COPD

COPD : 

COPD AKM Mosharraf Hossain Prof of Respiratory Medicine Department of Medicine, BSMMU Drmosharraf_hossain@yahoo.com 08/10/11

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Definition of COPD

Lung Anatomy: 

Lung Anatomy Bronchopulmonary segment →Bronchi→ TB (Basic functional unit Acini 25000) →RB( Alveoli 300 million in each lung)

Lung Physiology: 

Lung Physiology

Innate Defence of Lung: 

Innate Defence of Lung EM showing respiratory epithelium with cilia © overlaid by mucus raft (M) EM showing alveolar macrophages patroling over alveolar spaces

Epidemiology: 

Epidemiology Globally 80 millions people suffer from mod-severe COPD. Among white males, airflow limitation was present in 14.2% of current smokers, 6.9% of ex-smokers, and 3.3% of never smokers. Among white females, the prevalence of airflow limitation was 13.6% in smokers, 6.8% in exsmokers , and 3.1% in never smokers. Airflow limitation was more common among white smokers than among black smokers.

Morbidity and Mortality: 

Morbidity and Mortality

Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998: 

Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998 0 0.5 1.0 1.5 2.0 2.5 3.0 Proportion of 1965 Rate 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 –59% –64% –35% +163% –7% Coronary Heart Disease Stroke Other CVD COPD All Other Causes Source : NHLBI/NIH/DHHS

COPD Mortality by Gender, U.S., 1980-2000: 

COPD Mortality by Gender, U.S., 1980-2000 Number Deaths x 1000 Source: US Centers for Disease Control and Prevention, 2002

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Risk Factors for COPD Genetic predisposition Gender Age Respiratory infections Socioeconomic status Poor nutrition Abnormal lung growth and development Oxidative stress Comorbidities Tobacco smoke Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings Outdoor air pollution Occupational dusts, organic and inorganic

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12 Risk Factors for COPD Nutrition Infections Socio-economic status Aging Populations

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LUNG INFLAMMATION COPD PATHOLOGY Oxidative stress Proteinases Repair mechanisms Anti-proteinases Anti-oxidants Host factors Amplifying mechanisms Cigarette smoke Biomass particles Particulates Source : Peter J. Barnes, MD Pathogenesis of COPD

Effects of COPD: 

Effects of COPD

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Y Y Y Mast cell CD4+ cell (Th2 ) Eosinophil Allergens Ep cells ASTHMA Bronchoconstriction AHR Alv macrophage Ep cells CD8+ cell (Tc1) Neutrophil Cigarette smoke Small airway narrowing Alveolar destruction COPD Reversible Irreversible Airflow Limitation Source : Peter J. Barnes, MD

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Alveolar wall destruction Loss of elasticity Destruction of pulmonary capillary bed ↑ Inflammatory cells macrophages, CD8 + lymphocytes Source : Peter J. Barnes, MD Changes in Lung Parenchyma in COPD

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Chronic hypoxia Pulmonary vasoconstriction Muscularization Intimal hyperplasia Fibrosis Obliteration Pulmonary hypertension Cor pulmonale Death Pulmonary Hypertension in COPD Source : Peter J. Barnes, MD

Diagnose COPD: 

Diagnose COPD Consider a diagnosis of COPD for people who are: over 35, and smokers or ex-smokers, and have any of these symptoms: - exertional breathlessness - chronic cough - regular sputum production, frequent winter ‘bronchitis’ wheeze [2004]

Sputum: 

Sputum

Physical signs: 

Physical signs

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Differential Diagnosis: COPD and Asthma COPD ASTHMA Onset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise Largely irreversible airflow limitation Onset early in life (often childhood) Symptoms vary from day to day Symptoms at night/early morning Allergy, rhinitis, and/or eczema also present Family history of asthma Largely reversible airflow limitation

Differentials: 

Differentials

How to Investigate ?: 

How to Investigate ? Spirometry and bronchodilator reversibility test CXR- bulla, hyperinflation Echocardiography CT scan ABG Alpha-1-antitrypsin

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Spirometry Symptoms Exercise Impairment Dyspnea, Wheezing Cough  Sputum Exposure Tobacco Occupational Pollution

Spirometric Diagnosis of COPD : 

Spirometric Diagnosis of COPD COPD is confirmed by post–bronchodilator FEV 1 /FVC < 0.7 Post-bronchodilator FEV 1 /FVC measured 15 minutes after 400µg salbutamol or equivalent

Criteria for Normal Spirometric Values: 

Criteria for Normal Spirometric Values FEV 1 : % predicted > 80% FVC: % predicted > 80% FEV 1 /FVC: > 0.7

Normal Trace Showing FEV1 and FVC: 

Normal Trace Showing FEV 1 and FVC 1 2 3 4 5 6 1 2 3 4 Volume, liters Time, seconds FVC 5 1 FEV 1 = 4L FVC = 5L FEV 1 /FVC = 0.8

Spirometry: Obstructive Disease: 

Spirometry: Obstructive Disease Volume, liters Time, seconds 5 4 3 2 1 1 2 3 4 5 6 FEV 1 = 1.8L FVC = 3.2L FEV 1 /FVC = 0.56 Normal Obstructive

Bronchodilator Reversibility Testing: 

Bronchodilator Reversibility Testing Provides the best achievable FEV 1 (and FVC) Helps to differentiate COPD from asthma Must be interpreted with clinical history - neither asthma nor COPD are diagnosed on spirometry alone

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Bronchodilator Reversibility Testing in COPD Preparation Tests should be performed when patients are clinically stable and free from respiratory infection Patients should not have taken: inhaled short-acting bronchodilators in the previous six hours long-acting bronchodilator in the previous 12 hours sustained-release theophylline in the previous 24 hours

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Bronchodilator Reversibility Testing in COPD Spirometry FEV 1 should be measured (minimum twice, within 5%) before a bronchodilator is given The bronchodilator should be given by metered dose inhaler through a spacer device or by nebulizer to be certain it has been inhaled (…..continued)

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Bronchodilator Reversibility Testing in COPD Spirometry (continued) Possible dosage protocols: 400 µg β 2 -agonist, or 80-160 µg anticholinergic , or the two combined FEV 1 should be measured again: 10-15 minutes after a short-acting b 2 -agonist 30-45 minutes after the combination

HRCT-gross emphysema: 

HRCT-gross emphysema

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37 GOALS of COPD MANAGEMENT VARYING EMPHASIS WITH DIFFERING SEVERITY

Four Components of COPD Management: 

Four Components of COPD Management Assess and monitor disease Reduce risk factors Manage stable COPD Education Pharmacologic Non-pharmacologic Manage exacerbations

GOLD Therapy at Each Stage of COPD: 

GOLD Therapy at Each Stage of COPD FEV 1 /FVC <0.70 FEV 1 ≥80% predicted I: Mild II: Moderate III: Severe IV: Very Severe FEV 1 /FVC <0.70 50% ≤FEV 1 <80% predicted FEV 1 /FVC <0.70 30% ≤FEV 1 <50% predicted FEV 1 /FVC <0.70 FEV 1 <30% predicted or FEV 1 <50% predicted plus chronic respiratory failure Add regular treatment with one or more long-acting bronchodilators (when needed): Add pulmonary rehabilitation Add inhaled glucocorticosteroids if repeated exacerbations Add long-term oxygen if chronic respiratory failure Consider surgical treatments Global Initiative for Chronic Obstructive Lung Disease (GOLD). NHLBI/WHO Workshop report. www.goldcopd.com Active reduction of risk factor(s): influenza vaccination Add short-acting bronchodilator (when needed )

Model of Annual Decline of FEV1: 

Model of Annual Decline of FEV1 If smoking is stopped, subsequent loss is similar to that in healthy non-smokers

Smoking cessation (1): 

Smoking cessation (1) Smoking is not a bad habit, this is a chronic medical illness Treating tobacco use and dependence should be regarded as a primary and specific intervention. The key steps in intervention are: Ask Identify all tobacco users at every visit Advise Strongly urge all tobacco users to quit Assess Determine willingness to make a quit attempt Assist Help the patient with a quit plan, provide practical counselling, treatment and social support, recommend the use of approved pharmacotherapy Arrange Schedule follow-up contact ERS-ATS COPD Guidelines

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Brief Strategies to Help the Patient Willing to Quit Smoking ASSIST For the patient willing to make a quit ttempt, offer medication and provide or refer for counseling or additional treatment to help the patient quit. For patients unwilling to quit at the time, provide interventions designed to increase future quit attempts. ARRANGE For the patient willing to make a quit attempt, arrange for followup contacts, beginning within the first week after the quit date. For patients unwilling to make a quit attempt at the time, address tobacco dependence and willingness to quit at next clinic visit.

LTOT in COPD: 

LTOT in COPD Arterial blood gases measured in clinically stable patients on optimal medical therapy on at least two occasions 3 weeks apart: PaO2 ≤ 7.3 kPa (55 mmHg) irrespective of Pa CO2 and FEV1 ≤ 1.5 litres PaO2 7.3-8 kPa (55-60 mmHg) plus pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia Patient stopped smoking Use at least 15 hours/day at 2-4 litres/min to achieve a Pa O2 > 8 kPa (60 mmHg) without unacceptable rise in Pa CO2. It improves survival, reduces secondary polycythaemia and prevents progression of primary pulmonary hypertension.

Oxygen Therapy Equipment: 

Oxygen Therapy Equipment oxygen cylinders: Oxygen flow can be adjusted as the cylinders are equipped with an oxygen flow meter with ‘medium' (2 litres/minute) and ‘high' (4 litres/minute) settings. Oxygen concentrators: A concentrator is recommended for a patient who requires oxygen for more than 8 hours a day (or 21 cylinders per month). A nasal cannula is usually preferred for long-term oxygen therapy from an oxygen concentrator. It can, however, produce dermatitis and mucosal drying in sensitive individuals. Giving oxygen by nasal cannula allows the patient to talk, eat, and drink, but the concentration of oxygen is not controlled; this may not be appropriate for acute respiratory failure. When oxygen is given through a nasal cannula at a rate of 1–2 litres/minute the inspiratory oxygen concentration is usually low, but it varies with ventilation and can be high if the patient is underventilating.

Oxygen Therapy: 

Oxygen Therapy Oxygen should be regarded as a drug. It is prescribed for hypoxaemic patients to increase alveolar oxygen tension and decrease the work of breathing. High concentration oxygen therapy : with concentrations of up to 60%, is safe in uncomplicated cases of conditions such as pneumonia, pulmonary thromboembolism, and fibrosing alveolitis. Low concentration oxygen therapy : 24-28% is reserved for patients with ventilatory failure due to chronic obstructive pulmonary disease or other causes. Domicilliary oxygen therapy :

Pulmonary rehabilitation: 

ERS-ATS COPD Guidelines Pulmonary rehabilitation Pulmonary rehabilitation is a multidisciplinary programme of care that is individually tailored and designed to optimise physical and social performance and autonomy. Pulmonary rehabilitation should be considered for patients with COPD who have dyspnoea or other respiratory symptoms, reduced exercise tolerance, a restriction in activities because of their disease, or impaired health status. Pulmonary rehabilitation programmes include: exercise training, education, psychosocial/behavioural intervention, nutritional therapy, outcome assessment, promotion of long-term adherence to the rehabilitation recommendations.

Nutrition: 

ERS-ATS COPD Guidelines Nutrition Weight loss and a depletion of fat-free mass (FFM) may be observed in stable COPD patients. Being underweight is associated with an increased mortality risk. Criteria to define weight loss are: Weight loss >10% in the past 6 months or >5% in the past month. Nutritional therapy may only be effective if combined with exercise or other anabolic stimuli. Underweight BMI <21 kg · m -2 ;age >50 yrs Normal weight BMI >21 – 23 kg · m -2 Overweight BMI >23 kg · m -2 Obese BMI 23 kg · m -2

Surgery in COPD : 

ERS-ATS COPD Guidelines Surgery in COPD Patients with a diagnosis of COPD have a 2.7–4.7-fold increased risk of post-operative pulmonary complications. The further the procedure from the diaphragm, the lower the pulmonary complication rate. Smoking cessation at least 4–8 weeks pre-operatively and optimisation of lung function can decrease post-operative complications. Early mobilisation, deep breathing, intermittent positive-pressure breathing, incentive spirometry and effective analgesia may decrease postoperative complications .

Surgery for COPD : 

ERS-ATS COPD Guidelines Surgery for COPD Bullectomy and lung volume reduction surgery may result in improved spirometry, lung volume, exercise capacity, dyspnoea, health-related quality of life and possibly survival in highly selected patients. Lung transplantation results in improved pulmonary function, exercise capacity, quality of life and possibly survival in highly selected patients.

Sleep: 

ERS-ATS COPD Guidelines Sleep Sleep in COPD is associated with oxygen desaturation , which is predominantly due to the disease itself rather than to sleep apnoea. The desaturation during sleep may be greater than during maximum exercise. Sleep quality is markedly impaired in COPD, both subjectively and objectively. Management of sleep problems in COPD should particularly focus on minimising sleep disturbance by measures to limit cough and dyspnoea, and nocturnal oxygen therapy is rarely indicated for isolated nocturnal hypoxaemia . Hypnotics should be avoided, if possible, in patients with severe COPD.

Air travel: 

ERS-ATS COPD Guidelines Air travel Commercial airliners can cruise at >12,000 m (>40,000 feet) as long as the cabin is pressurised from 1,800–2,400 m (6,000–8,000 feet). This is equivalent to an inspired oxygen (O 2 ) concentration at sea level of ~15%. Patients with COPD can exhibit falls in arterial O 2 tension ( PaO 2 ) that average 25 mmHg (3.3 kPa ). Pre-flight assessment can help determine O 2 needs and the presence of co-morbidities. Most airlines will provide supplemental O 2 on request. There is increasing evidence that patients on long flights may be at increased risk for deep vein thrombosis.

Definition: 

ERS-ATS COPD Guidelines Definition COPD exacerbation is an acute and sustained worsening of patient’s baseline dyspnoea, cough and sputum amount with purulence sufficient to warrant a change in therapy .

Causes of COPD Exacerbation: 

Causes of COPD Exacerbation Viruses Bacteria Rhinoviruses Coronaviruses RSV Influenza virus Parainfluenza virus Haemophylus influenzae Streptococcus pneumoniae Moraxella catarrhalis Pseudomonas Staphylococcus Medicine International

Risk Factors for Pseudomonas: 

Risk Factors for Pseudomonas - Frequent administration of antibiotics (4 or more courses over the past year) - Recent hospitalization (2 or more days' duration in the past 90 days) - Isolation of Pseudomonas during a previous hospitalization - Severe underlying COPD (FEV1 <50 percent predicted)

Indications for Hospitalisation in COPD exacerbation: 

Indications for Hospitalisation in COPD exacerbation Inadequate response of symptoms to outpatient management Marked increase in dyspnoea Type II Respiratory failure Acute confusion Uncertain diagnosis Inadequate home care Presence of high-risk co-morbid conditions, including pneumonia, cardiac arrhythmia, congestive heart failure, diabetes mellitus, renal or liver failure

Outpatient/Community Management: 

Outpatient / Community Management Patient education Check inhalation technique Consider use of spacer devices Bronchodilators Short-acting β 2 -agonist and/or ipratropium MDI with spacer or hand-held nebuliser as needed Corticosteroids (the actual dose may vary) Prednisone 30–40 mg per os q day for 10 days Consider using an inhaled corticosteroid Antibiotics May be initiated in patients with altered sputum characteristics Choice should be based on local bacteria resistance patterns Amoxicillin/ ampicillin , cephalosporins Macrolides If the patient has failed prior antibiotic therapy consider: Amoxicillin/ clavulanate Respiratory fluoroquinolones

Hospital Management: 

Hospital Management Bronchodilators Short acting β 2- agonist ( albuterol , salbutamol ) and/or Ipratropium MDI with spacer or hand- held nebuliser as needed Inj Aminophylline (5mg/kg BW bolus then .5mg/kg/ hr maintainece dose) Supplemental oxygen (if saturation <90% to maintain 92-94%) Corticosteroids If patient tolerates, prednisone 30–40 mg per os q day for 10 days If patient can not tolerate oral intake, equivalent dose i.v. for up to 14 days Consider use inhaled corticosteroids by MDI or hand-held nebuliser Antibiotics ( based on local bacteria resistance patterns) May be initiated in patients that have a change in their sputum characteristics (purulence and/or volume) Amoxicillin / clavulanate Respiratory fluoroquinolones ( gatifloxacin , levofloxacin , moxifloxacin ) If Pseudomonas spp . and/or other Enterobactereaces spp . are suspected , consider combination therapy

Treatment in HDU/ICU: 

Treatment in HDU/ICU Supplemental oxygen Respiratory stimulant: Doxapram Ventilatory support : NIV, Mechanical Ventilation Bronchodilators Short-acting β 2- agonist ( albuterol , salbutamol ) and ipratropium MDI with spacer , two puffs every 2–4 h If the patient is on the ventilator , consider MDI administration, consider long-acting β- agonist Corticosteroids If patient tolerates oral medications , prednisone 30–40 mg per os q day for 10 days If patient can not tolerate , give the equivalent dose i.v . for up 14 days Consider use inhaled corticosteroids by MDI or hand- held nebuliser Antibiotics ( based on local bacteria resistance patterns) Choice should be based on local bacteria resistance patterns Amoxicillin / clavulanate Respiratory fluoroquinolones ( gatifloxacin , levofloxacin , moxifloxacin ) If Pseudomonas spp . and or other Enterobactereaces spp . are suspected consider combination therapy

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ERS-ATS COPD Guidelines

NIV in COPD Exacerbation: 

NIV in COPD Exacerbation

NIV-Contraindications : 

NIV- Contraindications NO absolute contraindications. Several are suggested: Coma or confusion Severe acidosis Significant comorbidity Radiological evidence of consolidation Vomiting, obstructed bowel Respiratory arrest, Cardiovascular instability, Recent facial or gastro-oesophageal surgery; craniofacial trauma and/or fixed naso -pharyngeal abnormality, burns, Extreme obesity .

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Inhaler Technique

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Theophylline Metabolism

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Alpha-1 antitrypsin augmentation therapy. Young patients with severe hereditary alpha-1 antitrypsin deficiency and established emphysema may be candidates for alpha-1 antitrypsin augmentation therapy. However, this therapy is very expensive, is not available in most countries, and is not recommended for patients with COPD that is unrelated to alpha-1 antitrypsin defficiency Alpha-1 antitrypsin augmentation therapy

Survival Improvement: 

Survival Improvement

COPD Prognosis:BMI and dyspnoea: 

COPD Prognosis:BMI and dyspnoea Body Mass Index (BMI) and dyspnoea have proved useful in predicting outcomes such as survival, and should thus be evaluated in all patients. BMI values < 21 kg · m -2 are associated with increased mortality. Functional dyspnoea can be assessed by the Medical Research Council dyspnoea scale: 0 Not troubled with breathlessness except with strenuous exercise. 1 Troubled by shortness of breath when hurrying or walking up a slight hill. 2 Walks slower than people of the same age due to breathlessness or has to stop for breath when walking at own pace on the level. 3 Stops for breath after walking about 100 m or after a few minutes on the level. 4 Too breathless to leave the house or breathless when dressing or undressing. ERS-ATS COPD Guidelines

Prognosis: 

Prognosis Variable 0 1 2 3 FEV1 SMWT MRC BMI ≥ 65 50-64 36-49 ≤ 35 ≥ 350 250-349 150-249 ≤ 149 0-1 2 3 4 >21 ≤21 The prognosis is inversely related to age and directly related to the post-bronchodilator FEV1. Additional poor prognostic indicators include weight loss and pulmonary hypertension. A patient with a BODE score of 0-2 has a mortality rate of around 10% at 52 months whereas a patient with a BODE score of 7-10 has a mortality rate of around 80% at 52 months.

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DO NOT SMOKE