Childhood asthma - etiopathogenesis,clinical manifestations and evaluation
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Childhood asthma - etiopathogenesis,clinical manifestations and evaluation



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Childhood asthma - etiopathogenesis,clinical manifestations and evaluation Childhood asthma - etiopathogenesis,clinical manifestations and evaluation Presentation Transcript

  • Dr. Lokanath Reddy Junior resident Dept of Paediatrics Kasturba Medical College Manipal CHILDHOOD ASTHMA - ETIOPATHOGENESIS CLINICAL FEATURES AND EVALUATION
  • CHILDHOOD ASTHMA  Definition  Epidemiology  Etiology  Pathogenesis  Clinical Manifestations  Differential diagnosis  Diagnosis and evaluation
  • DEFINITION Asthma* is a chronic inflammatory disorder of the airways that causes recurrent episodes of  wheezing  breathlessness  chest tightness  cough, particularly at night and/or early morning * Robbins and cotron’s pathologic basis of diseases
  • DEFINITION  These symptoms are usually associated with widespread but variable bronchoconstriction airflow limitation that is partly reversible spontaneously or with treatment
  • DEFINITION  The hallmarks of the disease are increased airway responsiveness to a variety of stimuli resulting in episodic bronchoconstriction inflammation of the bronchial walls and increased mucus secretion
  • EPIDEMIOLOGY STATISTICS* 1. Global Asthma Statistics  Accounts for about 1 in every 250 deaths worldwide ( 0.4%)  16 million (1.1% of total) DALYs (WHO, 2004)  ~ 300 million people worldwide currently have asthma * South Asia Network for Chronic Disease, New Delhi,
  • EPIDEMIOLOGY  Prevalence increases globally by 50% every decade*  Low prevalence rates (2%–4%) - Asian countries High prevalence rates (15%–20%)- Western world  Prevalence is rising sharply with increasing urbanisation and westernisation* * (Masoli et al. 2004). 1. Global Asthma Statistics
  • EPIDEMIOLOGY 2. Asthma statistics in India (WHO, 2004)  57,500 estimated total deaths / year  5.1 estimated deaths / 1,00,000 population  277 DALYs (disability adjusted life-year) / 100,000 population  Constitutes 0.2% of all deaths and 0.5% of National Burden of Diseases  Overall prevalence in India- 3% (30 million)* 3000/1lakh population *(Aggarwal et al. 2006).
  • EPIDEMIOLOGY  More prevalent in modern metropolitan cities and more affluent nations, and is strongly linked with other allergic conditions  In contrast, children living in rural areas of developing countries and farming communities are less likely to experience asthma and allergy.  Asthma prevalence is exceptionally high in five states: Tripura, Sikkim, Kerala,Mizoram,West Bengal
  • EPIDEMIOLOGY  Karnataka: 1000-2000 per 1,00,000  AP: 2000-3000 per 1,00,000  80% report disease onset prior to 6 years of age. However, of all children who have recurrent wheezing, only a minority go on to have persistent asthma in later childhood.  Allergy in young children has emerged as a major risk factor for the persistence of childhood asthma.
  • EARLY CHILDHOOD RISK FACTORS FOR PERSISTENT ASTHMA 1. Parental asthma (single-20%, both-60%) 2. Allergy Atopic dermatitis (eczema) Allergic rhinitis Food allergy Inhalant allergen sensitization 3. Severe lower respiratory tract infections requiring hospitalization Pneumonia Bronchiolitis 4. Wheezing apart from colds 5. Male gender 6. Low birth weight 7. Environmental tobacco smoke exposure 8. Possible use of acetaminophen (paracetamol) 9. Exposure to chlorinated swimming pools 10. Reduced lung function at birth 11. Eosinophilia (>4%)
  • ETIOLOGY  A combination of  Age  Environmental factors  Biological factors  Genetic factors
  • ETIOLOGY  Why asthma is common in children ??
  • AHR-Airway Hyper Responsiveness ETS-Environmental Tobacco Smoke.
  • ETIOLOGY A combination of environmental & genetic factors in early life shape how the immune system develops & responds to ubiquitous environmental exposures. Respiratory microbes, inhaled allergens & toxins can injure the lower airways Aberrant immune and repair responses to airways injury  persistent disease.
  • ETIOLOGY Prolonged pathogenic inflammation and aberrant repair of injured airways Lung dysfunction- Airway Hyperresponsiveness and reduced airflow In a growing lung adversely affect airway growth and differentiation Altered airways at mature ages Ongoing exposures worsen it
  • ETIOLOGY ENVIRONMENT 1.VIRUSES :  Injurious viral infections causing pneumonia & bronchiolitis are risk factors for persistent asthma in childhood Respiratory viruses causing recurrent wheezing 1. RSV 2. Rhinovirus 3. Influenza virus 4. Parainfluenza virus 5. Adenovirus 6. Human metapneumo virus
  • ETIOLOGY 2. AEROALLERGENS  Indoor and home allergens – Pollen,mites,dust etc.  Environmental tobacco smoke and air pollutants(ozone, sulfur dioxide)  Cold dry air & strong odors can trigger bronchoconstriction when airways are irritated.  Eliminating of offending allergen can lead to resolution of symptoms and sometimes “Cure” asthma.
  • ASTHMA TRIGGERS 1.Common viral infections of the respiratory tract 2.Aeroallergens in sensitized asthmatic patients Animal dander Indoor allergens Dust mites Cockroaches Molds 3.Seasonal aeroallergens Pollens (trees, grasses, weeds) Seasonal molds 4.Environmental tobacco smoke 5.Air pollutants Ozone Sulfur dioxide Particulate matter Wood- or coal-burning smoke Endotoxin, mycotoxins Dust ASTHMA TRIGGERS 6.Strong or noxious odors or fumes Perfumes, hairsprays Cleaning agents 7.Occupational exposures Farm and barn exposures Formaldehydes, cedar, paint fumes 8.Cold & dry air 9.Exercise 10.Crying, laughter, hyperventilation 11.Co-morbid conditions Rhinitis Sinusitis Gastroesophageal reflux
  • PATHOGENESIS 1. ATOPIC ASTHMA • Major etiologic factors in atopic asthma – Genetic predisposition to type I hypersensitivity “atopy” – Exposure to environmental triggers • Inheritance of susceptibility genes makes individuals prone to develop strong TH2 reactions against environmental antigens(allergens)
  • PATHOGENESIS Changes in airway in asthma  Increase in the no. of mucus-secreting goblet cells  Hypertrophy of submucosal glands  Basement membrane underlying the mucosal epithelium is thickened  Hypertrophy and hyperplasia of smooth muscle cells.
  • PATHOGENESIS Triggering of asthma (Priming or sensitization)  Allergen  TH2 cells  TH2 cells produce cytokines  IL-4 - stimulates the production of IgE;  IL-5-activates locally recruited eosinophils;  IL-13-stimulates mucus secretion from bronchial submucosal glands and also promotes IgE production by B cells.  IgE coats submucosal mast cells
  • PATHOGENESIS Immediate phase  Re-exposure to antigen  Ag-induced cross- linking of IgE bound to IgE receptors on mast cells  preformed mediators  directly or via neuronal reflexes Induce bronchospasm, by direct stimulation of subepithelial vagal (parasympathetic) receptors through both central and local reflexes (unmyelinated sensory C fibers). Increased vascular permeability and mucus production Recruit additional mediator-releasing cells from the blood
  • PATHOGENESIS Late phase  Largely consists of inflammation  Recruited leukocytes(N,E,B,L,M)  mediator release from leukocytes, endothelium, and epithelial cells.  Factors, particularly from eosinophils (e.g., major basic protein, eosinophil cationic protein), also cause damage to the epithelium.  Epithelial cells are known to produce a large variety of cytokines in response to infectious agents, drugs, and gases as well as to inflammatory mediators.
  • PATHOGENESIS  For example,eotaxin, produced by airway epithelial cells, is a potent chemoattractant and activator of eosinophils.  The major basic protein of eosinophils, in turn, causes epithelial damage and more airway constriction.  The long list of mediators in acute asthma can be subclassified by the clinical efficacy of pharmacologic intervention with inhibitors or antagonists of the mediators.
  • PATHOGENESIS MEDIATORS ACTION 1. Leukotrienes C4, D4, and E4 Extremely potent • prolonged bronchoconstriction • increased vascular permeability • increased mucus secretion 2. Acetylcholine, released from intrapulmonary parasympathetic nerves. Airway smooth muscle constriction by directly stimulating muscarinic receptors. 3. Histamine A potent bronchoconstrictor 4. prostaglandin D2 Bronchoconstriction and vasodilatation 5. platelet-activating factor Aggregation of platelets and release of histamine and serotonin from their granules. 6. IL-1, TNF, and IL-6, chemokines (e.g., eotaxin), neuropeptides, nitric oxide, bradykinin, and endothelins. chemoattractants and activators of eosinophils.
  • GENETICS  Asthma: A complex genetic trait in which multiple susceptibility genes interact with environmental factors to initiate the pathologic reaction.  Why Individual variability in symptoms ??  considerable variability in the expression of these genes and in the combinations of polymorphisms  More than 100 genes, many of these affect the immune response or tissue remodeling.  Some genes may influence the development of asthma, while others modify asthma severity or the patient’s response to therapy.
  • GENETICS  chromosome 5q: near the gene cluster encoding the cytokines IL-3, IL-4, IL-5, IL-9, and IL-13 and the IL-4 receptor. The receptor for LPS (CD14), and the gene for β2-adrenergic receptor also map here.  IL-13 gene: Polymorphisms in the IL-13 gene have the strongest and most consistent associations with asthma or allergic disease.  CD 14 gene: A gene encoding the monocyte receptor for endotoxin.Polymorphism of this TT genotype of CD14 shows variable response in different conditions
  • GENETICS • TT GENOTYPE OF CD14 : TH1 Vs TH2 RESPONSE(HYGEINE HYPOTHESIS) • High endotoxin levels  TH2 type, thus favoring more brisk IgE production and a predisposition to allergy. • Low endotoxin levels  TH1 type  protective against asthma or allergic sensitization • These studies indicate that the relationship between genotype and phenotype is context dependent, and help explain some of the discrepant results of association studies in different populations.
  • GENETICS • Class II HLA alleles: produce IgE antibodies against some but not all antigens, such as ragweed pollen. • ADAM-33: ADAM-33 belongs to a subfamily of metalloproteinases related to collagenases. It is expressed by lung fibroblasts and bronchial smooth muscle cells. • It is speculated that ADAM-33 polymorphisms accelerate proliferation of bronchial smooth muscle cells and fibroblasts, thus contributing to bronchial hyperreactivity and subepithelial fibrosis.ADAM-33 is also associated with decline in lung functions.
  • GENETICS • β2-adrenergic receptor gene: This also maps to 5q and variations in this gene are associated with differential in vivo airway hyper-responsiveness and in vitro response to β-agonist stimulation. • IL-4 receptor gene: Mutliple polymorphic variants in the gene encoding the alpha-chain of the IL-4 receptor are associated with atopy, elevated total serum IgE, and asthma.
  • GENETICS • Mammalian chitinase family: Chitinases are enzymes that cleave chitin, a polysaccharide contained in many human parasites and the cell walls of fungi. • In humans the chitinase family includes members with and without enzymic activity. • One member with activity, acidic mammalian chitinase, is up-regulated in and contributes to TH2 inflammation. • Another chitinase family member with no enzymatic activity, YKL-40, is associated with asthma. Serum levels of YKL-40 correlate with the severity of asthma
  • MORPHOLOGY • Status asthmaticus : Lungs are overdistended because of overinflation, with small areas of atelectasis. • Macroscopic: Occlusion of bronchi and bronchioles by thick, tenacious mucus plugs. • Histology: The mucus plugs contain whorls of shed epithelium, which give rise to the well-known spiral shaped mucus plugs called Curschmann spirals. • Numerous eosinophils and Charcot-Leyden crystals are present; the latter are collections of crystalloid made up of an eosinophil lysophospholipase binding protein called galectin-10.
  • MORPHOLOGY • “AIRWAY REMODELING” include: – Overall thickening of airway wall – Sub-basement membrane fibrosis (due to deposition of type I and III collagen beneath the classic basement membrane composed of type IV collagen and laminin) – Increased vascularity – An increase in size of the submucosal glands and mucous metaplasia of airway epithelial cells – Hypertrophy and/or hyperplasia of the bronchial wall muscle (this has led to the novel therapy of bronchial thermoplasty which reduces airway hyper- responsiveness for up to at least a year).
  • PATHOGENESIS 2. NON-ATOPIC ASTHMA – No evidence of allergen sensitization – Skin test results are usually negative. – A positive family H/O asthma is less common. – Respiratory infections due to viruses (e.g., rhinovirus, parainfluenza virus) are common triggers. – hyperirritability of the bronchial tree . – It is thought that virus-induced inflammation of the respiratory mucosa lowers the threshold of the subepithelial vagal receptors to irritants. – Inhaled air pollutants, such as SO2, ozone & NO2, may contribute to the chronic airway inflammation & hyperreactivity that are present in some cases.
  • PATHOGENESIS 3. DRUG-INDUCED ASTHMA • Aspirin-sensitive asthma, individuals with recurrent rhinitis and nasal polyps. (Sampter’s triad) • They are exquisitely sensitive to small doses of Aspirin as well as other NSAIDs, and they experience not only asthmatic attacks but also urticaria. • Mechanism: inhibiting the COX pathway of arachidonic acid metabolism without affecting the lipoxygenase route, thus tipping the balance toward elaboration of the bronchoconstrictor leukotrienes.
  • PATHOGENESIS 4. OCCUPATIONAL ASTHMA • Stimulated by fumes (epoxy resins, plastics), organic and chemical dusts (wood, cotton, platinum), gases (toluene), and other chemicals (formaldehyde, penicillin products). • Minute quantities of chemicals are required  to induce the attack usually occurs after repeated exposure. • Underlying mechanisms vary according to stimulus & include type I Hypersensitivity reaction.
  • LABORATORY FINDINGS PULMONARY FUNCTION TESTS • To confirm the diagnosis • To determine disease severity • Forced expiratory airflow measures are helpful in diagnosing and monitoring asthma and in assessing efficacy of therapy. – SPIROMETRY – PEFR
  • LABORATORY FINDINGS • Valid spirometric measures depend on a patient's ability to properly perform a full, forceful, and prolonged expiratory maneuver, usually feasible in children > 6 yr of age • If the FEV1 (forced expiratory volume in 1 sec) is within 5% on 3 attempts, then the highest FEV1 effort of the 3 is used. • In asthma, airways blockage results in reduced airflow with forced exhalation and smaller partial-expiratory lung volumes
  • LABORATORY FINDINGS • NON ASTHMATIC: No airflow limitation therefore no scooping. FEV1/FVC > 0.8 • ASTHMATIC : Note the “scooped” or concave appearance of the asthmatic expiratory flow- volume loops; with increasing obstruction, there is greater “scooping.” FEV1/FVC < 0.8 Measuring exhaled nitric oxide (FENO), a marker of airway inflam. in allergy-associated asthma, helps with anti-inflammatory management and in confirming the diagnosis of asthma.
  • LABORATORY FINDINGS FEV1, forced expiratory volume in 1 sec; FVC, forced vital capacity. LUNG FUNCTION ABNORMALITIES IN ASTHMA  Spirometry (in clinic): 1. Airflow limitation: Low FEV1 (relative to percentage of predicted norms) FEV1/FVC ratio <0.80 2. Bronchodilator response (to inhaled β-agonist): Improvement in FEV1 ≥12% and ≥200 mL* 3. Exercise challenge: Worsening in FEV1 ≥15%*  Daily peak flow or FEV1 monitoring: 1.Day to day and/or am-to-pm variation ≥20%*
  • LABORATORY FINDINGS PEFR monitoring devices -simple & inexpensive tools to measure airflow -monitoring PEFRs daily  indicator of asthma control • PEFR monitoring should be started by measuring morning & evening PEFRs (best of 3 attempts) for several weeks for patients to practice the technique, to determine a “personal best,” and to correlate PEF values with symptoms • PEFR variation >20% is consistent with asthma • Girls: 3.43 x ht – 180 lit/min • Boys: 2.98 x ht – 110 lit/min
  • LABORATORY FINDINGS  PEFR: Poorly controlled asthma
  • LABORATORY FINDINGS RADIOLOGY A) CHEST X RAY (PA & lateral views) normal, or subtle and nonspecific findings of hyperinflation (flattening of the diaphragms) and peribronchial thickening - helpful in identifying abnormalities that are hallmarks of asthma masqueraders (aspiration pneumonitis, hyperlucent lung fields in bronchiolitis obliterans), and complications during asthma exacerbations (atelectasis, pneumomediastinum, pneumothorax).
  • RADIOLOGY B) CT Scan: Bronchiectasis, clearly seen on HRCT scan  cystic fibrosis, allergic bronchopulmonary mycoses (aspergillosis), ciliary dyskinesias, or immune deficiencies.
  • NATURAL HISTORY  Onset can occur at any age but children & young adults are commonly affected age groups  5-10% of children with mild asthma go on to develop severe asthma later in life  Although Asthma cannot be cured, clinical episodes can largely be prevented & controlled by proper management.  Allergic rhinitis & skin allergy may coexist with or precede the onset of asthma.  Variability in the clinical course, persistence in some individuals and progression in others
  • TYPES OF ASTHMA CLINICAL CLASSIFICATION 1. TRANSIENT EARLY WHEEZING  Common in early preschool years  Recurrent cough/wheeze, primarily triggered by common respiratory viral infections  Tends to resolve during the preschool years, without increased risk of asthma in the later life  Reduced airflow at birth , S/O relatively narrow airways, improves by school age.
  • TYPES OF ASTHMA 2. PERSISTENT ATOPY ASSOCIATED ASTHMA  Begins in early preschool years  Associated with atopy in early preschool years:  Clinical: Atopic dermatitis in infancy, allergic rhinitis, food allergy  Biologic: Early inhalant allergen sensitization, Increased IgE, increased blood eosinophils  Highest risk for persistence into later childhood and adulthood  Lung function abnormalities: Those with onset < 3 yr acquire reduced airflow by school age  Those with later onset of symptoms, or with later onset of allergen sensitization, are less likely to experience airflow limitation in childhood
  • TYPES OF ASTHMA 3. NONATOPIC WHEEZING  Wheezing/coughing beginning in early life, often with respiratory syncytial virus infection; resolves in later childhood without increased risk of persistent asthma  Associated with bronchial hyperresponsiveness
  • TYPES OF ASTHMA 4. ASTHMA WITH DECLINING LUNG FUNCTION  Children with asthma with progressive increase in airflow limitation  Associated with hyperinflation in childhood, male gender
  • TYPES OF ASTHMA 5. LATE-ONSET ASTHMA IN FEMALES, ASSOCIATED WITH OBESITY AND EARLY- ONSET PUBERTY  Onset between 8 and 13 yr of age  Associated with obesity and early-onset puberty; specific for females
  • TYPES OF ASTHMA 6. OCCUPATIONAL-TYPE ASTHMA IN CHILDREN  Children with asthma ass. with occupational-type exposures known to trigger asthma in adults in occupational settings  E.g., endotoxin exposure in children raised on farms
  • CLINICAL FEATURES AND EVALUATION SYMPTOMS  Most common chronic symptoms  Intermittent dry coughing  expiratory wheezing  Older children  shortness of breath & chest tightness  Younger children  intermittent, non-focal chest pain  symptoms worse at night, especially during prolonged exacerbations  Daytime symptoms linked with physical activities or play,  self-imposed limitation of physical activities,  general fatigue (possibly due to sleep disturbance)  difficulty keeping up with peers in physical activities.
  • CLINICAL FEATURES AND EVALUATION HISTORY • Triggers: -physical exertion -hyperventilation (laughing) -cold or dry air -airways irritants • An environmental history is essential for optimal asthma management • Treatment H/O : symptomatic improvement with Rx with (Bronchodilators) supports the diagnosis of asthma.
  • CLINICAL FEATURES AND EVALUATION • Risk factors:  allergic conditions (allergic rhinitis, allergic conjunctivitis, atopic dermatitis, food allergies)  parental asthma  symptoms apart from colds • In clinic, quick resolution (< 10 min) or convincing improvement in symptoms & signs of asthma with administration of SABA
  • CLINICAL FEATURES & EVALUATION EXAMINATION Inspection: look of the child, retractions, respiratory rate, pattern of breathing Auscultation:  Expiratory wheezing and a prolonged expiratory phase - acute exacerbations • Crackles (or rales) and rhonchi - excess mucus production and inflammatory exudate in the airways.  Decreased breath sounds, commonly the right lower posterior lobe  regional hypoventilation owing to airways obstruction.
  •  Segmental crackles + poor breath sounds  lung segmental atelectasis  Severe exacerbations:  labored breathing and respiratory distress  inspiratory and expiratory wheezing  increased prolongation of exhalation,  poor air entry  suprasternal and intercostal retractions , nasal flaring, and accessory respiratory muscle use. • Status asthmaticus: silent chest CLINICAL FEATURES & EVALUATION
  • DIAGNOSIS CLINICAL FEATURES THAT INCREASE PROBABILITY OF ASTHMA More than one of the following symptoms: wheeze, cough, breathing difficulty, chest tightness, particularly if these symptoms: - frequent and recurrent - worse at night and in the early morning - occur in response to, or are worse after, exercise or other triggers, such as exposure to pets, cold or damp air, or with emotions or laughter - occur apart from viral infections Personal history of atopic disorder Family history of atopic disorder and/or asthma Widespread wheeze heard on auscultation History of improvement in symptoms or lung function in response to adequate therapy
  • DIAGNOSIS CLINICAL FEATURES THAT LOWER THE PROBABILITY OF ASTHMA Symptoms with viral infections only, with no interval symptoms Isolated cough in the absence of wheeze or breathing difficulty History of moist cough Prominent dizziness, light-headedness, peripheral tingling Repeatedly normal physical examination of chest when symptomatic Normal peak expiratory flow (PEF) or spirometry when symptomatic No response to a trial of asthma therapy Clinical features pointing to alternative diagnosis
  • DIFFERENTIAL DIAGNOSIS CLINICAL CLUES TO ALTERNATIVE DIAGNOSES IN WHEEZY CHILDREN PERINATAL AND FAMILY HISTORY POSSIBLE DIAGNOSIS Symptoms present from birth or perinatal lung problem Cystic fibrosis; chronic lung disease of prematurity; ciliary dyskinesia; developmental anomaly Family history of unusual chest disease Cystic fibrosis; neuromuscular disorder Severe upper respiratory tract disease Defect of host defence; ciliary dyskinesia SYMPTOMS AND SIGNS Persistent moist cough Cystic fibrosis; bronchiectasis; protracted bronchitis; recurrent aspiration; host defence disorder; ciliary dyskinesia Excessive vomiting Gastro-oesophageal reflux (± aspiration) Breathlessness with light-headedness and peripheral tingling Hyperventilation/panic attacks
  • DIFFERENTIAL DIAGNOSIS SYMPTOMS AND SIGNS POSSIBLE DIAGNOSIS Inspiratory stridor Tracheal or laryngeal disorder Abnormal voice or cry Laryngeal problem Focal signs in chest Developmental anomaly; post-infective syndrome; bronchiectasis; tuberculosis Finger clubbing Cystic fibrosis; bronchiectasis Failure to thrive Cystic fibrosis; host defence disorder; gastro-oesophageal reflux INVESTIGATIONS Focal or persistent radiological changes Developmental anomaly; cystic fibrosis; post-infective disorder; recurrent aspiration; inhaled foreign body; bronchiectasis; tuberculosis
  • EVALUATION IN EMERGENCY SETTING MILD MODERATE SEVERE SYMPTOMS 1.Breathlessness While walking At rest (softer cry, poor feeding) At rest (stops feeding) Can lie down Prefers sitting Sits upright 2. Talks in Sentences Phrases words 3. Alertness May be agitated Agitated Agitated, drowsy in SA
  • EVALUATION IN EMERGENCY SETTING SIGNS MILD MODERATE SEVERE 1. Respiratory rate increased increased >30 breaths/min 2. Use of accessory muscles, SSR Usually not commonly Usulally, (paradoxical thoracoabdominal – SA) 3. Wheeze Moderate; often only end- expiratory Loud; throughout exhalation Usually loud; throughout inhalation and exhalation Absence of wheeze-SA 4. Pulse rate (b/m) 100 100-120 >120, bradycardia-SA 5. Pulsus paradoxus Absent < 10mm Hg May be present 10-25mm Hg Often present,20-40mmHg Absence suggests respiratory muscle fatigue
  • EVALUATION IN EMERGENCY SETTING MILD MODERATE SEVERE FUNCTIONAL ASSESSMENT 1.PEFR >70% 40-69% <40% (<25%-SA) 2. PaO2 Normal >60mm Hg <60mm Hg, Cyanosis 3. PaCO2 <42 mmHg < 42mmHg >42mm Hg 4. SpO2 >95% 90-95% <90% Hypercapnia (hypoventilation) develops more readily in young children than in adults and adolescents
  • CLASSIFICATION OF ASTHMA SEVERITY INTERMITTENT PERSISTENT MILD MODERATE SEVERE IMPAIRMENT 1. Day time symptoms ≤2 days/week >2 days/week but not daily Daily Throughout the day 2. Nighttime awakenings - Age 0-4 yr 0 1-2/mo 3-4/mo >1/wk - Age >5 yr <2/month 3-4/mo >1/wk 7/wk 3. Short-acting β2-agonist use for symptoms ≤2 days/wk >2 days/wk but not daily, and not more than 1 on any day Daily Several times per day 4. Interference with normal activity None Minor limitation Some limitation Extreme limitation
  • CLASSIFICATION OF ASTHMA SEVERITY INTERMITTENT PERSISTENT MILD MODERATE SEVERE LUNG FUNCTION 1. FEV1 % predicted, age ≥5 yr Normal FEV1 between exacerbations, >80% predicted >80% predicted 60-80% predicted < 60% predicted 2. FEV1/FVC - Age 5-11 yr >85% >80% 75-80% <75% - Age >12 yr Normal Normal Reduced 5% Reduced >5% RISK Exacerbations requiring systemic steroids ≥ 2 exacerbations in 6 mo requiring systemic corticosteroids (or) ≥ 4 wheezing episodes/yr lasting >1 day and risk factors for persistent asthma - age 0-4 yr 0-1/yr - age >5yr 0-1/yr >2/yr >2/yr >2/yr
  • REFERENCES  Robbins and Cotran Pathologic Basis of Disease, Professional Edition, 8th ed.  Kliegman: Nelson Textbook of Pediatrics, 19th ed.  British Guideline on the Management of Asthma  Asthma : Sutapa Agrawal South Asia Network for Chronic Disease, New Delhi  Chernick: Kendig's Disorders of the Respiratory Tract in Children, 7th ed.