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COPDCHRONIC
OBSTRUCTIVE
PULMONARY DISEASE
SYNONYMS
Chronic obstructive pulmonary disease(COPD) is also called as chronic obstructive lung disease(COLD), chronic obstructive airway disease(COAD),chronic airflow obstruction(CAO).
DEFINITION Chronic obstructive pulmonary disease is a
progressive disease that makes it hard to breath. “progressive” means the disease get worse over time.
In COPD, less air flows in and out of the airways because of one or more of the following:
The airways and air sacs lose their elastic quality.
The walls between many of the air sacs are destroyed.
The walls of the airways become thick and inflamed.
The airways make more mucus than usual, which can clog them.
RISK FACTORS
Exposures: Cigarette smoking, pipe & cigar smoking is the
most important risk factor.
Breathing in second hand smoke, Air pollution, or chemical fumes or dust from the environment or workplace.
Previous Infectious diseases like HIV, tuberculosis
Poverty & malnutrition
Host factors: Genetic condition called alpha-1 antitrypsin
deficiency.(alpha-1 anti protease deficiency)
age:>40yrs
Airway hyperactivity as in asthma
Chronic bronchitis Emphysema
Incidence:
middle & late adult life More in male than females More in smokers than non smokers More in urban than in rural dwellers
CHRONIC BRONCHITIS
Chronic bronchitis is defined as condition associated with excessive tracheobronchial mucus production to cause productive cough for at least 3 months of the year for more than 2 consecutive years.
Chronic bronchitis is characterized by inflammation of airways extended from trachea to small airways, alveoli.
EMPHYSEMA
Emphysema is defined as abnormal permanent distension of air spaces distal to the terminal bronchiole with destruction of alveolar septa.
PATHOLOGY OF COPD Chronic bronchitis & Emphysema occurs as a
result of inflammatory process involving the airways and distal air spaces.
Smoking & other airway irritants cause neutrophils, macrophages, T-lymphocytes(CD8+) & other inflammatory cells accumulate in airways.
Once they activated, they trigger inflammatory response in which inflammatory mediators navigate to site to destroy & remove foreign debris
Repeated exposure to airway irritants cause ongoing inflammatory response which causes permanent inflammation of airways, chronic bronchitis.
In emphysema, oxidants produced by smoking & proteases produced by inflammatory macrophages, epithelial cell cause protease & anti protease imbalance which is responsible for breakdown of lungs fragile elastic lamina, destruction of alveolar septa.
Mediators: LTb4( attracts neutrophils, lymphocytes),TNFα, IL1β, IL6(amplify inflammatory response) & TGFβ(induce fibrosis in small airways)
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PATHOLOGICAL CHANGES
In chronic bronchitis:
Hypertrophy & hyperplasia of mucous producing glands.
Goblet cell hyperplasia
Reduction in ciliated cells
Mucosal edema & intra luminal mucous plug
Increased smooth muscle
Reduction in caliber of airways
Normal reid index 0.44±0.09Chronic bronchitis>0.51
In Emphysema:
Severe destruction of small airways, alveoli.
Destruction of alveolar septa.
Formation of large pockets called bullae.
CLASSIFICATION OF EMPHYSEMA
Centriacinar:
Destruction and distension are limited to respiratory bronchiole and alveoli closely related to them(with sparing of the periphery).
Predominantly found in upper lobe & superior segments of lower lobe, most frequently associated with cigarette smoking.
Panacinar:
Generalized destruction of both central & peripheral portion of acinus. Predominant in lower half of the lungs, mostly associated with alpha 1 antitrypsin deficiency.
Paraseptal:
Involves only distal acinus. It involves distal airway structures, alveolar ducts & sacs. Localized around septa of the lungs.
SYMPTOMS
Chronic bronchitis Emphysema
•Ongoing cough with mucus production(called smoker’s cough)
•Copious purulent sputum
•Breathlessness relatively late in onset
•Mucopurulent relapses more frequent
•Wheezing
•Chest tightness
•Minimal cough with expectoration
•Scanty mucoid sputum
•Breathlessness insidious in onset initially on Exertional, gradually even at rest
•Mucopurelent relapses less frequent
•Generalised Weakness
•lethargy
On examination:Inspection: Pt looks dyspnic Use of accessory muscles Barrel shaped chest (due to hyper inflation) Prolonged expiration Tripod positioning to facilitate action of accessory
muscles. Patients with advanced disease have paradoxical inward
movement of the rib cage with inspiration (Hoover's sign). Emphysema patients, termed "pink puffers" are thin and
non cyanotic at rest and have prominent use of accessory muscles
Chronic bronchitis patients are more likely to be heavy and cyanotic & termed as “blue bloaters”.
Palpation:
-decreased chest expansion
Percussion:
- hyper resonance on lung fields
Auscultation:
Decreased breath sounds
Normal vesicular breathing but prolonged expiration
Expiratory ronchi
Coarse crepitatons on both phases
INVESTIGATIONS
Chest X-Ray:
Not sensitive for Dx
To exclude other diseases
Hyper-inflation signs
Low set flat diaphragm
ABG: important for assessing patients with severe COPD.
Detect acute & chronic hypercapnia
Respiratory acidosis(pco2 raised, hypercarbia)
Pao2 is markedly reduced (hypoxemia) Measurement of serum α1AT level, normal level 2-4 g/l.
ECG: May show features of right atrial &ventricular hypertrophy.
Pulmonary function testing (spirometry):
Main method for diagnosing COPD.
low FEV1/FVC (< 70%)
Used for classification of COPD severity.Obstructive patternFEV1-reduced (<80%)FEV1/FVC-reduced (<70%)PEF-reducedTLC-increasedRV-increased
COMPLICATIONS OF COPD
Carbon dioxide narcosis: Persistant Co2 retention causes increase Paco2; hypercarbia, causes drowsiness, altered sensorium, headache.
Respiratory failure:
Type Ι respiratory failure(low Pao2, normal Paco2) occurs in mild to moderate COPD.
Acute or Chronic Type ΙΙ respiratory failure occurs in severe COPD.
Secondary polycythemia: Results from hypoxemia stimulating erythropoiesis.
COPD
HypoxaemiaHypercarbia
Pulmonary vasoconstriction
Pulmonary HTN
Chronic after load to R ventricle
RVH
RVF
Corpulmonale:
Clinical findings: peripheral edema
raised JVP
tender hepatomegaly
MANAGEMENT
General measures:
Cessation of smoking
Avoid lung irritants
Improve nutrition
Regular exercises
Chest physiotherapy.
Specific management:
Mild COPD: Add short acting β2 agonists like salbutamol 2-4mg or terbutaline 2.5-5mg 6 hourly.
Moderate COPD: Add long acting β-stimulants like salmetrol,2puffs of 25 mcg each 2-3 times a day, formetrol 2 puffs of 6 mcg each 1-3 times a day with short acting anti cholinergic like ipratropiumbromide 40-80μg 6 hourly or long acting anti cholinergic like tiotropium bromide 18μg once a day.
Severe COPD: Add inhaled glucocorticosteroids like beclomethasone/budesonide/fluticasone. If response is not satisfactory add systemic glucocorticosteroids like prednisolone/methyl prednisolone.
Very severe COPD: Long term O2, ventilatory support, management of cardiac failure, may consider surgical management.
Methylxanthines like aminophylline or theophylline can be administered when necessary.
Long term domiciliary oxygen therapy should be administered to patients with PaO2<55 mmhg, >16 hrs/day, 2-3ltr/min to maintain SaO2>90%. This reduses pulmonary hypertension, polycythemia, dyspnoea, hypoxaemia.
Antibiotics like tetracycline or ampicillin is needed when respiratory infection present, if no response sputum culture sensitivity to be done & antibiotic changed accordingly.
For out patients management doxycycline, amoxicilline-clavulanate can be given. Patients older than 65 years fluoroquinolones like levofloxacin, gemifloxacin, moxifloxacin can be given.
For hospitalised patients IV antibiotics like azithromycin or fluoroquinolones or third generation cephalosporins like ceftriaxone or cefotaxime should be administered.
Severe acute exacerbation of COPD:
Oxygen: Initial therapy should be maintaining SaO2 >90%, can be ).
Bronchodilators: Nebulisation of β2 agonists like salbutamol 2.5mg every 20 min & anti cholinergic agents like ipratropium bromide to be administered.
Antibiotics: Indicated if sputum volume & purulence is increased.
Most common organisms incluce S.pneumoniae, H.influenzae, M,catarrhalis.
patients with severe exacerbation third generation cephalosporins & fluoroquinolones or an aminoglycoside to be given.
Corticosteroids: IV or oral corticosteroids to be administered as they improve lung function & hypoxemia.
Aminophylline: should be administered if patient fails to respond to initial treatment with Nebulization of β2 agonists. . Given as a
loading dose of 5mg/kg/hr as an infusion.
Diuretics: should be administered to patients with gross cardiac failure.
Respiratory stimulants: Like Doxapram can be if patient is not responding to conventional agents. Dose 1.5-4mg/min as infusion.
Non-invasive positive pressure Ventilation(NIPPV): Ventilation should be tried with tight fitting face mask.
This is used in patient with normal mental status, stable cardiovascular function.
Indications- severe dyspnoea, use of accessory muscles, paradoxical abdominal motion, PH<7.35 mmhg, PaCo2> 45 mmhg, Respiratory rate>25/min.
Invasive mechanical ventilation: When NIV fails patient should be intubated for mechanical ventilation.
Indications- severe dyspnoea, use of accessory muscles, paradoxical abdominal motion, Respiratory rate>35/min
Severe acidosis-PH<7.25
Hypercapnia>60 mmhg
Hypoxia<40 mmhg
Altered sensorium
Respiratory arrest, unstable cardiovascular function, sepsis, hypotension, shock.
Surgical management:
Bullectomy
Lung volume reduction surgery(LVRS)-resection of damaged portion of lung, improves exercise tolerance but doesn’t improve life expectancy.
Lung transplantation- If FEV1<35% (PaO2< 60 mmhg), & PaCo2>50 mmhg.
GOLD Stage
Severity Spirometry Management
0 At Risk Normal Avoid risk factors
I Mild FEV1/FVC <0.7 and FEV1 80% predicted
Short acting β- 2 agonist
II Moderate FEV1/FVC <0.7 and 50% FEV1
<80% predictedLong acting β- 2 agonist/short or long acting anti cholinergics
III Severe FEV1/FVC <0.7 and 30% FEV1
<50% predictedAdd inhaled steroids/methylxanthines
IV Very Severe FEV1/FVC <0.7 and FEV1 <30% predictedorFEV1 <50% predicted with respiratory failure or signs of right heart failure
Add oxygen, ventilatory support, management of RHF
THANK YOU