Chronic Obstructive Pulmonary Disease By Abhinay Sharma Bhugoo Ml-610.
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Transcript of Chronic Obstructive Pulmonary Disease By Abhinay Sharma Bhugoo Ml-610.
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ChronicObstructive Pulmonary DiseaseBy Abhinay Sharma BhugooMl-610
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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
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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 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
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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
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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 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
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Venn diagram Venn diagram of chronic obstructive pulmonary disease (COPD).
1 21
3 45
6 78
9 10
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Histopathology of chronic bronchitis showing hyperplasia of mucous glands hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells
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Gross pathology of advanced emphysema. Large bullae 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 for
smokers
• Intravenous drug use• Pulmonary vascular damage
• Insoluble filler (eg, cornstarch, cotton fibers, cellulose, talc) contained in methadone or methylphenidate
• 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 individual’s risk of death risk of death or hospitalizationhospitalization
• History
• Multifactorial with • Individual lifestyle
• Socioeconomic factors
• Education / Knowledge
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Pathophysiological changes
This phenomenon is called dynamic hyperinflation
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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 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
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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.
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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
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Physical Examination
• Hyperinflation (barrel chest)
• Wheezing – Frequently heard on forced and unforced expiration
• Diffusely decreased breath sounds
• Hyperresonance on percussion
• Prolonged expiration phase
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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
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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 diffuse hypovascularity and bullae formationhypovascularity 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 with chronic 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 Acute exacerbationexacerbation
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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, Morexella
catarrhalis, 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 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
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bronchodilator
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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 : at ALL stage
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Post-bronchodilator
FEV1(% predicted)
Management based on GOLD
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bronchodilator
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Pulmonary rehabilitation
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Oxygen therapy
Oxygen therapy via nasal cannulaHome 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