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
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