"TO CORRELATE CLINICORADIOLOGICAL CHARACTERISTICS

OF BRONCHIECTASIS WITH PULMONARY HYPERTENSION"

DISSERTATION SUBMITTED TO

THE TAMIL NADU Dr. M.G.R MEDICAL UNIVERSITY, CHENNAI

IN PARTIAL FULFILLMENT OF THE REGULATIONS FOR THE

AWARD OF DEGREE OF M.D IN RESPIRATORY MEDICINE

BY

Dr.NAJMA MUHAMMED.K

GUIDE : DR.K.ANUPAMA MURTHY

DEPARTMENT OF RESPIRATORY MEDICINE

PSG INSTITUTE OF MEDICAL SCIENCES AND RESEARCH

PEELAMEDU, COIMBATORE – 641004

TAMILNADU, INDIA

"TO CORRELATE CLINICORADIOLOGICAL CHARACTERISTICS

OF BRONCHIECTASIS WITH PULMONARY HYPERTENSION"

DISSERTATION SUBMITTED TO

THE TAMIL NADU Dr. M.G.R MEDICAL UNIVERSITY, CHENNAI

IN PARTIAL FULFILLMENT OF THE REGULATIONS FOR THE

AWARD OF DEGREE OF M.D IN RESPIRATORY MEDICINE

BY

Dr.NAJMA MUHAMMED.K

GUIDE : DR.K.ANUPAMA MURTHY

DEPARTMENT OF RESPIRATORY MEDICINE

PSG INSTITUTE OF MEDICAL SCIENCES AND RESEARCH

PEELAMEDU, COIMBATORE – 641004

TAMILNADU, INDIA

"TO CORRELATE CLINICORADIOLOGICAL CHARACTERISTICS

OF BRONCHIECTASIS WITH PULMONARY HYPERTENSION"

DISSERTATION SUBMITTED TO

THE TAMIL NADU Dr. M.G.R MEDICAL UNIVERSITY, CHENNAI

IN PARTIAL FULFILLMENT OF THE REGULATIONS FOR THE

AWARD OF DEGREE OF M.D IN RESPIRATORY MEDICINE.

BY

Dr.NAJMA MUHAMMED.K

GUIDE : DR.K.ANUPAMA MURTHY

DEPARTMENT OF RESPIRATORY MEDICINE

PSG INSTITIUTE OF MEDICAL SCIENCES AND RESEASRCH

PEELAMEDU, COIMBATORE – 641004

TAMILNADU, INDIA

CERTIFICATE

This is to certify that the thesis entitled “TO CORRELATE

CLINICORADIOLOGICAL CHARACTERISTICS OF BRONCHIECTASIS

WITH PULMONARY HYPERTENSION” is a bonafide work of

DR.NAJMA MUHAMMED.K done under the guidance and supervision of

DR.ANUPAMA MURTHY MD(CHEST) in the Department of PSG Institute

of Medical Sciences and Research, Coimbatore in fulfilment of the regulations

of Dr.MGR Medical University for award of M.D .Degree in Tuberculosis and

Respiratory Diseases.

DR.K.ANUPAMA MURTHY

Professor & Head

Department of Respiratory Medicine

DR.RAMALINGAM

DEAN

DECLARATION

I hereby declare that this study dissertation entitled “TO CORRELATE

CLINICORADIOLOGICAL CHARACTERISTICS OF BRONCHIECTASIS

WITH PULMONARY HYPERTENSION” was prepared by me under the direct

guidance and supervision of Professor of Respiratory Medicine,

DR.K.ANUPAMA MURTHY, MD (CHEST),PSG Institute of Medical

Sciences & Research, Coimbatore.

This dissertation is submitted to the Tamil Nadu Dr.MGR Medical

University in fulfilment of the University regulations for the award of M.D.

Degree in Tuberculosis and Respiratory Diseases. This dissertation has not

been submitted for the award of any other Degree or Diploma.

DR.NAJMA MUHAMMED.K

CERTIFICATE BY GUIDE

This to certify that the thesis entitled “TO CORRELATE

CLINICORADIOLOGICAL CHARACTERISTICS OF BRONCHIECTASIS

WITH PULMONARY HYPERTENSION” is a bonafide work of

DR.NAJMA MUHAMMED done under my direct guidance and supervision in

the Department of Respiratory medicine, PSG Institute of Medical Sciences

and Research, Coimbatore in fulfilment of the regulations of DR.MGR Medical

University for the award of M.D .Degree in Tuberculosis and Chest Diseases.

DR.K.ANUPAMA MURTHY

Professor & Head

Department of Respiratory Medicine

ACKNOWLEDGEMENT

I shall forever remain indebted to my beloved teachers,

Dr.K.Anupama Murthy, Dr.Karthikeyan Ramaraju for their constant valuable

inputs guidance, patients support without which thesis would have been

impossible

A special mention to the Radiology and Cardiology departments for

their unyielding support and providing a good number of cases for this study. I

take this opportunity to thank all the above mentioned departments

Finally I thank all my patients, who cooperated at every step and

provided me the opportunity to conduct the study.

Thank you

Dr.Najma Muhammed.K

PLAGIARISM CERTIFICATE

This is to certify that this dissertation work titled “ TO

CORRELATE CLINICORADIOLOGICAL CHARACTERISTICS OF

BRONCHIECTASIS WITH PULMONARY HYPERTENSION” of the

candidate Dr. Najma Muhammed. K with registration number

201527151 for the award of MD in the branch of RESPIRATORY

MEDICINE. I personally verified the urkund.com website for the

purpose of Plagiarism check. I found that the uploaded thesis file

contains introduction to conclusion pages and result shows 7% of

plagiarism in the dissertation.

Signature of the guide

CONTENTS

SL.NO CONTENTS PAGE NO

1 INTRODUCTION 1-12

2 AIMS AND OBJECTIVES 13

3 MATERIALS AND METHODS 14-16

4 REVIEW OF LITERATURE 17-51

5 RESULTS 52-62

6 DISCUSSION 63-74

7 SUMMARY 75

8 LIMITATION 76

9 CONCLUSION 77

10 BIBLIOGRAPHY

11 ANNEXURE

I) ABBREVIATIONS

II) CONSENT FORM

III) PATIENTS INFORMATION FORM

IV) MASTER CHART

1

INTRODUCTION

Bronchiectasis is one of the most prevalent morbidity in any community

leading to recurrent lower respiratory tract infections. Bronchiectasis means

abnormal and permanent dilation of medium sized subsegmental bronchi from

fourth to ninth generations. First described by Laennec in 1819,Later by Sir

William Osler,late by 1800 and futher defined by Reid in 1950.Bronchiectasis

usually associated with mucosal thickening, mucus plugging and avariable

degree of hyperinflation of lung. Bronchiectasis is associated with common

and rare disease, which impact of muciliary clearance and immunity. Mucus

clearance and local defence mechanisms aganist microorganisms are important

in preventing recurrent pulmonary infection.Repeated infection causes damage

and impedes the clearance of mucus.The airway dilatation and impairement of

mucociliary clearance increases suspectibility for repeated infection in

lungs,resulting in chronic infection.The abnormal airway anatomy ,chronic

infection and mucus retension result in decline in respiratory function.

Bronchiectasis may be congenital or acquired. Pathogenesis has not

been well defined. The combination of a microbial insult and defect in host

defence may result in persistent bronchial infection and inflammation which

leads to further structures to prolonged infection,result in lung damage. Other

pathogenesis includes obstructive either intraluminal or extraluminal,

inflammatory conditions, immunological changes.Autoimmune disease also

have some association in pathogenesis of bronchiectasis. The prevalence of

2

bronchiectasis is 5-7 times greater in persons over 55years of age. In Indian

adult it is third commonest non –tubercular respiratory disease with the

incidence of 71per lakh.

PULMONARY HYPERTENSION

Pulmonary Hypertension is a common complication in chronic lung

disease. Most revised classification of pulmonary hypertension,chronic lung

disease or conditions with alveolar hypoxia are included in WHO Group III of

PH –related disease. In this category of chronic lung disease of a mixed

obstructive and restrictive pattern,which includes chronic bronchiectasis, cystic

fibrosis and syndrome characterized by combination of pulmonary fibrosis and

emphysema ,in which the prevalence of PH is almost 50%. Prevelance in India

of bronchiectasis with pulmonary hypertension 1% in occupational airway

disease,15% in Chronic obstructive pulmonary disease,2% in Obliterative

bronchiolitis.Global prevalence in bronchiectasis of pulmonary hypertension is

7-12%.

Alveolar hypoxia is major factor for pulmonary vasoconstriction.

Endothelial level is one of the most important leading pathway for

development of PH in chronic lung disease. Alveolar hypoventilation increases

acute pulmonary vasoconstriction and vasodilation causes physiological shunt.

Hypoxia causes pulmonary vasoconstriction leads to increase pulmonary

vascular resistance. Vasoconstriction is achieved through activation of

3

vasoconstrictor pathway or inactivation of a vasodilator pathway, or through

the effects of hypoxia on vascular smooth muscle.

Figure : 1 Chest radiograph showing markedly dilated pulmonary arteries

(arrows).

4

Figure 2 : Contrast-enhanced computed tomography of the chest of a patient with

pulmonary arterial hypertension associated with congenital heart disease (large atrial

septal defect). Massive dilatation of the pulmonary arterial trunk and branches (#). The

ratio of the diameter of aorta (Ao) to the diameter of main pulmonary artery

(PA) is >1.5.

5

Figure 3: Measurements of main pulmonary artery and ascending aorta at the level of

bifurcation. The main pulmonary artery (PA) size is typically taken at the level of the

bifurcation of the main pulmonary artery perpendicular to the vessel wall. The aortic

dimension of the ascending aorta is taken at the same level to calculate the PA to the

aortic diameter (PA/Ao) ratio. The diameter is determined using the internal diameter

in the contrast-enhanced image.

6

Chest radiography is not sensitive for the diagnosis of airway disease.In

most severe cases of patients with bronchiectasis,as dilation of large airways

which can be visualized . High –resolution computed tomography is more

sensitive test than chest radiography and is useful in diagnosis of airway

disease. The test is considered as gold standard for diagnosing bronchiectasis.

Greater variance in section thickness compared to HRCT sections obtained

only at 10mm intervals,leads to improve the detection of bronchiectasis. HRCT

technique compromises scanning for apex to base with 1-2mm cuts at 10mm

intervals.

Common finding in bronchiectasis include bronchial wall

thickening,centrilobular nodules mosaic attenuation by air trapping. Following

tomographic criteria are used for diagnosis of CT bronchiectasis

1) Bronchial internal diameter larger than 1.5times the diameter of adjacent

pulmonary artery

2) Bronchial visualization in the periphery 1-2cm from the paritel pleura

7

Figure 4: shows normal lung (right), bronchiectasis lung (left)

Figure 5 : Tracheobronchial Segments

8

TRACHEOBRONCHIAL TREE ANATOMY

Trachea divides into right- and left- primary main bronchi.

Each further divides into lobar bronchi which in turn give rise to segmental

bronchi - supply air to bronchopulmonary segments.

Segmental bronchi divide dichotomously, eventually giving rise to terminal

bronchioles which further terminates into respiratory bronchioles.

Originating from each respiratory bronchioles are 2-11 alveolar ducts leading

to the alveolar sacs which are extended as a group of alveoli.

Airway becomes progressively narrower, shorter and more numerous, and

Cross sectional area, enlarges.

Areas of tracheobronchial tree furthest from the trachea are collectively called

the "distal respiratory tree"

RIGHT MAIN BRONCHUS :

The right main bronchus is 2 cm long on average and has an internal diameter

of 10-16 mm. This is slightly larger than the diameter of the left main

bronchus.

The bronchus intermedius of the right bronchial tree is actually quite short ,

extending for 1.0-2.5 cm until its anterior wall extends into and becomes the

middle lobe bronchus. Its posterior wall extends into and becomes the right

lower lobe bronchus.

9

Volume loss caused by pleural effusion, atelectasis, elevated right

hemidiaphragm, as well as traction or torsion from a fibrotic or scarred upper

lobe often cause shortening of this bronchus.

The RIGHT UPPER LOBE BRONCHUS Right upper lobe bronchus divides into

a. The apical bronchus

b. The anterior bronchus

c. The posterior bronchus

Distally just beyond the bronchus intermedius, another division occurs into :

The middle lobe bronchus with its anterior direction, dividing into

a) medial and b) lateral segmental bronchus

RIGHT LOWER LOBE BRONCHUS

The right lower lobe bronchus divides immediately into

a) Superior segmental bronchus (just across from the right middle

lobebronchus), and

b) Medial basal segmental bronchus a bit more distally and along its

medial wall.

10

Finally dividing into three lower lobe bronchi

(Three musketeers):

c) Antero-basal

d) Latero-basal

e).Postero-basal

LEFT MAIN BRONCHUS

The left main bronchus is usually 4-5cm long (Right. 2cm long). Its lumen is

narrower and relatively horizontal. The usual length of the left

lower lobe bronchus beyond the origin of the superior segmental bronchus is

1cm.

Divides into upper and lower lobe bronchus.

Left upper lobe bronchus divides into apicoposterior and anterior.

Lingular – supr division, inferior division.

Left Lower lobe bronchus divides into apical,anterior basal, posterior basal,

lateral basal segments.

11

Figure 6 : Bronchopulmonary segments

According to CT findings bronchiectasis is classified as Cylindrical

(bronchial dilation),Varicose (with focal constrictions along airways)or Cystic

(saccular dilations at the end of bronchus).

Echocardiography is commonly used to estimate systolic pulmonary

artery pressure and to diagnose pulmonary hypertension in patients with

advanced lung disease.It used as conventional clinical echocardiographic

equipment,with 2.5 or 3.5mHz transducers.Indicative of PH on echocardiogram

include increased systolic pulmonary artery hypertension or tricuspid

regurgitant jet,right atrial and ventricular hypertrophy,small left ventricular

dimension and dilated pulmonary artery. Echocardiography has been found to

non-invasive it is preferred mortality to diagnose pulmonary hypertension.

Invasive hemodynamic assessment by RHC is pivotal in the evaluation of any

12

patient with suspected PAH. Right –Heart catherization is typically performed

after the non invasive testing for PH.

Physiological parameters such as pulmonary function test that are

characteristic of an obstructive disorder, confirming initial involvement of

small airways. With progression of disease, a mixed functional disorder or a

restrictive disorder can be found due to progressive destruction of pulmonary

parenchyma that is characterised by recurrent infectious exacerbations and

massive destruction of the small airways. 6-minute walk test enabling the

evaluation of the degree of respiratory discomfort, in terms of determination of

subjective rates according to the perfection of individual. This a vertical scale

to quatify from 0-10 in which 0 represents no symptoms, and 10 represents

maximum symptoms and providing an providing individual measurement of

the density of the exercise.

In conclusion high –resolution CT scan can be used for diagnosis extend

of involvement of segments of bronchiectasis. So predictors of clinical,

physiological and radiological correlation in patients with bronchiectasis will

help to determine predictors of pulmonary hypertension.

13

AIMS & OBJECTIVES

To correlate clinicoradiological characteristics of bronchiectasis with

pulmonary hypertension

OBJECTIVE

Primary Objective

To correlate clinicoradiological profile of bronchiectasis

Secondary Objective

To correlate clinicoradiological profile of bronchiectasis with severity of

pulmonary hypertension

To correlate clinicoradiological profile with physiological charecteristics of

bronchiectasis

14

MATERIALS AND METHODS

The study aim to correlate the clinicoradiological parameters of

bronchiectasis,and to assess the severity of exercise capacity and Pulmonary

Artery Hypertension in these patients.Clinical and radiological predictors will

facilitate futher understanding of pulmonary atery hypertension and thereby

affect treatment outcomes.

Study type

Prospective cross-sectional study

Study Duration

12months

Study Locale

PSG Institute of Medical Sciences and Research

Study Method

Convenience Sampling

Sample Size

40subjects

15

Inclusion Criteria

Age 18 to 65 years

Cases of Bronchiectasis diagnosed based on clinico radiological profile

Willing to participate in the study adhering to its protocol

Exclusion Criteria

Patients not having acute exacerbation or active infection

Patients with Primary PulmonaryHypertension(PPH)

Patients with pulmonary hypertension attributable to primary causes other than

bronchiectasis

Mental status not competent enough to consent for the study in the study

adhering to its protocol

16

STUDY METHODOLOGY

STEP 1:

Inclusion Criteria

STEP 2:

Informed Consent

STEP 3:

Clinical profilebronchiectasis (History, MMRC, BORG, SGRQ)

STEP 4:

Radiological profile of bronchiectasis

STEP 5:

FEV1 (measured with PFT),6MWT

STEP 6:

ECHO foe evaluation of pulmonary hypertension

STEP 7:

Analyze and Correlate

Data Analysis

Spss Software Version 24

17

REVIEW OF LITERATURE

Bronchiectasis is an important cause of respiratory morbidity but it has

generally a low profile. As it is a heterogeneous condition with a large number

of predisposing factors, long clinical history, the pathogenesis has not been

well defined. Bronchiectasis is defined as permanent and abnormal dilatation of

bronchi(1).In 1953,1.3 cases of bronchiectasis were reported in Bedford, a

similar prevalence of 1.5 cases per 1000 was found from the chest radiographs

obtained from routine miniature chest radiographs obtained from England and

Wales in 1956 during tuberculosis eradication campaign. It is described as

common in developing nations, but there is a lack of data on the actual

prevalence. Generally ,bronchiectasis appears to be more common in females,

with approximately two -thirds of patients in studies.

Most studies of bronchiectasis pathology were performed between 1920

and 1960,when there was readily available access to surgical and post mortem

tissue. Bronchiectasis was characteristed by dilatation of subsegmental airways,

which were tortuous, inflamed and obstructed by secretions. There was

generally damage to the bronchioles, often with associated fibrosis and

parenchymal destruction. The vascular supply to affected areas was derived

mainly from hypertrophy of bronchial arteries and their anastomoses with

pulmonary arteries.

18

Reid classified bronchiectasis(2) into three different types, based on

macroscopic appearance of pathology specimens:

1) Tubular (or cylindrical), in which there was smooth dilatation of

bronchus

2) Varicose, in which there were focal narrowings along a dilated

bronchus and

3) Cystic, in which there was progressive dialation of a bronchus,

which terminated in cysts or saccules. The main form currently

seen on HRCT is the tubular or cylindrical form.

Figure 7

19

Figure : 8 A–D, Normal bronchus (arrow) (A), cylindric bronchiectasis with

lack of bronchial tapering (arrow) (B), varicose bronchiectasis with string-of-

pearls appearance (arrow) (C), and cystic bronchiectasis (arrow) (D).

20

Most definitive pathology study was performed by Whitwell(3) in a

study “pathology and pathogenesis” in 1952 also described . He studied 200

operative lung samples from patients with bronchiectasis. He described the

bronchial wall to be infiltrated with inflammatory cells. Ciliated epithelium

was often replaced with squamous or columnar epithelium. The elastin layer

was deficient or absent and, in more severe cases, there was destruction of

muscle and cartilage, theses changes were responsible for bronchodilation.

He described three main forms of bronchiectasis:

1) Follicular 2) Saccular 3) Atelectactic.

1) Follicular bronchiectasis is acquired, it forms in presence of numerous

lymphoid follicles situated in thickened,usually cylindrically dialated

bronchial walls.

2) Saccular bronchiectasis characterised by presence of macroscopically

visible thin walled, saccular bronchial dilations.

3) Atelectatic bronchiectasis , it was predominantly right-sided with

follicular and saccular bronchiectasis, which involved the left lung

more commonly.

.

21

Figure : 9 Cystic fibrosis. A and B, Transverse (A) and coronal (B) images

show upper lobe predominance of cystic bronchiectasis(arrows) and

volume loss, enlarged lung volumes, and diffuse heterogeneous

attenuation.

22

Pathophysiology of Bronchiectasis

The dominant feature of bronchiectasis is airway inflammation in

association with bacterial infection. It has generally been thought that the

inflammation is secondary to unclearing infection. The “vicious cycle

hypothesis” was proposed by Cole at al(4) explain the development of

bronchiectasis. It compromised mucociliary clearance, allowing infection and

colonisation of the respiratory tract. Bacteria caused inflammation, which

damaged the respiratory tract, leading to more bacterial proliferation and more

inflammation or damage. Thus ongoing cycle developed which caused

progressive destruction of the lung. The current view is that a combination of

microbial insult and defect in host defence allow establishment of persistent

bronchial infection.

23

Figure : 9 Cycle of Infection and Inflammation of bronchiectasis

Mucocillary system:

Mucocillary system is apart of innate defence mechanism that clears

unwanted materials from the airways.It consists of cilia,periciliary fluid layer

and the mucus layer.Mucus is normally cleared by successful interaction of the

cilia in the mucus and this depends on the beat frequency of the cilia,the

mucus load and its physical properties ,and depeth of the periciliary fluid

layer.Abnormalities in any component of the mucociliary system can result in

abnormal mucociliary clearance.

24

Figure : 10 Components of the Mucociliary System

In bronchectasis, chronic inflammation in the airways results in an

increase in the size and number of mucus secretory cells, that is in hypertrophy

of the submucus glands and in hyperplasia and metaplasia of the globet cells

extending to the bronchioles that are normally free of mucus secretory cells.

Therefore in bronchiectasis there is excessive mucus secretion throughout the

conducting airways ,including the bronchioles where mucus does not exist in

the healthy state. The cilia cannot transport excessive load of mucus .

In a study done by Tsang et al in 2005 showed that cilia have been

found to beats slowly in bronchiectasis that is not related to genetic ciliary

defects then in healthy subjects, a feature that could relate to inflammatory

25

products such as neutrophil elastase or to bacterial products especially in those

colonized with pseudomonas.

Mucus in bronchiectasis can be highly viscoelastic and adhesive. These

physical properties are greatly influenced by the hydration at the airway

surface. Then the secreted mucus volume is excessive as bronchiectasis there

is an imbalance between mucins and available water. Daviskas et al and

Boucher et al studies showed that dehydration of airway mucus in

bronchiectasis is evident when the percentage of solids in sputum is greater

than the normal 2-3% .The increase in the percentage of solids in the mucus of

bronchiectasis patients in addition to causing impairement to its transport can

potentially inhibit the motility of neutrophilis within the mucus and thus their

ability to kill bacteria. When the solids where increased from normal 2.5% to

6.5%,neutrophilis failed to kill bacteria.

The increased production of mucus in bronchiectasis together with the

impairement of the mucociliary system leads to accumulation of mucus,

chronic cough, mucus plug formation, airway obstruction, bacterial

colonization and infections that fails to resolve completely. In bronchiectasis

,the failure of mucociliary system to transport mucus most likely relates to the

abnormal load of mucus and the abnormal physical properties of the mucus

rather that to the cilia or their movement being abnormal, except in patients

with genetic ciliary defects. When the mucociliary system fails cough becomes

a every important mechanism for clearing mucus. Cough become compromised

26

in patients with bronchiectasis due to highly viscoelastic and sticky mucus.

Due to severe airflow limitation in bronchiectasis cough becomes ineffective.

The impairement of the mucociliary system and the abnormal properties

of mucus in bronchiectasis have been documented in studies by Currrie et al,

Daviskas et al, Isawa et al using a radioaerosol technique and imaging with

gamma camera.

Effects of bacteria and pathogens

Bacteria have a number of effects on the respiratory tract of which the

best described is inhibition of mucociliary clearance.Hemophilius influenza,

Streptococcus pneumonia and Pseudomonas aeruginosa produce

mediators that inhibit ciliary function damage ciliary epithelieum and inhibit

mucus transport.Bacteria may destroy the epithelieum,release chetatic factors

to attract large number of neutrophilis and produce biofilms.Biofilms are best

described ibn pseudomonas infection,in which an impenetrable matrix is found

around the bacteria with severe damage to the underlying lung.

Neutrophilis are found in large numbers in bronchiectasis. Readet al

and Eller et al found that following injection with radiolabelled white cells

50% of the circulating neutrophilis pass into the bronchi. These neutrophilis are

most prevalent in the airway lumen and release mediators such as protease and

elastase which damages the bronchial wall elastin and epithelium. The

bronchial cell wall is infiltrated predominantly by a macrophages, which

appear to be the cells predominantly causing small airway obstruction.

27

Aetiology of Bronchiectasis

There are large number of causes that have been proposed to causes

bronchiectasis. Bronchiectasis is a heterogenous condition with a long clinical

history before the diagnosis is made, the exact role of causative factors is often

not clear. Certain causative factors are Post –infectious bronchiectasis, most

common causes described in the literature is childhood infection, particularly

with pneumonia, whooping cough and measles. This appears to be particularly

important in populations with poor health and recurrent infections. Infection

causes structural damage to the airways, allowing persistent infection results in

bronchiectasis. Seroprevalence in measles in unvaccinated populations

morethan 90% and whooping cough > 50%.Finally patients with immune

deficiency are more likely to have significant lung infections.

In a study by Whitwell et al(3), in 1952 a study of pathology and

pathogenesis of bronchiectasis described as mycobacterial infections, both

tuberculous and non – tuberculous have an association with bronchiectasis,

mechanism is probably due lymph node obstruction and atelectatic.

Bronchiectasis can develop abnormal mucociliary clearance caused primarily

by genetic ciliary defect. Approximately 50% of patients with primary ciliary

dyskinesia have Kartagener’s syndrome ,characterised by bronchiectasis,

sinusitis, and situs inversus. Another rare condition is Young’s syndrome,

characterised by azoospermia and bronchiectasis that is due to highly tenacious

secretions that are poorly cleared. Causes of obstruction include an inhaled

28

foreign body, slow growing tumour and twisting of an airway after lobar

resection.

In a study in described by Currie et al (6) in 1987 “Impaired

tracheobronchial clearance in bronchiectasis in studied retained that sputum

can contribute to obstruction which leads to an important role in bronchiectasis.

Immune dysfunction associated with bronchiectasis including HIV,

hypogammaglobulinaemia, type I major histocompatibility complex. Therefore

,malnutrition and socioeconomic factors may play a role in precipitating

immune dysfunction.

In a study Silva et al(41) in 1989,highlighted that othercauses strongly

associated with bronchiectasis such as Rheumatoid arthritis, Sjogrens

syndrome, Churg –Strauss syndrome and inflammatory bowel disease.

In a cohort study by Parr et al(38) in 2000,74 subjects with α1-Antitrypsin

deficiency that 70 subjects had evidence of radiological bronchiectasis and 20

had the syndrome of clinical bronchiectasis.

Microbiology of bronchiectasis

The microbiology of bronchiectasis is complex , with multiple

potential pathogens. The pattern of isolates varies between different

institutions. Previous studies have shown that the two major pathogens found

are H.Influenza,and P.aeruginosa .Other important pathogens include

Moxarella catarrhalis, S.pneumoniae,non –tuberculous mycobacteria and

Aspergillus species. A consistent finding is that, despite the presence of

purulent sputum,30-40% of specimens will fail to grow any pathogens.

29

As bronchiectasis progresses there appears to be a change in bacterial flora.

Subjects with mild disease usually have no pathogens isolated, while subjects

with moderate disease most commonly have H.Influenzae.In most severe

disease ,P.aeruginiosa is the dominant pathogen.

Assessment of bronchiectasis based on

Clinical features:

Severity of clinicopathologic events varies widely in patients with

bronchiectasis. Patients have exacerbations, with chronic sputum production

other symptoms include hemoptysis, especially during exacerbations and

breathlessness, characterized by mild to moderate airflow obstruction, lethargy

and reduced health status.

Clinical signs

Finger digital clubbing recognized as a sign of chronic suppurative lung

disease.Studies reports that prevalence of clubbing 1- 2%.Overall, suggests that

finger clubbing is now seen only in minority of patients with non –CF

bronchiectasis.Other clinical finding in bronchiectasis is coarse

crackles,reported upto 73% of patients in more recent studies.

30

Assessment of Functional status with physiological parameters

Bronchiectasis is chronic respiratory condition,characterised by cough

and sputum production together with physical fatigue and reduced exercise

tolerance.It causes diminished exercise capacity include dyspnea secondary to

dynamic hyperinflation,altered respiratory mechanics and decreased skeletal

muscle bulk.However ,there have been limited evaluation of physical function

in patients with bronchiectasis and influence on respiratory disease severity

and extent of disease on exercise capacity is notknown.

6-Minute Walk test

It is widely used to measure of functional status, as well as a predictor of

prognosis(32).With the clinical application suggested that simple measurement

reflected on the pulmonary and functional status of patients with

bronchiectasis,evaluation of the 6MWT in population has been limited.

A study done by Lee at al(33) in 2008,clinical determinants of the 6-Minute

Walk test in bronchiectasis provides a valuable information of the functional

status in a group of patients with mild to moderate bronchiectasis and also

indicates dynamic hyperinflation and increased work of breathing are

responsible of disease.In this study evidence of airflow obstruction measured

by using FEV1 and FVC associated 6minute walk test.

31

Pulmonary Functional Test

Patients with bronchiectasis generally have mild to moderate airflow

obstruction.Both adults and children have been shown to develop

progressively worsening airflow obstruction. Hogg et al have studied small

airways obstruction found the factor most associated with obstruction was the

presence of lymphoid follicles, which were similar.Airway reversibility may

also be common in bronchiectasis.Murpghy et al and Pang et al found

significant airway reversibility in 40% of subjects and two other studies found

a 30% and 69% of reversibility in bronchiectasis.

Functional impairement in bronchiectasis is related to the extent of lung

damage as determined by the number of bronchopulmonary segments involved.

Measurements of ventilatory capacity and lung volumes with

bronchographically proven bronchiectasis showed that airways obstruction is

constantly ventilatory defect.

Another smaller series shown that 71% of 34 patients with

bronchiectasis had airflow limitations in FEV1/forced vital capacity ratio is less

than 65%.

The findings showed that the presence of infection/inflammation was

associated with increased airways obstruction. In a study done by Taylor et

al,in 2010 about 204 patients showed that degree of airflow limitation has

been correlated positively with both the duration of symptoms and extent of

disease on CT examination. Reversibility of airflow limitation may present in

bronchiectasis.Lung function tests have diagnostic value in bronchiectasis but

32

are useful in measuring the extent of impairement and demonstrating

occasional response to bronchodilators or other treatments.The simple and

highly reproducible tests, such as FEV1 and FVC are also clinically useful and

reliable

MODIFIED BORG Dyspnea scale

This scale is an aid for the 6-minute walk test enabling the evaluation of the

degree of respiratory discomfort,in terms of determination of subjective rates

according to the perfection of individual.This a vertical scale to quatify from 0-

10 in which 0 represents no symptoms,and 10 represents maximum symptoms

and providing an providing individual measurement of the density of the

exercise.

Martinez gracia et al in 2000 in their study suggested an independent

impact of BORG score in assessing the lung extent in bronchiectasis.

33

Imaging in Bronchiectasis

Chest radiography is often the first imaging modality used to

investigate patients with suspected bronchiectasis(9)

Plain chest radiography

Radiographs are insensitive as a diagnostic tool for bronchiectasis,

and suggest the diagnosis in lessthan 50% of cases in studies. Plain chest

radiographic features have been described by Simon et al(1) in 1978,which

include :

Evidence of dilated bronchi

Ring Shadows: produced by dilated bronchi seen ‘end-on’.It may be

small, numerous widespread, sometimes referred as honeycomb lung. Larger

ring shadows

(0.5-2cm diameter) which contain fluid levels, formed by retained mucopus.

They may be localized or widespread, giving the radiographic appearance of

cystic lung.

Parrallel Lines: are produced by dilated bronchi viewed ‘side-on’. It is

fine parallel, air-contaning , hairline opacities. Tramline: there walls been

thickened rather than hairline, more numerous or crowded together, indicating

lobar shrinkage.

Solid tubular opacities: bronchi contain mucopus which may seen as

solid tubular, looking like a scaled –down column of tooth –paste. Gloved

34

finger shadow’s tangentially produce glove tending to have a rounded end,

representing a large dilated bronchus containing mucopus.

Bronchography

It was for many years for the investigation of choice, for confirming

bronchiectasis. Technique involves instillation of liquid contrast medium into

tracheobronchial tree, under general or local anaesthesia. Aqueous or oily

propyliodone was commonly used. Affected parts of lungs showed areas of

bronchial dilatation, described as cylindrical, fusiform, saccular. Changes seen

are found commonly in left lung and are bilateral in about one-third of cases.

Nowadays, bronchography is regarded as obsolete in most centres, HRCT

having been to be more satisfactory.

Computed tomography scanning with high resolution

It should be used to diagnose bronchiectasis as technique demonstrates the

airways in higher detail than standard computed tomography scanning. In a

study done by Naidich et al(9) and Mcguinness et al(10) ,in 1982 and 2002 have

established the use of standard criteria for diagnosis of bronchiectasis.

Most specific features are :

a) Internal diameter of a bronchus is wider than its adjacent pulmonary artery

b) Failure of bronchi to taper, and

c) Visualisation of the bronchi in outer 1-2cm of lung fields.

Less specific features include mucosal wall thickening, crowding of

bronchi and mucus impaction. Lobes most commonly involved in

bronchiectasis are lowerlobes.

35

High resolution computed tomography

It has become the investigation of choice in bronchiectasis. Earlier studies CT

was used for non- invasive and safe, this technique is used as alternative to

bronchography in the diagnosis of bronchiectasis. These showed that

conventional CT was less sensitive for diagnosing bronchiectasis than

bronchography ,the sensitivities for 10-mm slices at 20 mm intervals .Cooke

and colleagues found that conventional CT diagnosed bronchiectasis in 71% of

45 bronchiectatic lobes, sensitivity 71%,indicates that this form of CT cannot

be used to ruleout bronchiectasis. Development of thin section HRCT changed

this so that sensitivities increased to 82-97%. Recommended HRCT technique

comprises scanning from apex to base with 1-2mm cuts at 10mm intervals.

HRCT criteria for diagnosing bronchiectasis are bronchial dilatation,

and bronchial wall thickening. A bronchus is taken to be dilated if its internal

diameter is greater than that of pulmonary artery branch, measurements being

conventionally made in short axis of both the bronchus and the vessel.

Bronchial wall thickening is present if the thickness of the wall is at least equal

to the diameter of adjacent pulmonary artery branch. The occurence of

bronchial wall thickening prior to the development of bronchial dilatation is

described in patients with hypogammglobulinaemia. Air trapping on expiration

has been demonstrated as areas of increased transradiancy in patients with

severe bronchiectasis. Scanning during inspiration and expiration may

distinguish between an area of bronchiectasis and emphysematous blebs,or

bullae.

36

Most commonly involved in bronchiectasis are lowerlobes usually multiple

lobes are involved. HRCT has been found to have greater sensitivity than spiral

CT when applied to patients in whom bronchiectasis is suspected.

Figure : 11 shows signet ring sign seen in bronchiectasis

37

Treatment of Bronchiectasis

Antimicrobial therapy is required once a acute exacerbation is identified

.Patients who relapse quickly or frequently (>3times in 1year)with mucoid or

mucopurulent sputum are usually managed with short course of appropriate

antibiotics ,may also need longer term preventive therapy. Patients with

chronic purulent sputum usually require higher antibiotics and also need of

long term nebulised antibiotic therapy.

Prophylactic Therapy

Macrolides are the most common antimicrobials used in clinical practise.

Azithromycin twice weekly for 6months,has shown positive results, with

reduced 24-hour sputum volume and reduced number of exacerbations.

Postural Drainage

Physiotherapy ,including postural drainage of chest secretions,has been

regarded for many years is the mainstay in treatment of

bronchiectasis.Postural drainage has been shown in the short term to

increase rates of mucociliary clearance and to increase the expectoration of

sputum,in patients whose secretions are copious.It has also been found to

improve airway function .

Vaccination

In routine practises patients with bronchiectasis are vaccinated aganist

influenza. Evidence is minimal regarding the pneumococcal vaccine, 23 valent

pneumococcal vaccine as routine management in adults with bronchiectasis.

38

Surgical Treatment

Surgical treatment plays only a small role in management of bronchiectasis.

Surgery is indicated in the patients whose significantly disabled by persistent

sputum production, recurrent infective exacerbations or haemoptysis despite all

reasonable medical measures having been taken over a period of at least

12months.The disease should be confirmed radiologically, should be

sufficiently localized to one lung or to part of one lung to enable curative

resection and residual lung should be suffienctly healthy in terms of measured

lung function.

39

PULMONARY ARTERY HYPERTENSION

Pulmonary hypertension(28) is a rare, pathologically complex disease

characterized by a progressive increase in pulmonary arterial pressure

associated with variable degrees of pulmonary vascular remodelling,

vasoconstriction, and thrombosis. These changes leads to increased

pulmonary vascular resistance, and with right-sided heart failure and death.PH

is defined as an increase in mean pulmonary arterial pressure > 25mmHg at rest

assessed by right heart catherisation. Pulmonary hypertension is a common

complication in chronic lung disease which included in alveolar hypoxia in

WHO group III of PH-related disease.PH is a haemodynamic

pathophysiological state that can be found in multiple conditions.

The clinical classification of Pulmonary Hypertension has gone through

a series of changes the first version was proposed in 1973 by WHO. Evian -

Venice classification proposed in 1998-2003 on PAH. This is classified into

five groups according to pathological, patho physiological and therapeutic

characteristics. During Fourth World Symposium on PH held in 2008 in Dana

Point, new classification was derived.

40

Classification:

Updated Clinical Classification of Pulmonary Hypertension(28) :

1. Pulmonary arterial hypertension

1.1 Idiopathic PAH

1.2 Heritable :

1.2.1 Bone morphogenetic protein receptor type II(BMPR2)

1.2.2 ALK-1, endoglin

1.2.3 Unknown

1.3 Drug or toxin –induced

1.4 Associated with:

1.4.1 Connective Tissue Diseases

1.4.2 Human Immunodeficiency virus (HIV) infection

1.4.3 Portal hypertension

1.4.4 Congenital heart diseases

1.4.5 Schitosomiasis

1.4.6 Chronic haemolytic anemia

1.5 Persistent pulmonary hypertension of newborn

41

1. Pulmonary venocclussive disease and/pulmonary capillary

hemangiomatosis

2 . Pulmonary hypertension due to left- sided heart disease

3. Pulmonary hypertension due to lung disease and / hypoxia

4. Chronic thromboembolic pulmonary hypertension (CTEPH)

5. Pulmonary hypertension with multifactorial mechanisms

Normal pulmonary arteries have thin medial layer of circular muscle ,

with thickness less than 5% of diameter of vessel. Under physiological

condition pulmonary circulation is characterised by variable intimal

hyperplasia, medial hypertrophy, adventitial proliferation, and fibrosis that

occur in close proximity to plexiform lesions. These lesions results from

intimal proliferation and progresses from a cellular to a fibrotic lesion with

advancing disease. As the vascular pathology progresses, pulmonary vascular

resistance increases and pulmonary artery rises, in order to maintain cardiac

output. So as right ventricle is able to compensate for resistance, the pressure

continues to increases as the pulmonary vascular resistance increases. When

contractile reserve of the right ventricle is exhausted, right ventricular systolic

failure ensures. Various degrees on right ventricular diastolic dysfunction also

present in PH. A combination of reduced right ventricular output and diastolic

dysfunction resulting in impairing left ventricular filling and leads in

42

hemodynamic deterioration. Inflammation associated with underlying lung

disease is responsible for development of PH in hypoxic states.

Group 3: Pulmonary hypertension due to Lung Disease and /or Hypoxia

Pulmonary hypertension associated with disorders of the respiratory system or

hypoxemia is a category of PH that is caused mainly by inadequate

oxygenation of pulmonary arterial blood result of either parenchymal lung

disease, impaired control of breathing or residence at high altitude. Pulmonary

arterial pressure is modest and survival depends on the severity of the

pulmonary disease, rather than on the severity of the associated hypertension.

Pathophysiology

Pulmonary hypertension in the setting of chronic respiratory disease leads to

increased pulmonary vascular resistance when pulmonary artery wedge

pressure is normal. Increased pulmonary vascular resistance is usually

secondary to effects of hypoxia and destruction of the vascular bed in lung

parenchyma. While acute hypoxia leads to pulmonary vasoconstriction in the

small pre-capillary arteries, chronic hypoxemia results in pulmonary vascular

remodelling including medial hypertrophy and intimial proliferation of distal

pulmonary arteries. Additional it includes mechanical stress secondary to

hyperinflation, loss of capillaries, inflammation and endothelin –derived

vasoconstriction – vasodilator imbalance.

Moreover, significant number of lung disease and severe PH, other co-

morbidities may contribute pathogenesis of PH, such as left ventricular

43

diastolic dysfunction or chronic thromboembolic pulmonary hypertension.

Genetic factors may also play an important role for developing PH.

Mechanism of Pulmonary hypertension in Bronchiectasis

Alveolar hypoxia is a stimulus for pulmonary vasoconstriction. Most

important pathways leading to pulmonary hypertension is endothelial level in

chronic lung diseases. Alveolar hypoventilation precipitates acute pulmonary

vasoconstriction in some parts of lungs and vasodilation which causes

physiological shunt. Studies by Sylvester et al 2009,showed that

vasoconstriction is achieved through vasoconstrictor pathway or inactivation of

a vasodilator pathway, through the effects of hypoxia on vascular smooth

muscle.Studies by Jing et al ,2009in rats,exposed to hypoxia suggest that

hypoxia exposed arterioles develop smooth muscles in the walls of non

muscular pre capillary blood vessels which persist after the removal of the

stimulus and contributes to on going pulmonary hypertension.

Development of pulmonary hypertension may result in both

intermittent and chronic. The effector pathway suggested L-type calcium

channels, non –specific cation channels and voltage –dependent potassium

channels, whereas mitochondria and nicotinamide adenine dinucleotide

phosphate oxidase described as oxygen sensors. Reactive oxygen species,

redox couples and adenosine monophoshate – activated kinases are the

mediators of hypoxic pulmonary vasoconstriction. Endothelin -1 pathway,

nitric oxide pathway, and reactive oxygen species helps for development of

44

pulmonary hypertension. Studies by Bosc et al,in 2010 demonstrated that

Endothelin -1 is an important mediator of systemic hypertension in

intermittent hypoxic states.ROS are highly reactive and unstable free

radicals.Intermittent hypoxia stimulates the synthesis and release of ROS

through the tyrosine hydroxylase system leading to the development of

systemic hypertension. Studies Somer et al ,in 2008 showed that ROS was

also been implicated in the induction of Endothelin -1 and in angiostensinogen

synthesis with all theses agents believed to contribute to the development of

pulmonary hypertension induced by intermittent hypoxia.

Figure : 12

45

Pulmonary vascular remodelling

Studies by Orr et al in 2012, of the vasculature in hypoxic pulmonary

hypertension demonstrated changes including intimal thickening, medial

hypertrophy and muscularization of small arterioles. When the balance between

apoptosis and proliferation of endothelial cells in the pre – capillary pulmonary

blood vessles, altered the proliferation, and overall resistance pattern is

increased.Studies by Pak et al 2007,in neonatal calves and rodent models

showed that chronic hypoxia triggers endothelial cell proliferation .Acute

hypoxia triggers adventitial fibroblast proliferation within hours of exposure

while medial hypertrophy and hyperplasia takes longer to develop. Fibroblasts

stimulated by chronic hypoxia can transform into smooth muscle cells.Chronic

hypoxia in rat models results in doubling of muscular arteries with proliferation

into non muscularized vessels.

Role of systemic inflammation

Inflammation associated with underlying lung disease may be partly

responsible for the development of pulmonary hypertension in hypoxic states.

Inflammatory cells have been detected in local vascular structures, evidence of

systemic inflammation with raised inflammatory makers, such as CRP, and

TNF-α .Studies by Chao et al in 2009,in rats exposed to hypoxia ,alveolar

macrophages play a critical role in the inflammatory process ,with

inflammation occurring in the presence of reduced alveolar PaO2.

46

Diagnosis of Pulmonary Hypertension

The evaluation process with suspects PH requires a series of

investigations confirm the diagnosis, clarify the clinical group of PH to

evaluate functional and hemodynamic impairment.

Clinical presentation

Symptoms includes breathlessness, fatigue, weakness, angina and syncope.

Physical signs of PAH include left parasternal lift second heart sound,

pansystolic murmur of tricuspid regurgitation. Lung sounds are usually normal.

Right –Heart catheterization

Invasive hemodynamic assessment by RHC is pivotal in the evaluation of any

patient with suspected PAH. Right –Heart catherization is typically performed

after the non invasive testing for PH. In RHC essential measurements include:

o Oxygen saturation

o Right atrial pressure

o Pulmonary artery pressure

o Left sided filling pressure

o Cardiac index/Cardiac output

o Systolic blood pressure

o Heart rate

o Response to acute vasodilators

47

In recent study of 94 patients with bronchiectasis,31 patients (32.9%)had

PH,defined as systolic Pulmonary artery pressure of ≥40mmHg on Doppler

echocardiography100.Significant correlation was obseverd between right

ventricular dimensions and systolic pulmonary artery pressure(r=0.74)while

RV dimension were inversely related to PaO2 values(r=0.37).

Chest radiograph

In 90% of patients with PAH the chest radiograph is abnormal at time of

diagnosis. Findings include loss of peripheral blood vessels. Right atrium and

ventricle enlargement more seen in advanced cases. Chest radiograph allows

associated moderate –to – severe lung disease, or pulmonary venous

hypertension due to left heart disease. The degree of PH in any given patient

doesnot correlate with extent of radiographic abnormalities.

Pulmonary Function Tests

This testing is a necessary part of initial evalutation of all patients with

pulmonary hypertension, to exclude or characterised the underlying airway or

parenchymal lung disease. Patients with PAH usually have decreased lung

diffusion capacity for carbon monoxide and mild to moderate reduction of lung

volumes. A decrease in lung volume together with a decrease in diffusion

capacity for carbon dioxide tension, may indicate pulmonary hypertension.

48

Echocardiography

Doppler echocardiography should performed as a noninvasive

screening test to detect elevated pulmonary artery pressure. It provides an

estimation of right ventricular function and pulmonary artery pressure and can

reveal other underlying cardiac abnormalities. Signs indicative of pulmonary

hypertension on echocardiogram include increased pulmonary artery

hypertension or tricuspid regurgitant jet, right atrial and ventricular

hypertrophy, flattening of intraventricular septum, small left ventricular

dimension and dilated pulmonary artery. Echocardiography is useful in disease

progression, removing the need for repeated pulmonary artery

catheterizations.

Patients with suspected pulmonary hypertension, right-sided heart

catheterization is required to confirm the presence of PH, to establish the

specific diagnosis, and to determine the severity and prognosis of pulmonary

hypertension. It also can be used to evaluate for vasoreactivity and guide

therapy. A acute response to a vasodilator is defined as a fall in pulmonary

artery hypertension of at least 10mm Hg to 40mm Hg or less, with an

increased or unchanged cardiac output. Eysmann et al(30) proven that right

heart catherization is required to perform presence of PH, for diagnosing

purposes.

In a study conducted by Abdulaziz et al(20) in 2008 found that systolic

pulmonary artery pressure was higher in cystic bronchiectasis with right and

left ventricular dysfunction.

49

Study showed correlation between HRCT score and SPAP and FEV%.It

showed SPAP could be a predictor of future pulmonary hypertension .Patient

with cystic bronchiectasis have significantly higher impairement of pulmonary

physiology as compared with cylindrical bronchiectasis patients.

Figure 13 :Echocardiography demonstrating right ventricular enlargement.

Figure : 14

50

Approach to therapy

Treatment goals for patients with pulmonary hypertension include

reduction in clinical signs, and symptoms and improvement in exercise

tolerance, hemodynamics, and quality of life, with decreased need for

hospitalization and longer survival. Long term oxygen administration has been

shown partially to reduce the progression of pulmonary hypertension.

Phosphodiesterase Type -5 Inhibitors

Pulmonary vasodilating effects of nitric oxide are mediated through

cGMP.Nitric oxide activates guanylate cyclise,which increases cGMP

production.Cyclic GMP causes vasorelaxation,but effects are attenuated by

rapid degradation of cGMP by phoshodiesterase.Sildenafil and Tadalafil inhibit

phosphodiesterase type 5,thus enhancing relaxation and growth inhibition of

vascular smooth muscle cells..both have demonstrated improvement in exercise

capacity and functional class.

Endothelin Receptor Antagonists

Endothelin -1 is a potent vasoconstrictor and smooth muscle mitogen, that is

over expressed in the plasma and lung tissue of patients with pulmonary

hypertension.

o Bosentan is a oral nonselective endothelin receptor antagonist,

o Ambrisentan is a oral selective endothelin type A receptor antagonist, both of

these agents have been shown to improve exercise capacity, functional class,

and time to clinical worsening.

51

Prostanoids

Prostacylin is a potent vasodilator and inhibitor of platelet activation and

smooth muscle proliferation. Three prostanoids have been shown to improve

exercise capacity, quality of life, hemodynamics are epoprostenol,treprostinil,

and iloprost.

Thus the above mentioned studies shows that alveolar hypoxia in

bronchiectasis is a potent stimulus for pulmonary vasoconstriction was leading

to the development of pulmonary artery hypertension and bronchiectasis

patients with pulmonary hypertension have worse survival than bronchiectasis

subjects without pulmonary hypertension.Studies also found that extent and

severity of bronchiectasis correlated strongly with severity of airflow

obstruction. Clinical determinants of the 6-Minute Walk test in bronchiectasis

provides a valuable information of the functional status in a group of patients

with mild to moderate bronchiectasis and also indicates dynamic hyperinflation

and increased work of breathing are responsible of disease.

52

RESULTS

We present our study results under following description

1. Distribution of study variables

2. Comparison of the variables within the study population

3. Correlation of variables in the study population

DISTRIBUTION OF VARIABLES IN STUDY POPULATION

A total of 40 patients were recruited for the study. In that 19 patients were

cystic, 11 were cylindrical and 10 were varicose. Out of 40 patients 17 were

male (42.5%) and 23 were female (57.5%). The mean age group of the study

was 45-55 years. The average age was 5510 years. Among the study

population 13 patients had history of smoking and 2 patients had history of

alcohol intake.

Socio-demographic details N=40

Age 5510 years

Gender Male

Female

17 (42.5%) 23(57.5%)

BMI Male

Female

22 24

53

Table 1.a. DISTRIBUTION OF PATIENTS BASED ON GENDER

Among the study population, out of 40 patients ,17 were male(42.5%) and were 23 female(57.5%).

Gender Numb

er of

patien

ts

Percent

age

Male 17 42.5%

Female

23 57.5%

0

5

10

15

20

25

MALE FEMALE

DISTRIBUTION BASED ON GENDER

NUMBER

54

Table 1.b. DISTRIBUTION OF PATIENTS BASED ON AGE

Among 40 patients, most of the patients in the age group of 40 to 60 year old.

The mean age of the study population was 5510 years. Distribution of patients

in the age group of less than 40 years and more than 40 years as given below.

Age group Number of patients Percentage

<40 6 15%

40-60 20 50%

>60 14 35%

TABLE 1.c. DISTRIBUTION OF PATIENTS BASED ON BMI

Among 40 patients the average BMI was 23.6 kg/m2. The mean BMI of male

patients was 22 kg/ m2 and for female it was 24 kg/m2. There was no

significant correlation between the BMI and extent of bronchiectasis.

BMI(mean)

Male 22

Female 24

55

TABLE IIa DISTRIBUTION OF PATIENTS BASED ON THE TYPE OF

BRONCHIECTASIS

The extent of bronchiectasis analyzed and based on the involvement of number

of chambers we classifies the patients into 3 different groups. The distribution

of patients is demonstrated in the following table.

CLASS NUMBER OF PATIENTS TOTAL PERCENTAGE

MALE FEMALE

CYSTIC 6 13 19 47.5%

CYLINDRICAL 7 4 11 27.5%

VARICOSE 4 6 10 25%

56

II b . CORRELATION OF NUMBER OF SEGMENTS INVOLVED AND

TYPE OF BRONCHIECTASIS

Among the 40 patients, we studied the number of lung segment involved in

each patient . In that the patients in the cystic group showed more number of

segment involvement than other groups.

The current study shows no significance in correlation between the

radiological findings and extent of bronchiectasis. The patients in cystic group

shows negative correlation of (r = -0.03), which shows the extent of

bronchiectasis cant be predicated using radiological findings.

Group of patients No of segment involved

<4 4

Cystic 10 9

Cylindrical 4 6

Varicose 11 0

57

II c .CORRELATION OF HRCT SCORE WITH TYPE OF

BROCHIECTASIS

The HRCT score done based 3 parameters

Bronchial dilation

Mucus thickness

Bronchial thickness

Among the parameters bronchial thickness was rare among the study

population. Most of the patient had high HRCT score.

The patients in cystic group shows significant correlation with the HRCT

findings (r=0.23) and extent of bronchiectasis. The positive correlation of

HRCT score was statistically significant only in cystic group compared to

others.

58

III. a .CORRELATION OF TYPE OF BROCHIECTASIS WITH

FEV1/FVC RATIO

Among the 40 patients, based on extent of bronchiectsis patients were

distributed into 3 different groups. In the 3 groups,cystic group shows the

FEV1/FVC ratio was significantly low (p≤0.05). In cylindrical group also the

ratio was low but it was not statistically significant.

Group of patients Mean FEVI/FVC P value

Cystic 34.815 0.04

Cylindrical 38.7114 0.3

Varicose 74.0716 0.68

59

III.b. CORRELATION OF 6 MINUTE WALK TEST AND FEV1/FEC IN

STUDY POPULATION

In our study we observed a significant correlation between the 6 minute walk

test and the pulmonary function test. Patients with altered PFT shows low score

in six minute walk test .There was a positive correlation (r=0.25) in the study

population with significant alteration in the FEV1/FVC . The 6 minute walk

test was found to be useful in patients with bronchiectasis in predicting the

severity.

According to the walking distance the patients were scored based on the

following criteria

Distance Score

>350 0

250-349 1

150-249 2

≤149 3

We consider walking distance more than 400m as normal. Among the study

population a total of 11 patients got score 3 , 5 got 2 , 7 got a score of 1 and 17

got score zero. There was no patient covered a walking distance of 400 m

among the study participants. The significant correlation of FEV1/FVC ratio

with 6 minute walk test shows p value (p<0.01)

60

III.c. CORRELATION OF MODIFIED MEDICAL RESEARCH

COUNCIL DYSPNEA SCALE (MMRC) WITH TYPE OF

BRONCHIECTASIS

Among the study population while correlating the MMRC score , there was

more patients coming under MMRC score of 2 . The patients in cystic group

showed a high MMRC score as compared to the cylindrical but it was not

statistically significant (p=0.8). the mean MMRC score in the study population

was 2.

III.d. CORRELATION OF MODIFIED BORG DYSPNEA SCALE

SCORE (BORG) WITH TYPE OF BRONCHIECTASIS

Among the study population while correlating the BORG score there was more

patients coming under the score of 4 . In the current study there was no

significant correlation between the BORG score and extent of bronchiectasis

(p=0.98). The mean score of the entire study population was 4.

61

IV A. DISTRIBUTION OF PATIENTS BASED ON INCIDENCE OF

PAH WITHIN THE STUDY POULATION

The incidence of PAH in the study population based on the extent of bronchiectasis is given below.

PAH CLASS Number of patients

<25 33

>25 7

0

5

10

15

20

25

30

35

<25>25

62

IV B .CORRELATION OF TYPE OF BRONCHIECTASIS WITH

PULMONARY ARTERY HYPERTENSION

In the current study we found few patients with significant high incidence of

PAH , mostly in the cystic group. But while comparing with the other groups it

was not statistically significant and shows no correlation in the cylindrical

group of patients (p=0.9). The extent of bronchiectasis may be affected by

pulmonary artery hypertension in cystic group of patients (r=0.07).

IV C.CORRLATION OF HRCT SCORE AND SEVERITY OF

PULMONARY ARTERY HYPERTENSION

In our study we analyzed that pulmonary hypertension seen commonly in

advanced bronchiectasis , particularly cystic disease than other 2 groups. On

analyzing our study found that there is no significant correlation between

HRCT score with incidence of pulmonary hypertension.

63

DISCUSSION

The important findings in our study were as follows

1. Correlate clinicoradiological characteristics of bronchiectasis with pulmonary

hypertension

2. To correlate clinicoradiological profile of bronchiectasis with severity of

pulmonary hypertension and physiological characteristics of bronchiectasis

Bronchiectasis is most prevalent morbidity in community with lower

respiratory tract infection. When they are impaired due to repeated infection

causes damage which impedes the clearance of mucus.

The aim of our study was to evaluate the clinicoradiological parameters of

bronchiectasis and to assess the severity of exercise capacity and pulmonary

artery hypertension in the patients. Clinical and radiological predictors will

facilitate further understanding of pulmonary artery hypertension and thereby

affect prognosis. We found that the predictors like (Clinical,

physiological,radiological) in patients of bronchiectasis who can develop

pulmonary hypertension.

SOCIODEMOGRAPHIC CHARACTERS

In our study 40 subjects were recruited in which 23 were female and 17 were

male with a mean age of 55±10 years. According to the epidemiological

studies the prevalence of bronchiectasis in india is 8.4% in the age group of 18-

65 years.

64

The current study was to analyse the correlation of variables in the study

population with extent of bronchiectasis. The variables were 1) FEV1/FVC 2)

HRCT 3) 6 Minute Walk Test 4) PAH 5) Modified Medical Research Council

Dyspnea Scale score 6) Modified BORG dyspnea scale score.

Based on the extent of bronchiectasis the patients were classified into 3

different groups. Which are cystic, cylindrical and varicose bronchiectasis.

Among the 3 groups 19 patients were in the cystic group ,11 were in the

cylindrical and 10 were in the varicose group. Cystic class of patients shows

more significant correlation with the variables than the other 2 groups.

The socio- demographic details were analysed and there was no significant

difference in the extent of bronchiectasis according to age or gender. The

average BMI was 22.47±5 and it was significantly correlated .

Singleton et al 87 patients found no statistical correlation between BMI and

bronchiectasis of patients. Ellis et al(36) in study conducted amongst 187

patients with bronchiectasis also found no significant correlation between BMI

and study groups.Similary no studies till date have proven the role of BMI in

assessing patients with bronchiectasis and correlating its significance in the

same.

Assessing the significance of smoking and alcohol intake in our study it was

found that,14 were smokers in 40 patients which was not statistically

significant with (p =0.443).Similarly alcohol intake while amongst the 40

65

patients had 5 patient had a history of alcohol intake. No significant correlation

was found between alcohol intake and study groups (p= 0.332).

Lindskog et al in 72 patients also reported similar findings that there was no

positive correlation between smoking and alcohol and the study groups.

Similarly no study has analyzed the relation between these parameters and

bronchiectasis. No significant correlation was found between alcohol intake

and study groups with( p = 0.327)

Cole et al (41)also reported similar findings that there was no positive

correlation between smoking and alcohol and study groups.Similarly no study

has analysed the relation between these parameters. Thus concluding that on

individual basis smoking and alcohol had no significance in differentiating

bronchiectasis and their presence could not be taken as a reliable indicator.

On analysing the symptomatology and nature of bronchiectasis, our study

found that 40 patients with breathlessness was seen in 25 patients(69.2%)cough

in 20 patients(46.2%),chest pain in 4 patients(30.8%) and hemoptysis 9

patients(2%).Correlating the symptomatology with bronchiectasis it was found

that symptomatology had no positive statistical significance.However all the

above mentioned studies concluded that symptomatology was inconclusive .

On analyzing haematological variables in our study,it was found that for

bronchiectasis group the mean values for haemoglobin (12.25 + 2.12),TLC

(9435+2234) , ESR (28.85+25.85)had no statistical significance in

differentiating bronchiectasis.There was no positive correlation between the

66

study groups on determining the haematological variables as was evidenced by

our study(P= 0.30).

Similar findings were noted by Perry et al(38) studied in 400 patients. Thus it

was proved that analysis of haematological parameters had no significant

impact on bronchiectasis. There was no study suggesting the haematological

variables have any effect in determining bronchiectasis.

CORRELATION OF NUMBER OF SEGMENTS INVOLVED AND

TYPE OF BRONCHIECTASIS

Among the 40 patients, most of the patient from cystic group showed more

number of segment involvement than other groups. There are 16 patients had

involvement of 3 segments and 3 had more than 4 segments involvement.

The current study shows no significance in correlation between the

radiological findings and extent of bronchiectasis. The patients in cystic group

shows negative correlation of (r = -0.03), which shows the extent of

bronchiectasis cant be predicated using radiological findings.

Mehmet A. Habesoglu et al in his study “Effect of radiological extent and

severity of bronchiectasis on pulmonary function” proved there is no

morphologic changes associated with bronchiectasis with lung function in

patients. He studied 71 patients, in that only 2 patient showed significant

radiological changes which was not significant.

67

CORRELATION OF HRCT SCORE WITH TYPE OF

BROCHIECTASIS

In our study the correlation between HRCT score and extent of bronchiectasis

showed significant correlation the cystic group of patients. The patients in

cystic group shows significant correlation with the HRCT findings (r=0.23) and

extent of bronchiectasis. The positive correlation of HRCT score was

statistically significant only in cystic group compared to others.

Gaik C. Ooi et al in his study “High-resolution ct quantification of

bronchiectasis: clinical and functional correlation” studied 60 patients in which

all patient underwent high resolution CT . This study establishes a link between

morphologic high-resolution CT parameters and clinical activity and emphasize

the role of bronchial wall thickening in patients with bronchiectasis.

68

CORRELATION OF TYPE OF BRONCHIECTASIS WITH

PULMONARY FUNCTION TEST (FEV1/FVC)

Among the 40 patients in the current study we observed a significant

correlation between the FEV1/ FVC and extent of bronchiectasis (p<0.05).

Patients were in cystic group those showed significant correlation with the

pulmonary function test while compared to cylindrical group.

The cystic group patient showed the significance with a p value of (P<0.05).our

study suggests that the severity of bronchiectasis can be predicated using the

pulmonary function tests.

Abdullaziz et al in the study “HRCT score in bronchiectasis: correlation with

pulmonary function with tests and pulmonary artery pressure” concluded that

there is a significantly lower FEV1/FVC in the cystic patients with a P value of

( p<0.0001).the mean of FEV1 and FVC % compared in cystic and cylindrical

group which shows significant difference in the mean values. In this study the

FEV1/FVC suggested as a diagnostic tool for bronchiectasis.

69

CORRELATION OF 6 MINUTE WALK TEST AND FEV1/FEC IN

STUDY POPULATION

In our study we analysed the significance of 6 minute walk test in correlation

with bronchiectasis. If the patients have significant PFT alteration , those

patients showed lowest score in 6 minute walk test.

The 6 minute walk test was found to be useful in patients with bronchiectasis in

predicting the severity. There is a positive correlation (r=0.25) between these

two factors in the entire study population and it was statistically significant

(p<0.01) .6 MWT is widely used to measure the functional status, used as

predictor in respiratory conditions.

In a study Lee et al in his study “ clinical determinants of the six minute walk

test in bronchiectasis” suggested that evidence of expiratory flow limitation,

which indicates dynamic hyperinflation and increased work of breathing are

responsible of disease. In this study evidence of airflow obstruction measured

by using FEV1 and FVC associated 6 minute walk test.

Jenkins et al in his study Six-minute walk test in pulmonary rehabilitation: do

all patients need a practice test?proven that Respiratory diagnosis influences

the magnitude of the learning effect for the 6MWT. The findings support the

recommendation of a practice 6MWT at baseline assessment in order to

provide an accurate measure of the effects of rehabilitation on 6MWD.

70

CORRELATION OF MODIFIED MEDICAL RESEARCH COUNCIL

DYSPNEA

SCALE (MMRC) WITH TYPE OF BRONCHIECTASIS

Among the study population while correlating the MMRC score there was

more patients coming under MMRC score of 2 . The patients in cystic group

showed a high MMRC score as compared to the cylindrical but it was not

statistically significant (p=0.8). the mean MMRC score in the study population

was 2.

There was studies suggesting that there is significant correlation between

MMRC and pulmonary function in obese patients. There was no study

supporting this correlation in stable bronchiectasis. In the current study MMRC

score was not showing any significant benefit in assessing the extent of

bronchiectasis.

71

CORRELATION OF MODIFIED BORG DYSPNEA SCALE SCORE

(BORG) WITH TYPE OF BRONCHIECTASIS

Among the study population while correlating the BORG score there was more

patients coming under the score of 4 . In the current study there was no

significant correlation between the BORG score and extent of bronchiectasis

(p=0.98). The mean score of the entire study population was 4.

Martinez gracia et al (n= 56) in their study “Dissociation of lung function,

dyspnea ratings and pulmonary extension in bronchiectasis” suggesting an

independent impact of BORG score in assessing the lung extent in

bronchiectasis.

72

CORRLATION OF HRCT SCORE WITH SEVERITY OF

PULMONARY ARTERY HYPERTENSION

In our study we analysed that pulmonary hypertension seen commonly in

advanced bronchiectasis ,particularly cystic disease. On analyzing our study

found that there is no significant correlation between HRCT score with

incidence of pulmonary hypertension.

Alzeer et al in his study “ right and left ventricular function and pulmonary

artery pressure in patient with bronchiectasis” 109 patients reported that 32.9%

of stable patients with bronchiectasis had pulmonary hypertension was higher

in cystic bronchiectasis with concomitant right and left ventricular

dysfunction.In this study SPAP was positively correlated with HRCT

score(r=0.23)Moreover high HRCT score not only reflects lung damage in

these patients,but it can also be associated with pulmonary hypertension.

Helbich et al, in his study “ evaluation of CT findings in cystic fibrosis”

reported similar findings that are correlated with score of all patients

(n=107).It has statistically significant positive relationship between the scores

and SPAP for all patients (p=<0.05)mean global score (8.67+ 2.9) for patients

whose SPAP value <40mmHg .

Abdullaziz et al (20) were in 94 patients ;62 were cystic and 32 were

cylindrical with mean age of 53.4+ 17.5 SD years. Forced vital capacity and

Forced expiratory volume 1 second (FEV1%)were lower in cystic

patients(p<0.0001)as compared with cylindrical patients.

73

David et al(16) in a study conducted in 261 patients with significant

bronchiectasis, it was found that score and extent of bronchiectasis have

comparison, but according to the other scores bronchial thickening

significantly decreased in studies. Silverman et al found in cystic disease were

found to have significantly higher HRCT score with other scores. Atilla et

al(41) in study conducted amongst 97 with patients with HRCT score is

increased in cystic type when comparing to other significant scores of HRCT.

74

CORRELATION TYPE OF BRONCHIECTASIS WITH PULMONARY

HYPERTENSION

In our study we analysed the incidence of systolic pulmonary artery pressure

was high in the study population .CT signs in bronchiectasis patients with

pulmonary hypertension showed enlarged of pulmonary artery. Some patients

with cystic bronchiectasis shows PAH but there was no significant correlation

between PAH and extent of bronchiectaisis in the current study. The correlation

coefficient showed positive correlation (r=0.07) but was not statistically

significant (p=0.9).

Devaraj et al , in his study “ pulmonary hypertension in patients with

bronchiectasis: prognostic significance of CT signs”studied on 91 patients

analysed that enlargement of pulmonary artery hypertension showed a highly

prognostic indicator in evaluation of patients with bronchiectasis.

Abdullaziz et al found that systolic pulmonary artery pressure was higher in

cystic bronchiectasis with right and left ventricular dysfunction.Study showed a

correlation between HRCT score and systolic pulmonary artery

hypertension.SPAP could be a predictor of future pulmonary hypertension.

In a study Hassan et al mentioned that right ventricular diameter was

significantly greater in cystic bronchiectasis and was positively correlated with

pulmonary hypertension. Study concluded that cystic bronchiectasis is

associated with more severe lung function impairment.

75

SUMMARY

In our study we included 40 patients in that 17 were male and 23

were female. The variables used in the study were age, gender, BMI, the HRCT

findings, pulmonary artery hypertension, 6 minute walk test, pulmonary

function test, MMRC score and BORG score.Among the 40 patients we

distributed the patients based on 3 different groups cystic, cylindrical and

varicose. We analysed sociodemographic variables found in bronchiectasis

There was a significant correlation between the pulmonary

function test and extent of bronchiectasis with (p<0.05)pulmonary

hypertension.As we compared to the other groups in cystic group the

correlation was more significant. Also the pulmonary function tests shows

significant positive correlation with HRCT score and 6 minute walk test.There

was a significant correlation between 6 minute walk test with extent of

bronchiectasis (r=0.25).There was no significant correlation between the extent

of involvement and pulmonary artery hypertension with extent of

bronchiectasis. Also the MMRC score and BORG score was not proved to be

an effective tool in assessing the extent of bronchiectasis.

76

LIMITATIONS

1. HRCT is the gold standard for diagnosing bronchiectasis, there is no

significant correlation between HRCT score and incidence of pulmonary

hypertension.

2.The gold standard for diagnosing pulmonary artery hypertension is Right –

heart catherisation, but in our study the severity of PAH was assessed by

Echocardiography,because Right heart-catherisation was invasive.

4. Eventhough six minute walk test was found to be useful in patients with

bronchiectasis in predicting the severity ,the test was difficult in patients with

severe pulmonary hypertension.

4.Sample size was less.

77

CONCLUSION

1. The patient with cystic bronchiectasis are develop pulmary artery hypertension

and MMRC score was higher in cystic group.

2. Pulmonary function test (FEV1/FVC and post FVC) has good significant

correlation and thereby it shows a strong predictor of Pulmonary hypertension.

3. 6Minute Walk Test (<400Mts) has good significant correlation.

4. Simple bedside and outpatient test like 6minute walk test/ Pulmonary Function

test can help to predict onset of pulmonary hypertension in bronchiectasis.

However further study need to be increase the sample size and use of Bio-

Markers.

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ANNEXURES

PFT - Pulmonary function Test

HRCT - High Resolution Computed Tomography

PAH - Pulmonary Artery Hypertension

FVC - Forced vital capacity

FEV1 - Forced Expiratory volume at 1 second

MMRC - Modified Medical Research Council

BORG - BORG Dyspnea scale

6MWT - Six minute Walk test

PSG Institute of Medical Science and Research, Coimbatore Institutional Human Ethics Committee

INFORMED CONSENT FORMAT FOR STUDENT RESEARCH PROJECTS I NAJMA MUHAMMED.K MD(Respiratory Medicine) 2015 batch PG student of the PSG Institute of Medical Sciences & Research (PSG IMS&R), I am carrying out a study on the topic To Correlate Clinicoradiological Characteristics of Bronchiectasis With Pulmonary Hypertension. as part of my student research project being carried out under the aegis of the Department of Respiratory Medicine My /Our research guide is : Dr.Anupama Murthy.K Designation : Professor and Head,

Department of respiratory Medicne The justification for this study is: COPD occurs worldwide,but it is a major health problem principally in societies where smoking is common.Its incidence is on the rise and WHO estimates that by 2020 it will be the 5th most prevalent disease worldwide and 3rd most common cause of death.COPD is a systemic disease with various extrapulmonary manifestations of which cardiac complication forms the leading cause of mortality and morbidity.so by early assessment of cardiac function by echocardiography, which is one of the best non invasive tests, prompt management can be initiated and helps in monitoring the patient. The aims of this study are: To correlate clinicoradiological characteristics of

bronchiectasis with pulmonary hypertension and to correlate the spirometric findings

with echocardiographic changes.

Sample size : 40. Respondents are (population group & age group): ____________________. Location : Department of Respiratory Medicine, PSG-IMSR. We request you to kindly cooperate with us in this study. We propose collect background information and other relevant details related to this study. We will be carrying out (strike off items that are not applicable): Initial interview (specify approximate duration):_ 10 minutes.

Health education sessions: Number of sessions: _ ONE. Approximate duration of each session: _ 10 minutes. Clinical examination (Specify details and purpose): YES, General and system wise examination as a part of routine work up. Echocardiogram : To assess pulmonary hypertension 6MWT Pulmonary Function Test : To determine physiological parameters BORG Scale,MMRC Blood sample collection : NA Specify purpose, discomfort likely to be felt and side effects, if any: Medication given, if any, duration, side effects, purpose, benefits: Final interview (specify approximate duration):_________ mts. If photograph is taken, purpose: Benefits from this study, if any: How the results will be used: If you are uncomfortable in answering any of our questions during the course of the interview / biological sample collection, you have the right to withdraw from the interview / study at anytime. You have the freedom to withdraw from the study at any point of time. Kindly be assured that your refusal to participate or withdrawal at any stage, if you so decide, will not result in any form of compromise or discrimination in the services offered. You will continue to have access to the regular services offered to a patient. You will NOT be paid any remuneration for the time you spend with us for this interview / study. The information provided by you will be kept in strict confidence. Under no circumstances shall we reveal the identity of the respondent or their families to anyone. The information that we collect shall be used for approved research purposes only. Consent: The above information regarding the study, has been read by me/ read to me, and has been explained to me by the student investigators from the PSG IMS&R. Having understood the same, I hereby give my consent to them to interview me. I affixing my signature / left thumb impression to indicate my consent and willingness to cooperate in this study. Respondent ID: _________. Signature / Left thumb impression of the Respondent. Signature of the Interviewer with date

Thesis Project

Title : Clinico Radiological Correlation of Bronchiectasis with Pulmonary Hypertension

Department of Respiratory medicine

PSG IMSR

Case Record Form

Name: ………………………………………. Informant: …………………………............

Age / sex: …………………………………… CRC. No : ………………………………….

Father’s / Husband’s name: …………………………………………………………………………...

Address: ……………………………………... Height: …………. Weight: ……………....

………………………………………………... BMI: ………………………………………

………………………………………………... PSG OP No: ________________________

Marital status: Married Unmarried Widow/widower

No. of family members: …………………… Adults ………. Children ……… (< 12 years)

Dwelling {lived for most part (>70%) of the subject’s life} Urban / Rural/High altitude

Education : Illiterate Read & write

Primary school High school

Higher secondary Graduate

Postgraduate Professional / Fellow / Doctorate

Occupation : employed unemployed retired housewife

Present : ………………………………………………… Duration : …………………

Past : (1) ………………………………………… Duration : …………………

(2) ………………………………………... Duration : …………………

Total monthly family income: ………………………

What is your contribution to total monthly family income? …………………… %

Socioeconomic status(Modified prasad’s classification):

Personal History :

Diet: vegetarian / mixed

If mixed diet how frequently you take animal food?

Daily / weekly / fortnightly / monthly / occasional

Smoking: Yes / No ( presence of regular smoking for at least one year and / or smoked at

least 100 cigarettes / beedies / others in his / her lifetime)

If yes, beedi/ cigarette/ hukka /others

No of beedies / cigarettes per day ………………………….

Age at started …………………………………………………

If ex-smoker, when stopped …………………………………

Alcohol : Yes / No

If yes, Quantity ……………………ml

Frequency ……………………

If stopped when …………………………..

Other informations : Drugs / narcotics abuse

Tobacco / pan chewing

Sexual promiscuity

Disease specific details : Bronchiectasis/Pulmonary Hypertension

Primary Symptoms:

Cough……………………………………………………………………….

Sputum(colour,quantity,foul smelling)……………………………………..

Breathlessness……………………………………………………………….

Hemoptysis…………………………………………………………………..

Chest Pain…………………………………………………………………….

Fever………………………………………………………………………….

Wheeze………………………………………………………………………..

Other symptoms:

Upper respiratory symptoms…………………………………………………..

Weight loss…………………………………………………………………….

Growth retardation…………………………………………………………….

Gastrointestinal symptoms……………………………………………………..

Infertility………………………………………………………………………..

History suggestive of asthma……………………………………………………

Details(Age,Duration,Family history)………………………………………….. …………………………………………………………………………………..

……………………………………………………………………………………

Type of medications Inhaled/Dry powered

In ABPA – h/o oral steroids

h/o high inhaled steroids

Treatment Details

Duration of respiratory symptoms suggestive of bronchiectasis

When was the diagnosis established with HRCT

Are you on any treatment for respiratory symptoms ?............Yes/No

If yes………………………………………………………………………

Treatment Details:

Medical Treatment:

Antibiotic’s used………..…..YES/NO

If yes duration & frequency……………………………………………………………………………

Bronchodilators- Inhaled/Oral &Duration……………………………………………………………..

Mucolytics………………………………………………………………………………………………Steroids used…………………..YES/NO

Postural drainage………………………………………………………………………………………..

Vaccination……………………………………………………………………………………………..

Pulmonary vasodilators used …….YES/NO

If yes details…………………………………………………………………………………………….

Oxygen therapy…………………YES/NO

If yes short burst or LTOT

Surgical Treatment……………...YES/NO

If yes give details ………………………………………………………………………………………

Details of exacerbation for bronchiectasis:

No. of ED visits for an acute exacerbation in the past one year (both PSG and GP clinics / hospitals)

( In the past one year, have you ever received emergency injectables / nebulized bronchodilators for your respiratory illness, in emergency departments of any hospitals / GP clinics? )

No ED visit ≤ 5 ED visits (…………..) >5 ED visits (………....)

No. of hospitalizations:

mm / yy

Reason

duration

ICU stay

Mech vent

Remarks

Past history / Co-existing illness:

Infection - Tuberculosis /Measles/Bacterial/Viral/Retroviral……………………………….. …………… Congential Disease………………………………………………………………………………………….. Lung Disease –COPD/ILD/Sleep disorder/Developmental abnormalities………………………………. Allergic Rhinitis/Sinusitis………………………………………………………………………………… Congenital heart disease /LVD/Valvular heart disease/Hypertension GERD / Acid peptic disease………………………………………………………………………………… Diabetes mellitus……………………………………………………………………………………………. Hypo/hyperthyroidism……………………………………………………………………………………… Other endocrine disorders…………………………………………………………………………………... Connective tissue disorder……………………………………………………………………………. Metabolic disorder…………………………………………………………………………………………….. Cerebro vascular diseases…………………………………………………………………………………... Kidney diseases……………………………………………………………………………………………... Obstetric history / Gynecological illnesses…………………………………………………………........... Surgical illnesses .………………………………………………………………………………………… Congenital anomalies……………………………………………………………………………………….. Others………………………………………………………………………………………………………..

Family History: (mention relationship where relevant)

Atopic diseases……………………………………………………………………………………………... Hypertension………………………………………………………………………………………………... Diabetes mellitus……………………………………………………………………………………………. Hypo/hyperthyroidism……………………………………………………………………………………… Other endocrine disorders…………………………………………………………………………………... Lung diseases ………………………………………………………………………………………………. Heart diseases……………………………………………………………………………………………….. Kidney diseases……………………………………………………………………………………………... Obstetric history / Gynaecological illnesses…………………………………………………………........... Surgical illnesses……………………………………………………………………………………………. Congenital anomalies………………………………………………………………………………………

Congenital disease – Cystic fibrosis/ Kartagener’s/ Young’s/

Hypogammaglobulenemia………………………………………………………………………

Alpha1antitrypsindeficiency………………………………………………………………………….

Others……………………………………………………………………………………… Malignancy………………………………………………………. Foreign body aspiration/Inhalation of toxic fumes………………………………………………………. Infertility…………………………………………………………………………………… Others………………………………………………………………………………………………………..

Physical examination

1. Vitals:

Pulse rate: …………………….. Respiratory rate: …………………….

B.P.: …………………………. Temperature: ………………………..

O2 saturation: ………………...

2. General examination:

Built Pallor cyanosis clubbing JVP Edema Lymph nodes

3. Respiratory system:

4. Cardiovascular System:

5. Others system

INVESTIGATIONS:

Hemogram Hb

TC DC

Platelet ESR

Sr.Urea Sr.Creatine

Urine Routine

X-ray chest PA view:

Normal /Abnormal

Unilateral/Bilateral

Zone Involved

Upper Mid Lower

Appearance Tooth paste Tramline FingerGlove Sign Honeycomb

Pulmonary function test:

Spirometry: prebronchodilator postbronchodilator

FVC

FEV1

FEV1/ FVC

ECHO EF RA /RV dilation RVSP

Others

HRCT Lungs Lobe involved upper middle Lower

Type

Unilateral /Lateral

Bronchial dilation

Associated features:

7. ITEM WEIGHTS Note: 1. This is given for information only. The Excel-based system and other computerised scoring systems use these weights. 2. The wording of the item may not correspond exactly with the wording in the current version of the questionnaire. PART 1 1) Over the last year, I have coughed: Most 80.6 Several 63.2 A few 29.3 Only 28.1 Not 0.0 2) Over the last year, I have brought up phlegm (sputum): Most 76.8 Several 60.0 A few 34.0 Only 30.2 Not 0.0 3) Over the last year, I have had shortness of breath: Most 87.2 Several 71.4 A few 43.7 Only 35.7 Not 0.0 4) Over the last year, I have had attacks of wheezing: Most 86.2 Several 71.0 A few 45.6 Only 36.4 Not 0.0 5) During the last year, how many severe or very bad unpleasant attacks of chest trouble have you had? More than three 86.7 3 attacks 73.5 2 attacks 60.3 1 attack 44.2 None 0.0 6) How long did the worst attack of chest trouble last? a week or more 89.7 3 or more days 73.5 1 or 2 days 58.8 less than a day 41.9 7) Over the last year, in an average week, how many good days (with little chest trouble) have you had? None 93.3 1 or 2 76.6 3 or 4 61.5 nearly every day 15.4 every day 0.0

8) If you have a wheeze, is it worse in the morning?

No 0.0 Yes 62.0 PART 2 9) How would you describe your chest condition? The most important problem I have 83 .2 Causes me quite a lot of problems 82.5 Causes me a few problems 34.6 Causes no problem 0.0 10) If you have ever had paid employment? My chest trouble made me stop work 88.9 My chest trouble interferes with my work or made me change my work 77.6 My chest trouble does not affect my work 0.0 11) Questions about what activities usually make you feel breathless. Sitting or lying still 90.6 Getting washed or dressed 82.8 Walking around the home 80.2 Walking outside on the level 81.4 Walking up a flight of stairs 76.1 Walking up hills 75.1 Playing sports or games 72.1 12) More questions about your cough and breathlessness. My cough hurts 81.1 My cough makes me tired 79.1 I get breathless when I talk 84.5 I get breathless when I bend over 76.8 My cough or breathing disturbs my sleep 87.9 I get exhausted easily 84.0 13) Questions about other effects your chest trouble may have on you. My cough or breathing is embarrassing in public 74.1 My chest trouble is a nuisance to my family, friends or neighbours 79.1 I get afraid or panic when I cannot get my breath 87.7

I feel that I am not in control of my chest problem 90.1 I do not expect my chest to get any better 82.3 I have become frail or an invalid because of my chest 89.9 Exercise is not safe for me 75.7 Everything seems too much of an effort 84.5 14) Questions about your medication. My medication does not help me very much 88.2 I get embarrassed using my medication in public 53.9 I have unpleasant side effects from my medication 81.1 My medication interferes with my life a lot 70.3

15) Questions about how activities may be affected by your breathing. I take a long time to get washed or dressed 74.2 I cannot take a bath or shower, or I take a long time 81.0 I walk more slowly than other people, or I stop for rests 71.7 Jobs such as housework take a long time, or I have to stop for rests 70.6 If I walk up one flight of stairs, I have to go slowly or stop 71.6 If I hurry or walk fast, I have to stop or slow down 72.3 My breathing makes it difficult to do things such as walk up hills, carry things up stairs, light gardening such as weeding, dance, play bowls or play golf 74.5 My breathing makes it difficult to do things such as carry heavy loads, dig the garden or shovel snow, jog or walk at 5 miles per hour, play tennis or swim 71.4 My breathing makes it difficult to do things such as very heavy manual work, run, cycle, swim fast or play competitive sports 63.5

16) We would like to know how your chest trouble usually affects your daily life. I cannot play sports or games 64.8 I cannot go out for entertainment or recreation 79.8 I cannot go out of the house to do the shopping 81.0 I cannot do housework 79.1 I cannot move far from my bed or chair 94.0 17) Tick the statement which you think best describes how your chest affects you. It does not stop me doing anything I would like to do 0.0 It stops me doing one or two things I would like to do 42.0 It stops me doing most of the things I would like to do 84.2 It stops me doing everything I would like to do 96.7

SL.NO NAME IP NO: OP NO: AGE SEX BMI MARITAL FAMILYDWELLING

EDUCAT OCCUPAT

INCOME DIET SMOKING ALCOHOL SPUTUM COUGH DYSPNEA HEMOPTY ASTHMA DURATN HB TLC RDW ESR CLUBBNG BORG MMRC HRCT SEGMNT TYPE ECHO RVSP RA/RV OTHERS FEVI/FVC PRE FEVI PRE FVC POSTFEV1 POSTFVC SAD 6MWT CXR SIDE ZONE SGRQ TS SYMPTM ACTIVTY IMPACT ANTIBIOT BRONCH MUCOLYT STEROIDS PST DRANG VACCNT VASODIL O2 SURGRY NO EXAC PST H/O FAMI H/O SPO2

1KALYANSUNDER

I15011934 o10007708 55 1 1 1 4 1 4 1 22000 2 2 0 1 1 II 0 1 10 9.8 7500 14.2 59 0 3 2 1 3 1 1 1 0 0 88 46 43 53 50 47 0 1 2 3 21.15 47.2 12.45 17.91 1 1 0 1 0 1 0 0 0 2 1 0 97%

2ZUHASABBER

I10042805 O10082611 20 2 1 0 5 1 6 0 30000 2 0 0 1 1 II 1 1 15 11.5 10,400 14.6 19 0 3 3 1 3 1,2 1 1 0 0 91 42 46 45 45 34 0 1 2 2 18.63 32.9 12.38 17.72 1 1 1 0 1 1 0 0 1 4,5 1 0 95%

3ROSLY

I16025693 O04026080 72 2 1 0 1 1 3 0 4000 2 0 0 1 1 III 0 1 7 12.1 12,600 14.2 22 0 9 4 1 2 1 1 0 0 0 64.6 45 53 46 56 27 2 1 2 2 31.69 78.98 13.54 27.26 1 1 0 1 0 0 0 0 0 2 1 0 96%

4PUSPHA

I16013715 O13081200 36 2 1 1 4 1 3 0 8000 2 0 0 1 1 II 0 1 15 11.5 9600 15.5 55 0 4 2 1 4 1 1 0 0 0 53.2 44 73 45 72 16 0 1 2 1 25.54 42.08 12.98 27.54 1 1 0 0 1 1 0 0 0 2 1 1 96%

5RAMALINGHM

I16024512 O10018010 41 1 1 1 4 1 2 1 8000 2 0 0 1 1 II 0 1 4 10.1 8200 12.6 140 0 2 2 1 3 2 1 1 0 0 61 31 43 30 41 12 0 1 2 2 26.18 56.49 12.2 24.67 1 1 0 0 0 0 0 0 1 2 1 10 95%

6RAMASAMY

I15010056 O11048936 65 1 1 1 4 1 2 3 10000 2 0 0 1 1 II 0 1 4 16.4 5400 16.9 8 0 3 2 1 1 1 1 1 0 0 47 76 72 73 72 72 1 1 2 2 22.97 47.62 21.78 11.54 1 1 0 0 0 1 0 0 0 2 1 0 96%

7RANGASAMY AR

I16019123 O16040355 75 1 1 1 6 2 3 0 10000 2 0 0 0 0 I 0 0 1 11.7 7000 15.1 46 1 3 2 1 1 2 1 0 0 0 69 61 75 63 72 27 0 1 2 3 24.48 54.72 12.11 22.09 1 1 0 0 0 1 0 0 0 1 0 0 96%

8SUMATHY

I16020298 O12014068 50 2 1 1 4 1 8 1 20000 2 0 0 1 1 II 0 1 3 10.3 6400 17.8 27 0 3 2 1 2 1 1 1 0 0 81.4 36 40 40 43 20 0 1 1 2 28.64 61.24 12.98 27.39 1 1 0 0 1 1 0 1 1 3 4 0 85%

9PALANISAMY

I16019526 O15014856 60 1 1 1 4 2 3 1 8000 2 2 0 1 1 II 0 1 45 10 7700 13.9 45 1 4 3 1 1 1 1 0 0 0 64.9 38 48 43 53 19 0 1 2 1 28.92 67.72 12.21 26.32 1 1 0 0 0 0 0 0 1 2 0 1 96%

10MAHALINGHAM

I15030049 O15069676 67 1 1 1 4 2 3 1 15000 2 0 0 1 1 II 0 0 3 14.7 14,100 13.4 79 0 2 3 1 2 2 1 0 0 0 52.8 24 38 24 36 11 0 1 2 2 23.38 46.18 12.27 22.58 1 1 0 0 0 1 0 0 0 3 1 0 97%

11NANJAMMAL P

I16014790 O16019216 75 2 1 1 4 1 0 0 10000 2 0 0 1 1 II 0 0 10 12.3 7,300 16 55 0 5 3 1 2 1 1 3 0 0 72.4 36 40 36 38 24 0 1 2 2 22.4 37.44 12.57 23.33 0 1 0 1 0 0 0 1 0 2 10 0 98%

12THULASIMMAL

I15033105 O10095425 52 2 1 1 3 1 3 1 4000 2 0 0 1 1 II 0 1 10 13.4 16,900 14.7 21 0 4 2 1 3 2 1 1 0 0 84.4 40 43 44 44 25 0 1 2 2 31.05 76.76 12.77 27.19 1 1 0 0 0 1 0 0 1 2 2 0 96%

13RANGARAJ

I16022726 O15077383 56 1 1 1 6 1 3 0 10000 2 0 0 1 1 III 0 1 0 13.2 7,300 14.1 5 0 4 3 1 2 1 1 2 0 0 47 18 42 43 48 7 0 1 2 3 30.58 75.78 12.76 26.6 1 1 0 0 0 1 0 0 0 2 3 0 96%

14NANJAMMAL

I16021729 O13035857 65 2 1 1 6 2 0 0 5000 2 0 0 1 1 II 0 0 0 14.2 6,900 13.5 20 0 2 4 1 3 2 1 1 0 0 74.5 39 46 39 43 43 3 1 1 1 22.45 32.69 12.21 25.09 1 1 1 0 0 1 0 0 0 4 1 0 96%

15SUBRAMANI

I16019861 O15084046 39 1 1 1 4 1 0 1 4000 2 0 0 1 1 I 0 0 0 11.6 6,300 15 12 0 3 2 1 2 2 1 0 0 0 77.7 44 47 45 48 30 0 1 1 1 21.09 54.52 12.11 15.75 1 1 0 0 0 0 0 0 0 1 0 0 97%

16MALLAN

I16023276 O16050895 64 1 1 1 4 1 5 0 3500 2 0 0 0 0 II 0 0 0 12.8 8,800 14.4 2 0 3 1 1 2 1,2 1 0 0 0 90 65 76 69 76 35 0 1 2 2 17.53 42.82 12.45 12.51 0 0 0 0 0 0 0 0 0 0 3,4 0 98%

17ESWARAN

I16018784 O10093271 38 1 1 0 2 2 3 1 8000 2 1 1 0 0 III 0 0 30 8.9 8,900 11.4 56 1 4 3 1 2 2 1 0 0 1 74 108 82 106 80 46 0 0 0 0 29.56 65.7 12.57 27.95 1 1 1 0 0 0 0 0 0 1 2,3 1 97%

18SRINIVASAN

I16019273 O02020134 76 1 1 1 4 1 4 1 20000 2 0 0 1 0 I 0 1 20 12.5 6,100 14.8 0 0 3 2 1 6 2 1 0 0 0 87 55 51 59 54 54 0 1 2 3 30.45 76.73 12.45 26.25 1 1 0 0 0 0 0 0 0 1 1,2 1 98%

19VALLIYATHAL

I15007629 O15014663 50 2 1 1 1 2 0 1 2250 2 0 0 1 0 I 0 1 3 11.8 5,900 13.6 25 0 3 2 1 4 1 1 0 0 0 109 71 64 79 68 76 0 1 2 3 19.36 39.51 12.45 17.01 1 1 0 0 0 0 0 0 0 1 1 0 96%

20PONGIYANNAN

I16024301 0II036905 63 1 1 1 3 2 0 1 10000 2 0 0 1 1 I 0 1 0 12.4 6,100 14.4 39 0 4 2 1 2 2 1 1 0 0 69 48 57 53 67 25 0 1 1 1 17.34 24.33 12.37 17.99 1 1 0 0 0 0 0 0 0 2 1 1 98%

21PALANIMMAL

I16013698 O10006029 56 2 1 1 4 2 0 0 10000 2 0 0 1 1 I 0 1 49 11.2 11,600 13 103 0 3 2 1 2 2 1 1 1 0 85 58 67 80 90 25 1 1 1 3 22.86 49.99 12.45 20.31 1 1 1 0 1 1 0 0 0 2 4 0 97%

22SIVABAKIYAM

I16013703 O13035215 47 1 1 1 3 1 3 1 5000 2 0 0 1 1 II 0 1 10 12.9 11,200 14.7 4 0 4 2 1 6 2 1 0 0 0 81 68 82 68 80 52 0 1 2 4 18.94 43.33 12.37 15.07 1 1 0 0 0 0 0 0 1 3 1 0 98

23GOVINDRAJ

I15026273 O97040946 74 1 1 1 4 1 4 1 10000 2 0 0 1 1 II 0 0 0 12.2 10,200 12.4 60 0 3 2 1 3 1 1 1 0 0 68 58 65 58 69 35 0 1 2 2 18.62 32.92 12.37 17.72 0 1 0 0 0 0 0 0 0 2 1 0 98

24TAMILSELVI

I6017694 O13039091 51 2 1 0 1 2 0 0 5000 2 0 0 1 1 II 0 1 4 13.2 5,800 13.1 23 0 3 2 1 4 3 1 1 0 0 71 84 84 101 80 95 0 1 1 2 18.53 40.6 12.71 14.95 1 1 1 0 0 1 0 0 0 0 4,5,7 1 92%

25RANGAMMAL

I6017694 O12081156 55 2 1 1 4 2 2 4 5000 2 0 0 1 0 II 0 0 6 6.4 10,900 14.3 20 0 3 2 1 2 2 1 2 0 0 93 24 26 24 22 17 2 1 1 3 26.78 52.19 12.47 27 0 1 0 0 0 0 0 0 0 2 1 0 95%

26VIJYANIRMALA

i16019091 O15063397 23 2 0 0 4 1 6 0 8000 2 0 0 1 1 II 0 1 15 13.4 13,700 12.6 23 0 3 2 1 2 1 1 0 0 0 75 41 46 49 66 36 0 1 1 2 18.21 33.26 12.19 16.94 1 1 1 0 1 1 0 0 1 0 0 0 97

27THANGAMMAL

i15012857 o15028202 66 2 1 0 4 1 0 0 8000 2 0 0 1 1 II 0 1 2 13.6 11,000 14.3 29 0 4 3 1 3 3 1 0 0 0 82 59 53 85 74 36 1 1 2 4 18.77 34.02 12.21 17.75 1 1 0 0 0 0 0 0 0 1 1 0 95%

28ELANGOTHI

I16018483 O09064727 56 2 1 1 4 1 2 0 20000 2 0 0 1 1 II 0 0 1 12.5 9,400 14.8 16 0 3 4 1 3 1 1 0 0 0 50 44 44 44 45 34 0 1 2 3 15.53 19.56 12.11 15.53 1 0 0 0 0 0 0 0 0 0 1 0 98%

29KRISHNAN E.S

I16017715 O16037440 70 1 1 1 4 1 3 0 10000 2 1 0 1 1 II 0 1 4 14.3 11,000 13.6 9 1 3 2 1 2 2 1 1 0 0 47 19 43 43 47 25 0 1 2 4 18.94 43.33 12.37 15.08 1 1 0 0 0 0 0 0 0 2 1 0 96%

30RAMASAMY

I17024509 O17044794 65 1 1 1 3 1 0 1 12000 2 1 0 1 1 III 0 0 3 11.1 9,400 15.6 31 1 2 3 1 2 1 1 1 0 0 92 25 25 24 22 18 2 1 2 3 17.2 32.25 11.19 15.9 1 1 0 1 0 1 0 0 0 2 3 0 93%

31KALIAMMAL

I16025842 O16001737 52 2 1 0 2 1 0 0 4000 2 0 0 0 1 II 0 1 3 15.9 12,900 15.9 7 0 3 4 1 3 1 1 1 0 0 50 43 44 44 45 63 1 0 1 4 18.62 32.92 12.36 17.7 0 1 0 1 0 1 0 0 0 2 3 0 97%

32JAYANTHI

I16028445 O09096706 42 2 1 1 3 1 4 1 10000 2 0 0 0 1 III 0 1 2 8.2 5,900 29 94 1 3 2 1 2 1 1 1 0 0 71 86 85 100 80 95 0 1 2 2 24.76 52.14 12.45 26 0 1 0 1 1 1 0 0 0 3 2,3 1 96%

33SELLATHAL

I16018386 O15077108 50 2 1 1 3 2 2 1 8000 2 1 0 1 0 II 0 1 10 15.1 8,900 13.1 67 1 2 2 1 3 2 1 1 0 0 47 19 43 43 38 35 0 1 1 3 30.45 76.73 12.45 26.25 1 1 1 0 0 0 0 0 0 2 3 1 97%

34JAYALAKSHMI

I16019716 O14081743 45 2 1 1 3 1 3 1 4000 2 0 0 1 1 II 0 1 3 14.1 11,100 13.7 16 1 2 3 1 2 2 1 0 0 0 90 65 76 65 67 25 0 1 2 3 29.58 64.7 12.6 26.94 1 1 0 0 0 0 0 0 0 3 2 1 96%

35VELLINGIRI

I17004121 O14014318 50 1 1 1 4 1 2 1 8000 2 0 1 1 1 II 0 1 2 12.9 6,800 13.9 61 0 3 2 1 2 3 1 1 0 0 50 44 44 45 50 35 0 1 2 2 22.4 37.44 12.57 23.33 1 1 0 0 0 1 0 0 1 2 3 1 97%

36BAGYAM

I16021790 O11017929 72 2 1 1 4 2 1 4 8000 2 0 0 1 1 II 1 4 5 11.3 11,800 16.1 23 0 4 2 1 3 2 1 1 0 0 74 68 76 72 80 47 0 1 2 2 28.07 57.2 13 27.56 0 0 0 0 0 0 0 0 0 0 1,4,5 0 94%

37SIVAKAMI

I16000708 O12030255 54 2 1 1 4 2 2 1 12,000 2 3 0 1 1 II 0 0 4 12.6 7,200 12.2 27 0 4 3 1 2 3 1 0 0 0 83 29 29 31 31 116 0 1 1 2 31.05 76.76 12.77 27.19 1 0 0 1 1 0 0 0 0 1 0 0 98%

38SAVITHIRI

I15038020 O15086817 57 2 1 1 4 0 3 1 10,000 2 3 0 1 2 II 3 0 1 13.1 13,100 13.9 43 0 0 0 1 1 1 1 0 0 0 55.3 41 58 46 68 17 0 1 1 2 19.66 40.22 12.11 17.53 1 0 1 1 0 0 0 0 0 2 2 1 98%

39VALLIYATHAL

I15007629 O15014663 56 2 1 1 2 1 1 2 10,000 0 2 0 1 1 I 0 2 3 0 3 2 1 2 2 1 0 0 0 109 71 64 76 68 66 0 1 2 3 19.36 39.51 12.45 17.01 1 0 1 1 1 0 0 0 1 3 3 1 97%

40VINITHA

I16026762 O14010999 29 2 1 1 4 1 6 1 20,000 2 0 0 1 2 2 5 2 2