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STUDY OF PEAK EXPIRATORY FLOW RATE AND
PULMONARY SCORE IN EVALUATION OF ACUTE
EXACERBATION OF ASTHMA IN THE AGE GROUP OF
5-18 YEARS
by
Dr. CHAITRA RAO B
Dissertation Submitted to the
Rajiv Gandhi University Of Health Sciences, Karnataka, Bangalore
In partial fulfillment of the requirements for the degree of
DOCTOR OF MEDICINE IN PAEDIATRICS
Under the guidance of
Dr. CHANDRAKALA P, MBBS, MD
Associate Professor
DEPARTMENT OF PAEDIATRICS
KEMPEGOWDA INSTITUTE OF MEDICAL SCIENCES
AND RESEARCH CENTRE
BANGALORE
2013
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Rajiv Gandhi University of Health Sciences, Karnataka
DECLARATION BY THE CANDIDATE
I hereby declare that this dissertation/thesis entitled “ STUDY OF PEAK
EXPIRATORY FLOW RATE AND PULMONARY SCORE IN EVALUATION
OF ACUTE EXACERBATION OF ASTHMA IN THE AGE GROUP OF 5-18
YEARS " is a bonafide and genuine research work carried out by me under the
guidance of Dr. CHANDRAKALA P, Associate Professor, Kempegowda Institute
of Medical Sciences and Research Centre , Bangalore.
Signature of the Candidate
Name: Dr CHAITRA RAO
B
Date:
Place: Bangalore
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Rajiv Gandhi University of Health Sciences, Karnataka
CERTIFICATE BY THE GUIDE
This is to certify that the dissertation entitled “ STUDY OF PEAK EXPIRATORY
FLOW RATE AND PULMONARY SCORE IN EVALUATION OF ACUTE
EXACERBATION OF ASTHMA IN THE AGE GROUP OF 5-18 YEARS " is a
bonafide research work done by Dr. CHAITRA RAO B in partial fulfillment of the
requirement for the degree of MD PAEDIATRICS
Date:
Place: Bangalore
Signature of the Guide
Name: Dr CHANDRAKALA P
Designation & Department
IV
Rajiv Gandhi University of Health Sciences, Karnataka
ENDORSEMENT BY THE HOD, PRINCIPAL/HEAD OF THE
INSTITUTION
This is to certify that the dissertation entitled “STUDY OF PEAK EXPIRATORY
FLOW RATE AND PULMONARY SCORE IN EVALUATION OF ACUTE
EXACERBATION OF ASTHMA IN THE AGE GROUP OF 5-18 YEARS" is a
bonafide research work done by Dr. CHAITRA RAO B under the guidance of Dr.
CHANDRAKALA P , Associate Professor , Kempegowda Institute of Medical
Sciences and Research Centre , Bangalore.
.
Place:
Seal & Signature of the Principal
Name: Dr M K SUDARSHAN
Date:
Place: Bangalore
Date:
Place: Bangalore
Seal & Signature of the HOD
Name: Dr A C RAMESH
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COPYRIGHT
Declaration by the Candidate
I hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall
have the rights to preserve, use and disseminate this dissertation / thesis in print or
electronic format for academic / research purpose.
©Rajiv Gandhi University of Health Sciences, Karnataka
Date:
Place: Bangalore
Signature of the Candidate
Name: Dr CHAITRA RAO B
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ACKNOWLEDGMENT
First, I thank God Almighty for all the grace he has bestowed upon me. This
dissertation is the culmination of the help, encouragement and guidance from a
number of people. I would like to thank them all.
It gives me immense pleasure to express my deep sense of gratitude and
indebtedness that I feel towards my teacher and guide Dr. CHANDRAKALA P,
Associate Professor of Paediatrics, Kempegowda Institute of Medical Sciences and
Research Centre, Bangalore, for her valuable suggestions, guidance, great care and
attention to detail that she has so willingly shown in the preparation of this
dissertation. I consider it to be a discrete privilege to have her as my guide and
teacher.
I am extremely thankful to Dr, M. K. SUDARSHAN, Dean, Principal and
Professor of Community medicine, for giving me an opportunity to conduct this
study.
I acknowledge and express my humble gratitude and sincere thanks to my
beloved teacher Dr. A. C. RAMESH, Professor and H.O.D, for his constant help to
undertake this study.
I thank Dr. SURESH, Medical Superintendent, Dr. (Capt.)
G.S.VENKATESH, Medical Director and Dr. VEERANNA, AMO, for allowing me
to conduct this study in their institute.
I owe a great deal of respect and gratitude to Dr. SRINIVASA S, Professor,
Dr. YASHODHA H.T, Professor, Dr. MURALI B. H, Associate Professor,
Dr. POORNIMA SHANKAR, Associate Professor, Department of Paediatrics, for
their scholarly suggestions and allround encouragement.
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I am immensely thankful to Dr. MADHU.G.N, Dr. H. S. RAMYA,
Dr. HARISH .J, Dr. SIVASHARANAPPA, Dr. GIRISH, Dr. SRINIVAS,
Dr. MOHAN KUMAR and Dr. CHAITRA, Assistant Professors in the Department
of Paediatrics for their kind guidance during the course.
I thank Dr. TANVIR, Dr. SHYLAJA and Dr. SNEHA, Senior Residents in
the Department of Paediatrics for their valuable support.
I thank Dr. LINGARAJ, Dr. MANJUNATH M. N, Dr. MANJUNATH V.
C, Dr. SANTOSH, Dr. DEVANG, Dr. GIRIJA, Dr. SHARANYA and all my other
Post graduate colleagues for their wholehearted support.
On a personal side, special thanks to my husband, Dr. I. S. SHRINIDHI, for
his patience, constant encouragement and support in the process of learning.
I shall forever be indebted to my parents, my in laws, my sister and friends for
their constant encouragement and support.
I am thankful to Mr PURANDER and Mr. BAABU for their cooperation.
Finally, I thank all my patients who formed the back bone of this study
without whom this study would not have been possible.
Date:
Place: Bangalore
Signature of the Candidate
Name: Dr CHAITRA RAO B
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LIST OF ABBREVIATIONS USED
AHR - Airway Hyperresponsivity
API -Asthma Predictive Index
AUC - Area under receiver operating characteristic curve
CAES - Clinical Asthma Evaluation Score
CAS - Clinical Asthma Score
CI -Confidence Interval
CO - Carbon monoxide
CO2 - Carbon dioxide
CSF - Cerebrospinal Fluid
CSGS - Clinical Symptom Grading System
CSS - Clinical Severity Score
DPI - Dry Powder Inhaler
ED - Emergency Department
FENO - Fractional Exhaled Nitric Acid
FEV1 - Forced Expiratory Volume in 1 second
FRC - Functional Residual Capacity
GINA - Global Initiative for Asthma
H+ - Hydrogen ions
H2O - Water
HFA -Hydroflouroalkanes
ICON -international consensus on on paediatric asthma
ICS - Inhaled Corticosteroid
ICU - Intensive Care Unit
IV - Intravenous
LABA - Long acting beta agonist
LTRA - Leukotriene Receptor Antagonist
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MPFM - mini-Wright peak flow meter
N2 - Nitrogen
NAEP - National Asthma Education Programme
O2 - Oxygen
OCS - Oral Corticosteroid
PaCO2 - Partial Pressure of arterial carbon dioxide
PaO2 - Partial Pressure of arterial oxygen
PASS - Paediatric Asthma Severity Score
PEFR - Peak Expiratory Flow Rate
PFM - Peak Flow Meter
PFT - Pulmonary Function Test
PI - Pulmonary Index
pMDI - pressurised metered dose inhaler
PRACTALL- practical allergy consensus report
PRAM - Preschool Respiratory Assessment Measure
PS - Pulmonary Score
RADI - Respiratory Distress Assessment Index
Raw - Airway resistance
RFO - Resistance to forced oscillation
RV - Residual Volume
SABA - Short acting beta agonist
SaO2 - Saturation of oxygen
SCIT - Subcutaneous Immunotherapy
SIT - allergen Specific Immunotherapy
SLIT - Sublingual Immunotherapy
SPSS - Statistical Product and Service Solutions
TLC - Total Lung Capacity
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ABSTRACT
Background & Objectives: Numerous asthma scoring systems have been devised
which combine a number of physical signs to estimate the severity of an acute asthma
exacerbation. Although more than 16 scoring systems exist, many are difficult to use.
The pulmonary score was developed to provide ‘‘user-friendly’’ measure of asthma
severity for children with acute asthma exacerbation. The objective of the study is to
study the efficacy of pulmonary score in assessing the severity of acute exacerbation
of asthma in comparison to peak expiratory flow rate and to compare pulmonary score
with peak expiratory flow rate.
Methods: The study sampled 50 children, aged 5–17 years, with mild to moderate
acute exacerbation of asthma. The PEFR (best of three attempts) and the PS were
measured before and after treatment at 5, 10 and 15 minutes. The PS includes
respiratory rate, wheezing, and retractions, each rated on a 0–3 scale. Pre- and post-
treatment PEFR and PS score were compared using paired t-tests to establish
construct validity. Correlation of pre- and post-treatment PSs with PEFRs was
measured to establish criterion validity.
Results: The mean predicted PEFR improved with treatment by 21.2% (from 50.8%
to 72.0% of predicted) (p <0.0001) at 15 minutes. The mean PS improved by 2.8
(from 4.8 to 2) (p < 0.0001) at 15 minutes. Pre- and post-treatment PSs were
significantly correlated with PEFRs. The correlation of pre-treatment PEFR and PS is
r = -0.497 (p = 0.000), that for post treatment at 15 minutes is r = -0.589 (p = 0.000).
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Interpretation & Conclusion: These data support the construct and criterion
validities of the PS as a measure of asthma severity among children. The PS is a
practical substitute to estimate airway obstruction in children who are too young or
too sick to obtain PEFRs.
Keywords: asthma; severity score; paediatric; validation; pulmonary score; PEFR.
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TABLE OF CONTENTS
SERIAL
NO
CONTENT PAGE NO
1 INTRODUCTION 1
2 OBJECTIVES 4
3 REVIEW OF LITERATURE
3.1 HISTORY 5
3.2 ANATOMY OF RESPIRATORY SYSTEM 12
3.3 PHYSIOLOGY OF RESPIRATORY SYSTEM 25
3.4 TYPES OF PULMONARY FUNCTION TEST 29
3.5 ASTHMA 31
3.6 PEAK FLOW METER 42
3.7 PULMONARY SCORING SYSTEM 49
4 MATERIALS AND METHODS
4.1 SOURCE OF DATA 52
4.2 INCLUSION CRITERIA 52
4.3 EXCLUSION CRITERIA 52
4.4 METHOD OF COLLECTION OF DATA 52-53
4.5 STATISTICAL METHODS 54
5 RESULTS 55
6 DISCUSSION 69
7 CONCLUSION 74
8 SUMMARY 75
9 BIBLIOGRAPHY 76
10 ANNEXURE
10.1 CONSENT FORM 81
10.2 ETHICAL CLEARANCE FOR DISSERTATION
STUDY
82
10.3 PROFORMA 83
10.4 KEY TO MASTER CHART 88
10.5 MASTER CHART 91
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LIST OF TABLES
Sl.No Tables Pages
1. Asthma control 33
2. Inhaled steroid dose equivalence 39
3. Assessment of Exacerbation Severity 41
4. Paediatric Respiratory Assessment Measure (PRAM) 50
5. Pulmonary Index Score 50
6. Characteristics of Validated Pulmonary Scores 51
7. Pulmonary Score 53
8. Mean and SD of PEFR &PS 55
9. Paired T Test for Construct Validity 55
10. Age distribution with Sex 58
11. Distribution of Socioeconomic status 59
12. Number of Days Missed in School in Last 12 months 60
13. Number of times child being treated in emergency in last 12 months 61
14. Number of times child being hospitalised overnight or longer in
last 12 months 62
15. Incidence of previous attacks 63
16. Triggering factors 64
17. Seasonal Variation 65
18. Associated factors 66
19. Type of medication used 67
20. Predicted Improvement of PEFR in Percentage 68
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LIST OF FIGURES
Serial no. Figures page nos.
1. Development of respiratory tree 13-14
2. Bronchopulmonary segments 17
3. Surface marking of lung 18
4. Regional distribution of cell types in respiratory tract epithelium 23
5. Alveoli and bronchiole 24
6. Classification of asthma 32
7. Pathogenesis of asthma 34
8. Treatment of asthma 37
9. Pharmacotherapy of asthma 38
10. PEFR instrument 43
11. Scatter Diagram for PEFR and PS before treatment 56
12. Scatter Diagram for PEFR and PS at 5 min 56
13. Scatter Diagram for PEFR and PS at 10 min 57
14. Scatter diagram for PEFR and PS at 15 min 57
15. Age Distribution with Sex 58
16. Distribution of socioeconomic status 69
17. Number of days missed in school in last 12 month 60
18. Number of times child being treated in emergency in last 12 months 61
19. Number of times child being hospitalised overnight or longer in
last 12 months 62
20. Incidence of Previous attacks 63
21. Triggering Factors 64
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22. Seasonal Variation 65
23. Associated factors 66
24. Predicted Improved of PEFR in Percentage 68
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1. INTRODUCTION
Bronchial asthma is undoubtedly one among the recurrent and chronic diseases of
childhood which calls for the attention of the paediatrician. Several epidemiological
studies have shown that the prevalence of this condition is increasing in developing
countries and India is no exception. The prevalence has increased to nearly 20- 30
percent in many parts of our country.
The availability of new diagnostic methods, a better understanding of the
pathophysiology of asthma and introduction of a number of drugs, both oral and
inhaled has revolutionized the management of asthma in children. It has also
increased the burden on the paediatrician to keep abreast with the advances as well as
educate the parents on the subjects.
But to the utter frustration of the paediatrician, parents are reluctant to use
these drugs in children because of the
(i) Expense
(ii) Widespread belief among parents that these aerosols are habit forming in
the long run and
(iii) Difficulty in convincing the parents that the preventive aerosols are to be
used even when the child is asymptomatic.
Typically wheezing attacks in young children are episodic, and interval
symptoms are frequently absent. Most children who wheeze before two years of age
rarely wheeze later and only a minority have symptoms three to five years after their
initial illness. Another group who wheeze in early life and still continue to have
wheezing at the age of six years have been noted to have a higher incidence of atopy
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and greater bronchial hyper-responsiveness (sensitivity). This group probably
represents the early onset of asthma in children.
Susceptibility to the development of asthma depends on the interaction of
multiple genes, coupled with environmental exposures. Understanding the precise role
of environmental exposures in the development of asthma is absolutely critical to
reducing the burden of this disease in children.
Accurate measurement of the severity of an acute asthma exacerbation is
important to guide initial treatment and to monitor response to subsequent therapy.
Clinical evaluation coupled with experience does not always accurately determine the
degree of airway obstruction. The most accurate method to measure severity is
spirometry, in which a number of pulmonary functions such as forced vital capacity
(FVC) and forced expiratory volume in 1 second (FEV1) are measured.
Unfortunately, spirometry requires special equipment not often available in the
emergency department, as well as staff trained to perform and interpret the results. In
the emergency department the peak expiratory flow rate (PEFR) is often used to
estimate the degree of airway obstruction in lieu of spirometry. However, spirometry
and PEFR are difficult methods for younger children to perform, or children of any
age with severe obstruction. Finally, some older children have difficulty performing
the expiratory manoeuvres for either PEFR or spirometry.
A number of asthma severity measures or scoring systems have been established
which combine a number of physical signs, such as respiratory rate and accessory
muscle use, to form an aggregate score that estimates the severity of an acute asthma
exacerbation. Although more than 16 severity scoring systems exist, many are
difficult to use. For example, some severity measures require blood gas analyses;
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others require numerous objective measures, or demanding assessments such as
inspiratory/expiratory ratios. Few scoring systems have been rigorously validated.
The pulmonary score (PS) was developed to provide a „„user-friendly‟‟ measure of
asthma severity for children with an acute asthma exacerbation.
The purpose of this study is to validate the pulmonary score as a measure of airway
obstruction in children presenting to the emergency department for treatment of an
acute asthma exacerbation.
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2. OBJECTIVES
To study the efficacy of pulmonary score in assessing the severity of acute
exacerbation of asthma in comparison to peak expiratory flow rate.
To compare pulmonary score with peak expiratory flow rate in measuring the
outcome of management of acute exacerbation of asthma.
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3. REVIEW OF LITERATURE
3.1 HISTORY
In 1984, Becker A B et al, published in his article” The pulmonary index.
Assessment of a clinical score for asthma” used a clinical score, the pulmonary index
(PI), in the emergency room assessment of children with acute asthma. The PI was
derived from respiratory rate, wheezing, inspiratory-expiratory ratio, and use of
accessory muscles. Patients were treated with a beta-adrenergic drug and were
assessed before and at 15-minute intervals after treatment using clinical examination,
PI, and spirometry. The PI before treatment correlated significantly with the mean
percent of forced expiratory volume in the first second to forced vital capacity ratio.
The PI 30 minutes after treatment correlated significantly with all tests of pulmonary
function performed. The PI is a simple score that is easily derived from clinical
observation1.
In 1988 , Baker M D , published “Pitfalls in the use of clinical asthma scoring” in
which he evaluated the correlation of the Wood-Downes-Lecks clinical asthma score
(CAS) with outcome in 210 consecutive known asthmatic children presenting to an urban
emergency department for treatment of acute asthma. CAS was assigned before each
treatment phase and before disposition from the emergency department and Ten-day
follow-up information was collected by telephone. While no differences in pre-treatment
CASs were found between outcome groups, disposition CASs were found to be
significantly higher in patients eventually admitted to the hospital as opposed to those
discharged home. However, CASs were not effective in identifying either those patients
who required prolonged hospitalization (greater than 24 hours) or those who sustained
ongoing disability following discharge home from the emergency department. These data
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indicate that the CAS alone is not a reliable indicator of severity of acute asthma of
childhood as judged by subsequent disability 2.
In 1992, Kimura Y et al, published in his article “Relationship between arterial
blood gas tensions and a clinical score in asthmatic children”. Clinical scoring system
devised by Mitsui was used in the study. This scoring system is constructed by
evaluating only the clinical symptoms and signs such as dyspnoea, wheezing,
auscultation of rales, speech impairment, cyanosis and mental status. All patients were
less than 5 years old. The clinical scores had a statistically significant correlation with
PaO2. High scores definitely were associated with hypoxemia but low scores did not
exclude hypoxemia. Scores showed good correlation with the values of PaCO2
compared with the values of PaO2. Scores under 3 were associated with PaCO2
values less than 40 mmHg; scores over 7, with PaCO2 over 40 mmHg.
Reproducibility was good, and there was a good relationship between scores and
blood gas tensions in individuals. Rales correlated with PaO2. Dyspnoea and cyanosis
had good correlation with PaCO2 3.
In 1996, Parkin P C et al, published “Development of a clinical asthma score
for use in hospitalized children between 1 and 5 years of age”. The objective was to
develop a clinical asthma score (CAS) for use in hospitalized children between 1 and
5 years of age. Formal approaches to item selection and reduction, reliability,
discriminatory power, validity and responsiveness were used. The final CAS
consisted of five clinical characteristics: respiratory rate, wheezing, in drawing,
observed dyspnoea and inspiratory-to-expiratory ratio. Interrater reliability was high
(weighted kappa = 0.82), and the CAS was discriminatory (Ferguson's delta = 0.92).
The CAS was valid, with a strong correlation with length of hospital stay (Spearman's
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correlation = 0.47, p < 0.05) and drug dosing interval (Spearman's correlation = -0.58,
p < 0.01). The CAS was responsive, with a significant change in CAS from admission
to discharge (Wilcoxon signed rank test, p < 0.01). This score, for use in hospitalized
preschool children, is reliable, discriminatory, valid, and responsive4.
In 2000, Chalut DS et al, published “The Preschool Respiratory Assessment
Measure (PRAM): a responsive index of acute asthma severity” A prospective cohort
study was performed in 217 children aged 3 to 6 years who presented with acute
asthma. Respiratory resistance measured by forced oscillation served as a gold
standard. Children were randomized to either the test group, in which multivariate
analyses were performed to elaborate the PRAM, or the validation group, in which the
characteristics of the PRAM were tested. For the test group (N = 145), the best
multivariate model contained 5 variables: wheezing, air entry, contraction of scalene,
suprasternal retraction and oxygen saturation. In the validation group (N = 72), the
PRAM correlated substantially with the change in resistance (r = 0.58) but modestly
with the percentage predicted resistance measured before (r = 0.22) and after
bronchodilation (r = 0.36). A change of 3 (95% CI: 2.2, 3.0) indicated a clinically
important change. PRAM appears to be a responsive but moderately discriminative
tool for assessing acute asthma severity. This measure, designed for preschool-aged
children, has been validated against a concurrent measure of lung function 5.
In 2002, Sharon R Smith et al, studied “Validation of the Pulmonary Score:An
Asthma Severity Score for Children” The study enrolled a convenience sample of
children, aged 5–17 years with acute asthma exacerbations. The PEFR and the PS
were measured before and after the first albuterol treatment by a physician and a nurse
from a pool of 45 trained observers. The PS includes respiratory rate, wheezing, and
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retractions, each rated on a 0–3 scale. Forty-six subjects completed the study. Mean
percent predicted PEFR improved after treatment by 20.7% (p = 0.0001), and mean
PS by 1.5 for nursing-obtained scores (p < 0.0001) and 1.9 for physician-obtained
scores (p < 0.0001). Pre- and post-treatment PSs were significantly correlated with
PEFR. The PS is a practical substitute to estimate airway obstruction in children who
are too young or too sick to obtain PEFRs 6.
In 2004, Gorlick MH et al, published “Performance of a novel clinical score,
the Pediatric Asthma Severity Score (PASS), in the evaluation of acute asthma” This
was a prospective cohort study of children treated for acute asthma at two urban
paediatric emergency departments . A total of 852 patients were enrolled at one site
and 369 at the second site. Clinical findings were assessed at the start of visit, after
one hour of treatment, and at the time of disposition. Peak expiratory flow rate
(PEFR) (for patients aged 6 years and older) and pulse oximetry were also measured.
Composite scores including three, four, or five clinical findings were evaluated, and
the three-item score (wheezing, prolonged expiration, and work of breathing) was
selected as the PASS. Interobserver reliability for the PASS was good to excellent
(kappa = 0.72 to 0.83). There was a significant correlation between PASS and PEFR
(r = 0.27 to 0.37) and pulse oximetry (r = 0.29 to 0.41) at various time points. The
PASS was able to discriminate between those patients who did and did not require
hospitalization, with area under the receiver operating characteristic curve of 0.82.
Finally, the PASS was shown to be responsive, with a 48% relative increase in score
from start to end of treatment and an overall effect size of 0.62, indicating a moderate
to large effect 7.
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In 2004, Birken CS et al, published “Asthma severity scores for preschoolers
displayed weaknesses in reliability, validity, and responsiveness” A Medline search
was used to identify published asthma severity scores for use in preschool children.
The measurement properties of the scores (item development, reliability, validity,
responsiveness, and usability) were evaluated using a published framework. Ten
asthma severity scores were identified, with 19 different clinical variables used as
items. Interrater agreement was assessed by five scores. Only two scores--Clinical
Asthma Score (CAS) and Respiratory Distress Assessment Index (RDAI)--reported
good agreement based on weighted kappa-statistics (0.64-0.90). Construct validity
was reported by the CAS, Clinical Asthma Evaluation Score (CAES), the Clinical
Symptom Grading System (CSGS), and the Preschool Respiratory Assessment
Measure (PRAM). Correlation coefficients between asthma severity scores and
clinical measures (length of stay, drug dosing interval, O2 saturation, health
professional assessment, PaO2, PaCO2) ranged from 0.47 to 0.70. Responsiveness
was formally demonstrated for two scales (PRAM, CAS). Most asthma severity scales
for use in preschool children have been informally developed. Recently developed
scores (CAS, PRAM) have more rigorously evaluated their measurement properties8.
In 2008, Ducharme FM et al, studied “The Pediatric Respiratory Assessment
Measure: a valid clinical score for assessing acute asthma severity from toddlers to
teenagers”. In a prospective cohort study, they examined the validity, responsiveness,
and reliability of the PRAM in children aged 2 to 17 years with acute asthma. The
study involved more than 100 nurses and physicians who recorded the PRAM on
triage, after initial bronchodilation, and at disposition. Predictive validity and
responsiveness were examined using disposition as outcome. The PRAM was
recorded in 81% (n = 782) of patients at triage. The PRAM at triage and after initial
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bronchodilation showed a strong association with admission (r = 0.4 and 0.5,
respectively; P < .0001), thus supporting its ability to distinguish across severity
levels. The responsiveness coefficient of 0.7 indicated good ability to identify change
after bronchodilation. The PRAM showed good internal consistency (Cronbach alpha
= 0.71) and inter-rater reliability (r = 0.78) for all patients and across all age groups9.
In 2004, Gorlick MH et al, published “Difficulty in obtaining peak expiratory
flow measurements in children with acute asthma”, a prospective cohort study. PEFR
was to be measured in all children age 6 years and older before therapy and after each
treatment with inhaled bronchodilators. Registered respiratory therapists obtained
PEFR and evaluated whether patients were able to perform the manoeuvre adequately.
456 children, 6 to 18 years old (median 10 years), were enrolled; 291 (64%) had
PEFR measured at least once. Of those in whom PEFR was attempted at least once,
only 190 (65%) were able to perform adequately. At the start of therapy, 54%
(142/262) were able to perform PEFR. Of the 120 who were unable to perform
initially, 76 had another attempt at the end of the ED treatment, and 55 (72%) were
still unable to perform. A total of 149 patients had attempts at PEFR both at the start
and end of treatment, of these, only 71 (48%) provided valid information on both
attempts. Patients unable to perform PEFR were younger (mean +/- SD = 8.7 +/- 2.8
years) than those who were able to perform successfully (11.2 +/- 3.2 years) and those
with no attempts (10.0 +/- 3.4 years). Children admitted to the hospital were more
likely to be unable to perform PEFR (58/126 = 46%) than those discharged from the
ED (43/330 = 13%, P < 0.0001)10
.
In 2010, Serge Gouin et al, published “Prospective evaluation of two clinical
scores for acute asthma in children 18 months to 7 years of age”, a prospective cohort
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study among 18 months to 7 years of age who had an asthma exacerbation. The
primary outcome was a length of stay (LOS) of >6 hours in the ED or admission to
the hospital. Clinical findings and components of the PRAM and the PASS were
assessed by a respiratory therapist (RT) at the start of the ED visit and after 90
minutes of treatment. During the study period, 3,845 patients were seen in the ED for
an asthma exacerbation. Moderate levels of discrimination were found between a LOS
of >6 hours and/or admission and PRAM (area under the receiver-operating
characteristic curve [AUC] = 0.69, 95% confidence interval [CI] = 0.59 to 0.79) and
PASS (AUC = 0.70, 95% CI = 0.60 to 0.80) as calculated at the start of the ED visit.
Significant similar correlations were seen between the physician's judgment of
severity and PRAM (r = 0.54, 95% CI = 0.42 to 0.65) and PASS (r = 0.55, 95% CI =
0.43 to 0.65)11
.
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3.2 ANATOMY OF RESPIRATORY SYSTEM
Development of respiratory system 12
The respiratory system is an outgrowth of the ventral wall of the foregut, and the
epithelium of the larynx, bronchi and alveoli are of endodermal origin. The
cartilaginous and muscular components are mesodermal origin. In the fourth week of
development the trachea is separated from the gut by the oesophagotracheal septum,
thus dividing the foregut into lungs anteriorly and oesophagus posteriorly.
Complete development of the respiratory system occurs through three distinct
processes-
1) Morphogenesis or formation of all the necessary structures: Morphogenesis of
the respiratory system is divided into five periods that includes- Embryonic
periods (4-6 weeks), Pseudo glandular period (6-16 weeks), Canalicular period
(between 16 weeks and 26-28 weeks), Saccular period (26 weeks to birth) and
Alveolar period (32 weeks of gestation-2 years of age). Morphogenesis of
respiratory system is regulated by some genes (HOX gene family) and
expression of some of these genes is controlled by retinoic acid. This may be
related to possible therapeutic role of retinoic acid at later stages of lung
development or in injured lungs.
2) Adaptation to air breathing: The transition from placental dependence to
autonomous gas exchanges requires adaptive changes in the lungs. These
changes include the production of surfactant in the alveoli, the transformation
of the lung from a secretory to a gas exchanging organ and establishment of
parallel pulmonary and systemic circulations.
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3) Post natal development: The post natal development of the lungs can be
divided into two stages-
First stage extends from birth to 18 months, in this stage there is
disproportionately increase in the surface and volume of the compartments involved
in gas exchange. This process is particularly active during early infancy and, contrary
to the previous belief may reach completion within the first 2 years instead of the first
8 years of life.
Second stage, all compartments grow more proportionately to each other.
Alveolar and capillary surface expand in parallel with somatic growth. Final size of
the lungs depends on factors such as subject‟s level of activities and prevailing states
of oxygenation (altitude).
FIGURE 1: DEVELOPMENT OF RESPIRATORY TREE
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Development of the respiratory tree and diaphragm. A-C, Development of the
endodermal respiratory tree D, Major epithelial populations in the early embryo from
a left dorsolateral view. The lung buds are bulging into the laterally placed
pericardioperitoneal canals. E, F, Formation of the diaphragm: E shows the
diaphragmatic components from a left dorsolateral view, and F shows the
diaphragmatic components viewed from above.
15
Division of respiratory system
A. According to functions of the respiratory system
Air conducting division: Composed of small cavity, nasopharynx, larynx, trachea,
bronchi and bronchioles.
Respiratory division: Composed of respiratory bronchioles, alveolar ducts, atrium,
alveolar sac and alveoli
B. According to size of the airway
Large airway: When size is more than 2mm.
Small airway: When size is less than 2mm.
C. Clinical division of respiratory system
Upper respiratory tract: This includes the nose, nasopharynx and oropharynx
Lower respiratory tract: This includes inlet of larynx, larynx, trachea, bronchi and
lungs. Clinical division largely related to spread of infection rather than any further
anatomical concept. But some authors describe upper respiratory tract includes nose
to larynx (up to lower border of cricoid cartilage) & lower respiratory tract includes
trachea to lungs 16
.
16
Lungs 13
The lungs are a pair of respiratory organs situated in the thoracic cavity. They
are spongy in texture and right lung is about 60 gm heavier than the left. Both lungs
have apex, base, costal & medial surfaces, and anterior, posterior & inferior borders.
Right lung is divided by two cleft (oblique& horizontal fissure) into 3 lobes; left lung
is divided by a single cleft (oblique fissure) into two lobes. The left upper lobe has a
lingular segment corresponding to the middle lobe of the right lung. Each lung has a
hilum through which principal bronchi enter the lungs along with arteries, and veins
and lymphatic‟s come out.
Each lung lobe is divided into bronchopulmonary segments which are defined
as the tertiary or segmental bronchi together with the portion of the lung lobe they
supply. These bronchopulmonary segments, ten in number in right lung and nine in
left lung, are roughly pyramidal in shape, their apices towards the hilum, their bases
lying on the surface of the lung.
The trachea bifurcates into right and left principal bronchi. The right principal
bronchus, shorter and more vertical than the left, is about 2.5 cm long and enters the
root of the right lung opposite the 5th
thoracic vertebra. The left principal bronchus,
narrower than the right, is nearly 5 cm long and enters the root of the lung opposite
the 6th
thoracic vertebra. On entering the lungs, the primary bronchi giving rise to 3
bronchi in the right lung and two in the left lung, each of which supplies a pulmonary
lobe. Each lobar bronchus gives of repeated branches to supply bronchopulmonary
segment, and by further ramification it ends to atrium. Atrium then leads to rounded
alveolar sacs.
17
The wall of the intrathoracic airways contains a spiral layer of smooth muscle
which is functionally a syncytium. On contraction, this smooth muscle produces
narrowing and shortening of airway.
FIGURE 2:BRONCHOPULMONARY SEGMENTS
18
FIGURE 3: SURFACE MARKING OF LUNG
19
Blood supply
The bronchial arteries supply nutrition to the bronchial tree and to the pulmonary
tissue. Bronchial system drains mainly into the pulmonary venous system. The
pulmonary circulation serves the respiratory function and the bronchial arteries are the
source of nutrition.
Nerve supply
Lung tissue is supplied by sympathetic nerves derived from T2
–T5
and
parasympathetic nerves derived from vagus.
Lymphatics
There are two sets of lymphatics, both drains into the bronchopulmonary nodes:
Superficial vessels drain the peripheral lung tissue beneath the pulmonary pleura and
flow round the borders of the lung and margins of the fissures.
Deep lymphatic‟s drain the bronchial tree, pulmonary vessels and connective tissue,
septa and accompany them towards the hilum, where they drain into the
bronchopulmoanry nodes. From upper lobes lymphatic‟s drain to superior
tracheobronchial lymph nodes and from lower lobes to the inferior tracheobronchial
lymph nodes.
20
Anatomical difference between the lungs of children and adult (14)
The anatomical differences between the lungs of child and the lungs of the adult:
1. Conducting airways are proportionately larger than the respiratory airways in
children compared with adult.
2. Airway resistance is more in the newborn and young child than in adult.
3. The diameter of the conducting airways are small in the infant than adult and
more easily obstructed by inflammation, by mucus secretion and by the
foreign bodies.
4. The chest wall and supportive structure of infants are softer so that chest wall
retraction during respiratory distress is greater in infants than in older patients.
5. Airway of young infant contains relatively more mucous glands than the
airway of adult and there are also age differences in the composition of the
mucus. Increased volume of mucus possibly contributes to airway obstruction
in infants.
6. The airway is probably more collapsible in response to pressure changes in
early life than in adult.
7. In infants, the collateral pathway of ventilation (the pores of Kohn and canal
of Lambert are less developed but in adult they are well developed and prevent
collapse distal to occlusion of small bronchus or bronchioles.
21
Diaphragm(15)
The diaphragm is a curved musculofibrous sheet that separates the thoracic
from the abdominal cavity. Its mainly convex upper surface faces the thorax, and its
concave inferior surface is directed towards the abdomen. The positions of the domes
or cupola of the diaphragm are extremely variable as they depend on body build and
the phase of ventilation. Thus the diaphragm will be higher in short, fat people than in
tall, thin people, and over inflation of the lung, as occurs for example in emphysema,
causes marked depression of the diaphragm. Usually, after forced expiration the right
cupola is level anteriorly with the fourth costal cartilage and therefore the right nipple,
whereas the left cupola lays approximately one rib lower. With maximal inspiration,
the cupola will descend as much as 10 cm, and on a plain chest radiograph the dome
coincides with the tip of the sixth rib. In the supine position, the diaphragm will be
higher than in the erect position, and when the body is lying on one side, the
dependent diaphragm will be considerably higher than the uppermost one.
Microstructure of trachea, bronchi and lungs16
The conducting airways are lined internally by a mucosa, and the epithelium
lies on a thin connective tissue lamina propria. External to this is a sub mucosa, also
composed of connective tissue, in which are embedded airway smooth muscle,
glands, cartilage plates (depending on the level in the respiratory tree), vessels,
lymphoid tissue and nerves. Cartilage is present from the trachea to the smallest
bronchi but is absent (by definition) from bronchioles.
The extra pulmonary and larger intrapulmonary passages are lined with
respiratory epithelium, which is pseudo stratified, predominantly ciliated, and
22
contains interspersed mucus-secreting goblet cells. There are fewer cilia in terminal
and respiratory bronchioles, and the cells are reduced in height to low columnar or
cuboidal. The epithelium of smaller bronchi and bronchioles is folded into
conspicuous longitudinal ridges, which allow for changes in luminal diameter.
Six distinct types of epithelial cell have been described in the conducting airways,
namely, ciliated columnar, goblet, Clara, basal, brush and neuroendocrine .
Lymphocytes and mast cells migrate into the epithelium from the underlying
connective tissue
The epithelium of the alveoli is flat and called type I and type II pneumocytes.
Type I cells completely cover the luminal surface of the alveoli and type II secretes
surfactant. The air in the alveoli is separated from capillary blood by 3 layers of cells
and membrane referred to collectively as the blood-air barrier:
The cytoplasm of the epithelial cells
The fused basal lamina of closely apposed epithelial and endothelial cells.
The cytoplasm of the endothelial cells.
Particles of less than 300 Da size, if lipid soluble are readily absorbed. Breaks in the
intercellular junction may enhance absorption. Cigarette smoke is a potent cause of
such breaches. Exposure to smoke in early childhood may lead to increase respiratory
disease by this mechanism.
23
FIGURE 4: Regional distribution of cell types in respiratory tract epithelium
24
FIGURE: 5 ALVEOLI AND BRONCHIOLE
25
3.3 PHYSIOLOGY OF RESPIRTORY SYSTEM17
The obvious goal of
respiratory system is to provide oxygen to the tissues and to remove carbon dioxide.
To achieve this, respiration can be divided into four major functional events:
1) Pulmonary ventilation, which means the inflow and outflow of air between the
atmosphere and the lung alveoli.
2) Diffusion of oxygen and carbon dioxide between the alveoli and blood.
3) Perfusion of the lungs by the flow of blood through the pulmonary capillary
which transport O2
and CO2
to and from the cell.
4) Regulation of ventilation and other factors of respiration.
Pulmonary ventilation
Mechanics of pulmonary ventilation: The lungs can be expanded and contracted in
two ways- 1) by downward and upward movement of the diaphragm to lengthen or
shorten the chest cavity and 2) by elevation and depression of the ribs to increase and
decrease the anteroposterior diameter of the chest cavity.
The mechanics of respiration is done by the process of inspiration and expiration.
Inspiration is an active process. The movement of the diaphragm account for about
75% of changes in intrathoracic volume. Diaphragmatic contraction increases vertical
diameter of the chest cavity and contraction of external intercostals muscles draw the
ribs laterally thereby increasing transverse diameter (Bucket handle effect) and
elevates the anterior end of the ribs thereby draw the sternum forward and increase the
anteroposterior diameter of the chest cavity (Pump handle effect) . During quiet
breathing the intrapleural pressure at the base of the lungs which is about –2.5 mm Hg
26
(relative to atmospheric) at the start of inspiration, decreases to about –6 mm Hg. The
lungs are pulled into a more expanded position. The pressure in the airway becomes
slightly negative and air flows into the lung. At the end of inspiration, the lung recoil
pulls the chest back to the expiratory position, where the recoil pressures of the lungs
and chest wall balance. The pressure in the airway 12 becomes slightly positive and
air flows out of the lungs. Expiration during the quiet breathing is positive in the sense
that no muscles which decreases intrathoracic volume contract. However, there is
some contraction of the inspiratory muscles in the early part of expiration. This
contraction exerts a breaking action on the recoil forces and slows expiration. This
expiration is a passive process, accompanied by elastic recoil of lung and chest wall.
Work of breathing: The work of inspiration can be divided into three different
fractions 1) that required to expand the lungs against its elastic forces, called the
elastic work or compliance works 2) that required to overcome the viscosity of the
lungs and chest wall structures, called tissue resistance work; and 3) that required to
overcome airway resistance, called airway resistance work. During quiet respiration
no muscle work is performed during expiration. In heavy breathing or when airway
resistance used tissue resistance are great, expiratory work does occur. This is
especially true in asthma in which airway resistance increases many fold. During
nasal breathing in infancy, about 50% total resistances are nasal, 25% from glottis and
large central airway and remainder 25% from peripheral. Thus infant are prone to
respiratory difficulty with upper airway obstruction.
Compliance of the lungs: The extent to which the lung expands for each unit increase
in transpulmonary pressure is called their compliance (Stretchability). The normal
27
total compliance of both lungs in an adult averages about 200 ml/Cm of H2O pressure,
that is 1 cm of H2O transpulmonary pressure changes – lungs expands 200 millilitres .
Surfactant: Surfactant is a surface tension lowering agent lining the interior of the
alveoli produced by type II alveolar epithelial cells. Surfactant is a mixture of
Dipalmitoylphosphatidyl choline (DPPC), phosphatidylglycerin, other lipid and
proteins. It prevents collapse of the alveoli at expiration and prevents pulmonary
oedema. Surfactant is important at birth for normal breathing.
Dead space and uneven ventilation: Since gas exchange in the respiratory tract
occurs only in the terminal portions of the airways, the volume of air that merely fills
the conducting passage without taking part in the gas exchange is called the dead
space. In an average man it is equal to 150 ml and children are 2.2 ml/Kg (18).
Because of this dead space, the amount of air ventilating the alveoli or alveolar
ventilation is (500-150) X12 or 4.2L/m. Because of the dead space, rapid, shallow
breathing produces much less alveolar ventilation than slow, deep respiration at the
same respiratory minute volume (tidal volume time‟s respiratory rate).
It is convenient to distinguish between the anatomic dead space (respiratory tract
volume excluding the alveoli) and the physiological (total) dead space (volume of air
not equilibrating with blood). In health, the two dead spaces are identical; but in
disease states, some of the alveoli may be underperfused or some may be
overventilated. The volume of air in the nonperfused alveoli and any volume of air in
the alveoli in excess of that necessary to arterialize the blood in the alveolar
capillaries are part of the physiological dead space.
28
Lung volumes and capacities: The amount of air that moves into the lungs with each
inspiration or the amount that moves out with each expiration is called the “tidal
volume”. The air inspired with a maximal inspiratory effort in excess of tidal volume
is the “inspiratory reserve volume”. The volume expelled by an active expiratory
effort after passive expiration is the “expiratory reserve volume” and the air left in the
lungs after a maximal expiratory effort is the “residual volume”. The space in the
conducting zone of the airways occupied by gas that does not exchange with blood in
the pulmonary vessels is the “respiratory dead space”. The volume of air that can be
forcefully expired after a normal expiration is called “inspiratory capacity” and the
volume of air that remains in lung after a normal expiration is called “functional
residual capacity” which is the sum of expiratory reserve volume and residual
volume. ”Total lung capacity” is the volume of air that remain in lungs after forceful
inspiration “The vital capacity” is the amount of air that can be forcefully inspired
after a forceful inspiration, is frequently measured clinically as an index of pulmonary
function. The fraction of the vital capacity expired in 1 second is „timed vital
capacity‟, also called “forced expired volume in 1 second or FEV1” gives additional
information; the vital capacity may be normal but the FEV1 greatly reduced in
diseases such as asthma. The amount of air inspired per minute is “pulmonary
ventilation” or “respiratory minute volume” is normally about 6 L (500 ml/breathX12
breaths)
Regulation of respiration: Rhythmical discharges originating from the „respiratory
centre‟ in the brain stem provide the basis for co-ordinated respiratory movements.
From the respiratory centre impulses travel in the autonomic fibres to reach the spinal
motor neurons which drive the respiratory muscles. Impulses mediating conscious
changes in breathing travel via the pyramidal tracts. The activity of the respiratory
29
centre is modified by a variety of chemical and neural stimuli so that respiration can
meet the changing metabolic needs of the body. Chemical stimuli arises from
peripheral and central chemoreceptor‟s, sensitive to changes in H+, CO2 and O2
concentration of the blood. Ventilation is increased when the peripheral
chemoreceptors in carotid and aortic bodies are stimulated by hypercapnia, acidosis or
hypoxia. Central chemoreceptors in the brain stem are stimulated by increased in H+
concentration of CSF. A rise in PCO2 of the arterial blood is accompanied by
increasing acidity of both blood and CSF, and therefore stimulates both central and
peripheral chemoreceptors.
3.4 TYPES OF PULMONARY FUNCTION TESTS18
1. Ventilator function can be assessed by :
Spirometry: It will give the results of the volumes and flow rates, flow
volume loops peak expiratory flow rate, Volume-Time Curve combined
resistance of lung and airway.
Bronchial provocative tests: Aerosol bronchodilators, histamine,
methacholine and exercise challenge.
Peak expiratory flow rate (PEFR): Can be measured by peak flow meter.
Plethosmography: To see will give the results of total lung capacity (TLC),
Functional residual capacity (FRC), and Residual volume (RV), and Air
way resistance (Raw), total lung volume.
Gas dilution: (helium dilution in closed circuit or N2 wash out in an open circuit)
- For lung volumes (Total lung capacity).
Oesophageal pressure: For lung volumes (Total lung capacity)
30
Single breath or multiple breath nitrogen (N2) washes out: To see distribution of
ventilation
Forced oscillator: To see respiratory resistance (airway, lung and chest wall
resistance)
Pneumotachograph: To see flow.
2. Diffusion of gas (Gas exchange) can be assessed by-
Blood gas analysis: To see gas exchange. O2 and CO2 through the
respiratory membrane.
Measurement of diffusing capacity: The carbon monoxide (CO) method.
Pulse oximetry: To see oxygen saturation.
3. Perfusion can be assessed by catheterization.
4. Ventilation-perfusion can be assessed by radionuclide lung.
31
3.5 ASTHMA24
DEFINITION: Asthma is a chronic inflammatory disorder associated with
variable airflow obstruction and bronchial hyper responsiveness. It presents with
recurrent episodes of wheeze, cough, shortness of breath, and chest tightness.
Definitions often include more details, such as specific cell types (e.g. mast
cells, eosinophils, etc.), timing of symptoms (particularly at night or early morning),
and reversibility (often), or triggers (viral infection, exercise, and allergen exposure).
The relative importance of each of these additional elements can be argued;
nevertheless, they are neither necessary for nor exclusive to asthma and therefore do
not add appreciably to the sensitivity or specificity of the previously mentioned,
generally accepted elements.
32
FIGURE 6: CLASSIFICATION:
Paediatric asthma is a diverse condition and several factors can be used for its
classification. Important changes in clinical presentation take place in relation to
age (upper left). Although limits are arbitrary and may differ between
individuals, infancy, preschool age, school age and adolescence are generally
considered as milestones. Phenotypes (upper right) may result from different
underlying pathophysiologies (endotypes), however, there is considerable
overlap and possible changes over time. Severity (lower left) can range from
very mild to life-threatening; although not necessarily discrete, a stepwise
approach has been used to characterize severity and inform treatment initiation.
More recently, the level of control (lower right) of both current symptoms and
risk of future morbidity is preferred as a measure, towards which asthma
management is evaluated.
33
TABLE 1: ASTHMA CONTROL
Pathogenesis and pathophysiology
There is general agreement that asthma is a disease of chronic inflammation,
airway hyper responsiveness, and chronic structural changes known as airway
remodelling.
Persistent asthma is universally regarded as a disease of chronic airway
inflammation. Increased populations of mast cells, eosinophils, lymphocytes,
macrophages, dendritic cells, and others contribute to inflammation. Structural cells
such as epithelial cells and smooth muscle cells may also contribute to the
inflammatory milieu. The inflammatory and structural cells collectively produce
mediators such as cytokines, chemokines, and cysteinyl leukotrienes that intensify the
inflammatory response and promote airway narrowing and hyper responsiveness.
AHR is associated with excessive smooth muscle contraction in response to
nonspecific irritants and viral infections, and for allergic individuals, exposure to
specific allergens. Neural mechanisms, likely initiated by inflammation, contribute to
AHR.
34
FIGURE 7: PATHOGENESIS OF ASTHMA
Acute episodes of airway narrowing are initiated by a combination of oedema,
infiltration by inflammatory cells, mucus hyper secretion, smooth muscle contraction,
and epithelial desquamation. These changes are largely reversible; however, with
disease progression, airway narrowing may become progressive and constant.
Structural changes associated with airway remodelling include increased smooth
muscle, hyperaemia with increased vascularity of subepithelial tissue, thickening of
basement membrane and subepithelial deposition of various structural proteins, and
loss of normal distensibility of the airway. Remodelling, initially described in detail in
adult asthma, appears to be also present in at least the more severe part of the
spectrum in paediatric asthma.
Natural history: Among children who wheeze before the age of 3 years, the majority
will not experience significant symptoms after the age of 6 years. Nevertheless, it
appears that decrements in lung function occur by the age of 6 years, predominantly
35
in those children whose asthma symptoms started before 3 years of age. The Asthma
Predictive Index (API) uses parental history of asthma and physician diagnosis of
atopic dermatitis as major criteria, along with peripheral blood eosinophilia, wheezing
apart from colds, and physician diagnosis of allergic rhinitis as minor criteria, to
predict disease persistence at the age of 6 years, in children younger than 3 years with
a history of intermittent wheezing. As shown in at least three independent
populations, the API holds a modest ability to predict disease persistence into early
school age. Infants with recurrent wheezing have a higher risk of developing
persistent asthma by the time they reach adolescence, and atopic children in particular
are more likely to continue wheezing. In addition, the severity of asthma symptoms
during the first years of life is strongly related to later prognosis. However, both the
incidence and period prevalence of wheezing decrease significantly with increasing
age.
Diagnosis and differential diagnosis
History:
Recurrent respiratory symptoms (wheeze, cough, dyspnoea and chest tightness)
Typically worse at night or early morning , exacerbated by exercise , viral infection ,
smoke , dust , pets , mold , dampness , weather changes , allergens
Personal history of atopy (eczema, food allergy, allergic rhinitis)
Family history of asthma or atopic diseases
36
Physical examination:
Chest auscultation for wheezing
Signs of other diseases such as eczema
Evaluation of lung function-spirometry and PEFR with reversibility testing
Evaluation of atopy (skin prick test or serum IgE)
Studies for exclusion of other diagnosis (chest x ray)
Therapeutic trial
Evaluation of airway inflammation (FENO, sputum eosinophils)
Evaluation of bronchial hyper responsiveness (nonspecific bronchial challenge:
methacholine , exercise)
Differential diagnosis
Infectious and Immunological disorders
Allergic bronchopulmonary aspergillosis, anaphylaxis, bronchiolitis, immune
deficiency, recurrent respiratory tract infections, rhinitis, sinusitis, sarcoidosis,
tuberculosis.
Bronchial pathologies
Bronchiectasis, bronchopulmonary dysplasia, cystic fibrosis, primary ciliary
dyskinesia
37
Mechanical obstruction
Congenital malformations, enlarged lymph nodes or tumours, foreign body aspiration,
laryngomalacia/tracheomalacia, vascular rings/laryngeal webs, vocal cord
dysfunction.
Other systems
Congenital heart disease, gastroesophageal reflux disease, neurogenic (aspiration),
psychogenic cough
FIGURE 8: TREATMENT
Asthma management should
be „holistic‟, including all
the elements necessary to
achieve disease control:
patient and parent education,
identification and avoidance
of triggers, use of appropriate medication with a well-formed plan, and regular
monitoring, are all crucial for success. Management should be adapted to the available
resources.
38
FIGURE 9: PHARMACOTHERAPY
The stepwise approach to asthma treatment in childhood aims at disease control.
Reliever medication should be used at any level of severity/control, if symptoms
appear/exacerbate.
Step 0: mildest spectrum of the disease, no controller medication is needed.
Step 1: use of one controller medication
Step 2: use of two medications, or a double dose of inhaled steroid, can be
used.
Step (3-4): In more difficult cases, increase of inhaled steroid dose, alone or in
combination with additional medication is needed
Step (5): Oral corticosteroids are kept as the last resort, for very severe patients.
Among biological treatments, Omalizumab has specific indications for children
at step 3 or higher. Stepping up or down should be evaluated at regular intervals,
39
measured by level of control. Treatment adherence, exposure to triggers and
alternative diagnoses should always be considered before stepping up. It should be
stressed that medications in each step are not identical, in either efficacy or safety, and
preferred choices can be described, especially for different age groups.
TABLE 2: INHALED STEROID DOSE EQUIVALENCE
Inhaled medication delivery devices:
0-5 years: pMDI with static treated spacer and mask or mouthpiece.
>5 years: pMDI with static treated spacer and mouthpiece, DPI (rinse or gargle
after inhaling ICS), breath actuated pMDI
Nebuliser: second choice at any age
Immunotherapy
Allergen-specific immunotherapy (SIT) involves the administration of
increasing doses of allergen extracts to induce persistent clinical tolerance in patients
with allergen-induced symptoms. Subcutaneous immunotherapy (SCIT) has been
shown to be clinically effective in allergic asthma, leading to a significant reduction in
40
symptoms, airway hyper responsiveness, and medication requirements. These effects
are generally considered to be greatest when standardized, single-allergen extracts of
house dust mites ,animal dander, grass, or tree pollen are administered, whereas
definitive evidence is currently lacking for the use of multi-allergen extracts and for
mold and cockroach allergens.
In clinical practice, allergen is typically administered for 3–5 years. A specific
age limit, above which SIT can be initiated, has not been clearly defined; PRACTALL
suggests that it may represent an acceptable intervention above 3 years of age, while
GINA <5 years suggests that no recommendation can be made at this age, because of
scarce evidence.
SIT has some important advantages over conventional pharmacological
treatment; first, it is the closest approach to a causal therapy in allergic asthma;
second, its clinical effect has been shown to persist after discontinuation of treatment;
and third, SIT has been linked with a preventive role against the progression of
allergic rhinitis to asthma and the development of sensitization to additional allergens.
Apart from common local side effects at the injection site, systemic reactions
(including severe bronchoconstriction) may occasionally occur, and these are more
frequent among patients with poor asthma control. SIT is not recommended in severe
asthma, because of the concern of possible greater risk for systemic reactions.
According to GINA, the option of immunotherapy should only be considered when all
other interventions, environmental and pharmacologic, have failed.
However, in such unresponsive condition, the efficacy of immunotherapy is
neither warranted.
41
Sublingual immunotherapy (SLIT) is painless and child friendly in terms of
administration route, offering the desirable option of home dosing and a more
favourable safety profile compared to SCIT.
Asthma exacerbation definition
An exacerbation of asthma is an acute or sub acute episode of progressive
increase in asthma symptoms, associated with airflow obstruction.
TABLE 3: ASSESSMENT OF EXACERBATION SEVERITY
42
3.6 PEAK FLOW METER
A peak flow meter is a small hand-held
device that measures how fast a person can blow
air out of the lungs when there is forceful
exhalation, after maximum inhalation. This
measurement is called the „peak expiratory
flow‟ (PEF). The peak flow meter helps to
assess the airflow through the airways and thus
help to determine the degree of obstruction
along them.
The measurement of PEF was pioneered
by Dr Martin Wright who produced the first
meter specifically designed to measure this
index of lung function. Since the original design
was introduced in the late 1950s, and the subsequent development of a more portable,
lower-cost version (the „Mini-Wright‟ peak flow meter), other designs and copies
have become available across the world. Brands of electronic peak flow meters are
also being marketed.
A peak flow meter (Figure 10) consists of a housing which has within it a
channel along which a pointer is movable to a distance dependent on the lung function
of the patient using the meter. Positioned adjacent to the channel, are two or more
indicators which move along an axis parallel with the channel. Each indicator presents
to view, two visually distinguishable areas defining a boundary that can be set at a
43
point along the path of the pointer to indicate limit positions relating to lung function.
This indicates to the user when to take remedial action
Physiological consideration and historical background
The basis of most of the various single-breath methods is the same: the
volume of air expired is measured against time by means of a spirometer with either a
recording drum or a timing device. There are some differences of opinion about the
most suitable interval of time over which to measure the volume and about the
relative merits of a recording drum or a timing device, but it is generally agreed that
methods of this kind are clinically valuable. All the methods, however, suffer from the
disadvantage that the necessary apparatus is cumbersome and normally requires
connection to an electric supply. Attention has therefore been directed to the
possibility of using the maximum forced expiratory flow rate (or “peak flow rate”),
instead of what is in effect the average for a limited time, as a measure of ventilator
capacity; such a measurement seemed likely to lend itself to the use of a simpler
instrument, consisting merely of a flow meter with a device for recording the
maximum flow.
According to Donald (1953) the empirical use of a measurement of this kind is
very old. “The physician asked a patient with respiratory disease to whistle or blow a
candle out was crudely assessing the maximum respiratory velocities”.
Donald suggested that a “simple, whistle-like instrument” might be developed
and might become a standard clinical tool.
44
Later on the instrument, called a “pneumometer” incorporates an aneroid manometer
fitted with a device for recording the maximum flow rate. Rates up to about 700
L/min. can be recorded.
Pneumotachograph has led to many observations of the expiratory flow pattern
but no systematic attempt to use the peak flow rate as a physiological measurement in
its own right appears to have been made. Pneumotachograph themselves have had
very low resistances (of the order of 2 mm. H2O/100 L/min) which gave a linear
relationship between flow and pressure. Both the earlier and the latest forms of
pneumotachograph suffer from the disadvantage of being fairly complicated and not
easily portable. A much simpler and more robust and portable instrument, designed
specifically for measuring the peak flow rate, called by them the “puffmeter”. Wright
and McKerrow described the peak flow meter in 1959. Since that time the instrument
has been used widely and has been found reliable over long periods. The Wright peak
flow meter depends upon the rotation of a vane attached to a spiral spring. Movement
of the vane uncovers an annular orifice and the point at which pressure behind the
vane balances the force of the spring depends upon the flow rate. The standard
Wright‟s peak flow meter ranges from 50-1000 L/min and weight 900 gm. Later on
various portable smaller and cheaper instruments suitable for domiciliary practice
have been developed.
The peak flow gauge (Ferraris Development and Engineering Co. Ltd, London
N18 3JD, UK) correlates closely with the PFM (Bhoomkar et al, 1975) but is too
bulky to be carried easily. The pulmonary monitor (Perks et al, 1981; Vitalograph Ltd,
Maids Moreton House, Buckingham MK18 ISW, UK) is pocket-sized, reliable and
gives reproducible values that correlate well with the PFM (Haydu et al, 1976).
45
Unfortunately the monitor has a scale differing from the standard PFM. This would
make comparison between trials difficult. Lastly a mini-Wright peak flow meter
(MPFM) has become available (Airmed, Clement Clarke)
Mini-Wright Peak Flow Meter (mWPFM)
This instrument is simpler version of the Wright peak flow meter now used
worldwide. Measurements with this instrument correlate well with peak expiratory
flow rate measurements from the larger Wright peak flow meter (AirMed,Ltd.,
Harlow, England), with observed correlation generally higher than 0.90. The
instrument is a light plastic Cylinder measuring 15x5cm weighing 72 gm (without
mouth piece). It consists of a spring piston that slides freely on a rod within the body
of the instrument. The piston drives an independent sliding indicator along a slot
marked with a scale graduated, low range from 50-350 L/min and high range from 60-
800 L/min. The indicator records the maximum movement of the piston, remaining in
that position until return to zero by the operator. In use the machine must be held
horizontally with air vents uncovered. The instrument may be cleaned easily in
running water or in a detergent solution. Details of washing and sterilization methods
are supplied in leaflet along with the meter. Studies involving long term use of this
device, particularly the MiniWright peak flow meter, have demonstrated that
performed well for many months and with as many as 4000 blows. Performance of
accuracy of the miniWright peak flow meter meets national asthma education
programme (NAEP) guideline variation <± 5% with standard Wright peak flow meter
(Clement Clarke int. Ltd, 1997)
46
Factors affecting the peak expiratory flow rate (PEFR) (18)
Anthropometric measurements: Standing height is the best single predictor in
childhood for PEFR. It has more or less linear relationship with weight, body surface
area and chest expansibility.
Age and Sex: Age has linear relationship with PEFR but sex has no significant
relation with PEFR in children when height is considered. But age has curvilinear in
male and linear relationship in female of adult. When only age is considered, PEFR
differs in both sexes.
Malnutrition: Current malnutrition impairs the PEFR and chronic malnutrition is
associated with reduction in PEFR/Age, perhaps because of slow growth of the large
airways.
Environmental effect: Smoking and environmental tobacco smoke increases airway
variability, thereby affect pulmonary function test as a PEFR. Summer time
particulate air pollution has independent effect on PEFR and is associated with
decline in PEFR in children.
Respiratory tracts and thoracic cage: The PEFR occurs early in the expiration and is
dependent on personal effort, large airway resistance, and possible compressive effect
of the manoeuvre on the intrathoracic airway. Thoracic cage deformity and respiratory
tract infection including microfilaremia has adverse effect on PEFR
Types of peak flow meters (19)
There are several brands of peak flow meters available which all perform the
same function. However, there are two major types: the low-range peak flow meter
47
for small children between 4 and 9 years of age, and for adults with severely impaired
lung function; and the standard-range peak flow meter for older children, teenagers,
and adults.
It is important that the doctor or healthcare provider prescribes the appropriate
device for each individual. Adults have larger airways than children. If given a low-
range peak flow meter, they will continually have maximum peak flow rates even
when having severe shortness of breath. This may jeopardise proper management
What is a normal peak flow rate?
Normal peak flow rates vary according to age, height, and sex. However, a
patient‟s normal score should be within 20% of a person of the same age, sex, and
height who does not have asthma.
The „normal peak flow‟ or „personal best‟ is the highest consistent peak flow
reading over a 2 –3-week period when the patient does not have asthma symptoms. It
serves as a standard against which other readings are measured. By checking the
patient‟s personal best when he does not have symptoms, changes can be recognised
and reduced PEF can be monitored. In addition, when the PEF remains at a high level,
it helps to reassure the individual that the asthma is under control.
Clinical use of the peak flow meter
Diagnosis of asthma
Variability: Diurnal Variation of at least 15% of established maximum is assumed to
be indicative of asthma.
Bronchodilator response: a bronchodilator response greater than 15% in PEF is
indicative of asthma
48
Exercise testing: a fall of PEFR greater than 15% is indicative of asthma
Occupational asthma: In occupational asthma there is a progressive fall in peak flow
rates over several days and failure to return fully to normal. There is also progressive
recovery on work cessation over several days, with or without medication
Monitoring disease progress
Self-management plan
How to use the peak flow meter
1. Set the cursor to zero. Do not touch the cursor when breathing out.
2. Stand up and hold the peak flow meter horizontally in front of the mouth.
3. Take a deep breath in and close the lips firmly around the mouthpiece, making
sure there is no air leak around the lips.
4. Breathe out as hard and as fast as possible.
5. Note the number indicated by the cursor.
6. Return cursor to zero and repeat this sequence twice more, thus obtaining
three readings.
The highest or best reading of all three measurements is the peak flow at that time
Limitations of a peak flow meter
Results are sometimes not reproducible over a long period and there may be inter-
model variation in the values of readings obtained. It is also effort dependent. It
primarily assesses the airflow in the larger airways and not in the medium and smaller
airways and thus can underestimate the degree of airflow limitation, particularly as
airflow limitation and gas trapping worse.
49
3.7 PULMONARY SCORING SYSTEM
Guidelines for the management of acute paediatric asthma hinge on the objective
assessment of asthma severity, generally measured by lung function tests such as peak
expiratory flow rate or spirometry.
Unfortunately, these lung function tests are nearly impossible to obtain in preschool-
aged children because of poor coordination and in 35% to 50% of school-aged
children, because of severity of illness or poor familiarity with the technique. With
preschool-aged children representing over half the patients treated for acute asthma. It
is estimated that three quarters of asthmatic children cannot perform standard lung
function tests in the emergency setting. To enable the clinical application of asthma
guidelines, it is thus crucial to find alternative ways to measure asthma severity and
response to treatment, valid for children aged 2 to 17 years.
Clinical scores can serve as simple and inexpensive tools to assess asthma severity for
the entire paediatric age span. More than 18 clinical scores for assessing acute asthma
have been reported, many of which were developed ad hoc without formal validation.
Birken et al identified the Preschool Respiratory Assessment Measure (PRAM) in
preschool-aged children.It was developed and validated against respiratory resistance
and proved discriminative and responsive to change in children aged 3 to 6 years.
Subsequently, the Paediatric Asthma Severity Score (PASS) proved reliable, valid,
and responsive to change in children aged 1 to 18 years. The authors cautioned users
that the 6-point PASS may not be sensitive enough to identify small but clinically
important changes in status. Conversely, the PRAM had not been validated in school-
aged children and lacked a formal assessment of reliability.
50
TABLE 4:PAEDIATRIC RESPIRATORY ASSESSMENT
MEASURE(PRAM)(20)
SIGNS 0 1 2 3
SUPRASTERNAL
MUSCLE
CONTRACTION
Absent Present
SCALENE MUSCLE
CONTRACTON
Absent Present
AIR ENTRY Normal Decreased at
bases
Widespread
decrease
Absent/minimal
WHEEZING Absent Expiratory
only
Inspiratory and
expiratory
Audible without
stethescope or silent
chest
O2% OR =
95%
92%-94% <92%
TABLE 5: PULMONARY INDEX SCORE (21, 22)
CLINICAL
ASTHMA
SCORE
RESPIRATORY
RATE
WHEEZING INSPIRATORY/
EXPIRATORY
RATIO
USE OF
ACCESSORY
MUSCLE
0 <30 None 5:2 0
1 31-45 Terminal expiration
with stethescope
5:3 -5:4 + or-
2 46-60 Entire expiration
with stethescope
1:1 ++
3 >60 Inspiration and
expiration without
stethescope
<1:1 +++
51
TABLE 6
CHARACTERISTICS OF VALIDATED PULMONARY SCORES
(23)
52
4. MATERIALS AND METHODS
4.1 Source of the data:
The study was conducted over a period of 1 year 6 months from December
2011 to June 2013 at the Department of Paediatrics, Kempegowda Institute of
Medical Sciences, and Bangalore after obtaining consent from the Institutional
Ethical Committee. It was a prospective comparative study in which 50
asthmatic children presenting with mild to moderate exacerbation of asthma in
the age group of 5 to 18 years were selected after taking informed consent.
Sample size was based on the average attendance in outpatient department and
inpatient admissions.
4.2 Inclusion criteria :
Children in the age group of 5-18 years presenting to the paediatrics
department with mild to moderate exacerbation of asthma.
Parents willing to give signed informed consent.
4.3 Exclusion criteria :
Suspected or known immunosuppressive, cardiac and neurological condition
affecting pulmonary function and other chronic pulmonary disease.
Children who are not able to perform peak expiratory flow rate.
4.4 Method of collection of data :
Known asthmatic children in the age group of 5-18 years presenting with mild
to moderate acute exacerbation of asthma to the KIMS Paediatric department were
selected. Prior to starting treatment, they were initially assessed by measuring
peak expiratory flow rate and pulmonary score.
53
Pulmonary score is assessed by 3 variables -respiratory rate, wheezing, use of
accessory muscle-each variable is awarded 4 scores-0, 1, 2, 3 summed up to 9.
TABLE 7: PULMONARY SCORE
SCORE RESPIRATORY
RATE
WHEEZE USE OF ACCESSORY
MUSCLE
0 ≤20 None No retraction
1 21-35 Terminal
expiration with
stethescope
Intercoastal/subcoastal
retraction
2 36-50 Entire expiration
with stethescope
Intercoastal/subcoastal
retraction + suprasternal
retraction
3 >50 Both inspiration
and expiration
with or without
stethescope
2 + use of ala nasi
PEFR measured using mini Wright Peak Flow Meter EU Scale before starting
treatment and best of the 3 readings considered. Observed PEFR was expressed as
the percentage of normal PEFR which was taken based on height and
sex19
.Treatment started according to standard protocol of asthma management.
Patients reassessed about 5 minutes after first dose of bronchodilator therapy, then
at 10 minutes, 15 minutes and for inpatients at the time of discharge by doing
PEFR and pulmonary score. Improvement in PEFR values is compared with that
of pulmonary score. Detailed history was taken and examination including
anthropometry was done with the help of predesigned case recording proforma to
ascertain severity, triggering factors and associated factors with asthma.
54
4.5 Statistical methods:
Pearson correlation coefficient is used to find negative correlation coefficient
between pulmonary score and peak expiratory flow rate before and after
treatment. Paired T test and Analysis of variance is used to measure the significant
improvement in peak expiratory flow rate and pulmonary score after treatment.
Statistical software: The statistical software namely SPSS was used for the
analysis of data and Microsoft word and Excel have been used to generate graphs,
tables etc.
55
5. RESULTS
Fifty children were evaluated, ranging from 5 to 17 years of age, with a mean
age of 9.7 years. PEFR and PS were evaluated before and after treatment at 5,
10 and 15 minutes for each patient. There was a significant change in PEFR
and PS before and after treatment (Table 8); as airway obstruction improved
with treatment, the PS should decrease and the PEFR should increase.
TABLE 8: MEAN AND SD OF PEFR &PS
Peak expiratory flow rate Pulmonary score
Before
treatment
At 5
minutes
At 10
minutes
At 15
minutes
At
discharge
Before
treatment
At 5
minutes
At 10
minutes
At 15
minutes
At
discharge
Mean 50.8 62.9 64.5 72 82.9 4.8 3.8 3.1 2 1.27027
SD 2.2 3.8 3.6 2.4 6.04 0.7 0.6 0.6 0.6 0.450225
The mean predicted PEFR improved with treatment by 21.25% from 50.8% to
72.0% of predicted (p <0.0001) by 15 minutes. The mean PS improved by 2.8 (p <
0.0001) from 4.8 to 2 by 15 minutes.
TABLE 9: PAIRED T TEST FOR CONSTRUCT VALIDITY
PAIRED VARIABLES T-Value P-Value
PEFR before treatment and PEFR at 5 minutes -24.043 .000
PEFR before treatment and PEFR at 10 minutes -26.171 .000
PEFR before treatment and PEFR at 15 minutes -107.350 .000
PEFR before treatment and PEFR at discharge -28.467 .000
PS before treatment and PS at 5 minutes 16.398 .000
PS before treatment and PS at 10 minutes 21.603 .000
PS before treatment and PS at 15 minutes 29.121 .000
PS before treatment and PS at discharge 41.909 .000
56
The PS had a significant negative correlation with the PEFR; i.e., as the PEFR
increased, the PS decreased. The correlation of pre-treatment PEFR and PS is r = -
0.497 (p = 0.000) (Fig. 11), that for post treatment at 5 minutes is r= -0.599 (p=0.000)
(fig 12), at 10 minutes is r= -0.592 (p=0.00007) (Fig 13) and at 15 minutes is r = -
0.589 (p = 0.000) (Fig.14).
FIGURE 11: SCATTER DIAGRAM FOR PEFR AND PS BEFORE
TREATMENT
0
1
2
3
4
5
6
7
40.0 45.0 50.0 55.0 60.0
PEFR and PS before treatment
SBT
PEFR
PS
0
1
2
3
4
5
6
50.0 55.0 60.0 65.0 70.0
PEFR and PS at 5 minutes
S5M
PEFR
PS
57
FIGURE 12: SCATTER DIAGRAM FOR PEFR AND PS AT 5 MIN
FIGURE 13: SCATTER DIAGRAM FOR PEFR AND PS AT 10 MINUTES
FIGURE 14: SCATTER DIAGRAM FOR PEFR AND PS AT 15 MINUTES
0
0.5
1
1.5
2
2.5
3
3.5
4
4.5
50.0 55.0 60.0 65.0 70.0 75.0
PEFR and PS at 10 minutes
S10M
PEFR
PS
0
0.5
1
1.5
2
2.5
3
3.5
65.0 70.0 75.0 80.0
PEFR and PS at 15 minutes
S15M
PEFR
PS
58
TABLE 10: AGE DISTRIBUTION WITH SEX
AGE(YEARS) MALE FEMALE TOTAL
5-9 13(26%) 12(24%) 25(50%)
10-15 14(28%) 9(18%) 23(46%)
>15 2(4%) 0 2(4%)
TOTAL 28(58%) 22(42%) 50(100%)
FIGURE 15: AGE DISTRIBUTION WITH SEX
In our study males constituted 58% (n=29) and females constituted 42% (n=21)
among the study group. There is equal distribution of cases between 2 age groups of
5-9 years (50%) and 10-15 years (46%). Only 4% (n=2) of cases were 17 years old.
0
10
20
30
40
50
60
5-9 years 10-15 years >15 years TOTAL
TO
TA
L N
O O
F P
AT
IEN
TS
AGE
MALE
FEMALE
TOTAL
59
TABLE 11: DISTRIBUTION OF SOCIOECONOMIC STATUS
SOCIOECONOMIC CLASS
LOWER 18(36%)
LOWER UPPER 15(30%)
MIDDLE 17(34%)
TOTAL 50
FIGURE 16: DISTRIBUTION OF SOCIOECONOMIC STATUS
In our study, majority 66% (n=33) of cases belong to lower socioeconomic status
according to modified Kuppuswamy classification, of which 36% (n=18) belonged to
lower class and 30% (n=15) belonged to lower upper class.34% (n=17) belonged to
middle class.
36%
30%
34%
SOCIOECONOMIC STATUS
LOWER
LOWER UPPER
MIDDLE
60
TABLE 12: NUMBER OF DAYS MISSED IN SCHOOL IN LAST 12 MONTHs
1-2 DAYS 18(36%)
3-5 DAYS 8(16%)
6-9 DAYS 8(16%)
10-14 DAYS 9(18%)
>15 DAYS 7(14%)
FIGURE 17: NUMBER OF DAYS MISSED IN SCHOOL IN LAST 12 MONTH
In our study, majority of children i.e 36% (n=18) missed only 1-2 days of school and
only 12% (n=6) children missed school for more than 15 days.
0
2
4
6
8
10
12
14
16
18
1-2 DAYS 3-5 DAYS 6-9 DAYS 10-15 DAYS >15 DAYS
NO
OF
CA
SES
61
TABLE 13: NUMBER OF TIMES CHILD BEING TREATED IN
EMERGENCY IN LAST 12 MONTHS
1 TIME 19(38%)
2 TIMES 13(26%)
3 TIMES 8(16%)
4 TIMES 6(12%)
5 OR MORE 4(8%)
FIGURE 18: NUMBER OF TIMES CHILD BEING TREATED IN
EMERGENCY IN LAST 12 MONTHS
In this study, 64% (n=32) of cases have taken 1-2 times treatment in
emergency department and only 6% (n=3) cases had taken treatment for more than 5
times in emergency department.
0
2
4
6
8
10
12
14
16
18
20
ONCE TWICE THRICE 4 TIMES 5 OR MORE
TOTA
L N
UM
BER
OF
PA
TIEN
TS
NUMBER OF TIMES
62
TABLE 14: NUMBER OF TIMES CHILD BEING HOSPITALISED
OVERNIGHT OR LONGER IN LAST 12 MONTHS
1 TIME 28(56%)
2 TIMES 14(28%)
3 TIMES 2(4%)
4 TIMES 1(2%)
5 OR MORE -
FIGURE 19: NUMBER OF TIMES CHILD BEING HOSPITALISED
OVERNIGHT OR LONGER IN LAST 12 MONTHS
In this study, 56% (n=28) cases were admitted once in the last 12 months, 28%
(n=14) cases were admitted twice, 4% (n=2) cases were admitted thrice and 2% cases
0
5
10
15
20
25
30
ONCE TWICE THRICE 4 TIMES 5 OR
MORE
TO
TA
L N
UM
BE
R O
F P
AT
IEN
TS
NUMBER OF TIMES OF HOSPITALISATION
63
admitted 4 times in the last 12 months. No cases were admitted for 5 or more times in
1 year.
TABLE 15: PREVIOUS ATTACKS
INTERMITTENT 22(44%)
MILD PERSISTENT 20(40%)
MODERATE PERSISTENT 7(14%)
SEVERE PERSISTENT 1(2%)
FIGURE 20: PREVIOUS ATTACKS
In our study, 44% (n=22) of cases had intermittent type and 40% (n=20) of
cases had mild persistent type of asthma, 14% (n=7) cases had moderate persistent
and 2% (n=1) had severe persistent asthma.
0
5
10
15
20
25
INTERMITTENT MILD PERSISTENT MODERATEPERSISTENT
SEVERE PERSISTENT
TOTA
L N
UM
BER
OF
PA
TIEN
TS
SEVERITY OF ASTHMA
64
TABLE 16: TRIGGERING FACTORS
DUST 30(60%)
SMOKE 5(10%)
EXERCISE 6(12%)
FOOD 4(8%)
CHALK DUST 6(12%)
FIGURE 21: TRIGGERING FACTORS
In this study, dust (60%) constituted the major triggering factor. Other triggering
factors were exercise 12% (n=6), chalk dust 12% (n=6), smoke 10% (n=5), food 8%
(n=4).
0
5
10
15
20
25
30
35
DUST SMOKE EXERCISE FOOD CHALKDUST
TOTA
L N
UM
BER
OF
CA
SES
TRIGGERING FACTORS
65
TABLE 17: SEASONAL VARIATION
RAINY 33(66%)
WINTER 31(62%)
SPRING 12(24%)
SUMMER 5(10%)
ALL SEASONS 5(10%)
FIGURE 22: SEASONAL VARIATION
Majority of cases showed seasonal variation with maximum exacerbations
occurring during rainy (66%, n=33) and winter (62%, n=31) season. About 24% cases
(n=12) showed exacerbation during spring, 10% (n=5) each during summer and all
seasons in our study.
0 5 10 15 20 25 30 35
RAINY
WINTER
SPRING
SUMMER
ALL SEASONS
TOTAL NUMBER OF PATIENTS
SEA
SON
AL
VA
RIA
TIO
N
66
TABLE 18: ASSOCIATED FACTORS
ALLERGIC RHINITIS 28(56%)
ATOPIC DERMATITIS 8(16%)
URTICARIA 2(4%)
FAMILY HISTORY OF ASTHMA 26(52%)
FAMILY HISTORY OF ALLERGIC
RHINITIS
4(8%)
LOW BIRTH WEIGHT 7(14%)
FIGURE 23: ASSOCIATED FACTORS
Majority of cases are associated with allergic rhinitis (56%, n=28) and family history
of asthma (52%, n=26). Atopic dermatitis was present in 16% (n=8) of cases, low
ALLERGIC RHINITS
ATOPIC DERMATITIS
URTICARIA
FAMILY HISTORY OF ASTHMA
FAMILY HISTORY OF ALLERGIC RHINITIS
LOW BIRTH WEIGHT
0 5 10 15 20 25 30
ASS
OC
IATE
D F
AC
TOR
S
TOTAL NUMBER OF CASES
67
birth weight in 14% (n=7) of cases, family history of allergic rhinitis in 8% (n=4) of
cases and urticaria in 4% (n=2) of cases in this study.
TABLE 19: TYPE OF MEDICATION USED
MODE OF DELIVERY MEDICATIONS USED NUMBER
INHALER ONLY SALBUTAMOL 9(18%)
SALMETEROL/FLUTICASONE 12(24%)
FORMOTEROL/BUDESONIDE 2(4%)
NEBULISATION ONLY SALBUTAMOL 11(22%)
SALBUTAMOL/BUDESONIDE 11(22%)
ORAL BRONCHODILATOR 8(16%)
STEROID 0
In our study, 18% (n=9) cases used only salbutamol as inhaler, 24% (n=12)
used combination of salmeterol and fluticasone and 4% (n=2) used formoterol and
budesonide combination as inhaler. 22% (n=11) cases used salbutamol and
budesonide nebulisation during attacks. Only 16% (n=8) used oral bronchodilators as
treatment.
68
TABLE 20: PREDICTED IMPROVEMENT OF PEFR IN PERCENTAGE
Improvement(% of
predicted PEFR)
5 min(no of
cases)
10 min(no of
cases)
15 min(no of
cases)
5-10 18(36%) 11(22%) -
11-15 22(44%) 21(42%) -
16-20 10 (20%) 18(36%) 15(30%)
>20 - - 35(70%)
FIGURE 24: PREDICTED IMPROVEMENT OF PEFR IN PERCENTAGE
In our study, only 70% of cases showed improvement in PEFR by >20% after 15
minutes of treatment. At 5 minutes, 36% cases showed improvement in PEFR by 5%
to 10%, 44% cases showed improvement by 11% to 15% and 20% cases showed
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
5 min 10 min 15 min
36 22
0
44
42
0
20 36
30
0 0
70
TOTA
L N
UM
BER
OF
CA
SES
IN %
TIME INTERVALS
>20%
16% to 20%
11% to 15%
5 % to 10%
69
improvement by 16% to 20%. At 10 minutes, 22% cases showed improvement in
PEFR by 5% to 10%, 42% cases showed improvement by 11% to 15% and 36% cases
showed improvement by 16% to 20%.
6. DISCUSSION
The present study was a hospital based prospective study conducted at Paediatric
department of Kempegowda Institute of Medical Sciences from December 2011 to
June 2013. Fifty patients presented with mild to moderate acute exacerbations of
asthma in the above mentioned period were included in the study.
Among the study group, there were only 2 cases of 17 years and both of them
were males. 50% of cases were in the age group of 5-9 years and 46% of cases
were in the age group of 10-15 years. Since only those who can blow PEFR were
included in the study, children below 5 years were excluded and older children
selected. So the mean age group of presentation was 9.7±3.1 years.
Male children were 56% (n=28) and females 44 % (n=22) which was comparable
to studies conducted in India25, 26
. The reason for male gender predominance
during childhood is not known. It would be due to genderwise difference in
airways patency due to hormonal differences.
36% of cases belonged to lower class, 30% of cases belonged to lower upper class
and 34% of cases belonged to middle class. Majority (66%) of asthma cases
belonged to lower socioeconomic status as reported in Indian Journal of
Paediatrics by Paramesh H27
. But in a study conducted in Pune city they have
proved that asthma is more common in higher socioeconomic class according to
hygiene hypothesis and excessive consumption of junk foods with lack of physical
exercise28
.
70
In the last 12 months, many (36%) children missed 1-2 days of school and 14%
children missed school for more than 15 days, 64% of children had taken
treatment in emergency department 1-2 times and only 8% were treated in
emergency department more than 5 times. 56% of cases were hospitalised once in
the last 12 months and no cases were hospitalised more than 5 times in one year.
These datas describe the severity of asthma of our study group.
Children with persistent asthma(56%) are more when compared to children with
intermittent asthma (44%).This is explained by the increasing incidence of
persistent asthma as reported by Paramesh H.29,30
Dust was the most common triggering factor-60%, followed by chalk dust (12%),
smoke (10%) and cold foods (8%).In a study in Lebanon, parents cited dust as the
most common triggering factor for asthma.31
Majority (66%) of the cases showed seasonal variation as a cause for triggering
asthma attacks30
.Asthma exacerbations were more during rainy season (66%) and
winter season32
(62%).Similar results were reported in a study conducted in rural
India25
.Asthma didn‟t show any seasonal variation in 10% of cases.
In Latin America, the prevalence of isolated allergic rhinitis (without asthma
coexistence) is up to 20%33
, and in asthmatic patients it ranges from 28%33
to
95%. In our study, 56% of asthmatic children had allergic rhinitis, prevalence
similar to that reported in Peruvian school children34,35
.16% children had atopic
dermatitis which is explained by the study “on atopic march‟‟36
.Family history of
asthma was present in 52% of cases37,38,39
. Although asthma is known to run in
families, the identification of an asthma gene has been elusive with over 100
genes found to be associated with asthma.
71
Average Absolute Eosinophil Count of my study group is 583.52 (SD ±380.59),
68% of patients had absolute eosinophil count>450 cells/mm3 and only one
patient had a count of 2920 cells/mm3. Peripheral blood eosinophilia in asthmatic
patients has been recognised since the early 1900s but individual eosinophil
counts have shown wide variation in patients who are clinically stable40
.
Majority of children were well aware of inhaler (46%) and nebulizer (60%)
therapy. 24% of children were taking long acting beta agonist and steroid
combination inhaler. 22% were taking salbutamol and budesonide nebulisations
during acute attacks. But this doesn‟t determine the educational status and
awareness of parents as the study sample was very small.
In our study, by 5 minutes of nebulization majority (44%) cases showed
improvement in PEFR by 11-15%, by 10 minutes 42% cases showed
improvement by 11-15% and 36% cases showed improvement by 16-20% and by
15 minutes 70% cases showed improvement by more than 20%.In our study, first
treatment for all cases were combination of salbutamol and budesonide
nebulisation and then treatment protocols according to severity was started.
The PS passed two formal tests of validity. We evaluated the construct and the
criterion validities of the PS.
Construct validity (the degree to which an instrument measures the construct or
characteristic under investigation) in this study is the degree to which the PS
measures airway obstruction. To establish construct validity, we compared the
pre- and post-treatment PSs and the pre- to post-treatment PEFRs. The PEFRs are
an established method to measure airway obstruction and improved with treatment
from a mean predicted PEFR of 50.2% to 72% (p = 0.000). It is assumed that if
the PEFR improves with treatment, the degree of airway obstruction decreases.
72
The PS should reflect this change, indicated by a decrease in numerical score. The
PS decreased with treatment from a mean of 4.8 to 2.0 (p = 0.000).
Criterion validity is the degree to which an instrument correlates with an
established criterion. The PEFR was used as the established criterion and both the
PEFR and the PS were measured at the same time. The correlations between the
pre-treatment PS and PEFR is r = -0.497. The post-treatment correlations is r = -
0.589 at 15 minutes. The PEFR was chosen as the established criterion because it
is often used to determine the severity of an asthma exacerbation.
Although pulmonary function tests (PFTs) may provide a better measure of
airway obstruction, PFTs require special equipment and training for a staff to
interpret. Both PEFRs and PFTs require cooperation from children to obtain
accurate measures of airway obstruction. The PS is a simple objective method to
assess the severity of an acute asthma exacerbation in children. The score is a
composite of physical findings commonly used in the assessment of children with
asthma: respiratory rate, wheezing, and accessory muscle use. These three
components are easy to obtain in children and require little additional training for
staff to learn.
The correlations between the PSs and PEFRs ranged from -0.497 to -0.589 and are
similar to the correlations found when other clinical scoring systems have been
compared with estimates of lung function or signs of respiratory distress. The
clinical severity score (CSS) was compared with arterial oxygen saturation and
FEV1, with correlations of r = 0.49 and r = 0.52, respectively41
. The asthma
severity score (ASS) correlated with oxygen saturation (r = -0.45) and FEV1 (r = -
0.54)42
. These correlations may seem lower than what is expected; however, all of
these scoring systems are based on physical signs (components) that do not
73
actually measure airway obstruction. So it is not surprising that, when compared
with measures of actual airway obstruction, there is limited correlation.
Furthermore, when the clinical appearance of a child with asthma improves with
treatment, the underlying obstruction may not improve to normal for several
weeks. This makes comparing measures of airway obstruction with clinical scores
difficult. The delayed improvement of airway obstruction helps explain why some
children in this study had PSs suggestive of mild severity but had lower than
expected PEFRs.
Despite their flaws, objective clinical scoring systems do play a role in helping to
estimate the degree of obstruction for children with asthma when true measures of
obstruction are not readily available.
Children with significant respiratory distress are likely to have difficulty
performing PEFRs because they cannot inhale completely before exhaling
forcefully. One reason the PS correlated better with the PEFR after bronchodilator
therapy may be that the child‟s ability to perform PEFRs improved with lessening
airway obstruction.
LIMITATIONS:
The PS was compared with the PEFR, which is a substitute for spirometry.
It is likely that any measure of severity requiring expiratory maneuvers would
be difficult to obtain in a patient with severe obstruction. The patient would
have trouble getting enough air entry during inspiration to have a meaningful
expiratory measurement, either PEFR or Spirometry measures.
Only older children who could perform PEFRs were included.
74
Since not all patients were inpatients and there was no uniformity in treatment
after first dose of bronchodilator, PEFR and PS could not be compared at the
time of discharge.
Application of the PS to a younger group, and those with more severe
presentations, may be avenues of further research.
7. CONCLUSION
The PS is a convenient simple method of assessing airway obstruction. The PS
appears to correlate better with lesser airway obstruction than greater airway
obstruction; i.e. the PS has higher post-treatment correlations, which makes
the PS a good tool to assess mild severity and the response to treatment. No
scoring system is perfect, but some method of assessing severity in children is
needed when spirometry testing is not obtainable. The PS appears to be an
objective and simple scoring system for the assessment of airway obstruction
for children. The PS has been validated by two standard tests of validity.
Construct validity of the PS through correlation of the pre- and post-treatment
scores and criterion validity by correlation between the PS and the PEFR were
established. Therefore, the PS can be used to assess airway obstruction in
children who are unable to perform other measures, such as PEFRs, and may
be used to guide therapy and to evaluate a child‟s response to treatment.
75
8.SUMMARY
A comparative prospective study was conducted in the Paediatric Department
of Kempegowda Institute of Medical Sciences to validate the PS as a measure to
assess the severity of asthma and child‟s response to treatment. The score is a
composite of physical findings commonly used in the assessment of children with
asthma: respiratory rate, wheezing, and accessory muscle use.
A total of 50 patients in the age group of 5-17 years with mild to moderate
exacerbation of asthma were randomly selected. PEFR and PS measured at the same
time before treatment and at 5 minutes, 10 minutes, and 15 minutes after treatment
and at the time of discharge. The recorded PEFR is expressed as the percentage of
normal PEFR. Normal PEFR calculated by referring to age, sex and height based
charts. Detailed history was taken and anthropometric parameters were recorded
according to the predesigned case proforma.
As airway obstruction improved with the bronchodilator therapy, PEFR
increased and PS decreased significantly. Pre- and post-treatment PEFRs and PSs
were compared using paired t-tests to establish construct validity. Significant negative
correlation was found between pretreatment PEFR and PS and post treatment PEFR
76
and PS which validated the score through criterion validity. Findings of this study
suggested that PS can be used as a tool to measure asthma severity and to guide
therapy.
9. BIBLIOGRAPHY
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A. Prospective Evaluation of Two Clinical Scores for Acute Asthma in Children
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Bangladesh, 5-15 Years.
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Pune
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Score for Assessing Acute Asthma Severity from Toddlers to Teenagers, Paediatric
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Severity Score (PASS), in the Evaluation of Acute Asthma. ACAD EMERG MED
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Guruprasad, Prevalence of asthma in school children in rural India, Ann Thorac
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81
10 ANNEXURE
10.1 CONSENT FORM
I/We the attendees of ………………. have been explained about the study by
name “STUDY OF PEAK EXPIRATORY FLOW RATE AND PULMONARY
SCORE IN EVALUATION OF ACUTE EXACERBATION OF ASTHMA IN
AGE GROUP OF 5 - 18 YEARS” in the language which we understand and in
which we ordinarily converse with the people. I/We have been explained that the
PEFR measurement would be done by the investigator for the study. I/We fully
understand the purpose of the study and willingly consent to participate in the study.
I/We further understand that we have the option to withdraw from the study at
any time without explaining the reason for the same.
82
I/We have been assured about maintenance of confidentiality about the
information rendered for the project.
Date:
Place: Signature:
(RELATIONSHIP WITH THE CHILD)
10.2 ETHICAL CLEARANCE FOR DISSERTATION STUDY
83
10.3 PROFORMA
84
STUDY OF PEAK EXPIRATORY FLOW RATE AND
PULMONARY SCORE IN EVALUATION OF ACUTE
EXACERBATION OF ASTHMA IN AGE GROUP OF 5 - 18
YEARS
NAME: AGE: SEX:
TELEPHONE NUMBER: IP / OP NUMBER:
ADDRESS:
HEIGHT: WEIGHT: BMI:
CHEST CIRCUMFERENCE: BEFORE TREATMENT: INSPIRATION
EXPIRATION
AFTER TREATMENT: INSPIRATION
EXPIRATION
SOCIO – ECONOMIC STATUS:
I. HAS ANY DOCTOR OR MEDICA PROVIDER EVER TOLD YOU THAT YOUR CHILD
HAS ASTHMA? Y / N
II. HOW MANY DAYS DID YOUR CHILD MISS SCHOOL LAST YEAR DUE TO HIS /
HER ASTHMA?
O 0 DAYS 1 – 2 DAYS 3 -5 DAYS 6 – 9 DAYS 10 – 14 DAYS 15 OR
MORE
III. HOW MANY TIMES HAS YOUR CHILD BEEN TREATED IN THE EMERGENCY
DEPARTMENT FOR ASTHMA IN THE PAST TWELVE MONTHS?
0 TIMES 1 TIME 2 TIMES 3 TIMES 4 TIMES 5 OR
MORE
IV. HOW MANY TIMES HAS YOUR CHILD BEEN HOSPITALISED OVERNIGHT OR
LONGER FOR ASHTMA IN THE PAST TWELVE MONTHS?
0 TIMES 1 TIME 2 TIMES 3 TIMES 4 TIMES 5 OR
MORE
V. IN THE PAST MONTH, DURING THE DAY, HOW OFTEN HAS THE CHILD GOT:
85
2 TIMES A
WEEK /
LESS
>2 TIMES A
WEEK
EVERYDAY
(ATLEAST
ONCE)
CONSTANTLY
(ALL THE
TIME)
COUGH
BREATHLESSNESS
WHEEZE
VI. IN THE PAST MONTH, DURING THE NIGHT, HOW OFTEN DOES YOUR CHILD
WAKE UP DUE TO
2 TIMES A
MONTH /
LESS
>2 TIMES A
MONTH
EVERYDAY
(ATLEAST
ONCE)
CONSTANTLY
(ALL THE
TIME)
COUGH
BREATHLESSNESS
WHEEZE
VII. WHAT TRIGGERS YOUR CHILD‟S ASTHMA OR MAKES IT WORSE?
- DUST - SMOKE
- ANIMAL DANDER - COCKRACHES
- GRASS / POLLEN - MOULD
- CHALK / CHALK DUST - STRONG SMELLS / PERFUMES
- FOOD - STRESS
- EXERCISE / SPORTS - CHANGE IN WEATHER
VIII. FOR EACH SEASON OF THE YEAR TO WHAT EXTENT DOES YOUR CHILD
USUALLY HAVE ASTHMA SYMPTOMS?
A LOT A LITTLE NONE
RAINY
WINTER
SPRING
SUMMER
IX. HISTORY SUGGESTIVE OF
86
1. ALLERGIC RHINITIS - Y / N
2. ATOPIC DERMATITIS - Y / N
3. URTICARIA - Y /N
4. BRONCHILITIS - Y / N
X. FAMILY HISTORY
1. ASTHMA - Y / N
2. ATOPIC DERMATITIS - Y / N
3. ALLERGIC RHINITIS - Y / N
4. SMOKING HISTORY - Y / N
XI. NEONATAL HISTORY
a. BIRTH WEIGHT –
b. PREMATURITY
c. RDS / TTPN
XII. DOES YOUR CHILD USE A PEAK FLOW METER? Y / N
XIII. DO YOU KNOW WHAT YOUR CHILD‟S PERSONAL BEST PEAK FLOW NUMBER IS?
_________
XIV. TREATMENT:
MEDICATION NAME HOW MUCH WHEN IT IS
TAKEN
1
2
3
4
XV. DEVICE USED TO DELIVER MEDICATION? _______________________
GENERAL PHYSICAL EXAMINTAION:
87
VITALS –
HEART RATE – RESPIRATORY RATE –
BLOOD PRESSURE - TEMPERATURE –
HEAD TO TOE EXAMINATION:
SYSTEMIC EXAMINATION:
RS –
INSPECTION –
NOSTRILS – NASAL CAVITY –
ORAL CAVITY – EAR –
TRACHEA – CHEST SYMMETRY –
RETRACTIONS –
PALPATION –
CHEST MOVEMENTS –
CHEST MEASUREMENTS – ANTEROPOSTERIOR:
TRANSVERSE:
HEMITHORAX: RIGHT – LEFT –
VOCAL FREMITUS –
PERCUSSION –
AUSCULTATION –
AIR ENTRY –
VOCAL RESONANCE –
BREATH SOUNDS –
ADVENTITIOUS SOUNDS –
CVS –
P/A –
CNS –
INVESTIGATIONS:
CHEST XRAY –
88
ABSOLUTE EOSINOPHIL COUNT –
PEAK EXPIRATORY FLOW RATE:
BEFORE TREATMENT
AFTER TREATMENT
5 MINUTES
10 MINUTES
15 MINUTES
AT THE TIME OF DISCHARGE
PULMONARY SCORE:
SCORE RESPIRATORY
RATE
WHEEZE USE OF ACCESSORY MUSCLE
0 <20 NONE NO RETRACTION
1 21-35 TERMINAL
EXPIRATION
WITH
STETHOSCOPE
SUBCOASTAL/INTERCOASTAL RETRACTION
2 36-50 ENTIRE
EXPIRATION
WITH
STETHOSCOPE
SUBCOASTAL/INTERCOASTAL+SUPRASTERNAL
RETRACTION
3 >50 INSPIRATION
AND
EXPIRATION
WITHOUT
STETHOSCOPE
USE OF ALA NASI
BEFORE TREATMENT
AFTER TREATMENT
5 MINUTES
10 MINUTES
15 MINUTES
AT THE TIME OF DISCHARGE
89
10.4 KEY TO MASTER CHART
SL - Serial Number
F - Female
M - Male
BMI- Body Mass Index
SE- Socioeconomic status
L - Lower class
LU - Lower upper class
M - Middle class
Symptoms:
A-How many days did your child miss school last year due to his / her asthma?
B- How many times has your child been treated in the emergency department for
asthma in the past twelve months?
C- How many times has your child been hospitalised overnight or longer for ashtma
in the past twelve months?
D- In the past month, during the day, how often has the child got asthma symptoms?
1-2 times a week / less, 2->2 times a week, 3-Everyday (atleast once), 4-
constantly
E- In the past month, during the night, how often does your child wake up due to
asthma symptoms?
1-2 times a month / less, 2->2 times a month, 3-Everyday (atleast once), 4-
constantly
TR - Triggering factors
D - Dust
C -Chalk powder
90
S - Smoke
E - Exercise
F - Food
SV - Seasonal variation
R - Rainy
W - Winter
S - Summer
SP - Spring
AS - All seasons
AH - Associated history
AR - Allergic rhinitis
AD - Atopic dermatitis
U - Urticaria
FH - Family history
A - Asthma
AR - Allergic rhinitis
(P) - Paternal
(M) - Maternal
(s) - Sibling
LBW - Low birth weight
T - Treatment
S - Salbutamol
B - Budesonide
SM - Salmeterol
FM - Formoterol
91
F - Fluticasone
T - Terbutaline
O - Oral
N - Nebulisation
I -Inhaler
AEC - Absolute Eosinophil Count
PEFR - Peak expiratory flow rate
BT - Before treatment
AT - After treatment
R -Respiratory rate
W - Wheezing
A -Use of accessory muscle
10.5 MASTER CHART
SL NAME AGE SEX BMI SE SYMPTOMS TR SV AH FH LBW T AEC
A B C D E
1 SAI SHAKTHI 10 F 14 LU 6-9D 2 1 2 2 D R AR A(P) ~~ S/B N 584
2 BAANU PRAKASH 13 M 15 LU ≥15 5 2 3 3 D R SP S ~~ ~~ ~~ SM/F I 782
3 SHASHANK 5 M 14 LU ≥15 3 1 3 3 D W S AD ~~ ~~ SM/F I 762
4 PRAVEEN 13 M 14 L 6-9D 2 1 2 2 C W ~~ ~~ ~~ SM/F I 612
5 BHARATH RAGHAVENDRA REDDY 14 M 19 L 1-2D 1 0 1 1 ~~ R AR ~~ ~~ S O 2920
6 ARVIND DAS 8 M 14 LU 1-2D 1 0 1 1 ~~ R AR ~~ ~~ S O 552
7 RAKESH 14 M 18 M 3-5D 5 1 1 3 E S R W AD U A(M) ~~ S O 784
8 HARBINA TAJ 11 F 13 L ≥15 5 2 3 3 C E AS AR A(s) ~~ SM/F I 734
9 IRFAN 7 M 20 L 6-9D 5 1 2 2 ~~ AS AR ~~ ~~ S/B N 418
10 SEHAN 5 F 14 LU ≥15 5 3 3 3 ~~ R SP S ~~ A(P) LBW S/B N 684
11 JAYANTH 6 M 15 M 1-2D 1 1 1 2 D R W AR A(P) ~~ S N 368
12 SAYEED 10 M 15 L 10-14D 5 3 3 3 D C S R W AR A(P) ~~ S/B N 784
13 ZUHAIB 17 M 25 M 1-2D 1 1 1 1 ~~ R AR A(P) ~~ FM/B I 388
14 KEERTHANA 9 F 18 M ≥15 5 4 2 2 D W SP S AR A(P) ~~ S/T O 492
15 KALYAN RAM 9 M 17 L 1-2D 2 0 1 1 ~~ AS U ~~ ~~ T O 288
16 THOUSIF 7 M 19 M 1-2D 1 0 1 1 ~~ AS AD ~~ ~~ T O 298
17 KIRAN 6 M 12 LU 10-14D 3 1 2 2 D E AS AR ~~ ~~ S/B N 376
18 CHANDANA 8 F 16 M 3-5D 3 1 1 2 D R ~~ ~~ ~~ S N 576
19 ZOYA KULSUM 10 F 17 L 1-2D 1 1 1 1 D F W AR ~~ ~~ S N 398
20 SAI ABHIRAM 10 M 13 L 1-2D 2 1 2 2 D W AR A(P) ~~ S N 598
21 CHANDANA 9 F 18 M 1-2D 1 1 1 1 ~~ R ~~ ~~ ~~ S N 484
22 VANITHA 11 F 19 L ≥15 3 2 3 3 D C R W AD ~~ ~~ SM/F I S I 820
23 SIMRAN FATHIMA 9 F 11 L ≥15 5 2 4 4 S R ~~ A(P) ~~ SM/F I S I 902
24 RABEENA 10 F 18 LU 10-14D 5 2 2 2 S W ~~ AR ~~ S N 542
25 AYESHA 9 F 12 L 1-2D 2 1 1 1 D W ~~ A(P )AR(P) LBW S/B N 425
26 SAANVI 11 F 18 ML 3-5D 2 1 2 2 ~~ R W AR A(P) LBW S N 652
27 ARVIND 10 M 15 L 1-2D 1 1 1 1 F W ~~ ~~ ~~ S I 582
28 NISHANTH 6 M 15 ML 1-2D 1 1 1 1 D R W AR ~~ LBW S N 282
29 HEMANTH 12 M 15 ML 10-14D 3 2 2 2 E W AR A(M) ~~ S/B N 574
30 SHREYA 8 F 15 ML 1-2D 2 1 1 2 ~ R AR A(M) ~~ T O 562
31 AKASH 11 M 16 L 3-5D 4 1 1 1 D R W AR ~~ ~~ S I 578
32 AYESHA BANU 11 F 13 L 10-14D 4 2 2 2 D R W SP AD A(M) ~~ SM/F I 526
33 CHANDINI 8 F 17 L 3-5D 3 1 2 2 E R W AR ~~ ~~ SM/F I 580
34 ABHINAV 10 M 13 LU 1-2D 2 1 1 1 D W SP ~~ A(M) ~~ S I 474
35 ZAARA KHANUM 10 F 16 LU 1-2D 1 1 1 1 D R W SP ~~ A(M) ~~ S I 388
36 YUNIS KHAN 14 M 15 L 1-2D 2 0 1 1 D R W SP AR ~~ ~~ S O 296
37 M D FOUZAN 8 M 16 M 6-9D 3 2 2 2 D R W SP AR AD A(P) ~~ SM/F I 358
38 AYESHA 8 F 15 M 3-5D 3 2 2 2 ~~ R W AR A(P) ~~ S I 534
39 KIRAN 7 M 12 LU 10-14D 5 2 2 2 D F E R W SP ~~ A(P) AR(P) ~~ S/B N 542
40 KEERTHANA 6 M 13 LU 10-14D 5 2 2 2 D R SP S AR A(P) ~~ S/B N 534
41 VARSHINI 6 F 19 LU 1-2 D 2 1 1 2 D S F R AR ~~ ~~ S I 530
42 REEBA 5 F 13 M 6-9 D 2 1 1 1 D R ~~ A(P) LBW S N 372
43 RAMESH 14 M 19 M 6-9 D 2 1 2 2 D R W AR A(M) ~~ S N 532
44 REENATH 5 F 12 LU 6-9 D 2 1 2 2 D R W AR A(P) ~~ SM/F I 256
45 RANJITH 14 M 16 LU 6-9 D 2 1 2 3 D C R W SP AR AD A(P) AR(P) ~~ S/B N 856
46 IMPANA 6 F 17 L 3-5 D 1 1 2 2 D R SP AD ~~ LBW SM/F I 521
47 FIROZ 17 M 26 M 3-5 D 1 2 1 1 ~~ W AR ~~ ~~ FM/B I 388
48 FARHAN PASHA 10 M 15 L 10-14D 5 2 3 3 D C R W ~~ A(P) ~~ SM/F I S I 886
49 SRAJAN 6 M 15 ML 1-2D 1 1 1 1 D R W AR ~~ LBW S N 282
50 HUZAIFA 10 F 18 LU 10-14D 5 2 2 2 D W ~~ ~~ ~~ S/B N 520
SL NAME PEFR L/MIN PULMONARY SCORE
BT
AT BT
AT
5MIN 10MIN 15MIN DISCHARGE 5MIN 10MIN 15MIN DISCHARGE
1 SAI SHAKTHI 148(57%) 175(68%) 175(68%) 200(77.5%) 210(81.4%) 5 R2W2A1 4 R1W2A1 3 R1W1A1 2 R1W1 1 R1
2 BAANU PRAKASH 135(47.5%) 185(65%) 185(65%) 195(68.6%) ~~ 5 R2W2A1 4 R2W1A1 4 R2W1A1 3 R1W1A1 ~~
3 SHASHANK 72(50%) 88(61%) 88(61%) 105(73%) 110(76.4%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
4 PRAVEEN 160(58%) 180(65.7%) 180(65.7%) 215(78.5%) 220(80%) 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1 1 R1
5 BHARATH RAGHAVENDRA REDDY 120(50%) 155(65%) 160(67%) 174(73%) ~~ 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 ~~
6 ARVIND DAS 100(52%) 120(62%) 135(70%) 145(75%) 155(80.3%) 4 R1W2A1 3 R1W1A1 2 R1W1 1 R1 1 R1
7 RAKESH 150(49.5%) 200(66%) 205(67.8%) 210(69.5%) ~~ 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 ~~
8 HARBINA TAJ 108(47.2%) 138(60%) 148(64.3%) 158(68.6%) ~~ 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 ~~
9 IRFAN 85(48.4%) 118(66.6%) 118(66.6%) 128(72.7%) ~~ 5 R2W2A1 4 R2W1A1 2 R1W1 1 R1 ~~
10 SEHAN 60(52.1%) 75(65.2%) 75(65.2%) 86(74%) 96(82.6%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
11 JAYANTH 95(51%) 112(60.3%) 112(60.3%) 134(72%) 160(86.2%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
12 SAYEED 115(48%) 138(57.5%) 142(59%) 166(69.3%) 180(75%) 6 R2W2A2 4 R2W1A1 4 R2W1A1 3 R1W1A1 2 R1W1
13 ZUHAIB 210(53%) 255(64.4%) 255(64.4%) 290(73.3%) 335(84.5%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
14 KEERTHANA 106(52%) 135(65.6%) 140(68.2%) 150(73%) ~~ 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 ~~
15 KALYAN RAM 112(52.8%) 144(67.3%) 144(67.3%) 155(72.4%) 195(91.3%) 5 R2W2A1 4 R2W1A1 2 R1W1 1 R1 1 R1
16 THOUSIF 86(50.9%) 112(66.8%) 112(66.8%) 125(74%) 155(92.3%) 4 R2W1A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
17 KIRAN 92(53.5%) 106(62.1%) 106(62.1%) 128(74.8%) 150(87.2%) 4 R2W1A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
18 CHANDANA 88(51.4%) 110(64%) 110(64%) 125(72.6%) 138(80%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
19 ZOYA KULSUM 120(48.9%) 160(65.7%) 165(67.6%) 175(71.4%) ~~ 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 ~~
20 SAI ABHIRAM 112(50%) 140(62.5%) 160(71% 160(71%) 180(80%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
21 CHANDANA 92(51.3% 120(66%) 120(66%) 130(72.2%) 170(94.4%) 4 R1W2A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
22 VANITHA 108(47.2%) 150(65.5%) 150(65.5%) 160(69.8%) 170(74.2%) 5 R2W2A1 3 R1W1A1 3 R1W1A1 2 R1W1 2 R1W1
23 SIMRAN FATHIMA 110(50%) 145(65.7%) 155(70.4%) 160(72.7%) 165(75%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 2 R1W1
24 RABEENA 125(51%) 160(65.2%) 165(67.3%) 180(73.5%) 210(85.7%) 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1 1 R1
25 AYESHA 105(51.2% 132(64.3%) 132(64.3%) 145(70.7%) 172(84%) 4 R1W2A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
26 SAANVI 112(50%) 135(60% 135(60%) 155(68.8%) 175(78%) 6 R2W2A2 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1
27 ARVIND 110(50%) 135(61.3%) 145(66%) 155(70.45%) 175(79.5%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
28 NISHANTH 75(50%) 100(66.6%) 100(66.6%) 110(73.3%) 144(96%) 4 R1W2A1 3 R1W1A1 2 R1W1 1 R1 1 R1
29 HEMANTH 135(47.5%) 155(54.5%) 160(56.3%) 190(66.9%) 230(80.9%) 6 R2W2A2 5 R2W2A1 4 R2W1A1 3 R1W1A1 4 R1W1A1
30 SHREYA 90(51.7%) 110(63.2%) 115(66%) 125(71.8%) 140(80.5%) 5 R2W2A1 4 R2W1A1 4 R2W1A1 3 R1W1A1 2 R1W1
31 AKASH 110(48.8%) 120(53.3%) 125(55.5%) 155(68.8%) 180(80%) 6 R2W2A2 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1
32 AYESHA BANU 115(51%) 135(60%) 140(62.2%) 160(71%) 180(80%) 5 R2W2A1 4 R1W2A1 3 R1W1A1 2 R1W1 1 R1
33 CHANDINI 85(50%) 100(58.8%) 110(64.7%) 125(73.5%) 135(79.4%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
34 ABHINAV 120(54.5%) 145(66%) 145(66%) 165(75%) 185(84%) 4 R1W2A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
35 ZAARA KHANUM 120(48.9%) 138(56.3%) 148(60.4%) 175(71.4%) ~~ 6 R2W2A2 5 R2W2A1 3 R1W1A1 1 R1 ~~
36 YUNIS KHAN 155(50.9%) 200(65.5%) 210(68.8%) 220(72.2%) 285(93.4%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
37 M D FOUZAN 105(51.5%) 120(58.8%) 120(58.8%) 155(75.9%) 175(85.8%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
38 AYESHA 95(50%) 115(60.5%) 120(63.1%) 135(71%) 150(79.2%) 5 R2W2A1 4 R1W2A1 4 R2W1A1 3 R1W1A1 2 R1W1
39 KIRAN 88(51.2%) 100(58.1%) 108(62.7%) 125(72.6%) 140(81.3%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
40 KEERTHANA 74(48%) 90(58.4%) 90(58.4%) 105(68%) 125(81.6%) 6 R2W2A2 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1
41 VARSHINI 60(52.1%) 80(69.5%) 80(69.5%) 85(73%) 95(81.8%) 4 R2W1A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
42 REEBA 65(50%) 86(66.4%) 86(66.4%) 90(69.2%) 110(84.6%) 4 R1W2A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
43 RAMESH 144(50.7%) 164(57.7%) 170(60.2%) 200(70.4%) 225(79.4%) 4 R1W2A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
44 REENATH 68(51.1%) 88(66.4%) 88(66.4%) 98(74.2%) 125(94.4%) 4 R1W2A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
45 RANJITH 144(50.7%) 170(60.2%) 170(60.2%) 200(70.4%) 210(74%) 5 R2W2A1 4 R2W1A1 4 R2W1A1 3 R1W1A1 2 R1W1
46 IMPANA 62((53.9%) 75(65.2%) 75(65.2%) 85(73.9%) 94(81%) 4 R2W1A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1
47 FIROZ 240(53.3%) 290(64.4%) 300(66.6%) 330(73.3%) ~~ 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 ~~
48 FARHAN PASHA 118(49.1%) 136(57%) 145(60.4%) 166(69.3%) 180(75%) 6 R2W2A2 5 R2W2A1 4 R2W1A1 2 R1W1 2 R1W1
49 SRAJAN 75(50%) 100(67.3%) 100(67.35) 108(72%) 144(96.4%) 5 R2W2A1 4 R2W1A1 3 R1W1A1 2 R1W1 1 R1
50 HUZAIFA 126(52.1%) 158(65.2%) 158(65.2%) 178(73.5%) 205(84.7%) 4 R2W1A1 3 R1W1A1 3 R1W1A1 2 R1W1 1 R1