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.