ChronicObstructive Pulmonary DiseaseBy Abhinay Sharma BhugooMl-610

Why COPD is Important ?• COPD is the only chronic disease that is showing

progressive upward trend in both mortality and morbidity

• It is expected to be the third leading cause of death by 2020

• Approximately 14 million Indians are currently suffering form COPD*

• Currently there are 94 million smokers in India• 10 lacs Indians die in a year due to smoking related

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

Disease Trajectory of a Patients with COPD

Symptoms

Exacerbations

Exacerbations

ExacerbationsDeterioration

End of Life

New Definition• Chronic obstructive pulmonary disease (COPD) is

a preventable and treatable disease state characterised by airflow limitation that is not fully reversible.

• The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, primarily caused by cigarette smoking.

• Although COPD affects the lungs, it also produces significant systemic consequences.

ATS/ERS 2004

introduction

COPD is a disorder in which subsets have dominant features of

chronic bronchitis chronic productive cough for 3 months 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 fibrosiswithout obvious fibrosis

Obstructive Airway Disease

Asthma

Explosion in

research

Revolution in

therapy

COPD

Little research

(? neglect)

Few advances in

therapy

introduction

• The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines (GOLD) guidelines define COPD as a disease state characterized by

• Airflow limitation that is not fully reversiblenot fully reversible, is usually progressive, and

• Associated with an abnormal inflammatory response of the lungs to inhaled noxious particles or gases

Venn diagram Venn diagram of chronic obstructive pulmonary disease (COPD).

1 21

3 45

6 78

9 10

Histopathology of chronic bronchitis showing hyperplasia of mucous glands hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells

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

At high magnification, loss of alveolar walls and dilatation of airspaces in emphysema can be seen.

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 for

smokers

• Intravenous drug use• Pulmonary vascular damage

• Insoluble filler (eg, cornstarch, cotton fibers, cellulose, talc) contained in methadone or methylphenidate

• Cocaine or heroin

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

Prognosis

• For assess an individual’s risk of death risk of death or hospitalizationhospitalization

• History

• Multifactorial with • Individual lifestyle

• Socioeconomic factors

• Education / Knowledge

Pathophysiological changes

This phenomenon is called dynamic hyperinflation

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 Postbronchodilator FEV1/FVC

Postbronchodilator FEV1% predicted

At risk >0.7 >80

Mild COPD <0.7 >80

Moderate COPD

<0.7 50-80

Severe COPD <0.7 30-50

Very severe COPD

<0.7 <30

Characteristic i/ii

• Cough

• worsening dyspnea

• progressive exercise intolerance

• 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 combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease.

Characteristic ii/ii

• Hx of more than 40 pack-yrs of smoking was the best best single predictor single predictor of airflow obstruction

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

• Wheezing on auscultation

• Self-reported wheezing

Physical Examination

• Hyperinflation (barrel chest)

• Wheezing – Frequently heard on forced and unforced expiration

• Diffusely decreased breath sounds

• Hyperresonance on percussion

• Prolonged expiration phase

characteristics allow differentiation

Chronic bronchitis(blue bloaters)

• obese• Frequent cough and

expectoration• Use of accessory muscles of

respiration 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

Differentials diagnosis

• Alpha1-Antitrypsin def

• Bronchitis

• Emphysema

• Nicotine Addiction

• Pulmonary Embolism

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

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

COPD: Hyperinflation, depressed diaphragm, increased retrosternal space, and hypovascularity of lung parenchyma are demonstrated.

Emphysema : increased AP diameter, increased retrosternal airspace, and flattened diaphragm on lateral chest radiograph.

A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragm on posteroanterior chest radiograph

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

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

treatment

• Acute exacerbation

• Stable COPD• Rx base on severity of disease

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 Acute exacerbationexacerbation

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

ACUTE EXACERBATION

treatment

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, Morexella

catarrhalis, Klebsiella pneumoniae ; Pseudomonas aeruginosa

• Machanical ventilation• Non-invasive positive pressure ventilation: NIPPV

• Invasive mechanical ventilation

Acute exacerbation : 1-3 wk onset

Treatment

• Short acting Beta2-agonist is first line but recommended combine of SABA and Anticholinergic for limited 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

bronchodilator

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

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

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

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

STABLE COPD

treatment

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

Treatment

• Avoidance of risk factor(s)

• Influenza vaccination

• Pneumococcal vaccination

Stable COPD : at ALL stage

Post-bronchodilator

FEV1(% predicted)

Management based on GOLD

bronchodilator

Pulmonary rehabilitation

Oxygen therapy

Oxygen therapy via nasal cannulaHome supplemental oxygen

Bilevel positive airway pressure (BiPAP)

“Bronchodilator medications are central to the symptomatic management of COPD”

GOLD Report 2003

Thank you