Dr. Lokanath Reddy
Junior resident
Dept of Paediatrics
Kasturba Medical College
Manipal
CHILDHOOD ASTHMA -ETIOPATHOGENESISCLINICAL FEATURES AND EVALUATION
CHILDHOOD ASTHMA
Definition Epidemiology Etiology Pathogenesis Clinical Manifestations Differential diagnosis Diagnosis and evaluation
DEFINITIONAsthma* is a chronic inflammatory disorder of the airways that causes recurrent episodes of
wheezing breathlessness chest tightness cough, particularly
at night and/orearly morning
* Robbins and cotron’s pathologic basis of diseases
DEFINITION
These symptoms are usually associated withwidespread but variable bronchoconstrictionairflow limitation that is
partly reversiblespontaneously or with treatment
DEFINITION
The hallmarks of the disease areincreased airway responsiveness to a
variety of stimuliresulting in episodic bronchoconstrictioninflammation of the bronchial walls and increased mucus secretion
EPIDEMIOLOGYSTATISTICS*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, http://sancd.org/uploads/pdf/Asthma_factsheet.pdf
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
EPIDEMIOLOGY2. 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 ResponsivenessETS-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.
ETIOLOGYProlonged pathogenic inflammation and aberrant repair of injured airways
Lung dysfunction- Airway Hyperresponsiveness and reduced airflow
Altered airways at mature agesOngoing exposures worsen it
ETIOLOGYENVIRONMENT1.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
ETIOLOGY2. 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
ETIOLOGY
ETIOLOGY
Cord blood IgE levels were high in first born babies
POSSIBLE ANTENATAL INFLUENCES ON THE DEVELOPMENT OF ASTHMA AND ALLERGY
PATHOGENESIS
PATHOLOGICAL CLASSIFICATION• ATOPIC ASTHMA• NON ATOPIC ASTHMA• DRUG INDUCED ASTHMA• OCCUPATIONAL ASTHMA
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 cellsHypertrophy of submucosal glandsBasement membrane underlying the
mucosal epithelium is thickenedHypertrophy 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
PATHOGENESISImmediate phase Re-exposure to antigen Ag-induced cross-
linking of IgE bound to IgE receptors on mast cells preformed mediators directly or via neuronal reflexesInduce 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 phaseLargely 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
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).
PATHOGENESIS2. 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.
PATHOGENESIS3. 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.
PATHOGENESIS4. 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
SPIROMETRY AIRFLOW LIMITATION BRONCHODILATOR RESPONSE EXERCISE CHALLENGE
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 FINDINGSPEFR 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
LABORATORY FINDINGS
RADIOLOGYA) 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
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 CLASSIFICATION1. 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 ASTHMA2. 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 EVALUATIONSYMPTOMS Most common chronic symptoms
Intermittent dry coughingexpiratory 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 distressinspiratory and expiratory wheezingincreased prolongation of exhalation,poor air entrysuprasternal and intercostal retractions ,
nasal flaring, and accessory respiratory muscle use.
• Status asthmaticus: silent chest
CLINICAL FEATURES & EVALUATION
DIAGNOSISCLINICAL 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
DIAGNOSISCLINICAL 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 perinatallung problem
Cystic fibrosis; chronic lung diseaseof 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; protractedbronchitis; recurrent aspiration; hostdefence disorder; ciliary dyskinesia
Excessive vomiting Gastro-oesophageal reflux (± aspiration)
Breathlessness with light-headedness andperipheral 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-infectivesyndrome; 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; recurrentaspiration; 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 exhalationAbsence of wheeze-SA
4. Pulse rate (b/m) 100 100-120 >120, bradycardia-SA
5. Pulsus paradoxus
Absent< 10mm Hg
May be present10-25mm Hg
Often present,20-40mmHgAbsence 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 SEVERITYINTERMITTENT 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.