Chronic Obstructive Pulmonary Disease (COPD)

Chronic Obstructive Pulmonary Disease(COPD) is defined as a preventable and treatable lung disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. The pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases. Related diagnoses include chronic bronchitis (cough and sputum on most days for at least 3 consecutive months for at least 2 successive years) and emphysema (abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis). Extrapulmonary manifestations include impaired nutrition, weight loss and skeletal muscle dysfunction .

Epidemiology

Globally, as of 2010, COPD affected approximately 329 million people (4.8% of the population). The disease affects men and women almost equally, as there has been increased tobacco use among women in the developed world. The increase in the developing world between 1970 and the 2000s is believed to be related to increasing rates of smoking in this region, an increasing population and an aging population due to less deaths from other causes such as infectious diseases. Some developed countries have seen increased rates, some have remained stable and some have seen a decrease in COPD prevalence. The global numbers are expected to continue increasing as risk factors remain common and the population continues to get older.  Between 1990 and 2010 the number of deaths from COPD decreased slightly from 3.1 million to 2.9 million and became the fourth leading cause of death. In 2012 it became the third leading cause as the number of deaths rose again to 3.1 million. In some countries, mortality has decreased in men but increased in women. This is most likely due to rates of smoking in women and men becoming more similar. COPD is more common in older people; it affects 34-200 out of 1000 people older than 65 years, depending on the population under review.

Risk Factors

1.      Tobacco smoke –about 95%

2.      Occupation : coal miners, fumes

3.      Outdoor or indoor air pollution—dust , smoke

4.      Low socioeconomic condition

5.      Infections

6.      Genetic predisposition –α-1 antitrypsin deficiency.

Pathophysiology

COPD has both pulmonary and systemic components The changes in pulmonary and chest wall compliance mean that collapse of intrathoracic airways during expiration is exacerbated, during exercise as the time available for expiration shortens, resulting in dynamic hyperinflation. Increased V./Q. mismatch increases the dead space volume and wasted ventilation. Flattening of the diaphragmatic muscles and an increasingly horizontal alignment of the intercostal muscles place the respiratory muscles at a mechanical disadvantage. The work of breathing is therefore markedly increased, first on exercise but, as the disease advances, at rest too. Emphysema may be classified by the pattern of the enlarged airspaces: centriacinar, panacinar and periacinar. Bullae form in some individuals. This results in impaired gas exchange and respiratory failure.

Clinical Features

Symptoms :

1. Age : usually >40 years
2. Persistent cough (for at least 3 consecutive months for at least 2 successive years).
3. Sputum production(scanty mucoid , or mucopurulent or purulent )
4. Breathlessness Repeated similar attacks in past

Signs :

In the case of  COPD there was many sign seen they can vary from person to persons the main signs are given below on point wise manner to fast memorize .

Ø  Vitals :- tachycardia patient have on  tachypnoea, presence or absence of fever

Ø  General physical examination  :

a.      Patient dyspnoeic and restless

b.      Polycythaemia : plethora

c.       Central cyanosis

d.      Pedal edema may be present ( with features of RHF)

e.      Flapping tremors (due to high CO2)

f.        Use of accessory muscles of respiration

g.      Tracheal tug present

Ø  3. Respiratory system examination :

a)      Inspection :Use of accessory muscles of respiration,Indrawing of costal margin and intercostal spaces ,“Pursed lip” breathing

b)      b.Palpation :Increased AP diameter, barrel shaped chest, Diminished chest expansion Tracheal tug can be observe.

c)      Percussion :Hyperresonant lung fields were found while doing percussion.

d)      Auscultation :on auscultation diminished vesicular breath sounds with prolonged expiration, fine crepitations (more in chronic bronchitis predominant),wheeze ( more in emphysema predominant) heard through stethoscope.

Investigation

1.      CBC : Hb-- increased,PCV –leucocytosis

2.       Sputum : GM stain, C/S, AFB staining

3.      Chest X- ray: Hyper inflated lung fields
       with tubular heart flat diaphragm and emphy
        sematous bulla may be seen

4.       Spirometry :

FEV1  <80 %

FEV1/FVC <70%

5.       ECG : P -Pulmonale

6.      Other :- ECHO CT scan can be done

Management

1. General management :

a.      Cessation of smoking:

Every attempt should be made to highlight the role of smoking in the development and progress of COPD, advising and assisting the patient toward smoking cessation (p. 99). Reducing the number of cigarettes smoked each day has little impact on the course and prognosis of COPD, but complete cessation is accompanied by an improvement in lung function and deceleration in the rate of FEV1 decline (Fig. 19.27 and Box 19.30). In regions where the indoor burning of biomass fuels is important,the introduction of non-smoking cooking devices or the use of alternative fuels should be encouraged.

b.      O2 if cyanosed patient

c.       Nebulisation

2               2.  Pharmacologic management

A.     Bronchodilator therapy:

a.      Short acting bronchodilators : salbutamol , terbutaline

b.      Ipatropium bromide, Tiotropium

c.       Long acting bronchodilators : salmeterol, Formoterol

d.      Theophylline and its derivatives

Bronchodilators are more effective in nebulization form . If nebulization not available use as inhalers(MDI)

B.      Corticosteroids

Ø  They reduce the frequency and severity of exacerbations.

Ø  Inhaled corticosteroids ( fluticasone, budesonide )

Ø  Oral( prednisolone ) or IV corticosteroids (IV hydrocortisone) during exacerbations.

C.      Antibiotics

Usually during exacerbations

1.      Cap Amoxicillin 250-500 mg 8 hrly or

2.      Co –trimoxazole 960 mg 12 hrly   for 7-10 days

Or Azithromycin 500 mg od for 5 days

Different types of antibiotics are in practice now

D.     Additional Treatment

a.      Diuretics : frusemide if pedal edema present.

b.      Chest physiotherapy- postural drainage

c.       Lung volume reduction surgery

d.      Lung Transplantation

Complications

ü  Cor pulmonale

ü  Pneumothorax by rupture of subpleural blebs

ü  Respiratory failure

ü  Pulmonary hypertension

ü  Lung carcinoma  Rare

Refrences

ü  Davidsons prinviple and practice of medicine

ü  Wikipedia