A Dissertation on
"A STUDY OF SERUM ELECTROLYTES AND RED CELL DISTRIBUTION WIDTH IN ACUTE EXACERBATION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE PATIENTS"
Dissertation Submitted to
THE TAMILNADU Dr.M.G.R. MEDICAL UNIVERSITY CHENNAI - 600 032
Ｃ
With partial fulfillment of the regulations for the award of the degree of M.D. GENERAL MEDICINE
BRANCH-I
COIMBATORE MEDICAL COLLEGE, COIMBATORE
MAY 2019
DECLARATION
I Solemnly declare that the dissertation titled “A STUDY OF SERUM ELECTROLYES AND RED CELL DISTRIBUTION WIDTH IN ACUTE EXACERBATION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE PATIENTS” was done by me from JULY 2017 to JUNE 2018, during the academic year 2016-2019. under the guidance and supervision of Prof.Dr.K.SIVAKUMAR M.D., Professor, Department of General Medicine, Coimbatore Medical College and Hospital, Coimbatore.
This dissertation is submitted to The Tamilnadu Dr.M.G.R. Medical University towards the partial fulfilment of the requirement for the award of MD degree in General Medicine (Branch 1)
Place: Coimbatore Dr.M.Ramanan
Date:
ETHICAL COMMITTEE CERTIFICATE
CERTIFICATE I
Certified that this is the bonafide dissertation done by Dr.M.RAMANAN from July 2017 to June 2018 during the academic year
2016 to 2019 and submitted in partial fulfillment of the requirements for the
Degree of M.D., General Medicine, Branch I of The Tamilnadu Dr.M.G.R. Medical University, Chennai.
Date: Prof.Dr.K.SIVAKUMAR M.D.,
Guide & Professor
Department of General Medicine
Date: Prof.Dr.KUMAR NATARAJAN M.D., Professor & Head of Department
Department of General Medicine
Date: Prof.Dr.B.ASOKAN M.S.,M.Ch(Plastic)
Dean
Coimbatore Medical College Coimbatore
CERTIFICATE – II
This is to certify that this dissertation work titled “A study of serum electrolytes and red cell distribution width in acute exacerbation of
chronic obstructive pulmonary disease patients” of the candidate DR.M.RAMANAN with registration Number- 201611313 for the award of
M.D in the branch of General Medicine I personally verified the urkund.com website for the purpose of plagiarism Check. I found that the uploaded thesis file contains from introduction to conclusion pages and result shows 2% (Two percentage) percentage of plagiarism in the dissertation.
Guide & Supervisor sign with Seal.
ACKNOWLEDGEMENT
I wish to express my sincere thanks to our respected Dean Prof.Dr.B.ASOKAN M.S.,MCh, (Plastic Surgery) for having allowed me to conduct this study in our hospital.
I express my heartfelt thanks and deep gratitude to the Head of the Department of General Medicine Prof.Dr.KUMAR NATARAJAN M.D., for his generous help and guidance in the course of the study.
I sincerely thank my Professor and Guide Prof.Dr.K.SIVAKUMAR M.D., for constant support, invaluable guidance and encouragement throughout my study and post graduate programme.
I am extremely grateful to Prof.Dr.S.KEERTHIVASAN M.D., HOD, Department of Thoracic Medicine for his valuable help and cooperation and allowing me to use institutional facilities.
I am extremely grateful to, Prof.Dr.LALITHA M.D., HOD, Department of Pathology, for their valuable help and cooperation and allowing me to use institutional facilities.
I am extremely grateful to, Prof.Dr.C.MURALI M.D.,HOD, Department of Radiology, for their valuable help and cooperation and allowing me to use institutional facilities.
I am extremely grateful to, Prof.Dr.MANIMEGALAI M.D.,HOD, Department of Pathology, for their valuable help and cooperation and allowing me to use institutional facilities.
I sincerely thank all the Asst. Professors Dr.S.BALAJI M.D., and Dr.K.SIVAKUMAR M.D., for their guidance and help.
I thank all my PATIENTS, who formed the backbone of this study without whom this study would not have been possible.
Lastly, I am ever grateful to the ALMIGHTY GOD for always showering His blessings on me and my family.
Dr.M.Ramanan
LIST OF ABBREVIATIONS USED
RDW – Red Cell Distribution Width
COPD - Chronic Obstructive Pulmonary Disease
HRCT – High resolution computed tomography
BODE – Body Mass Index, Airflow Obstruction, Dyspnea and Exercise
FEV1 - Forced Expiratory Volume in One second
FVC - Forced Vital Capacity
WHO - World Health Organization
GOLD - Global Initiative for Chronic Obstructive Lung Disease
MMRC - Modified Medical Research Council
BMI - Body Mass Index
HB - HEMOGLOBIN
6WMT-Six Minute Walk Distance
RBC – Red blood cells
PAH-Pulmonary Artery Hypertension
ABG – Arterial Blood Gas Analysis
TABLE OF CONTENTS
SL.NO TITLES PAGE.NO
1 INTRODUCTION 1
2 OBJECTIVES OF STUDY 2
3 REVIEW OF LITERATURE 3-31
4 MATERIALS & METHODS 32-33
5 RESULTS AND OBSERVATIONS 34-90
6 DISCUSSION 91-97
7 SUMMARY 98
8 CONCLUSION 99
9 BIBLIOGRAPHY 100-105
10 ANNEXURES
A1.PROFORMA 106 – 107
A2.CONSENT FORM 108-111
A3.KEYS TO MASTER CHART 112-115
A4.MASTER CHART 116-122
LIST OF TABLES
SI NO NAME OF THE TABLES PAGE NO
1 AGE AND GENDER DISTRIBUTION OF STUDY GROUPS
34
2 ASSOCIATION OF SMOKING WITH DISEASE OUTCOME
34
3 HEMOGLOBIN AND RDW AMONG STUDY GROUPS 35 4 SERUM ELECTROLYTES AMONG STUDY GROUPS 35
5 AGE CATEGORY OF CASES 36
6 AGE CATEGORY OF CASES VS RDW 37
7 AGE CATEGORY OF CASES VS SERUM SODIUM 38 8 AGE CATEGORY OF CASES VS SERUM POTASSIUM 39
9 GENDER OF CASES 40
10 GENDER OF CASES VS RDW 41
11 GENDER OF CASES VS SERUM SODIUM 42
12 GENDER OF CASES VS SERUM POTASSIUM 43
13 SMOKING OF CASES 44
14 CASES WITH FEVER 45
15 CASES WITH COUGH 46
16 CASES WITH CREPITATIONS 47
17 CASES WITH WHEEZING 48
18 CASES WITH CLUBBING 49
19 CASES WITH PEDAL EDEMA 50
20 X RAY FEATURE OF CASES 51
21 X RAY FEATURE OF CASES VS RDW 52
22 X RAY FEATURE OF CASES VS SERUM SODIUM 53 23 X RAY FEATURE OF CASES VS SERUM POTASSIUM 54
24 HEMOGLOBIN STATUS AMONG CASES 55
25 HEMOGLOBIN STATUS AMONG CASES VS RDW 56 26 HEMOGLOBIN STATUS AMONG CASES VS SERUM
SODIUM
57
27 HEMOGLOBIN STATUS AMONG CASES VS SERUM POTASSIUM
58
28 FEV1 OF CASES 59
29 FEV1 OF CASES VS RDW 60
30 FEV1 OF CASES VS SERUM SODIUM 61
31 FEV1 OF CASES VS SERUM POTASSIUM 62
32 FEV1/FVC OF CASES 63
33 FEV1/FVC OF CASES VS RDW 64
34 FEV1/FVC OF CASES VS SERUM SODIUM 65 35 FEV1/FVC OF CASES VS SERUM POTASSIUM 66
36 BMI CATEGORY OF CASES 67
37 BMI CATEGORY OF CASES VS RDW 68
38 BMI CATEGORY OF CASES VS SERUM SODIUM 69 39 BMI CATEGORY OF CASES VS SERUM POTASSIUM 70 40 SIX MINUTE WALK TEST AMONG CASES 71 41 SIX MINUTE WALK TEST AMONG CASES VS RDW 72 42 SIX MINUTE WALK TEST AMONG CASES VS SERUM
SODIUM
73
43 SIX MINUTE WALK TEST AMONG CASES VS SERUM POTASSIUM
74
44 MMRC AMONG CASES 75
45 MRC AMONG CASES VS RDW 76
46 MRC AMONG CASES VS SERUM SODIUM 77
47 MRC AMONG CASES VS SERUM POTASSIUM 78
48 BODE AMONG CASES 79
49 BODE AMONG CASES VS RDW 80
50 BODE AMONG CASES VS SERUM SODIUM 81
51 BODE AMONG CASES VS SERUM POTASSIUM 82
52 GOLD AMONG CASES 83
53 GOLD AMONG CASES VS RDW 84
54 GOLD AMONG CASES VS SERUM SODIUM 85 55 GOLD AMONG CASES VS SERUM POTASSIUM 86
56 OXYGEN SATURATION AMONG CASES 87
57 OXYGEN SATURATION AMONG CASES VS RDW 88 58 OXYGEN SATURATION AMONG CASES VS SERUM
SODIUM
89
59 OXYGEN SATURATION AMONG CASES VS SERUM POTASSIUM
90
60 COMPARISON BETWEEN COPD AND CONTROL GROUPS
91
61 CHARACTERISTICS OF THE STUDY POPULATION 92 62 CLINICAL FEATURES AT PRESENTATION 93 63 CORRELATION OF RDW WITH SEVERIT Y OF COPD 94 64 SERUM ELECTROLYTES IN COPD PATIENTS IN
VARIOUS STUDIES
96
65 CORRELATION BETWEEN SEVERITY OF COPD AND SERUM SODIUM AND SERUM POTASSIUM
96
LIST OF CHARTS
SL NO NAME OF CHARTS PAGE NO
1 AGE CATEGORY OF CASES 36
2 AGE CATEGORY OF CASES VS RDW 37
3 AGE CATEGORY OF CASES VS SERUM SODIUM 38 4 AGE CATEGORY OF CASES VS SERUM
POTASSIUM
39
5 GENDER OF CASES 40
6 GENDER OF CASES VS RDW 41
7 GENDER OF CASES VS SERUM SODIUM 42 8 GENDER OF CASES VS SERUM POTASSIUM 43
9 SMOKING OF CASES 44
10 CASES WITH FEVER 45
11 CASES WITH COUGH 46
12 CASES WITH CREPITATIONS 47
13 CASES WITH WHEEZING 48
14 CASES WITH CLUBBING 49
15 CASES WITH PEDAL EDEMA 50
16 X RAY FEATURE OF CASES 51
17 X RAY FEATURE OF CASES VS RDW 52
18 X RAY FEATURE OF CASES VS SERUM SODIUM 53 19 XRAY FEATURE OF CASES VS SERUM
POTASSIUM
54
20 HEMOGLOBIN STATUS AMONG CASES 55
21 HEMOGLOBIN STATUS AMONG CASES VS RDW 56 22 HEMOGLOBIN STATUS AMONG CASES VS SERUM
SODIUM
57
23 HEMOGLOBIN STATUS AMONG CASES VS SERUM POTASSIUM
58
24 FEV1 OF CASES 59
25 FEV1 OF CASES VS RDW 60
26 FEV1 OF CASES VS SERUM SODIUM 61 27 FEV1 OF CASES VS SERUM POTASSIUM 62
28 FEV1/FVC OF CASES 63
29 FEV1/FVC OF CASES VS RDW 64
30 FEV1/FVC OF CASES VS SERUM SODIUM 65 31 FEV1/FVC OF CASES VS SERUM POTASSIUM 66
32 BMI CATEGORY OF CASES 67
33 BMI CATEGORY OF CASES VS RDW 68
34 BMI CATEGORY OF CASES VS SERUM SODIUM 69 35 BMI CATEGORY OF CASES VS SERUM
POTASSIUM
70
36 SIX MINUTE WALK TEST AMONG CASES 71 37 SIX MINUTE WALK TEST AMONG CASES VS RDW 72 38 SIX MINUTE WALK TEST AMONG CASES VS
SERUM SODIUM
73
39 SIX MINUTE WALK TEST AMONG CASES VS SERUM POTASSIUM
74
40 MMRC AMONG CASES 75
41 MRC AMONG CASES VS RDW 76
42 MRC AMONG CASES VS SERUM SODIUM 77 43 MRC AMONG CASES VS SERUM POTASSIUM 78
44 BODE AMONG CASES 79
45 BODE AMONG CASES VS RDW 80
46 BODE AMONG CASES VS SERUM SODIUM 81 47 BODE AMONG CASES VS SERUM POTASSIUM 82
48 GOLD AMONG CASES 83
49 GOLD AMONG CASES VS RDW 84
50 GOLD AMONG CASES VS SERUM SODIUM 85 51 GOLD AMONG CASES VS SERUM POTASSIUM 86
52 OXYGEN SATURATION AMONG CASES 87
53 OXYGEN SATURATION AMONG CASES VS RDW 88 54 OXYGEN SATURATION AMONG CASES VS SERUM
SODIUM
89
55 OXYGEN SATURATION AMONG CASES VS SERUM POTASSIUM
90
LIST OF FIGURES
SL.NO NAME OF FIGURES PAGE.NO
1 RENE LAENNEC WITH STETHOSCOPE 3
2 HUTCHINSON AND HIS WATER SPIROMETER 4 3 DIFFERENT SEGMENTS OF RESPIRATORY
SYSTEM
6
4 BRONCHOPULMONARY SEGMENT 7
5 PULMONARY CIRCULATION 9
6 LUNGS LYMPHATIC SUPPLY 10
7 SPIROGRAM OF LUNG VOLUME CHANGES 10
8 TYPES OF COPD 13
9 PATHOGENESIS OF ALPHA 1 ANTITRYPSIN DEFICIENCY
17
10 PATHOGENESIS OF COPD 18
11 PATHOGENIC MECHANISM IN COPD 19
12 MODIFIED MRC DYSPNEA SCALE 20
13 MECHANISM OF COR PULMONALE 20
14 SYSTEMIC MANIFESTATIONS 21
15 CAUSES OF ACUTE EXACERBATION 22
16 SPIROMETRY 22
17 GOLD STAGING OF COPD 23
18 BODE INDEX 24
19 CHEST X RAY 24
20 SMOKING CESSATION AND FEV1 PREDICTION 26
21 TREATMENT OPTIONS IN COPD 28
22 CALCULATION OF RDW 29
1
INTRODUCTION
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of airways causing obstruction of air flow to lungs. It is a preventable and treatable condition. But it remains to be an important cause of morbidity and mortality worldwide.
The red cell distribution width (RDW) is commonly done in all patients as a part of complete blood count and it indicates the range of variation of RBC volume.
Commonly in clinical practice RDW is used in differentiating between different types of anemia. However recent studies have proved the emergence of RDW as strong predictor of poor survival in patients with established heart failure and coronary artery disease. RDW has also been recently proposed as a marker of immune activation correlating with levels of interleukin-6 and tumour necrosis factor alpha. This increased level of immune activation as seen is patients with raised RDW may be the common link between raised RDW and poor prognosis in COPD patients with acute exacerbation. Therefore, this study aims to study this association between severity of acute exacerbation of COPD and RDW levels.
Serum sodium and serum potassium are commonly deranged in patients with acute exacerbation of COPD. But their role as a prognostic factor in COPD patients is poorly studied. Due to lack of clear information about the factors affecting prognosis of COPD, poor prognosis is seen in patients with acute exacerbation of COPD.Therefore we also assessed the relationship between Serum electrolytes and various indices used to measure the severity of acute exacerbation of COPD.
2
OBJECTIVES OF THE STUDY
To study the relationship between Red cell distribution width and various indices to assess the severity of acute exacerbation of COPD.
To also study the serum sodium and potassium levels in patients with acute exacerbation of COPD and in their healthy controls.
3
REVIEW OF LITERATURE
HISTORY – COPD
Arteams (260 AD) described many pulmonary diseases in which
‘pneumodes’ might be same as emphysema,chronic bronchitis or bronchial asthma leading to congestive heart failure.
British born Charles Badham was the first one to describe chronic bronchitis and emphysema1.
Rene Laennec explained the correlation between emphysema with chronic bronchitis in mid 1800.
Figure no 1- Rene Laennec with stethoscope Invention of spirometer is by John Hutchinson in 1846.
Hutchinson’s instrument was able to measure only the vital capacity. 100 years from Hutchinson’s spirometer, Tiffeneau added the important parameter of timed vital capacity to lung function test.
4
Figure no 2- Hutchinson and his Water Spirometer
In 1959, at a gathering of prominent doctors named Ciba Guest, they proposed a definition of COPD.
T.T. Higgins had studied men between ages of 25 and 64 to understand the relationship between respiratory symptoms and smoking2.
In 1959 The Medical Research Council used the term “chronic bronchitis”
in their publications to define expectoration when others causes like tuberculosis and bronchiectasis have been ruled out, to patients who have coughed up sputum on most days during at least for 3 consecutive months in 2 successive years3.
In 1964-1973 Boushy and colleagues published papers on prognostic factors in COPD and the prognostic significance of Lung function tests in COPD4.
In 1977 Boushy SF et al. studied in 136 patients with COPD, the correlation between pulmonary function tests, arterial oxygen pressure and arterial carbon dioxide tension with hemodynamic parameters5.
5
ANATOMY
Respiratory system consists of
1. upper respiratory pathway and 2. lower respiratory pathway
UPPER RESPIRATORY PATHWAY
Components of upper respiratory pathway - nose, paranasal sinuses, pharynx, and larynx.
Upper respiratory pathways are used - 1. as a passage for the air to flow.
2. Filtration of air, protection of airways, phonation and coughing.
LOWER RESPIRATORY PATHWAY Trachea
Trachea is a 5-inch sized tube made mainly of hyaline cartilage arranged as C shaped rings and it begins from cricoid cartilage and is divided into two at the level of angle of louis and pseudo stratified ciliated columnar type of epithelium is seen6. It consists of around sixteen to twenty cartilaginous rings, which prevents collapse of the airways. Trachea divides at level of carina to form the 5cm long left side main bronchus and about 1 -3 cm long right-side bronchus.
The right bronchus is wider, shorter in length and more vertically placed and so
6
right lung is most commonly affected by aspiration7. Bronchi then divides into secondary and to tertiary bronchi. Tertiary bronchi again divides into multiple terminal bronchioles8.
The air passage is divided into 23 segments, the first 16th serve as passage for air and 16th to 23rd segments serves for the purpose of gaseous exchange.
Figure No:3- Different segments of Respiratory system
A Broncho pulmonary segments is a part of lungs which is supplied by an individual segmental bronchus. Right lung is formed by 10 bronchopulmonary segments, while left lung consists of 8 -9 lobes. Each Broncho pulmonary segment has its own blood supply from pulmonary and bronchial arteries9.
7
Figure No:4- Bronchopulmonary Segment
8
ALVEOLI
Alveoli are the respiratory unit of lungs.
Lungs consists of 600 million alveoli.
The epithelium of alveoli contains 2 different types of cells.
Type 1 cells – squamous epithelial cells, which covers the surface of majority of alveoli.
Type II cells- Pneumocytes, which secretes surfactant which reduce surface tension inside the alveoli
PULMONARY CIRCULATION
Blood from right atrium enters the right ventricle which is pumped into pulmonary artery which in turn reaches the pulmonary capillaries. In the pulmonary capillaries exchange of oxygen with carbon dioxide occurs. The oxygenated blood in turn is carried to the Left atrium and then to left ventricle and blood is pumped through major arteries for supply all over the body10.
Dual blood supply for lungs -
1. pulmonary arteries supply venous blood
2. Bronchial arteries which give oxygenated blood
9
Figure No: 5-Pulmonary Circulation LYMPHATIC SYSTEM
Lymphatic’s is divided into
1. SUPERFICIAL PLEXUS and 2. DEEP PLEXUS
● Visceral pleura is drained by Superficial plexus and peri -bronchial tissues by deep plexus.
● Lymphatic’s will initially flow towards hilum and then to the extrapulmonary lymph nodes, which is finally emptied into thoracic duct.
● Lymphatics are absent in alveoli11.
10
Figure No: 6- Lungs – lymphatic supply PHYSIOLOGY
Figure no: 7 – Spirogram of lung volume changes
11
Lung volumes
Various normal lung volumes are -
1) Tidal volume: The amount of air inspired in or expired out during quiet breathing (500-750 ml).
2) Residual volume: The volume of air remaining in lungs at the end of a maximal forceful expiration (1.3 litres).
3)Inspiratory reserve volume: Maximum air that can be inspired in at end of normal inspiration (2 litres).
4) Expiratory reserve volume: Maximum air that can be expired out after normal expiration (1 litre).
Lung Capacities
5) Vital capacity: Maximum amount of air that can be expelled after deep inspiration (3.5 litres).
6) Functional residual capacity: (RV+ ERV). The amount of air which is remaining in lungs at end of normal expiration (2.5 litres).
7)Inspiratory capacity: (IRV+ TV) It is the maximum amount of air that can be inspired after normal tidal expiration (2.5 litres).
8) Total lung capacity:(TV+IRV+ERV) It is amount of air in lungs after maximum inspiration (5 litres).
12
Spirometry is the most important test of airflow limitation in patients with COPD12. It enables differentiation between restrictive, obstructive and proximal airway disease.
1. FEV1 (Forced expiratory volume in one second): It is the volume exhaled at end of first second of forced expiration13,14. Decline in FEV1 has the most predictive value in COPD15,16. FEV1 starts decreasing with age at about 30 ml/year and this increases to 45 ml/year in smokers17.
2. FVC (Forced vital capacity): amount of air forcefully exhaled from lungs after maximum inspiration.
3. FEV1/FVC: It is a very important parameter in COPD. It is a ratio of FEV1 to FVC expressed as a percentage. A value below 70% is diagnostic of COPD18. CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
DEFINITION
The American Thoracic Society (ATS) defines COPD as a disease process involving progressive chronic airflow obstruction because of chronic bronchitis, emphysema or both19.
13
COPD is of two types, namely
1. CHRONIC BRONCHITIS
2. EMPHYSEMA.
Figure no: 8 – Types of COPD
• Bronchitis is defined as presence of chronic productive cough on most of the days for a minimum of 3 months/year for at least 2 years20.
• Can be present without significant airflow limitation.
• Emphysema is defined as abnormal permanent dilatation of distal air spaces, distal to terminal bronchioles, accompanied by destruction of alveolar walls and without obvious fibrosis.
• Always associated with significant airflow limitation.
14
CLASSIFICATION
A. TRUE EMPHYSEMA
1) Centriacinar-Focal destruction limited to respiratory bronchioles and central portion of acinus. Commonly seen in smokers. Most common in upper lobes.
2) Panacinar- Most severe form commonly involving the lower lungs. It involves the entire alveolus distal to terminal bronchiole.
3) Paraseptal – Distal acinus is commonly involved.
4) Irregular – any pattern of involvement may occur.
5) Mixed type
B. OVER INFLATION.
1) Compensatory over inflation:
In this condition one part of lungs may be destroyed while the other part may have compensatory increase in function and size. septal walls are usually preserved but distention of alveolar sac is seen.
2) Infantile lobar emphysema:
It is a type of obstructive over inflation seen in a neonate having congenital hypoplasia involving bronchial cartilage or in infants with respiratory distress.
15
3) Senile hyperinflation
In elderly population, the lungs become hyperinflated because of loss of elastic tissue in lungs as a result of ageing. It is also called as senile emphysema.
Cigarette smoking is most important correlate with COPD21, cigarette consists of many different types of free radicals, causing inflammatory changes, resulting in COPDs pathological and clinical features. Pipe and Cigar smokers have a high mortality and morbidity rates for COPD than non smokers22.British Thoracic Society guidelines suggest most patients with COPD have at least 20 pack years smoking history23.Obstruction of small airway is the earliest demonstrable defect in a smoker24.
CAUSES OF COPD
Environmental factors
• Tobacco smoke.
• Occupational exposures
• Low socioeconomic status
• Infections: adenovirus may cause disturbance of local inflammatory response;
• Smoking cannabis
16
Host factors
• Airway hyper-reactivity.
• Alpha 1 Anti proteinase deficiency (AT) is the only known genetic risk factor for developing COPD.
Risk factors for development of COPD include
• TOBACCO SMOKING. Smoking is the leading cause for COPD.Passive smoking is another important risk factor.
• OCCUPATIONAL EXPOSURE TO CHEMICALS AND DUSTS. The exposure to chemicals is another important risk factor of COPD.
• AGE. COPD develops progress gradually over age. So, People above 40 years are more prone to develop COPD
• ALPHA-1 ANTITRYPSIN DEFICIENCY
Alpha-1-antitrypsin is a polymorphic glycoprotein which responsible for majority of anti-protease activity by inhibiting neutrophil elastase, governed by gene on 14q32 chromosome. Both liver and lungs are affected in patients with alpha 1 anti-trypsin deficiency since the enzyme acts on both. Nearly 80 % had a family history with autosomal recessive inheritance.
17
Figure No: 9- Pathogenesis of alpha 1 antitrypsin deficiency
It predominantly affects lower lobes and causes panacinar emphysema.
PATHOGENESIS
Most of COPD patients have overlapping of features of both chronic bronchitis and emphysema. Tobacco smoke and air pollutants are related to etiology of both of these conditions. The major mechanism is the permanent destruction of walls of the alveoli, and is closely linked to reduction in level of the enzyme serum alpha-1-antitrypsin, commonly referred to as protease-antiprotease imbalance hypothesis25.
18
Figure No: 10- Pathogenesis of COPD
1) Inflammation
Chronic inflammation is the most important mechanism involved in pathogenesis of COPD.Macrophages and neutrophil in alveoli gets activated and release inflammatory mediators like tumour necrosis factor, IL-8 and other chemokines which in turn damages the lung structures.
2) Young patients tend to develop emphysema due to alpha 1 antitrypsin deficiency. Imbalance between proteinases and anti-proteinases could cause result in emphysema due to damage to walls of the alveoli
Smoking has a seminal role in perpetuating oxidant-antioxidant imbalance in pathogenesis of emphysema.
• Tobacco smoke contains abundant reactive oxygen species, which deplete the antioxidant mechanisms thereby inciting tissue damage.
19
• Activated neutrophils also adds to the pool of reactive oxygen radical.
• Smokers also has a functional alpha 1 antitrypsin deficiency even in patients without enzyme deficiency26.
Figure No: 11- Pathogenic mechanism in COPD
CLINICAL FEATURES OF COPD
The classical symptoms of COPD are breathlessness on exertion, accompanied by cough and wheeze. Most patients have a smoking history of at least 20 pack years.
Cough
Cough and sputum production usually precede the onset of cough. Usually the presenting symptom is cough. Hemoptysis is a rare complication of COPD.
Volume of sputum is generally less than 60 ml but amount increases as disease progresses.
20
Shortness of breath
Breathlessness causes most disability and is associated with loss of function over time. The appearance of breathlessness indicates moderate to severe impairment of pulmonary function17.dyspnea is graded using modified MRC dyspnea scale
Figure No: 12-Modified MRC Dyspnea Scale
Cor pulmonale is hypertrophy of right ventricle usually resulting from parenchymal diseases of lungs, but can also arise from disease of pulmonary vasculature, recurrent pulmonary thromboembolism or chronic hypoxia.
Figure No: 13-Mechanism of Cor-pulmonale
21
The systemic manifestations of COPD includes depression, weakness, ischemic heart disease, hypertension, congestive cardiac failure, obesity, bone diseases and diabetes.
Figure No: 14- Systemic Manifestations
COPD – ACUTE EXACERBATION:
Exacerbation of COPD is sudden worsening of symptoms including breathlessness, cough and variation in quantity and colour of sputum. They may be associated by fever, myalgia or sore throat. Economic analysis shows that more than 70% of COPD related health care expenditures are due to exacerbations. The approach of the patients with acute exacerbation includes an assessment of severity of illness, identification of precipitating factors and initiation of treatment.
22
Figure No 15- Causes of acute exacerbation
INVESTIGATIONS 1) Pulmonary function testing
Spirometry is the most robust test of airflow limitation in COPD patients. It enables differentiation between restrictive and obstructive lung disease. Severity of COPD is also assessed with help of spirometry.
23
Figure No 16 - Spirometry
The COPD is diagnosed when airflow limitation demonstrated by post bronchodilator values of FEV1/ FVC less than 70 and also FEV1 less than 80%.
FEV1 is the single most important parameter in assessment of severity of COPD26,27.
PROGNOSIS Spirometry–
Fig No: 17- GOLD staging of COPD
BODE index is a composite index which helps to know the prognosis of COPD patients. It calculates the 4-year survival rate of patients and its components include FEV1, body mass index, MMRC scale and six-minute walk test.
24
Fig No:18- BODE Index Chest X- ray
Chest x ray is the first investigation usually done in COPD patients.
Fig No: 19-Chest X Ray
The diagnosis of COPD can be made in chest X-Ray by features suggestive of hyperinflation including
1.low flattened diaphragm 2.hyper lucent lung fields
25
3.increased Antero-posterior diameter 4.increased Retrosternal air
5.Vertical heart 2) Blood count
A blood count is done to assess the haemoglobin levels and to rule out infections by looking at total blood count.
3) Alpha 1 -antiproteinase
The level of these enzymes are studied usually only in young patients.
4) ABG and pulse oximetry
Arterial blood gas analysis is essential in COPD patients to know the degree of hypoxemia and hypercapnia and in acute exacerbation to determine the hydrogen ion concentration.
Pulse oximetry is used to find out oxygen saturation in the patients and most important investigation in management of the patients.
Fussell KM et al used ambulatory oximetry monitoring to assess the need for long term oxygen therapy28.
5) High resolution CT chest
HRCT is now being used as a prime diagnostic tool in COPD patients. The advantage of using HRCT is that it can detect COPD before it can be detected through chest x rays.
26
MANAGEMENT OF COPD:
NON – PHARMACOLOGICAL METHODS:
CESSATION OF SMOKING: In patients with early COPD, smoking cessation improves lung function initially and declines the annual decline of FEV1.
Fig No:20- Smoking cessation and FEV1 prediction
OXYGEN THERAPY
Oxygen therapy is a life saving measure in COPD and improves quality of life in patients with severe COPD29.Supplemental oxygen should be given to patients with PaO2 less than 55 mmHg or an oxygen saturation of 88 % or lower.
Oxygen therapy also decreases in hospital admissions and length of hospital stay of COPD patients30.
27
Patients with COPD may develop substantial decrease in nocturnal PaO2 and Nocturnal oxygen therapy might be indicated in all severe COPD patients to combat against nocturnal hypoxia31.
PULMONARY REHABILITATION THERAPY
Pulmonary rehabilitation improves exercise tolerance32.it includes patient and family education, smoking cessation, physiotherapy, exercise and psychosocial support.
NON-INVASIVE VENTILATION
• Non-invasive ventilation will increase the inspiratory pressure helping in better gaseous exchange, mainly used in acute exacerbation
VACCINATION STRATEGIES
Vaccinations can prevent serious illness and death in mainly elderly COPD patients. Influenza and pneumococcal vaccines are the two vaccines commonly used.
SURGERIES 1) Bullectomy
2) Lung volume reduction surgery (LVRS)-indications include, symptoms secondary to severe emphysema, marked hyperinflation and CT evidence of heterogenous emphysema.
28
3) Lung transplantation is the new therapy for advanced lung disease.
PHARMACOLOGICAL MANAGEMENT
Fig No: 21- Treatment Options in COPD
Patients are initially treated with an inhaled bronchodilators like beta agonist, often along with an anti-cholinergic agent. These can be administered together or separately depending on the severity of the exacerbation. The addition of methyl xanthines like theophylline may be considered but serum levels should be closely monitored in view of its toxicity.
Patients with COPD are often colonized with pathogens and many practitioners use antibiotics in moderate to severe exacerbation, even without any demonstratable infection.
Glucocorticoids are used in acute exacerbation of COPD and it has been shown to shorten recovery time, shorten the duration of hospital stay and reduce the chance of hospital readmission by preventing further exacerbations.
29
RED CELL DISTRIBUTION WIDTH – RDW
Red cell distribution width is measurement of coefficient of variation of red cell volume. Marked anisocytosis is considered when RDW is increased. The normal values for RDW are as follows
• RDW – SD – 39-46 fL
• RDW – CV – 11.5-14.5%
RDW is an estimate of variation in volume within population of red cells, expressed as 1 SD of red cell volume measurement divided by MCV. Instrument manufactures use RDW using different algorithms, so that reference range varies according to analyser model.
RDW-CV is calculated as follows
• RDW-CV % = 1 standard deviation of RBC volume/MCV x 100%
Fig no 22: Calculation of RDW
30
RDW is used routinely for –
• Increase in RDW helps in early diagnosis of nutritional anemia such as iron, folic acid or vitamin b12 deficiency as in most instances RDW is the first parameter to get affected in anemia.
• It helps in differentiating between iron deficiency anemia and thalassemia.RDW is increased in iron deficiency anemia
• It also helps in differentiating megaloblastic anemia caused by vitamin B12 or folate deficiency by its association with increased RDW from other causes of macrocytosis.
Over the past decade, RDW has been associated with incipient myocardial infarction and heart failure in the general population has emerged as the one of the strongest predictor of poor survival in patients with established heart failure and coronary artery disease33.
RDW has also been proposed as marker of immune activation correlating with levels of tumour necrosis factor alpha and interleukin – 6. The process of dysregulated hematopoiesis and inflammation may be linked, since interleukin – 6 is important for production of hepcidin in liver and thus may indirectly regulate iron metabolism34,35.
RDW is also been linked with increased risk of atherosclerosis, poor prognosis in sepsis and as a poor prognostic factor in COPD.The same mechanism mentioned above is also considered the reason for these association36,37.
31
SERUM ELECTROLYTES AND COPD
COPD patients are susceptible to have low serum sodium levels due to variety of reasons. Inappropriate activation of renin –angiotensin system in COPD patients and also elevation of plasma arginin vasopressin [AVP] could result in hyponatremia [Bauer et al,1965]. Use of medications, reduced oral intake and undernutrition seen during periods acute exacerbation of COPD are main reasons for development of hyponatremia in those pateints38,39. Chronic hypoxia and hypercapnia as a result of primary lung pathology, cardiac or renal failure and SIADH may also contribute to hyponatremia in those patients.
Whatever may be the cause, hyponatremia itself is a predictor of poor prognosis in acute exacerbation of COPD patients40.It may lead to CNS dysfunction, cardiac conduction defects, secondary renal failure and even death41 [Suri et al;2009]. Therefore, hyponatremia should be ruled out in all patients with COPD for early intervention and better prognosis.
Along with Hyponatremia, hypokalemia is another important co-morbidity in patients with COPD.It may be attributed to respiratory acidosis, metabolic alkalosis, long duration steroid therapy or use of beta 2 adrenergic agonists42.similar to hyponatremia prognosis is poor in patients with hypokalemia which may be attributed to cardiac arrhythmias or poor nerve- muscle conduction seen in this patients. Early correction of serum electrolytes is thus warranted in COPD patients to prevent fatal outcomes and improve survival43,44.
32
MATERIALS AND METHODS
SOURCE OF STUDY:
Data consists of primary data collected by the principal investigator directly from the cases of COPD with acute exacerbations admitted in the medical ward in Coimbatore Medical College and Hospital.
DESIGN OF STUDY: Comparative Cross sectional study PERIOD OF STUDY:ONE YEAR
METHODOLOGY:
This is a comparative cross-sectional study of 100 cases managed for COPD with acute exacerbations in the medical ward of Coimbatore Medical College and Hospital and 30 age and sex matched healthy community controls.
Informed and written consent was obtained from all the subjects involved in the study. Detailed history and physical examination were done in all patients as indicated in proforma. All the investigations were done with due permission from the Institutional Ethical Committee.
Inclusion criteria
1) All patients above age 18 years & diagnosed cases of COPD presenting with acute exacerbations.
Exclusion criteria
1) Patients below 18.
33
2) Known causes of electrolyte imbalance other than those caused by Chronic obstructive pulmonary disease or its treatment like known cases of diabetic ketoacidosis, Renal failure, primary hyperaldosteronism or mineralocorticoid excess.
3) Known cases of anemia, hepatic dysfunction, thyroid diseases.
4) Consent not given.
STATISTICAL METHODS
All the datas that were obtained were entered in MS Excel and statistical analysis was done using SPSS Software. Numbers and percentages are used in reporting Categorical values. Mean and standard deviation are used while reporting Numerical values. Statistical analysis was done using ANOVA, chi-square test and unpaired T test. Statistical significance was considered if p value was less than 0.05.
INVESTIGATIONS
1.ROUTINE COMPLETE BLOOD COUNT
Total count, Differential count, Hemoglobin levels, Red cell distribution width.
2.BLOOD BIOCHEMISTRY Random blood sugar
Renal function tests
Serum Sodium and serum Potassium 3. PULMONARY FUNCTION TESTS 4. Chest X ray PA view
5. Sputum analysis (if needed).
34
RESULTS
Table-1: Age and gender distribution of study groups.
Sl.
No.
Cases (N=100) n (%)
Controls (N=30)
n (%) 1 Age category in years
29 – 50 28 (28) 7 (23.3)
51 – 70 53 (53) 17 (56.7)
71 – 81 19 (19) 6 (20)
2 Gender
Male 60 (60) 18(60)
Female 40 (40) 12(40)
The age and sex were similar in both cases and controls.
Table-2: Association of smoking with disease outcome
Smoking Cases (N=100) n (%)
Controls (N=30)
n (%)
p value#
No 48 (66.7) 24 (33.3) 0.002*
Yes 52 (89.7) 6 (10.3)
Note: # p value based on chi-square test, * statistically significant (p<0.05).
Smoking was predominantly present in cases compared to controls.
35
Table-3: Hb and RDW among study groups.
Variable
Cases (N=100) Mean (SD)
Controls (N=30) Mean (SD)
p value#
Hb in g % 13.9 (1.9) 12.8 (1.4) <0.001*
RDW (mEq/L) 14.5 (0.9) 12.6 (0.9) <0.001*
Note: # p value based on independent sample t test, * statistically significant (p<0.05) Both haemoglobin and RDW were on higher side in cases compared to controls and
was statistically SIGNIFICANT with Mean RDW in cases was 14.5+0.9 and mean Hemoglobin was 13.9+1.9.
Table-4: serum electrolytes among study groups
Variable
Cases (N=100) Mean (SD)
Controls (N=30) Mean (SD)
p value#
Sodium (mEq/L) 130.6 (5.2) 141.6 (4.3) <0.001*
Potassium (mEq/L) 3.4 (0.4) 4.3 (0.4) <0.001*
Note: # p value based on independent sample t test, * statistically significant (p<0.05) Serum electrolytes in cases vs control were statistically SIGNIFICANT. Mean sodium
in Cases were 130.6+5.2 and mean potassium was 3.4+0.4.
36
Table-5: Age category of cases (N=100) Age category in years n & %
29 – 50 28
51 – 70 53
71 – 81 19
Chart-1: Age category of cases (N=100)
In this study, most of the cases [53%] were in age group of 51-70.
28
53
19
0 10 20 30 40 50 60
29 – 50 51 – 70 71 – 81
37
Table-6: Age category of cases vs RDW (N=100)
Chart-2: Age category of cases vs RDW (N=100)
In this study, Age categorization vs RDW was STATISTICALLY SIGNIFICANT with Maximum mean of RDW of 15.4 seen in 71-81 age group and mean of RDW was least in 29-50 age group.
14
14.5
15.4
13 13.5 14 14.5 15 15.5 16
29 – 50 51 – 70 71 – 81
Age category in years
DW
Mean SD
29 – 50 14 0.6
51 – 70 14.5 0.8
71 – 81 15.4 0.9
p value = 0.001 Significant
ANOVA
38
Table-7: Age category of cases vs serum sodium (N=100)
Chart-3: Age category of cases vs serum sodium (N=100)
In this study, Age categorization vs Serum sodium was STATISTICALLY SIGNIFICANT with mean serum sodium was least [126.8] in 71-81 age group.
134
130
126.8
122 124 126 128 130 132 134 136
29 – 50 51 – 70 71 – 81
Age category in years
serum sodium
Mean SD
29 – 50 134 4.6
51 – 70 130 4.7
71 – 81 126.8 5.2
p value = 0.001 Significant
ANOVA
39
Table-8: Age category of cases vs serum potassium (N=100)
Chart-4: Age category of cases vs serum potassium (N=100)
In this study, Age categorization vs serum potassium was statistically significant with mean serum potassium was least [3.1] in 71-81 age group.
3.7
3.4
3.1
2.8 2.9 3 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8
29 – 50 51 – 70 71 – 81
Age category in years
serum potassium
Mean SD
29 – 50 3.7 0.4
51 – 70 3.4 0.3
71 – 81 3.1 0.3
p value = 0.001 Significant
ANOVA
40
Table-9: Gender of cases (N=100)
Sl. No. Gender n & %
1 Male 60
2 Female 40
Chart-5: Gender of cases (N=100)
In this study 60% were males and 40% were females. The male to female ratio was 3:2.
60 40
Male Female
41
Table-10: Gender of cases vs RDW (N=100)
Chart-6: Gender of cases vs RDW (N=100)
Statistical analysis of Gender of cases vs RDW was not significant.
14.6
14.5
14.44 14.46 14.48 14.5 14.52 14.54 14.56 14.58 14.6 14.62
Male Female
Gender RDW
Mean SD
Male 14.6 0.8
Female 14.5 1.0
p value = 0.52 Not significant Independent sample t test
42
Table-11: Gender of cases vs serum sodium (N=100)
Chart-7: Gender of cases vs serum sodium (N=100)
Statistical analysis of gender of cases vs serum sodium was not significant.
129.8
131.8
128.5 129 129.5 130 130.5 131 131.5 132
Male Female
Gender Sodium
Mean SD
Male 129.8 5.4
Female 131.8 4.5
p value = 0.07 Not significant Independent sample t test
43
Table-12: Gender of cases vs serum potassium (N=100)
Chart-8: Gender of cases vs serum potassium (N=100)
Statistical analysis of gender of cases vs serum potassium was not significant.
3.5
3.4
3.34 3.36 3.38 3.4 3.42 3.44 3.46 3.48 3.5 3.52
Male Female
Gender Potassium
Mean SD
Male 3.5 0.4
Female 3.4 0.4
p value = 0.82 Not significant Independent sample t test
44
Table-13: Smoking of cases (N=100) Sl. No. Smoking n & %
1 Yes 52
2 No 48
Chart-9: Smoking of cases (N=100)
In this study,52% of cases were smokers and 48% were non-smokers.
52
48 Yes
No
45
Table-14: Cases with fever (N=100)
Sl. No. Fever n & %
1 Yes 35
2 No 65
Chart - 10: Cases with fever (N=100)
In this study only 35% of cases had fever and fever was absent in most of the cases.
35
65
Yes No
46
Table-15: Cases with cough (N=100)
Sl. No. Cough n & %
1 Yes 100
2 No 0
Chart-11: Cases with cough (N=100)
In this study all patients [100%] had history of cough.
100
0 0
20 40 60 80 100 120
Yes No
47
Table-16: Cases with crepitations (N=100)
Sl. No. Crepitations n & %
1 Yes 40
2 No 60
Chart-12: Cases with crepitations (N=100)
In this study crepitations was present in 40% of the cases and was absent in 60% of the cases.
40
60
Yes No
48
Table-17: Cases with wheezing (N=100)
Sl. No. Wheezing n & %
1 Yes 84
2 No 16
Chart-13: Cases with wheezing (N=100)
In this study, wheezing was present in majority of patients constituting 84% and was absent in only small number of cases [16%]
84 16
Yes No
49
Table-18: Cases with clubbing (N=100) Sl. No. Clubbing n & %
1 Yes 33
2 No 67
Chart-14: Cases with clubbing (N=100)
In this study, clubbing was present in 33% of cases and was absent in 67% of cases.
33
67
Yes No
50
Table-19: Cases with pedal edema (N=100) Sl. No. pedal edema n & %
1 Yes 29
2 No 71
Chart-15: Cases with pedal edema (N=100)
In this study pedal edema was absent in majority of patients constituting 71% and was present in only 29 % of cases.
29
71
Yes No
51
Table-20: X-ray feature of cases (N=100) Sl. No. X-ray feature n & %
1 Emphysema & chronic bronchitis
24
2 Emphysema 40
3 Chronic bronchitis 28
4 Normal 8
Chart-16: X-ray feature of cases (N=100)
In this study, patients with chest x ray suggestive of emphysema was seen in most cases constituting 40%, bronchitis with emphysema in 24%, bronchitis in 28% and chest x ray was normal in 8% of patients.
0 5 10 15 20 25 30 35 40 45
Emphysema &
chronic bronchitis
Emphysema Chronic bronchitis Normal
52
Table-21: X-ray feature of cases vs RDW (N=100)
Chart-17: X-ray feature of cases vs RDW (N=100)
Statistical analysis of chest x ray vs RDW was SIGNIFICANT with patients having high RDW showing x ray changes of both emphysema and chronic bronchitis.
15.2
14.4 14.4
13.7
12.5 13 13.5 14 14.5 15 15.5
Emphysema &
chronic bronchitis
Emphysema Chronic bronchitis Normal
X-ray feature RDW
Mean SD
Emphysema & chronic bronchitis
15.2 0.9
Emphysema 14.4 0.8
Chronic bronchitis 14.4 0.7
Normal 13.7 0.7
p value =0.001 Significant
ANOVA
53
Table-22: X-ray feature of cases vs serum sodium (N=100)
Chart-18: X-ray feature of cases vs serum sodium (N=100)
Statistical analysis of chest x ray vs serum sodium was SIGNIFICANT with patients having least mean sodium of 128.1+3.9 showing x ray changes of both emphysema and chronic bronchitis and mean sodium was in normal range in patients with normal chest x-rays.
128.1
131.1 130.3
136.7
122 124 126 128 130 132 134 136 138
Emphysema &
chronic bronchitis
Emphysema Chronic bronchitis
Normal
X-ray feature Sodium
Mean SD
Emphysema & chronic bronchitis
128.1 3.9
Emphysema 131.1 4.7
Chronic bronchitis 130.3 5.5
Normal 136.7 4.6
p value =0.001 Significant
ANOVA
54
Table-23: X-ray feature of cases vs serum potassium (N=100)
Chart-19: X-ray feature of cases vs serum potassium (N=100)
Statistical analysis of chest x ray vs serum potassium was SIGNIFICANT with patients having least mean potassium of 3.2+0.3 having x ray changes of both chronic bronchitis and emphysema and mean potassium was normal in patients with normal chest x rays.
3.2
3.5 3.5
3.8
2.9 3 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9
Emphysema &
chronic bronchitis
Emphysema Chronic bronchitis Normal
X-ray feature Potassium
Mean SD
Emphysema & chronic bronchitis
3.2 0.3
Emphysema 3.5 0.5
Chronic bronchitis 3.5 0.4
Normal 3.8 0.4
p value =0.002 Significant
ANOVA
55
Table-24: Haemoglobin status among cases (N=100) Haemoglobin status n & %
< 12 12
12 – 15 68
> 15 20
Chart-20: Haemoglobin status among cases (N=100)
In this study,68% had haemoglobin in normal range between 12-15 g/dL followed by 20% had haemoglobin in the higher range above 15 g/dL and 12% had haemoglobin below 12 g/dL.
12
68
20
< 12 12 – 15 > 15
56
Table-25: Haemoglobin status among cases vs RDW (N=100)
Chart-21: Haemoglobin status among cases vs RDW (N=100)
Study of haemoglobin levels vs RDW was statistically SIGNIFICANT. Patients with haemoglobin more than 15 g/dL had RDW on higher side indicating factors other than anemia has contributed to the rise in RDW in the cases.
14.2 14.2
15.6
13.5 14 14.5 15 15.5 16
< 12 12 – 15 > 15
Haemoglobin status RDW
Mean SD
< 12 14.2 0.7
12 – 15 14.2 0.6
> 15 15.6 0.9
p value =0.001 Significant
ANOVA
57
Table-26: Haemoglobin status among cases vs serum sodium (N=100)
Chart-22: Haemoglobin status among cases vs serum sodium (N=100)
Study of haemoglobin vs serum sodium was statistically SIGNIFICANT. Severe hyponatremia was seen in patients with haemoglobin more than 15 g/dL probably indicating chronic hypoxia leading to polycythemia in these group of patients.
132.3
131.8
125.6
122 124 126 128 130 132 134
< 12 12 – 15 > 15
Haemoglobin status Sodium
Mean SD
< 12 132.3 3.7
12 – 15 131.8 4.9
> 15 125.6 3.9
p value =0.001 Significant
ANOVA
58
Table-27: Haemoglobin status among cases vs serum potassium (N=100)
Chart-23: Haemoglobin status among cases vs serum potassium (N=100)
Statistical analysis of haemoglobin vs serum potassium was SIGNIFICANT.
Hypokalemia was more commonly noted in cases with haemoglobin more than 15 g/dL again probably indicating chronic hypoxia leading to secondary polycythemia.
3.6
3.5
3.1
2.8 2.9 3 3.1 3.2 3.3 3.4 3.5 3.6 3.7
< 12 12 – 15 > 15
Haemoglobin status Potassium
Mean SD
< 12 3.6 0.5
12 – 15 3.5 0.4
> 15 3.1 0.3
p value =0.003 Significant
ANOVA
59
Table-28: FEV1 of cases (N=100)
Sl. No. FEV1 n & %
1 Mild 14
2 Moderate 16
3 Moderately severe 24
4 Severe 28
5 Very severe 18
Chart-24: FEV1 of cases (N=100)
Most of the patients in this study had severe airflow obstruction constituting 28%, followed by moderately severe in 24%, very severe in 18%, moderate in 16% and mild in 14 % of cases.
14
16
24
28
18
0 5 10 15 20 25 30
Mild Moderate Moderately severe
Severe Very severe
60
Table-29: FEV1 of cases vs RDW (N=100)
Chart-25: FEV1 of cases vs RDW (N=100)
In this study, Statistical analysis of FEV1 vs RDW was SIGNIFICATN with p value of 0.001 and FEV1 was 13.6+0.4 in Mild obstruction,13.8+0.3 in moderate obstruction,14.0+0.3 in moderately severe obstruction.RDW was on the higher side in patients with severe and very severe airflow obstruction at 14.8+0.4 in severe and 15.9+0.8 in very severe obstruction.
13.6 13.8 14
14.8
15.9
12 12.5 13 13.5 14 14.5 15 15.5 16 16.5
Mild Moderate Moderately severe
Severe Very severe
FEV1 RDW
Mean SD
Mild 13.6 0.4
Moderate 13.8 0.3
Moderately severe 14.0 0.3
Severe 14.8 0.4
Very severe 15.9 0.8
p value =0.001 Significant
ANOVA
61
Table-30: FEV1 of cases vs serum sodium (N=100)
Chart-26: FEV1 of cases vs serum sodium (N=100)
In this study, statistical analysis of FEV1 vs serum sodium was SIGNIFICANT, with hyponatremia of 126.9+3.1 and 126.2+4.1 noted in severe and very severe airflow obstruction.
136.6
135.4
131.6
126.9
126.2
120 122 124 126 128 130 132 134 136 138
Mild Moderate Moderately severe
Severe Very severe
FEV1 Sodium
Mean SD
Mild 136.6 4.1
Moderate 135.4 2.8
Moderately severe 131.6 2.5
Severe 126.9 3.1
Very severe 126.2 4.1
p value =0.001 Significant
ANOVA
62
Table-31: FEV1 of cases vs serum potassium (N=100)
Chart-27: FEV1 of cases vs serum potassium (N=100)
In this study, statistical analysis of FEV1 vs serum potassium was SIGNIFICANT, with hypokalemia of 3.4+0.04,3.2+0.007 and 3.1+0.04 noted in moderately severe, severe and very severe airflow obstruction.
3.9 3.8
3.4 3.2 3.1
0 0.5 1 1.5 2 2.5 3 3.5 4 4.5
Mild Moderate Moderately severe
Severe Very severe
FEV1 Potassium
Mean SD
Mild 3.9 0.09
Moderate 3.8 0.10
Moderately severe 3.4 0.04
Severe 3.2 0.07
Very severe 3.1 0.04
p value =0.001 Significant
ANOVA
63
Table-32: FEV1/FVC of cases (N=100) Sl. No. FEV1/FVC n & %
1 Mild 31
2 Moderate 22
3 Severe 47
Chart-28: FEV1/FVC of cases (N=100)
Most the cases in our study are in severe category constituting 47%, followed by mild constituting 31% and moderate constituting 22%.
31
22
47
0 5 10 15 20 25 30 35 40 45 50
Mild Moderate Severe
64
Table-33: FEV1/FVC of cases vs RDW (N=100)
Chart-29: FEV1/FVC of cases vs RDW (N=100)
Statistical analysis of FEV1/FVC vs RDW was SIGNIFICANT, with RDW on the higher side at 15.2+0.8 noted in cases with severe airflow limitation.
13.7
14.2
15.2
12.5 13 13.5 14 14.5 15 15.5
Mild Moderate Severe
FEV1/FVC RDW
Mean SD
Mild 13.7 0.3
Moderate 14.2 0.5
Severe 15.2 0.8
p value =0.001 Significant
ANOVA
