Determinants of Acute Exacerbation of Asthma in Asthmatics

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					Determinants of Acute Exacerbation of Asthma
                in Asthmatics




          DEPARTMENT OF COMMUNITY MEDICINE

            TRIVANDRUM MEDICAL COLLEGE




                                         NATARAJAN R

                                         JEENO JAYAN

                                         VIJIN VARGHESE

                                         SARAN SOMAN
                                                                                     2



                         DEPARTMENT OF COMMUNITY MEDICINE
                         MEDICAL COLLEGE, TRIVANDRUM – 695011
                             Phone: 0471- 2528379, 2528417
                             E-mail:commedtvm@gmail.com
                             Website: www.commedtvm.org



                                 CERTIFICATE


Report of project work done in 2009 on Determinants of Acute Exacerbation of Asthma in
                                      Asthmatics.

   Guided By: -

   Dr.Tony Lawrence,
   Dept. of Community Medicine,
   Govt. Medical College, Thiruvananthapuram

                  Certified that this report is a bonafide record of the project
undertaken on Determinants of Acute Exacerbation of Asthma in Asthmatics by
Natarajan.R, Jeeno Jayan, Vijin Varghese and Saran Soman and was done during the
year 2009.




  Date:                                                           Dr. VIJAYAKUMAR

                                                Professor and Head of the Department

                                                   Department of Community Medicine

                                                Medical College, Thiruvananthapuram.
                                                                                       3




                                ACKNOWLEDGEMENT



We cannot express in words the indebtedness we owe to our esteemed teacher,
Dr.Vijayakumar, Head of Department, Community Medicine, Trivandrum Medical College
for his encouragement and guidance and providing us with an opportunity to do this
project.



No words can express the deepest sense of gratitude and thanks to our supervising
teacher, Dr.Tony Lawrence for his invaluable guidance, support and encouragement
throughout the period of project work right from its conception to completion.



We are also thankful to Dr. Sanjeev Nair, M.O, Department of Pulmonary Medicine,
Chest Disease Hospital, Pulayanarkotta; Dr. Arjun, Consultant, Chest and Thoracic
Clinic, S P Fort hospital; Dr.Mini ,Asthma Clinic, General Hospital for their support and
help in the form of advice and reference for this project.



The helpful discussions and suggestions provided by all the teachers and post graduates
in the Department of Community Medicine are sincerely acknowledged. We are also
thankful to all the friends for the help offered to us.



We are most indebted to the patients who took part in this study, but for whose
cooperation the project would not have been possible. We sincerely hope that the results
of this study will in some way contribute to the betterment in their management.
                                        4




                     CONTENTS



a. EXECUTIVE SUMMARY               5

b. INTRODUCTION                    7

c. REVIEW OF LITERATURE            10

d. OBJECTIVE                       12

e. METHODOLOGY                     13

f. RESULTS AND DISCUSSION          15

g. CONCLUSION AND RECOMENDATIONS   22

h. LIMITATIONS                     24

i. BIBLIOGRAPHY                    25

j. QUESTIONNAIRE                   27
                                                                                             5




                                  EXECUTIVE SUMMARY

Introduction



Asthma is a global health problem.300 million people suffer from asthma worldwide. By
2001 estimates, India had 25 million people suffering from asthma. This is likely to go up
by 50% by 2016.The World Health Organization has estimated that 15 million disability-
Adjusted Life Years (DALYs) are lost annually due to asthma, representing 1% of total
global disease burden. The prevalence of asthma is increasing worldwide. Extensive
studies have been carried out on Childhood Asthma and ‘Risk factors’ of Asthma, but
there is conflicting evidence about the ‘Trigger Factors’ (Determinants) of acute
exacerbation of asthma. The lack of clarity about these ‘Trigger Factors’ prompted us to
undertake this study in adult asthmatics.



Methodology



A case crossover design was used to achieve our objective. The study was conducted
from September to November 2009 at Chest Disease Hospital (Pulayanarkotta),Chest
and Thoracic Clinic(S P Fort Hospital) and Asthma Clinic(General Hospital).The study
was conducted on 50 asthmatic patients (>12 years of age) who reported with acute
exacerbation and those who came for review within 2 days of their last exacerbation. A
semi-structured questionnaire was used to interview them. A paired analysis was done
using McNemar test and the trigger factors of the asthmatic attack were identified. The
strength of association was measured using Odd’s ratio.



Result

After analysis, the following factors were found to have statistically significant association
with asthma exacerbation:


    Perceived Weather change (corrected OR-28, p-0.0001)

    Dust exposure (OR-18.000, p-0.0002)
                                                                                         6


    Respiratory Infection (OR-15.5, p-0.0001)

    Physical exertion (corrected OR-15, p-0.0005)

    Interruption of regular anti-asthmatic medication (corrected OR-10, p-0.0077)

    Exposure to Smoke (corrected OR-9, p-0.0133)

    Emotional and psychological stress (OR-5.000, p-0.0433)




Conclusion



In our setting, the most important trigger factors of acute asthma exacerbation are
perceived climate change, dust exposure, respiratory infection, physical exertion,
interruption of regular anti-asthmatic medication, exposure to smoke and emotional and
psychological stress. Hence appropriate measures have to be taken to mitigate these
factors in asthmatics. Also further studies are required to find out more about the trigger
factors of asthma exacerbation.
                                                                                         7




                                    INTRODUCTION

Asthma is a chronic inflammatory disorder of the airways that causes recurrent episodes
of wheezing, breathlessness, chest tightness and cough, particularly at night and/or in the
early morning. These symptoms are usually associated with widespread but variable
bronchoconstriction and airflow limitation that is at least partly reversible, either
spontaneously or with treatment. It is thought that inflammation causes an increase in
airway responsiveness (bronchospasm) to a variety of stimuli. Many cells and cellular
elements play a role in the inflammatory response.

Asthma is a global health problem.300 million people suffer from asthma worldwide. By
2001 estimates, India had 25 million people suffering from asthma. This is likely to go up
by 50% by 2016.The World Health Organization has estimated that 15 million disability-
Adjusted Life Years (DALYs) are lost annually due to asthma, representing 1% of total
global disease burden. Annual worldwide deaths from asthma have been estimated at
250,000 and mortality does not appear to correlate to its prevalence.

Social and economic factors are integral to understanding asthma and its care, whether
viewed from the perspective of individual sufferer, health care professional, or entities
that pay for health care. Absence from school and days lost from work are reported as
substantial social and economic consequences of asthma in studies from the Asia-Pacific
region, India, Latin America, United Kingdom and United States of America.



FACTORS INFLUENCING THE DEVELOPMENT AND EXPRESSION OF ASTHMA



Factors that influence the risk of asthma can be divided into those that cause the
development of asthma and those that trigger asthma symptoms; some do both. The
former include host factors (which are primarily genetic) and the latter are usually
environmental factors. However, the mechanisms whereby they influence the
development and expression of asthma are complex and interactive. For example, genes
likely interact with other genes and with environmental factors to determine asthma
susceptibility. In addition maturation of immune response and the timing of infectious
exposures during the first years of life are emerging as important factors modifying the
risk of asthma in genetically susceptible individuals.
                                                                                         8


Additionally, some characteristics have been linked to an increased risk of asthma, but
are not themselves true causal factors. The apparent racial and ethnic differences in the
prevalence of asthma reflect underlying genetic variances with a significant overlay of
socioeconomic and environmental factors. In turns the link between asthma and
socioeconomic status-with a higher prevalence in developed than in developing nations,
in poor compared to affluent populations in developed nations, and in affluent compared
to poor populations in developing nations-likely reflect lifestyle differences such as
exposure to allergens, access to health care, etc.

Much of what is know about asthma risk factors comes from studies of young children.
Risk factors of the development of asthma in adults, particularly de novo in adults who did
not have asthma in childhood, are less well defined.



HOST FACTORS

   1) Genetic factors-Multiple genes are involved in the pathogenesis of asthma and
      different genes may be involved in different ethnic groups.
   2) Obesity-Obesity has also been shown to be a risk factor of asthma. Certain
      mediators such as leptins may affect airway function and increase the likely hood
      of asthma development.
   3) Sex-Male sex is a risk factor for asthma in children. Prior to the age of 14, the
      prevalence of asthma is nearly twice as great in boys as in girls. As children get
      older the difference between the sexes narrows, and by adulthood the prevalence
      of asthma is greater in women than in men. The reason for this sex-related
      difference is not clear. However, lung size is smaller in males than in females at
      birth but larger in adulthood.



 TRIGGER FACTORS

The trigger factors are those which set off an acute attack in individuals who already have
asthma. They themselves are not the ‘cause’ of asthma. The triggers and risk factors of
asthma attacks are different for each person, and can even change over time in each
patient. Environmental, infectious and personal factors may all play a part in triggering
asthma attacks. The following are factors that are said to trigger an asthmatic attack:

       Respiratory Infections, usually viral such as colds, flu and bronchitis.
       Allergens, usually from house dust mites, pets or pollen.
       Play, exercise and undue physical exertion.
                                                                                      9


       Emotions, like excitement, fear and anger, stress.
       Irritants, such as air pollution.
       Tobacco smoke-active and passive smoking.
       Dust, Firewood smoke.
       Paint, cosmetics like talc, perfumes, etc.
       Weather changes such as cold spells.
       Food allergens, like peanuts, certain sea foods, food additives.
       Certain medications like aspirin, beta blockers and NSAIDs.
       Heart burn.




 Extensive studies have been carried out on Childhood Asthma and ‘Risk factors’ of
Asthma, but there is conflicting evidence about the ‘Trigger Factors’ (Determinants) of
acute exacerbation of asthma. The lack of clarity about these ‘Trigger Factors’ prompted
us to undertake this study in adult asthmatics.
                                                                                          10




                                REVIEW OF LITERATURE



The case crossover design was introduced in 1991 by Maclure M to study the transient
effect of brief exposure on the occurrence of a rare acute-onset disease. The argument is
that if there are precipitating events, these events should occur much more frequently
during a period immediately prior to the onset of disease than at a similar period which is
more distant from the disease onset. For example, it has been reported that physical
stress and mental stress may trigger sudden cardiac death. If this is true, one would find
that sudden cardiac death occurred more frequently during or shortly after strenuous
physical activity, or that there was an increase in informant-reported life stress either
acutely before sudden cardiac death or during the weeks before the event. Another
example is the alcohol consumption and injury. The effect of alcohol is transient and
alcohol use is usually associated with injury. Therefore, one would expect that the alcohol
consumption prior to injury increases the risk of injury.



 The design applies best if the exposure is intermittent, the effect on risk is immediate and
transient, and the outcome is abrupt. To estimate relative risk, the exposure frequency
during a window just before outcome onset is compared with exposure frequencies
during control times rather than in control persons. Self-matching of cases eliminates the
threat of control-selection bias and increases efficiency.



Case crossover design is a scientific way to ask and answer the question that “Was the
patient doing anything unusual just before the onset of the disease”. Like most of the
epidemiological studies we need to have control data to determine what "unusual" meant.
However, we can’t do the comparison among individuals since everyone is different.
Rather, the comparison should be done within the individual. In another words, we will
compare the individual’s activity before the disease onset to his/her usual activity. Thus
here, we have a "case" component and also a "control" component, but the information of
both components will come from the same individual.



We define the "case component" as hazard period which is the time period right before
the disease or event onset; and the "control component" as control period which is a
specified time interval other than the hazard period. The information of the individual
"exposed to certain activity or agent during the hazard period and control period will be
                                                                                       11


compared. If we collect such information from many subjects who had the disease or
event, we can test for consistent relationships between the disease and the exposure.



In 1993 Mittleman MA, Maclure M, Tofler G H ,et al. investigated the effect of heavy
physical exertion on the onset of MI and whether the risk of MI can be modified by regular
physical exertion, with the help of case crossover design.



In 1997 Gullette EC, Blumenthal JA, Babyak M, et al. studied the Effects of mental stress
on myocardial ischemia during daily life.

In 1998 Barbone F, McMahon AD, Davey PG, et al. studied the Association of road-traffic
accidents with benzodiazepine use.

In the same year, Meier CR, Jick SS, Derby, et al. studied the Association of Acute
respiratory-tract infections and risk of first-time acute myocardial infarction.
                                                                              12




                               OBJECTIVE

 To study the determinants of acute exacerbation of asthma in known asthmatics
                               aged above 12 years.
                                                                                                    13




                                       METHODOLOGY

Study design

Case Crossover Study

Study setting

1) Chest Disease Hospital, Pulayanarkotta

2) Chest and Thoracic Clinic, S P FORT Hospital

3) Asthma Clinic, General Hospital, Trivandrum

Study subjects

Case:

      “A case is defined as any clinically diagnosed asthmatic patient, above 12 years of
age, who falls within the time period of 72hrs before the onset of acute asthmatic attack.”



Control:

      “The same asthmatic patient, who was defined as the case, but falling within a time
period of 168 to 240hrs before the onset of the acute asthmatic attack.”




SELECTION OF PATIENTS

INCLUSION CRITERIA

Patients, who reported within 2 days of their asthma exacerbation *. (* as diagnosed by an expert
pulmonologist)
                                                                                          14

EXCLUSION CRITERIA

1) Patients< 12 years of age.

2) Patients suffering from other co-morbid respiratory conditions like tuberculosis,
pleural effusion, chronic obstructive pulmonary disease.

3) Patients who reported after 2 days of their exacerbation.

4) Those patients who had an asthmatic attack at any time in the 10 days prior to the
current exacerbation.

5) Patients who were terminally ill, unwilling or non cooperative.

Sample Size: Case- 50 ;      Control-50

Study Period: September-November 2009

Study Tool: A semi-structured questionnaire was used to interview the patients. It
consisted of socio-demographic variables and 16 variables (triggers) relevant to the
study.

Analysis:
A paired analysis of the data was carried out using McNemar test calculator and the
trigger factors of the asthmatic attack were identified. The strength of association of
various trigger factors was measured by Odds Ratio (b/c) from the 2x2 table.




Ethical consideration: Informed consent was obtained from all participants. All
information provided by them was kept confidential and used only for research
purposes.

                                RESULTS AND DISCUSSION

1) DUST EXPOSURE

                    CONTROL PERIOD

                         EXPOSED     UNEXPOSED
                                                                        15


HAZARD                      2             18
            EXPOSED

PERIOD                      1             29
           UNEXPOSED

Odds ratio : 18 ;     p value: 0.0002;    x2 : 13.474

2) RESPIRATORY INFECTIONS

                     CONTROL PERIOD

HAZARD                   EXPOSED    UNEXPOSED
                            10            31
            EXPOSED
PERIOD                      2             7
           UNEXPOSED

Odds ratio : 15.5 ;    p value: 0.0001;    x2 : 23.578

3) PASSIVE SMOKING

                     CONTROL PERIOD

HAZARD                   EXPOSED    UNEXPOSED
                            4             5
            EXPOSED
PERIOD                      3             38
           UNEXPOSED

Odds ratio : 1.66;     p value: 0.7237 ;       x2   : 0.125



4) PHYSICAL EXERTION

                     CONTROL PERIOD

                         EXPOSED    UNEXPOSED
HAZARD                      1             14
            EXPOSED
                            0*            35
PERIOD     UNEXPOSED


*Corrected Odds ratio : 15; p value : 0.0003 ;          x2    : 13.06

5) PERCEIVED WEATHER CHANGE

                     CONTROL PERIOD

                         EXPOSED    UNEXPOSED
                                                                        16


                          2              27
            EXPOSED
HAZARD
                         0*              21
           UNEXPOSED
PERIOD
*Corrected Odds ratio : 28 ; p value: 0.0001        ;   x2   : 25.037



6) SMOKE EXPOSURE

                  CONTROL PERIOD

HAZARD                 EXPOSED      UNEXPOSED
                          1              8
            EXPOSED
PERIOD                   0*              41
           UNEXPOSED

*Corrected Odds ratio : 9 ; p value: 0.0133 ;       x2   : 6.125



7) HEARTBURN (Gastro esophageal reflux)

                  CONTROL PERIOD

                       EXPOSED      UNEXPOSED
HAZARD                    4              3
            EXPOSED
                          2              41
PERIOD     UNEXPOSED


Odds ratio : 1.5; p value: 1.0000 ;   x2      : 0.000



8) EMOTIONAL STRESS

                  CONTROL PERIOD

                       EXPOSED      UNEXPOSED
HAZARD                    0              10
            EXPOSED
                          2              38
PERIOD     UNEXPOSED


Odds ratio : 5; p value: 0.0433 ;   x2    : 4.083

9) INTERRUPTION OFREGULAR ANTI-ASTHMATIC MEDICATION

                  CONTROL PERIOD
                                                                              17

                        EXPOSED    UNEXPOSED
HAZARD                     0           9
            EXPOSED

PERIOD                    0*          41
           UNEXPOSED


*Corrected Odds ratio : 10 ; p value : 0.0077 ;      x2      : 7.11



10) EXPOSURE TO ALLERGENS (grass pollen, animal dander, cockroach allergen)

                     CONTROL PERIOD

                        EXPOSED    UNEXPOSED
HAZARD                     0           0
            EXPOSED
                           0           50
PERIOD     UNEXPOSED


              Odds ratio : 0.000


11) INTAKE OF ALLERGIC FOOD ITEMS

                     CONTROL PERIOD

                        EXPOSED    UNEXPOSED
HAZARD                     0           2
            EXPOSED
                          0*          48
PERIOD     UNEXPOSED


*Corrected Odds ratio : 3 ; p value: 0.4795 ;   x2   : 0.5

12) INTAKE OF NEW FOOD

                     CONTROL PERIOD


                        EXPOSED    UNEXPOSED
HAZARD                     0           0
            EXPOSED
                           0          50
PERIOD     UNEXPOSED


Odds ratio : 0.000

13) SMOKING

                     CONTROL PERIOD
                                                                     18


                        EXPOSED   UNEXPOSED
HAZARD                     0          1
            EXPOSED
                          0*          49
PERIOD     UNEXPOSED


*Corrected Odds ratio : 2 ; p value: 1 ; x2 : 0.000



14) INTAKE OF MEDICATIONS OTHER THAN USUAL (NSAIDs, Beta Blockers)

                     CONTROL PERIOD

                        EXPOSED   UNEXPOSED
HAZARD                     0          0
            EXPOSED
                           0          50
PERIOD     UNEXPOSED


Odds ratio : 0.000

15) COSMETICS (deodorants, talc, perfumes)

                     CONTROL PERIOD

                        EXPOSED   UNEXPOSED
HAZARD                     0          0
            EXPOSED
                           0          50
PERIOD     UNEXPOSED


Odds ratio : 0.000

16) PAINT AND PAINT PRODUCTS

                     CONTROL PERIOD

                        EXPOSED   UNEXPOSED
HAZARD                     0          0
            EXPOSED
                           0          50
PERIOD     UNEXPOSED




Odds ratio : 0.000
                                                                                          19


                                       DISCUSSION

On analyzing the data, the following factors were found to be statistically significant
trigger factors of acute asthma exacerbation:

        Perceived weather change (OR-28*, p-0.0001)

        Dust exposure (OR-18.000, p-0.0002)

        Respiratory Infection (OR-15.5, p-0.0001)

        Physical exertion ( OR-15*, p-0.0005)

        Interruption of regular anti-asthmatic medication (OR-10*, p-0.0077)

        Exposure to Smoke (OR-9*, p-0.0133)

        Emotional and psychological stress (OR-5.000, p-0.0433)

                                                                 OR: Odd’s ratio; p=p value
                                                                              *corrected odds



From our study, Perceived weather change was identified as one of the trigger factors of
acute asthma exacerbation. 27 patients had felt “hot” or “cold” spells (change in weather
pattern) prior to the asthma exacerbation exclusively in the hazard period. Transient
worsening of asthma may occur as a result of exposure to risk factors for asthma
symptoms, or triggers, such as exercise, air pollutants1 and even certain weather
conditions2.



Exposure to dust and smoke from various sources too had a role in triggering asthma
exacerbations. Dust exposure included both indoor and outdoor sources. Smoke
exposure included firewood smoke, automobile exhaust and smoke from industries.



Clinical and experimental evidence suggests an important role for respiratory infections in
the development of asthma attacks. In our study too, we found respiratory tract infection
as a significant trigger. Respiratory infections have an important relationship to asthma as
they produce wheezing and increase symptoms in patients.
                                                                                         20


We were able to identify Physical exertion as an important asthmatic trigger. A study
conducted Dr. Shlomo Moshe from Tel Aviv University’s Sackler Faculty of Medicine
found an indisputable connection between asthma and exercise. 6



Smoking is an established trigger factor of acute asthmatic attack. Tobacco smoking
makes asthma more difficult to control, results in more frequent exacerbations and
produces a more rapid decline in lung function and increases risk of death 3. In our study,
smoking was not found to be a statistically significant trigger .This can be explained by
the fact that 31 of our subjects were females and the male subjects were either non
smokers or had abstained from smoking because of self identification of smoking as a
trigger factor.



A significant association was obtained between emotional stress and asthma
exacerbation. There is well documented evidence that emotional stress is a trigger factor
for asthma. Emotional stress may lead to asthma exacerbations, primarily because
extreme expressions (laughing, crying, anger / fear) can lead to hyperventilation and
hypocapnoea which can cause bronchospasm.



Up to 28% of adults with asthma , but rarely children with asthma, suffer from
exacerbations in response to aspirin and other NSAIDs. This syndrome is more common
in severe asthma4.In our study, a positive association between intake of such
medications and asthma attack could not be established. This may be because of the low
incidence of drug induced asthma or these drugs probably effect an exacerbation only on
long term intake.



The relationship of increased asthma symptoms, particularly at night, to gastro
oesophageal reflux remains uncertain, although this condition is nearly 3 times as
prevalent in patients with asthma compared to general population5. A positive correlation
was not obtained in this aspect in our study as well. This can be a real finding or it could
be due to the problem of sample size. Further studies are essential in this regard.
                                                                                      21


No cases with exposure to paint, cosmetics and allergens (grass pollen, pet dander)
could be elicited. Therefore, we cannot come to a conclusion about the role of these in
triggering an asthmatic attack in our setting. Further studies will help in decoding this
aspect.

No correlation was found between consumption of allergic food and asthma attack. This
may be explained by the fact that the incidence of food allergy related asthma is low and
usually severe. The patients being well aware of their food habits may have avoided the
sensitive food stuff.



A strong correlation was also present between Interruption of regular anti-asthmatic
medication and asthma exacerbation.
                                                                                           22




                         CONCLUSIONS & RECOMENDATIONS



Going through an intense period of preparation, data collection & analysis, we came
across some of the webs of intricate relationships among the triggers that solemnly or in
multitude precipitated an asthmatic attack which in itself varied in magnitude, proportions
and parts. We were able to pinpoint the trigger factors of asthmatic attack, accepting our
limitations. This is important when it comes to tackling the incidence of asthmatic attack,
which is in reality the heartbeat behind taking up this mission. In our setting, the most
important trigger factors of acute asthma exacerbation include:

      Dust exposure
      Respiratory Infection
      Physical exertion
      Perception of weather change
      Exposure to smoke
      Stress
      Interruption of regular anti-asthmatic medication

Based on the findings made above, the following suggestions are recommended for
reducing the incidence of acute exacerbations of asthma in known asthmatics.



The avoidance of as many allergens as possible to which the individual is sensitive is the
key aspect. For this, the patient must be helped in all possible aspects to identify his/her
own triggers. No one single approach is sufficient to reduce allergens; a multi factorial
approach is required.



Physical exertion triggers an asthmatic attack by hyperventilation. For those in whom
physical exertion is a trigger, activities like running, early morning jogging can be fateful.
Intense work outs can prove to be detrimental than beneficial. They must be advised to
limit their level of exertion and also refrain from activities that may require them to exert
beyond their capacity.
                                                                                          23


Respiratory infections being notorious for precipitating an attack should be promptly
treated with appropriate medication. This will help in combating the respiratory infections
from initiating an exacerbation. Susceptible individuals must, therefore, be advised to
avoid contact with various sources of infections and adopting a healthy lifestyle. Such
individuals must also be advised to seek treatment without any delay in case of a
respiratory tract infection.



Avoiding exposure to dust and smoke is the best possible way to prevent an asthmatic
attack in individuals who are sensitive to these triggers. Smoke from vehicle exhausts,
industries, and household smoke are few situations that we came across during our data
collection. Air filters and room air cleaners may help prevent some asthma symptoms.
Emphasis must be laid on personal protection measures (masks, handkerchiefs)
especially when these patients are engaged in activities like sweeping, cleaning and
dusting. Firewood smoke exposure can be reduced by use of tall chimneys in the kitchen
or by resorting to alternative smoke free fuels for cooking. Highly sensitive individuals
must refrain from engaging in activities that will increase their exposure to these triggers.
Maintaining the emission standards of vehicles will help in reducing environmental smoke
and this will help in the long run.



Stress being a Siamese twin of modern lifestyle is hard to combat, but never impossible.
The role of stress as an asthmatic trigger has to be studied further. Emphasis need to be
laid on management of stress at personal level and at the society level.



Asthmatics must be advised not to skip their prescribed medications. The medications
are particularly intended for the asthma control and should be taken without fail. The
doctor must ask the patient to come for periodic check ups and ensure patient adherence
and compliance to medications. The kith and kin of the patient have a major role in this
aspect.



Emphasis must also be laid on prompt rescue treatment of asthma attacks. Patients must
be taught how to use Rota halers and Space halers.
                                                                                       24




                                   LIMITATIONS




1) Sample size was not calculated statistically because of time constraints and lack of
   a pilot study in our setup to do so. Hence we took all cases which satisfied our
   inclusion and exclusion criteria, during our study period.

2) The exposure information was provided by the study participants. Recall bias may
   very possible occur as the information was not "recorded" and was recalled by the
   individuals.


3) The results obtained represent only relative risk but not an absolute risk.


4) The trigger factors of asthma exacerbation vary from one person to another and
   also from time to time within an individual. We were able to identify only those
   trigger factors that had precipitated the current attack in the individual. Whether the
   patient had other trigger factors could not be found out.
                                                                                                     25




                                        BIBLIOGRAPHY


a) Global initiative for Asthma (GINA)
                                             th
b) Robbins Pathological Basis of Diseases 7 Edition 723-27

c) Harrisons Textbook of Medicine

d) www.pitt.edu

e) www.wikipedia.org

f)   www.nih.gov

g) Case-crossover design in air pollution epidemiology J.J.K. Jaakkola, Institute of Occupational

     Health, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.

h) The case-crossover design: a method for studying transient effects on the risk of acute events.

     Maclure M. Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115.



1) Tillie-Leblond J, Gosset P,Tonnel AB. Inflammatory events in severe acute asthma. Allergy 2005

     60(1): 23-9

2) Newson R, Strachas D, Archibald E, Emberlin J, Hardaker P, Coller C. Acute asthma epidemics,

     weather and pollen in England.1987-1994. Eur Respin J1998; 694-701

3) Thomson N C, Chaudhari R, Livingston E Asthma and cigarette smoking Eur Respir J (2004) 24

     (5):822-33

4) Szczeklek A, Stevenson D D Aspirin induced asthma: advances in pathogenesis, diagnosis and

     management J Allergy Clin Immunol 2003: 111(5) 913-21

5) Hardig S M . Acid reflux and asthma . Curr Opin Pulm Med 2003:9 (1) 42-5

6) American Friends of Tel Aviv University (2009, January 7). Asthma Attacks Triggered By Exertion

     At Work And Play. Science Daily.
                                                                                                    26




                                           CONSENT FORM


Information to Participants

       We are Jeeno Jayan, Vijin Varghese, Natarajan R and Saran Soman, MBBS students of
Govt. Medical College, Trivandrum. We are doing a study to find out the Determinants of Acute
Exacerbation of Asthma in Asthmatics. For this study we need your co – operation and help
which you can provide by helping us fill out a questionnaire on the same. The filling of this
questionnaire will take about 15 minutes of your time.

       We assure you that the co-operation to this study is purely VOLUNTARY and all the details
you provide will be kept strictly confidential. A decision from your part on not participating in this
study will not affect your personal relationship with the institute or other services to which you
are otherwise entitled.

Consent by Participants

         I have read the information given above. I have been given the opportunity to ask
questions and doubts. All my questions have been answered to my satisfaction. Understanding
all of this, I am voluntarily participating in this research at my free will and also willing to answer
the questionnaire given along with.


                                                                       Signature: -
                                                                       Name: -

Date: -
                                                                                        27


                                  QUESTIONNAIRE



   SECTION A: (Sociodemographic pattern)



   Name:                 Age:   Sex:
   Address:
   Occupation:
   Educational status:
   Socioeconomic status:



   SECTION B


1) When were you diagnosed as asthmatic?
2) Any history of asthma in your family? Y/N
3) Did you suffer from asthma in your childhood?




   (Questions to Consider in the Diagnosis of Asthma as per GINA guidelines)

          Has the patient had an attack or recurrent attacks of wheezing?
          Does the patient have a troublesome cough at night?
          Does the patient wheeze or cough after exercise?
          Does the patient experience wheezing, chest tightness, or cough after
           exposure to airborne allergens or pollutants?
          Do the patient's colds “go to the chest” or take more than 10days to clear
           up?
          Are symptoms improved by appropriate treatment?
                                                                                               28




                                            SECTION C

Sl.                                   Hazard Period                   Control period
no
             Exposure            ________ to ________   (Y/N)   ________ to ________   (Y/N)

1      Dust as in cleaning,
      sweeping or others

2     Respiratory tract
      infections



3      Grass pollen, animal
      dander, cockroach
      allergen.

4     Smoking

5     Passive smoking

6     Physical exertion

7     Perception of Weather
      change

8     Intake of allergic food.


9     Intake of any new food
      stuff

10    Intake of medications
      (NSAIDs , aspirin)

11    Smoke

12    Emotional and
      psychological stress
                               29


13   Cosmetics (new
     perfumes, talc, etc)

14   Heart Burn

15   Paint products

16   Interruption of regular
     anti-asthmatic
     medication

				
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