Chronic Obstructive Pulmonary Disease

By Abhinay Sharma Bhugoo Ml-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 Exacerbations Deterioration

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

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 permanent enlargement of the air spaces distal to the terminal bronchioles, without obvious fibrosis

emphysema

introduction

Obstructive Airway Disease

Asthma
Explosion in research

COPD
Little research (? neglect) Few advances in therapy

Revolution in therapy

 The Global Initiative for Chronic Obstructive Lung Disease (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

introduction

1 5

2 4

3 6

8 7
9 10

Venn diagram of chronic obstructive pulmonary disease (COPD).

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

Gross pathology of advanced emphysema. 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.

 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 I/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

Etiology II/II

 For assess an individuals risk of death or hospitalization History Multifactorial with

Individual lifestyle Socioeconomic factors Education / Knowledge

Prognosis

This phenomenon is called dynamic hyperinflation

Pathophysiological changes

COPD classification based on spirometry

GOLD 2003
Severity Postbronchodilator FEV1/FVC Postbronchodilator FEV1% predicted

At risk
Mild COPD

>0.7
<0.7

>80
>80

Moderate COPD
Severe COPD Very severe COPD

<0.7
<0.7 <0.7

50-80
30-50 <30

SPIROMETRY is not to substitute for clinical judgment in the evaluation of the severity of disease in individual patients.

Characteristic i/ii

Typically combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease.
Systemic manifestations
decreased fat-free mass impaired systemic muscle function Osteoporosis Anemia Depression pulmonary hypertension cor pulmonale left-sided heart failure

Cough worsening dyspnea progressive exercise intolerance sputum production alteration in mental status Productive cough or acute chest illness Breathlessness Wheezing

 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 nearly ruled out
Self-reported smoking Hx of > 55 pack-yrs Wheezing on auscultation Self-reported wheezing

Characteristic ii/ii

 Hyperinflation (barrel chest) Wheezing Frequently heard on forced and unforced expiration Diffusely decreased breath sounds Hyperresonance on percussion

Prolonged expiration phase

Physical Examination

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

characteristics allow differentiation

 Alpha1-Antitrypsin def Bronchitis Emphysema Nicotine Addiction

Pulmonary Embolism

Differentials diagnosis

 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 i/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

Investigation ii/ii

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 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).

 Acute exacerbation Stable COPD

Rx base on severity of disease

treatment

 Severity evaluate

Mild to moderate
Hemodynamic stable

bronchodilator

Acute exacerbation

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

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

Treatment

ACUTE EXACERBATION
treatment

Treatment
Acute exacerbation : 1-3 wk onset
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

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

Treatment

Medication Beta2agonist

type Short

Onset (min) 3-5

duration (hour) 4-6

Route Inhale Oral IV Inhale Oral Inhale Inhale Inhale Oral IV

drug Salbutamol(ventolin) Terbutaline Fenoterol Procaterol Salmeterol Formoterol Ipratopium bromide Tiotropium (Spiriva) Theophylline Aminophylline

8-12 Long Anticholinergic Short Long 30-45 10-15 5 > 12 6-8 >24

Methylxanthine

bronchodilator

Uncertained in sustained release

 Systemic corticosteroid

Acute exacerbation : 1-3 wk onset

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

Treatment

 Oxygen
All pt with SpO2 < 90% keep SpO2 9094%

Limited S/E of Oxygen supplement

Acute exacerbation : 1-3 wk onset

hypoxic drive hypoventilation ventilation / perfusion mismatch deadspace )

Haldane effect
rightward displacement of the CO2hemoglobin dissociation curve in the presence of increased oxygen saturation, increasing the amount of CO2 dissolved in blood

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

Acute exacerbation : 1-3 wk onset

C/I of NIV
Uncooperation Cardiovascular instability Life-threatening hypoxemia Severe acidosis : pH < 7.25

Treatment

 Mechanical ventilation
Indication of Invasive mechanical ventilation
Respiratory failure

Acute exacerbation : 1-3 wk onset

Severe acidosis : pH < 7.25 RR > 35/min Accessory muscle used

with
C/I for NIV Fail NIV

Treatment

STABLE COPD
treatment

Treatment
Stable COPD : base on severity
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

 Avoidance of risk factor(s)

Stable COPD : at ALL stage

Influenza vaccination Pneumococcal vaccination

Treatment

Management based on GOLD

Post-bronchodilator FEV1 (% predicted)

Medication Beta2agonist

type Short

Onset (min) 3-5

duration (hour) 4-6

Route Inhale Oral IV Inhale Oral Inhale Inhale Inhale Oral IV

drug Salbutamol(ventolin) Terbutaline Fenoterol Procaterol Salmeterol Formoterol Ipratopium bromide Tiotropium (Spiriva) Theophylline Aminophylline

8-12 Long Anticholinergic Short Long 30-45 10-15 5 > 12 6-8 >24

Methylxanthine

bronchodilator

Uncertained in sustained release

Pulmonary rehabilitation

Oxygen therapy via nasal cannula

Home supplemental oxygen

Oxygen therapy

Bilevel positive airway pressure (BiPAP)

Bronchodilator medications are central to the symptomatic

management of COPD GOLD Report 2003

Thank you