This is a detailed ppt of childhood asthma

1. Dr. Lokanath Reddy
Junior resident
Dept of Paediatrics
Kasturba Medical College
Manipal
CHILDHOOD ASTHMA -
ETIOPATHOGENESIS
CLINICAL FEATURES AND
EVALUATION

2. CHILDHOOD ASTHMA
 Definition
 Epidemiology
 Etiology
 Pathogenesis
 Clinical Manifestations
 Differential diagnosis
 Diagnosis and evaluation

3. 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

4. DEFINITION
 These symptoms are usually associated with
widespread but variable bronchoconstriction
airflow limitation that is
partly reversible
spontaneously or with treatment

5. 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

6. 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,
http://sancd.org/uploads/pdf/Asthma_factsheet.pdf

7. 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

8. 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).

9. 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

10. 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.

11. 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%)

12. ETIOLOGY
 A combination of
 Age
 Environmental factors
 Biological factors
 Genetic factors

13. ETIOLOGY
 Why asthma is common in children ??

14. AHR-Airway Hyper
Responsiveness
ETS-Environmental Tobacco
Smoke.

15. 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.

16. 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

17. 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

18. 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.

19. 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

20. ETIOLOGY

21. ETIOLOGY
 Cord blood IgE levels were high in first born babies
POSSIBLE ANTENATAL INFLUENCES ON THE
DEVELOPMENT OF ASTHMA AND ALLERGY

22. PATHOGENESIS
PATHOLOGICAL CLASSIFICATION
• ATOPIC ASTHMA
• NON ATOPIC ASTHMA
• DRUG INDUCED ASTHMA
• OCCUPATIONAL ASTHMA

23. 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)

25. 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.

27. 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

29. 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

30. 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.

31. 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.

32. 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.

33. 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.

34. 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

35. 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.

36. GENETICS

37. 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.

38. 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.

39. 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

40. 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.

41. 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).

42. 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.

43. 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.

45. 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.

46. 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

47. LABORATORY FINDINGS
SPIROMETRY
 AIRFLOW LIMITATION
 BRONCHODILATOR RESPONSE
 EXERCISE CHALLENGE

49. 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

50. 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.

51. 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%*

52. 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

53. LABORATORY FINDINGS
 PEFR: Poorly controlled asthma

54. LABORATORY FINDINGS

55. 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).

56. RADIOLOGY

57. RADIOLOGY
B) CT Scan: Bronchiectasis, clearly seen
on HRCT scan  cystic fibrosis, allergic
bronchopulmonary mycoses
(aspergillosis), ciliary dyskinesias, or
immune deficiencies.

58. 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

59. 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.

60. 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

61. 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

62. 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

63. 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

64. 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

65. 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.

66. 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.

67. 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

68. 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.

69.  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

70. 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

71. 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

72. 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

73. 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

74. 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

75. 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

76. 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

77. 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

78. 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

79. 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.