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Chronic obstructive pulmonary disease2

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COPD CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Transcript
Page 1: Chronic obstructive pulmonary disease2

COPDCHRONIC

OBSTRUCTIVE

PULMONARY DISEASE

Page 2: Chronic obstructive pulmonary disease2

SYNONYMS

Chronic obstructive pulmonary disease(COPD) is also called as chronic obstructive lung disease(COLD), chronic obstructive airway disease(COAD),chronic airflow obstruction(CAO).

Page 3: Chronic obstructive pulmonary disease2

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.

Page 4: Chronic obstructive pulmonary disease2
Page 5: Chronic obstructive pulmonary disease2

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

Page 6: Chronic obstructive pulmonary disease2

Host factors: Genetic condition called alpha-1 antitrypsin

deficiency.(alpha-1 anti protease deficiency)

age:>40yrs

Airway hyperactivity as in asthma

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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

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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.

Page 9: Chronic obstructive pulmonary disease2

EMPHYSEMA

Emphysema is defined as abnormal permanent distension of air spaces distal to the terminal bronchiole with destruction of alveolar septa.

Page 10: Chronic obstructive pulmonary disease2

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

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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)

Page 12: Chronic obstructive pulmonary disease2
Page 13: Chronic obstructive pulmonary disease2

s

Page 14: Chronic obstructive pulmonary disease2

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

Page 15: Chronic obstructive pulmonary disease2

Normal reid index 0.44±0.09Chronic bronchitis>0.51

Page 16: Chronic obstructive pulmonary disease2

In Emphysema:

Severe destruction of small airways, alveoli.

Destruction of alveolar septa.

Formation of large pockets called bullae.

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Page 18: Chronic obstructive pulmonary disease2

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.

Page 19: Chronic obstructive pulmonary disease2

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.

Page 20: Chronic obstructive pulmonary disease2
Page 21: Chronic obstructive pulmonary disease2

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

Page 22: Chronic obstructive pulmonary disease2
Page 23: Chronic obstructive pulmonary disease2

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”.

Page 24: Chronic obstructive pulmonary disease2
Page 25: Chronic obstructive pulmonary disease2
Page 26: Chronic obstructive pulmonary disease2

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

Page 27: Chronic obstructive pulmonary disease2

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.

Page 28: Chronic obstructive pulmonary disease2

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

Page 29: Chronic obstructive pulmonary disease2

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.

Page 30: Chronic obstructive pulmonary disease2

COPD

HypoxaemiaHypercarbia

Pulmonary vasoconstriction

Pulmonary HTN

Chronic after load to R ventricle

RVH

RVF

Corpulmonale:

Page 31: Chronic obstructive pulmonary disease2

Clinical findings: peripheral edema

raised JVP

tender hepatomegaly

Page 32: Chronic obstructive pulmonary disease2
Page 33: Chronic obstructive pulmonary disease2

MANAGEMENT

General measures:

Cessation of smoking

Avoid lung irritants

Improve nutrition

Regular exercises

Chest physiotherapy.

Page 34: Chronic obstructive pulmonary disease2

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.

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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.

Page 36: Chronic obstructive pulmonary disease2

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.

Page 37: Chronic obstructive pulmonary disease2

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.

Page 38: Chronic obstructive pulmonary disease2

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.

Page 39: Chronic obstructive pulmonary disease2

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.

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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.

Page 41: Chronic obstructive pulmonary disease2

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.

Page 42: Chronic obstructive pulmonary disease2

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

Page 43: Chronic obstructive pulmonary disease2
Page 44: Chronic obstructive pulmonary disease2

THANK YOU


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