I

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

II

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

III

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

V

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

VI

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.

VII

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

VIII

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

IX

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

x

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).

xi

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.

xii

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

xiii

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

xiv

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

xv

22. Seasonal Variation 65

23. Associated factors 66

24. Predicted Improved of PEFR in Percentage 68

1

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

2

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;

3

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.

4

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.

5

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

6

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

7

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

8

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.

9

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

10

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

11

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

.

12

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.

13

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

14

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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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