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8/2/2019 Copd Abhinay

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Chronic

ObstructivePulmonary DiseaseBy Abhinay Sharma Bhugoo

Ml-610


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Why COPD is Important ?

COPD is the only chronic disease that is showingprogressive upward trend in both mortality andmorbidity

It is expected to be the third leading cause of death by2020

Approximately 14 million Indians are currently sufferingform COPD*

Currently there are 94 million smokers in India

10 lacs Indians die in a year due to smoking relateddiseases

*The Indian J Chest Dis & Allied Sciences 2001; 43:139-47


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Disease Trajectory of a

Patients with COPD

Symptoms

Exacerbations

Exacerbations

ExacerbationsDeterioration

End of Life


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New Definition Chronic obstructive pulmonary disease (COPD) is

a preventable and treatable disease statecharacterised by airflow limitation that is not fullyreversible.

The airflow limitation is usually progressive and isassociated with an abnormal inflammatoryresponse of the lungs to noxious particles orgases, primarily caused by cigarette smoking.

Although COPD affects the lungs, it also producessignificant systemic consequences.

ATS/ERS 2004


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introduction

COPD is a disorder in which subsets have dominant features of

chronic bronchitis

chronic productive cough for 3 months during each of 2 consecutive

years

emphysema permanent enlargement of the air spaces distal to the terminal

bronchioles, without obvious fibrosis


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Obstructive Airway Disease

Asthma

Explosion in

research

Revolution in

therapy

COPD

Little research

(? neglect)

Few advances in

therapy


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introduction

The Global Initiative for Chronic Obstructive LungDisease (GOLD) guidelines define COPD as a disease

state characterized by

Airflow limitation that is not fully reversible, is usually

progressive, and Associated with an abnormal inflammatory response of the lungs

to inhaled noxious particles or gases


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Venn diagram of chronic obstructive pulmonary disease (COPD).

1 213 45

6 789 10


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Histopathology ofchronic bronchitis showing hyperplasia of mucous glands andinfiltration of the airway wall with inflammatory cells


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Gross pathology ofadvanced emphysema. Large bullae are present on the surface of

the lung.


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At high magnification, loss of alveolar walls and dilatation of airspaces in emphysema

can be seen.


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Etiology I/II

Cigarette smoking- 90%

Environmental factors Biomass fuels with indoor cooking and heating

Traffic-related air pollution

Airway hyperresponsiveness

Alpha1-antitrypsin deficiency Panacinar emphysema

Premature emphysema at an average age of 53 years for nonsmokers and 40 years forsmokers

Intravenous drug use Pulmonary vascular damage

Insoluble filler (eg, cornstarch, cotton fibers, cellulose, talc) contained in methadone ormethylphenidate

Cocaine or heroin


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Etiology II/II

Immunodeficiency syndromes

Independent risk

Vasculitis syndrome Hypocomplementemic vasculitis urticaria syndrome (HVUS)

Connective tissue disorders

Cutis laxa is a disorder of elastin , various forms of inheritance

Marfan syndrome is an autosomal dominant inherited disease of type I

collagen

Ehlers-Danlos syndrome

Salla disease

Autosomal recessive storage disorder , sialic acid


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Prognosis

For assess an individuals risk of death or hospitalization

History

Multifactorial with

Individual lifestyle

Socioeconomic factors Education / Knowledge


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Pathophysiological changes

This phenomenon is called dynamichyperinflation


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COPD classification based on spirometry

GOLD 2003

SPIROMETRY is not to substitute for clinical judgment in the

evaluation of the severity of disease in individual patients.

Severity PostbronchodilatorFEV1/FVC

PostbronchodilatorFEV1% predicted

At risk >0.7 >80

Mild COPD 80

Moderate COPD


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Characteristic i/ii

Cough

worsening dyspnea

progressive exerciseintolerance

sputum production

alteration in mental status

Productive cough or acute

chest illness

Breathlessness

Wheezing

Systemic manifestations

decreased fat-free mass

impaired systemic muscle

function

Osteoporosis

Anemia

Depression

pulmonary hypertension

cor pulmonale

left-sided heart failure

Typically combination of signs and symptoms of

chronic bronchitis, emphysema, and reactive airwaydisease.


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Characteristic ii/ii

Hx of more than 40 pack-yrs of smoking was the best

single predictor of airflow obstruction

If all 3 signs are absent, airflow obstruction can be nearlyruled out Self-reported smoking Hx of > 55 pack-yrs

Wheezing on auscultation

Self-reported wheezing


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Physical Examination

Hyperinflation (barrel chest)

WheezingFrequently heard on forced and unforcedexpiration

Diffusely decreased breath sounds

Hyperresonance on percussion

Prolonged expiration phase


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characteristics allowdifferentiation

Chronic bronchitis(bluebloaters) obese

Frequent cough andexpectoration

Use of accessory muscles ofrespiration is common

Coarse rhonchi and wheezing

may be heard on auscultation signs of right heart failure

Cor pulmonale

edema and cyanosis

Emphysema(pink puffers)

thin with a barrel chest little or no cough

Breathing may be assisted by

pursed lips

patients may adopt the tripod

sitting position hyperresonant, and wheezing

may be heard

Distant Heart sounds


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Differentials diagnosis

Alpha1-Antitrypsin def

Bronchitis

Emphysema

Nicotine Addiction

Pulmonary Embolism


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Investigation i/ii

Pulmonary Function Tests

For diagnosis

Assessment of severity

Following its progress

ABG

Hypoxemia / hypercapnia

Acidosis

Serum Chemistries

Retain sodium /Lower potassium levels /bicarbonate

Chronic respiratory acidosis leads to compensatory metabolic alkalosis


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Investigation ii/ii

CBC Secondary polycythemia

Hct>52% in men or 47% in women

Alpha1-Antitrypsin all patients < 40 yrs or Fm Hx of emphysema at early age

Sputum Evaluation Streptococcus pneumoniae

Haemophilus influenzae

Moraxella catarrhalis

Pseudomonas aeruginosa

Chest Radiography +/- CT scan


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COPD: Hyperinflation, depressed diaphragm, increased retrosternal space, and

hypovascularity of lung parenchyma are demonstrated.


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Emphysema : increased AP diameter, increased retrosternal airspace, and flattened

diaphragm on lateral chest radiograph.


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A lung with emphysema shows increased anteroposterior (AP) diameter, increased

retrosternal airspace, and flattened diaphragm on posteroanterior chest radiograph


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A computed tomography (CT) scan shows hyperlucency due to diffusehypovascularity and bullae formation, predominantly in the upper lobes.


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Severe bullous disease as seen on a computed tomography (CT) scan in a patient withchronic obstructive pulmonary disease (COPD).


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treatment

Acute exacerbation

Stable COPD Rx base on severity of disease


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Treatment

Severity evaluate

Mild to moderate Hemodynamic stable

bronchodilator Pred 30-40 mg/dy for 7dy

Moderate to severe

Risk for respiratory failure

Accessory muscle used:paradoxical chest/abd motion

SpO2 < 90% or PaO2 < 60 mmHg

PaCO2 > 45 mmHg or pH < 7.35

Acute

exacerbation


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Treatment

Indication for admit

Severe exarcerbation

Severe stage of COPD New onset of : cyanosis, peripheral

edema

Unimprove after appropriated Tx

Multi-Comorbit : CAD, DM, HT

New onset Arrhythmia

Undefinite Diagnosis

Old age or Homeless


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ACUTE EXACERBATION

treatment


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Treatment

Bronchodilator

Beta2-agonist

Anticholinergic

Methylxantine

Corticosteroid

Systemic corticosteroids

Oxygen

All pt with SpO2 < 90% keep SpO2 90-94%

Antibiotic

Cover Streptococcus pneumoniae, Hemophilus influenza, Morexellacatarrhalis, Klebsiella pneumoniae ; Pseudomonas aeruginosa

Machanical ventilation

Non-invasive positive pressure ventilation: NIPPV

Invasive mechanical ventilation

Acute exacerbation : 1-3 wk onset


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Treatment

Short acting Beta2-agonist is first

line but recommended combine

of SABA and Anticholinergic forlimited S/E (palpitation,

tachycardia, tremor)

Fenoterol/Ipratropium bromide

Every 15-20 min in 1st hour then 4-6

hr interval

Addition SABA every 1-2 hr

Acute exacerbation

: 1-3 wk onset


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bronchodilator

Medication type Onset (min) duration(hour) Route drug

Beta2agonist Short 3-5 4-6 InhaleOral

IVSalbutamol(ventolin)

Terbutaline

Fenoterol

8-12 InhaleOral

Procaterol

Long 30-45 > 12 Inhale SalmeterolFormoterol

Anticholinergic Short 10-15 6-8Inhale

Ipratopium bromideLong 5 >24 Inhale Tiotropium (Spiriva)

Methylxanthine Uncertained in sustained release OralIV TheophyllineAminophylline


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Treatment

Systemic corticosteroid

Limited systemic inflammation and airway

inflammation

Decrease sputum eosinophil

Decrease serum CRP

Improve FEV1 and PaO2

Minimize treatment failure / Length of stay in Hospital/Exacerbation

No improve of mortality

Prednisoline 30-40 mg/dy for 7-14 dy or

Dexamethasone 5- 10 mg q 6 hr or Hydrocortisone 100-200 mg q 6 hr

Acute exacerbation : 1-3 wk onset


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Treatment

Oxygen

All pt with SpO2 < 90% keep SpO2 90-

94%

Limited S/E of Oxygen supplement

hypoxic drive hypoventilation

ventilation / perfusion mismatch

deadspace ) Haldane effect

rightward displacement of the CO2-

hemoglobin dissociation curve in the presence

of increased oxygen saturation, increasing the

amount of CO2 dissolved in blood

Acute exacerbation

: 1-3 wk onset


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Treatment

Machanical ventilation

Indication of NIV

accessory muscle with abd paradox

Acidosis pH 7.25-7.35 and/or PaCO2 > 45

mmHg

RR > 24 / min

C/I of NIV

Uncooperation

Cardiovascular instability

Life-threatening hypoxemia

Severe acidosis : pH < 7.25

Acute exacerbation

: 1-3 wk onset


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Treatment

Mechanical ventilation

Indication of Invasive mechanical

ventilation Respiratory failure

Severe acidosis : pH < 7.25

RR > 35/min

Accessory muscle used

with C/I for NIV

Fail NIV

Acute exacerbation

: 1-3 wk onset


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STABLE COPD

treatment


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Treatment

Bronchodilator

Beta2-agonist

Anticholinergic

Methylxantine

Corticosteroid

inhaled corticosteroids

Vaccination

Annual influenza vaccine

Pneumococcal vaccination

Pulmonary rehabilitation Improve quality of life

Oxygen therapy

Short term

Long term

surgery

Stable COPD : base on severity


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Treatment

Avoidance of risk factor(s)

Influenza vaccination

Pneumococcal vaccination

Stable COPD : atALL stage

Management based on GOLD


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Post-bronchodilator

FEV1

(% predicted)

Management based on GOLD


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bronchodilator

Medication type Onset (min) duration(hour) Route drug

Beta2agonist Short 3-5 4-6 InhaleOral

IVSalbutamol(ventolin)

Terbutaline

Fenoterol

8-12 InhaleOral

Procaterol

Long 30-45 > 12 Inhale SalmeterolFormoterol

Anticholinergic Short 10-15 6-8 Inhale Ipratopium bromideLong 5 >24 Inhale Tiotropium (Spiriva)

Methylxanthine Uncertained in sustained release OralIV TheophyllineAminophylline


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Pulmonary rehabilitation


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Oxygen therapy

Oxygen therapy via nasal cannula Home supplemental oxygen


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Bilevel positive airway pressure (BiPAP)


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Bronchodilator medications are central to the symptomatic

management of COPD

GOLD Report 2003


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Thank you

copd abhinay

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