnormal lung function tests. Consequences of the airway obstruction and other air flow limiting events include; hyperinflation with a decrease in lung compliance, alveolar hypoventilation, pulmonary  PATHOPHYSIOLOGY OF ASTHMA vasoconstriction and decreased production of surfactant. With persistence of obstruction, hypercapnea ,acidosis, respiratory failure and death may occur. A ball-valve obstructive phenomenon like barrel chest is demonstrated during acute exacerbation of asthma, while evidence of loss of lung volume is seen in severe chronic asthma.  PATHOPHYSIOLOGY OF ASTHMA -There are many factors that trigger obstruction in asthma and they vary from one patient to another. -The trigger factors include; Viral infections Dusts and pollutants including cigarette smoke Allergens- House dust mites, pollens, molds, animal danders, certain foods, spores, etc  PATHOPHYSIOLOGY OF ASTHMA Exercise Drugs Changes in weather patterns and cold dry air Psychological factors such as stress and emotion Perfumes  ASTHMA PHENOTYPES PHENOTYPE: The outward, physical manifestation of the organism DISEASE PHENOTYPE: Cluster of either clinical or pathologic features which tend to be associated and which are useful in some way such as in managing the patient or understanding the mechanism of the disease  ESTABLISHED ASTHMA PHENOTYPES IN CHILDREN ▪ Transient wheezing ▪ Non-atopic wheezing in toddlers ▪ Ig E mediated wheeze/asthma ▪ Late onset childhood asthma IMPORTANCE OF ASTHMA PHENOTYPES TO PREDICT: Response to treatment Propensity for accelerated loss of pulmonary function and development of fixed airflow obstruction Asthma with predominant involvement of the peripheral (distal) airways - (Small Airways Disease)  FEATURES OF CHILDHOOD ASTHMA Asthma is a dual component disease (inflammation and bronchospasm). Symptoms and signs depend on the severity of the disease. Common symptoms include: Wheeze Shortness of breath Chest tightness Cough  FEATURES OF CHILDHOOD ASTHMA The hallmark of asthma is that these symptoms tend to be: Variable Intermittent Worse at night Provoked by triggers including exercise.  FEATURES OF CHILDHOOD ASTHMA contd. Additional Information include: Personal and family history of asthma or other atopic conditions. Worsening of symptoms following exposure to recognize triggers. Worsening symptoms with drugs.  FEATURES OF CHILDHOOD ASTHMA contd. Signs of asthma include: Rhonchi (Bilateral, diffuse, expiratory, polyphonic) Reduced lung function i. Decreased peak flow ii. Obstructive pattern on Spirometry Evidence of hyperinflation(wide AP diameter, hyperresonance, diminished breath sounds)  ASTHMA MIMICS Age dependent Include: Reflux oesophagitis, Tracheosophageal fistula, etc. Bronchiolitis, Pneumonia, Sinusitis etc. Pulmonary tuberculosis, Laryngeal papilomatosis etc. Cardiac failure and dilated cardiomyopathies Inhaled foreign bodies Tracheomalacia and Bronchomalacia Vocal cord dysfunction  ASTHMA DIAGNOSIS Definitive diagnosis of asthma can be difficult to obtain in young children Majority (43.45%) present at age group 2-6 years. Asthma can be diagnosed in infancy  ASTHMA DIAGNOSIS CONTD. METHODS OF DIAGNOSIS History/clinical features Basic investigations Eosinophils Ig E levels: Total, specific Prick skin test Blood gas analysis  ASTHMA DIAGNOSIS CONTD. Pulse oximetry Chest radiography (when indicated) Stool for ova/parasite Lung function test PEFR Spirometry-FEV1, FVC, FEV25-75, FEV/FVC Provocation test- Exercise test, methacholine/histamine Others  ASTHMA DIAGNOSIS Objective measures are essential for a correct and adequate diagnosis of asthma and the methods include: Bronchodilator responsiveness Diurnal variability in airway caliber/volume Free running exercise (6 minutes running exercise)  Objective measurements Asthma diagnosis is based on demonstration of airway reversibility and variable airflow limitations as measured with a spirometer (FEV1 and FVC) or a peak expiratory flow (PEF) meter: FEV1/FVC ratio less than 75%; or PEFR less than 80% of predicted or best PEFR increase more than 15%; 15-20 mins after inhalation of a rapid acting β2- agonist  Objective measurements PEFR decrease more than 15% ; 15-20 mins after inhalation of cholinergic drug PEFR fall more than 15% (12.5% Oviawe et al) after a 6 minutes of sustained running or other exercise PEFR varies more than 20% from morning measurement upon rising to measurement 12 hrs later in patients taking bronchodilator (more than 10% in patient who is not on bronchodilator)  SEVERITY OF ASTHMA Asthmatic child often falls into one of 4 categories based on severity of disease (GINA guidelines). Intermittent Mild persistent (chronic) Moderate persistent (chronic) Severe persistent (chronic)  SEVERITY OF ASTHMA Majority of children (65% Benin series) have intermittent asthma Only 1% of children have severe persistent asthma (stunting of growth, marked limitations of activity, various chest deformities and symptoms everyday). ASSESSMENT OF SEVERITY OF INTERVAL ASTHMA SEVERITY LEVEL DAYTIME NIGHT EXACERBATIO PEF OR FEV1 PEF SYMPTO TIME NS VARIABILITY MS B/W SYMPTOMS EXACERB B/W ATIONS EXACERBAT IONS INFREQUENT None None Brief, mild, >80% two per At least 80% Once per >Twice per May affect At least 80% 20%-30% PERSISTENT week but not month but activity and predicted everyday not every sleep week MODERATE Daily >Once per At least twice 60-80% >30% PERSISTENT week per week; predicted restrict activity or affect sleep SEVERE Continual Frequent Frequent: ≤60% >30% PERSISTENT restrict activity predicted  SEVERITY OF ASTHMA EPISODE This enables the clinician to institute appropriate mode of therapy Four levels are identifiable: Mild: PEFR more than 75% predicted. Moderate: PEFR 50 - 75% predicted. Severe: PEFR 33 – 50% predicted. Life threatening: PEFR less than 33% predicted. INITIAL ASSESSMENT OF ACUTE ASTHMA SYMPTOMS MILD MODERATE SEVERE OR LIFE THREATENING CONFUSED No No Agitated or Altered consciousness OXIMETRY ON 94% 94%-90% Less than 90% PRESENTATION(SaO2) TALKS Sentences Phrases Words or Unable to speak PULSE RATE (BEATS/ Less than 100 100-200 More than 200 MINUTE) INITIAL ASSESSMENT OF ACUTE ASTHMA Contd. SYMPTOMS MILD MODERATE SEVERE OR LIFE THREATENING CENTRAL CYANOSIS Absent Absent Likely to be present WHEEZE INTENSITY Variable Moderate to loud Often quiet PEF( PREDICTED OR More than 60% 40%-60% Less than 40% PERSONAL BEST) FEV1 (PREDICTED) More than 60% 40%-60% Less than 40% MANAGEMENT OF CHILDHOOD ASTHMA MANAGEMENT GOALS Reduction/elimination of symptoms especially at night Reduction or elimination on activity at home, school, and leisure Utilization of treatments with low incidence of side effects Maintenance of optimal growth and development Improvement in quality of life Reduction in asthma mortality MANAGEMENT OF CHILDHOOD ASTHMA The various stages in the management of childhood asthma include: Environmental Manipulation Partnership in asthma management Pharmacotherapy Immunotherapy  Environmental Manipulation – Most children above five years with asthma have identifiable allergy – Identify precipitating trigger factors – Counsel both parents and children on avoidance methods e.g. elimination of house dust and house dust mite  Environmental Manipulation – Avoidance of cigarette smoking by parents and others – Discourage families with asthmatic children from acquiring pets or operating poultry farm – Consider removal of patients from environment if efforts at removal of allergens from the environment fail. Partnership in Asthma Management – Establish good partnership with patient, parent and teacher. It is often said that physicians do not manage a child’s asthma, rather parents manage the asthma. – Train the child and/or the parent to recognize the signs and symptoms of asthma Partnership in Asthma Management – Instruct parents and patients on the use of drugs and apparatus for asthma control e.g. inhaler, spacer devices, peak flow meters etc. – Encourage self-referral (to parents, doctors etc) and self-medication.  Pharmacotherapy – Numerous drugs “relievers and preventative” are now available for asthma treatment. – Ideal drugs are B2 agonists to combat bronchoconstriction and corticosteroids as anti inflammatory agents. – Inhaler method i.e. local therapy is the preferred delivery method for the drugs. Children have difficulty using conventional metered dose inhalers (MDI), and therefore  Pharmacotherapy spacer devices are recommended with MDI. The ideal delivery method involves direct inhalation from the canister e.g. fluticazone and seretide discus – Recent therapeutic developments include Salmeterol, Nedocromil Sodium, Budesonide, Leukotriene receptor antagonist e.g. Zafirlukast etc.  Pharmacotherapy Contd – Compliance with therapy is a major problem in the management of childhood asthma. Therefore, polypharmacy should be avoided. – Two inhalers comprising B2 agonist and corticosteroid in a twice daily dosage will suffice in most cases. – Rationally, a combination of long acting B2 agonist (LABA) e.g Salmeterol and inhaled corticosteroid (ICS) e.g. Fluticazone should  Pharmacotherapy Contd be the ultimate in the management of persistent asthma in childhood. - The dose of the chosen drug is often tailored to the severity of the asthma and in a step wise fashion. – Recently, the International Treatment Guidelines endorsed the combination of a long acting B2 agonist and an inhaled corticosteroid in a single inhaler “GINA 2002” An example is Seretide.  IMMUNOTHERAPY This involves the use of allergin-specific immunotherapy Allergens are given to patients in repeated and increasing doses to provide immune tolerance Two methods of administration include; - Subcutaneous immunotherapy (SCIT) - Sublingual immunotherapy (SLIT)  IMUNOTHERAPY Both of them reduces the use of quick reliever and long-term control medications Improves quality of life and FEV1 Anaphylactic reaction is a rare complication.  INITIAL MANAGEMENT OF CHILDREN WHO HAVE ACUTE ASTHMA TREATMENT MILD EPISODE MODERATE EPISODE SEVERE/LIFE THREATENING Hospital admission Probably not Probably required Yes. Consider necessary required intensive care. Supplementary O2 Probably not May be required Required. Monitor required monitor SaO2 Sao2. Arterial blood gases may be required. Salbutamol (100 µg 4-6 puffs( Children< 6 puffs(Children< 6puffs(