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Management of COPD The GOLD Perspective

Dr Mohammed Tarek Alam


Assistant Professor Department of Medicine

Introduction
Cigarette smoking is the primary cause of COPD.

The WHO estimates 1.1 billion smoker


worldwide, increasing to 1.6 billion by 2025 in low & middle-income countries.

In 2000,the WHO estimated 2.74 million deaths worldwide from COPD.

In 1990 ,COPD was ranked 12th as burden of disease, by 2020 it is projected to rank 5th

COPD is the only chronic disease that is showing progressive upward trend in both mortality and morbidity

Despite this burden, COPD is a Cinderella condition that receives limited recognition from both patients and physicians

Respiratory Medicine 2002; 96: S1-S31

GOLD
Global Initiative For Chronic Obstructive Lungs Diseases
Formed by WHO & US National Heart, Lung & Blood (NHLB) Institute.

GOLD formed
to standardize recommendations for diagnosis and management of COPD worldwide

GOLD
Increase awareness of COPD

Improve diagnosis, management, and prevention


Stimulate research

GOLD definition of COPD


Preventable and treatable disease with some significant extra pulmonary effects that may contribute to the severity in individual patients The pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases
This definition does not use the terms chronic bronchitis and emphysema and excludes asthma (reversible airflow limitation)

Definition. contd
Chronic bronchitis , defined as the presence of cough and sputum production for at least 3 months in each of 2 consecutive years, is not necessarily associated with airflow limitation. Emphysema, defined as destruction of the alveoli, is a pathological term that is sometimes (incorrectly) used clinically and describes only one of several structural abnormalities present in patients with COPD

Symptoms of COPD
Cough Sputum production Dyspnea on exertion

Episodes of acute worsening of these symptoms often occur

Chronic cough and sputum production often precede the development of airflow limitation by many years, although not all individuals with cough and sputum production go on to develop COPD

What Causes COPD?


Genetic Infection
Factors affecting lung growth

Risk is related to the total burden of inhaled particles a person encounters over his lifetime

A Toxic Cocktail

ASTHMA
Allergens

COPD
Cigarette smoke

Ep cells

Mast cell

Alv macrophage Ep cells

CD4+ cell (Th2)

Eosinophil

CD8+ cell (Tc1)

Neutrophil

Bronchoconstriction AHR

Small airway narrowing Alveolar destruction

Airflow Limitation Reversible Irreversible

Cigarette smoke Biomass particles Particulates

The True History


Host factors Amplifying mechanisms

LUNG INFLAMMATION

Anti-oxidants
Oxidative stress

Anti-proteinases

Proteinases

Repair mechanisms

COPD PATHOLOGY

Important inflammatory cells


Macrophages

T Lymphocyte CD8
Neutrophils

Eosinophils

Pathologic difference between Asthma and COPD

Asthma
Sensitizing agent (mite, dust, Pollen)

COPD
Noxious agent (Smoking)

Asthmatic Airway Inflammation CD4 T Lymphocyte, eosinophil Reversible airflow limitation

COPD Airway Inflammation CD8 T Lymphocyte Macrophage Neutrophil

Irreversible airflow limitation

Pulmonary and Systemic features of COPD


Enlargement of mucus secreting glands / increase in number of goblet cells / inflammatory cell infiltrate - increased sputum Loss of elastic tissue , inflammation and fibrosis in airway wall premature airway closure, gas trapping and dynamic hyperinflation changes in pulmonary and chest wall compliance Pulmonary vascular remodeling and impaired cardiac performance Unopposed action of proteases and oxidants leading to destruction of alveoli and appearance of emphysema

Dyspnea that is:

Diagnosing COPD
Consider COPD, and perform spirometry, if any of these indicators are present in a person over age 40.

Progressive (worsens over time) Usually worse with exercise Persistent (present every day) Described by the patient as an increased effort to breathe, heaviness, air hunger, or gasping.

Chronic Cough:
may be intermittent and may be unproductive

Chronic sputum production:


Any pattern of sputum production

History of exposure to risk factors:


Tobacco smoke Occupational dusts and chemicals Smoke from home cooking and heating fuel

Spirometry
When performing spirometry, measure:
Forced Vital Capacity (FVC), Forced Expiratoory Volume in one second (FEV1) Calculate the FEV1/FVC ratio. Spirometric results are expressed as % predicted using appropriate normal values for the persons sex, age, and height Patients with COPD typically show a decrease in bothFEV1 and FEV1/FVC ratio. Post bronchodilator FEV1 is recommended for the diagnosis and assessment of severity of COPD

COPD classification based on spirometry


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.

Physical signs

Large barrel shaped chest (hyperinflation) Prominent accessory respiratory muscles in neck and use of accessory muscle in respiration Low, flat diaphragm Diminished breath sound

Algorithm for Diagnosis at Primary Care


Pt reporting with respiratory symptoms Assess by -Detailed history -H/o exposure to risk factors -Physical examination Sputum for AFB +ve Treat as TB -ve Provisional Diagnosis of COPD Treat as COPD if suggestive

Spirometry

National Guidelines for Management of COPD at Primary Care Level

Differential diagnosis
Asthma early onset, symptoms vary, family history, allergy, rhinitis, eczema may be present Congestive heart failure
basilar creps, CxR shows dilated heart, pulmonary edema

Bronchiectasis
Large volumes of sputum Clubbing

Tuberculosis
Any age Abnormal CxR
High local prevalence

Obliterative bronchiolitis
Younger age, nonsmoker May have history of RA, fume exposure CT on expiration shows hypodense areas

Diffuse panbronchiolitis
Male and non smokers Almost all have chronic sinusitis CT and chest x-ray shows diffuse small centrilobluar nodular opacities and hyperinflation

Relieve symptoms Prevent progression of disease Improve exercise tolerance Improve health status Prevent and treat complications Prevent and treat exacerbations Reduce mortality Prevent or minimize side effects from treatment Cessation of cigarette smoking should be included as a goal throughout the management program

The goals of COPD management include

GOLD Workshop Report

Four Components of COPD Management


1. Assess and monitor disease
2. Reduce risk factors

3. Manage stable COPD


Education Pharmacologic

Non-pharmacologic

4. Manage exacerbations

1. Assess and Monitor Disease


Detailed medical history
Risk factors, past medical history, family history Pattern of symptom development History of exacerbations and hospitalization Presence of comorbidities Impact of disease Social and family support Possibilities for reducing risk factors Spirometry, chest x-ray, ABG, alpha-1 anti trypsin

COPD is usually a progressive disease. Lung function can be expected to worsen over time, even with the best available care. Symptoms and lung function should be monitored to follow the development of complications, to guide treatment, and to facilitate discussion of management options with the patient. Comorbidities are common and should be actively identified

2. Reduce Risk Factors


Smoking cessation is the single most effective and cost effective intervention to reduce the risk of developing COPD The 5 As
Ask about smoking at every visit Advise to quit strongly Assess willingness to quit Assist the patient in quitting Arrange follow up contact

3.Manage Stable COPD


Management should be guided by the following general principles:
Determine disease severity Implement a stepwise treatment plan Choose treatment according to national and cultural preferences

Patient education Pharmacologic treatment


Brochodilators short and long acting beta agonists and anti cholinergics Inhaled glucocorticoids Oral glucocorticoids Vaccines influenza yearly and pneumococcal every 5 years Antibiotics Mucolytics Antitussives

Non pharmacologic treatment


Rehabilitation Oxygen therapy long term administration of oxygen (>15 hours/day) in patients with chronic respiratory failure increases survival and has a beneficial impact on pulmonary hemodynamics, hematologic characteristics, exercise capacity, lung mechanics, and mental state

Initiate oxygen in patients with stage IV: very severe COPD if:
PaO2 is at or below7.3 kPa (55 mm hg) or Sao2 is at or below 88%, with or without hypercapnia or PO2 is between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg) or SaO2 is 88%, and if there is evidence of pulmonary hypertension, peripheral edema suggesting CHF, or polycythaemia (HCT >55%)

Surgical treatment
Bullectomy Lung Volume reduction surgery (LVRS)

4. Manage Exacerbations
Acute Exacerbation:
Acute exacerbation of COPD is defined as an event in the natural course of disease characterized by a change in the patients baseline dyspnoea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset and may warrant a change in regular medication in a patient with underlying COPD.

Common causes of exacerbation


Infection Air pollution

Unknown (1/3rd cases)

Diagnosis & assessment of severity


Clinical
1. Symptoms 2. Physical signs

Laboratory Parameters
1. 2. 3. 4. 5. Spirometry ABG CXR ECG Others

Clinical Parameters
Symptoms
Increase in
1. 2. 3. 4. 5. 6. Breathlessness Chest tightness Wheeze Cough & sputum with change of color Fever Other nonspecific symptoms

Clinical Parameters
Physical signs
1. 2. 3. 4. 5. 6. 7.

contd..

Signs of hyperinflation of lung Signs of Respiratory failure Signs of infection Signs of cor-pulmonale Paradoxical chest wall movements Haemodinamically instability Reduced alertness

Laboratory Parameters
Spirometry

PEFR < 100 L /min. or FEV1 < 1.00 L -- indicates a severe exacerbation
ABG

PaO2 < 60 mm of Hg and/or SaO2 < 90% when breathing in room air -indicates respiratory failure PaO2 < 50 mm of Hg, PaCO2 > 70 mm of Hg & PH < 7.3 --indicates a life threatening attack

Laboratory Parameters
CXR (P/A & Lateral)
-- to exclude other causes of dyspnoea

contd..

ECG
-- to exclude RVH, arrhythmia, IHD, pulmonary embolism

Spiral CT scan

Management
Home management
Hospital management
a) Management in emergency dept. b) Management in ICU

Antibiotics Bronchodilators Corticosteroids

Management (ABC Approach)

Home Management
Bronchodilator therapy
a) Increase dose & frequency b) Addition of anti-cholinergics c) Theophylline

Oral Glucocorticoids
40 mg prednisolone for 10 days

Home Management Contd


Antibiotics
specially sensitive to S. pneumoniae, H. influenzae & M. Catarrhalis Some common antibiotics used in COPD exacerbations Co-Amoxiclav Quinolone derivatives 2nd & 3rd generation cephalosporin

Antibiotic treatment
Oral Treatment Alternative treatment Parenteral treatment
Group-A: Patients not No antibiotic for only Co-amoxiclav; needing hospitalization one cardinal Macrolides; (mild COPD) symptom. If indicated Cephalosporins than beta-lactum, tetracycline, trimethprim/ sulfamethoxaole Group-B: Patients admitted to hospital (moderate to severe COPD without risk of P. aeruginosa) Co-amoxiclav Fluoroquinolones Co-amoxiclav; Cephalosporins; Fluoroquinolones

Group-C: Patients admitted to hospital (moderate to severe COPD with risk of P. aeruginosa)

Fluoroquinolone

Fluoroquinolone; Beta lactum with P. aeruginosa activity

Hospital Management
Indications for Hospital admission Marked increase in intensity of symptoms specially resting
dyspnea Failure to respond to initial home management Onset of new physical signs, e.g. Cyanosis, Peripheral edema Significant co-morbidities Insufficient home support Newly occurring arrhythmias

Management in emergency room


Assess severity by clinical & lab. parameters
Oxygen

therapy repeat ABG after 30 min. Bronchodilations : a) Increase dose & frequency b) Add anticholinergics c) Intravenous methyl xanthines Add Glucocorticoids IV/ oral Antibiotics IV/ oral NIPPV Monitor fluid balance & nutrition Treat associated conditions, e.g.. heart failure / arrhythmias Closely monitor condition of the patient

Hospital Management

contd..

Indications for ICU admission


Severe dyspnea that responds inadequately to initial emergency therapy Confusion, lethargy, coma Persistent or worsening hypoxemia
PaO2 < 50 mm & /PaCO2 > 70 mm of Hg PH < 7.3 despite supplemental O2

Management in ICU
Previous management of emergency
Room + Ventilatory support
a) Non-invasive (NIPPV) b) Invasive mechanical ventilation

Management in ICU
Selection criteria for NIPPV
(at least 2 should be present)

contd..

a) Moderate to severe dyspnoea with use of accessory muscles & paradoxical abdominal motion b) Moderate to severe acidosis (PH 7.3 7.35) & hypercapnia (PaCO2 45 60 mm of Hg) c) Resp. frequency > 25 breaths /min

Indications for Invasive Mechanical Ventilation


Severe dyspnoea with use of accessory muscles of resp. & paradoxical abdominal motion.

Resp. frequency > 35 breaths /min Life threatening hypoxaemia: PaO2 (<40 mm of Hg)
(pH <7.25)

Severe acidosis

& hypercapnic

PaCO2 >60 mm

Resp. arrest Somnolence, impaired mental status. Hypotension, Shock, CHF Other complications (Sepsis, metabolic abnormalities, pneumonia, pulmonary embolism, massive pleural effusion) NIPPV failure

When to Discharge a Patient from Hospital


Inhaled 2 agonist therapy is required no more frequently then every 4 hours

Patient is able to walk across the room

Pt. has been clinically stable for 12-24 hours


ABG have been stable for 12 24 hours Patient fully medication. understands correct use of

Conclusion
Cornerstones of management of
COPD exacerbation includes --

1. 2. 3. 4.

Adequate O2 supplementation Adequate Bronchodilation Proper antibiotics Ventilatory support

A timely intervention in acute exacerbation of COPD significantly reduces the morbidity & mortality.

Whats new
Experts believe that patients do best on "triple therapy," taking three different medications: a longacting beta-agonist, an inhaled corticosteroid, and the anticholinergic Spiriva (generic name tiotropium bromide). Pulmonary hypertension, or high blood pressure in the arteries leading to the lungs, is a common complication of COPD. The FDA has approved a new formulation of sildenafil called Revatio that's specifically for pulmonary hypertension.

Replacing oxygen with a mix of helium and oxygen. When 60 percent helium was combined with 40 percent oxygen -- making a mixture known as Heliox -- COPD patients were able to increase their exercise capacity by an average of 245 percent. Because helium is less dense than oxygen, it allows COPD sufferers to empty their damaged lungs more completely. Bronchoscopic surgery - Researchers are experimenting with using a bronchoscope-guided needle to create tiny holes through the airway walls. Miniature tubes called stents are then inserted to connect the smaller, collapsed airways with the healthier, bigger airways.

Roflumilast a new medication, (brand name Daxas) has been approved in Europe and USA for chronic bronchitis type ofCOPD. It targets PDE-4 and inhibits inflammation in COPD patients.

Key Points
COPD is preventable and treatable Encourage smokers to quit at every opportunity Dyspnea, cough, and sputum consider COPD Confirm with spirometry Four (4) components of COPD management Pharmacologic treatment Non-pharmacologic treatment Patient education is very important COPD often associated with exacerbations

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