Chronic Obstructive PulmonaryDisease

Dr. Akram Yousuf P.G (Med III)

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines define COPD is a disease state characterized by airflow limitation that is not fully reversible, is usually progressive, and is associated with an abnormal inflammatory response of the lungs to inhaled noxious particles or gases.

Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years (other causes of cough being excluded).

Emphysema is defined pathologically as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.

Difference:Airflow limitation in emphysema is due to loss of elastic recoil and decrease in airway tethering, whereas chronic bronchitis leads to narrowing of airway caliber and increase in airway resistance. Although some patients predominantly display signs of one of these diseases or the other, most fall somewhere in the middle of the spectrum between the 2 conditions.

Patient with chronic bronchitis have dec alveolar ventilation, with a low PaO2 and a high PaCO2. hence they are cyanosed and called Blue Bloaters

Emphysemetic patients have inc alveolar ventilation, a near normal PaO2 and a normal or low PaCO2. They are not Cynosed and called Pink Puffers .

Blue Bloaters have dec alveolar ventilation, with a low PaO2 and a high PaCO2. They are cyanosed but not breathless and may go on to develop cor pulmonale. Their respiratory centres are relatively insensitive to CO2 and they rely on hypoxic drive to maintain respiratory effort —supplemental oxygen should be given with care

Pink Puffers have inc alveolar ventilation, a near normal PaO2 and a normal or low PaCO2. They are breathless but are not cyanosed. They may progress to type 1 respiratory failure

Blue Bloaters V/S Pink Puffers

• Occupational exposures, such as coal, silica and cadmium

• Low Birth Weight Baby

• Childhood Infections or Maternal Smoking

• Recurrent Infections

• Low socioeconomic status

• Cannabis smoking

Presentation

• Most patients with chronic obstructive pulmonary disease (COPD) seek medical attention late in the course of their disease.

• Patients often ignore the symptoms because they start gradually and progress over the course of years.

• Patients typically present with a combination of signs and symptoms of chronic bronchitis, emphysema, and reactive airway disease.

Presentation

The common symptoms includes,

• Cough (The cough usually is worse in the mornings and produces a small amount of colorless sputum)

• Worsening Dyspnea (Breathlessness is the most significant symptom, but it usually does not occur until the 4th to 6th decade of life. By the time the FEV1 has fallen to 50% of predicted, the patient is usually breathless upon minimal exertion)

• Wheezing (Wheezing may occur in some patients, particularly during exertion and exacerbations)

Presentation

Systemic manifestations

• Muscular weakness,

• Perpheral edema,

• weight loss due to altered fat metabolism,

• increased osteoporosis.

Presentation

Some important clinical differences may help distinguish between the types of COPD:

• Classic findings for patients with chronic bronchitis include productive cough with gradual progression to intermittent dyspnea; frequent and recurrent pulmonary infections and progressive cardiac/respiratory failure with edema and weight gain.

• Classic findings for patients with emphysema include a long history of progressive dyspnea with late onset of nonproductive cough; occasional mucopurulent relapses; and eventual cachexia and respiratory failure.

Presentation

On Examination

• The sensitivity of a physical examination in detecting mild to moderate COPD is relatively poor.

• Patients with severe disease experience tachypnea and respiratory distress with simple activities.

• The respiratory rate increases in proportion to disease severity.

• Use of accessory respiratory muscles and paradoxical indrawing of lower intercostal spaces is evident (known as the Hoover sign).

• In advanced disease, cyanosis, elevated jugular venous pulse (JVP), and peripheral edema can be observed.

On Examination

On Inspection:

• The patient is dyspnoeic with pursuing of lips and resp rate of >30 br/mins.

• The chest is barrel shaped.

• Indrawing of lower intercostal space on inspiration due to low flat diaphragm.

• Suprasternal and Supraclavicular Excavation.

• Prominent accessory muscles of respiration may be seen.

On Examination

On Percussion:• Increased resonance in both lung fields.

• Obliteration of liver and cardiac dullness (liver dllness may be lower down)

On Auscultaion:

• Breath sounds may be diminished but vesicular with prolong expiration

• Rhonchi may be present if associated with chronic bronchitis

On Examination

On Examination

Chronic bronchitis Emphysema• Patients may be obese

• Frequent cough and expectoration are typical

• Use of accessory muscles of respiration is common

• Coarse rhonchi and wheezing may be heard on auscultation

• Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis

• Patients may be very thin with a barrel chest

• Patients typically have little or no cough or expectoration

• Breathing may be assisted by pursed lips and use of accessory respiratory muscles; patients may adopt the tripod sitting position

• The chest may be hyperresonant,

and wheezing may be heard

• Heart sounds are very distant

• Overall appearance is more like classic COPD exacerbation

Investigations

• Pulmonary function tests are essential for the diagnosis and assessment of the severity of disease, and they are helpful in following its progress.

• If post bronchodilators shows FEV1/FVC <70% of predicted, it may indicates the obstructive pattern of lung disease.

Lung function test: Spirometry

Arterial Blood Gas Analysis• provides the best clues as to acuteness and severity of disease

exacerbation.

• Patients with mild COPD have mild to moderate hypoxemia without hypercapnia. As the disease progresses, hypoxemia worsens and hypercapnia may develop

Serum Electrolytes • Patients with COPD tend to retain sodium. In addition, serum

potassium should be monitored carefully, because diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels.

• Chronic respiratory acidosis leads to compensatory metabolic alkalosis. In the absence of blood gas measurements, bicarbonate levels are useful for following disease progression

Sputum DR • In persons with stable chronic bronchitis, the sputum is

mucoid and macrophages are the predominant cells.

• With an exacerbation, sputum becomes purulent because of the presence of neutrophils

• A mixture of organisms often is visible with Gram stain.The pathogens cultured most frequently during exacerbations are Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis and Pseudomonas aeruginosa.

Alpha 1 Anti Trypsin : • Measure alpha1-antitrypsin (AAT) in all patients younger than 40

years or in those with a family history of emphysema at an early age. The diagnosis of severe AAT deficiency is confirmed when the serum level falls below the protective threshold value of 11 mmol/L (ie, in the range of 3-7 mmol/L)

Pulse Oximeter• when combined with clinical observation, this test can be a

powerful tool for instant feedback on a patient's status

Blood C.P• Chronic hypoxemia may lead polycythemia.

• A hematocrit greater than 52% in men or 47% in women is indicative of polycythemia.

• Correction of hypoxemia should reduce secondary polycythemia in patients who have quit smoking

Echocardiography:• Many patients with long-standing COPD develop secondary

pulmonary hypertension from chronic hypoxemia and vascular remodeling.

• This may result in eventual right-sided heart failure (cor pulmonale)

right-sided heart catheterization • may be performed to measure pulmonary artery pressures

directly and to gauge the response to vasodilators.

STAGING

Modified British Medical Research Council (mMRC) is used to assess the degree of Breathlessness in the patient of COPD.

GOLD criteria for assessing the severity of airflow obstruction (based on the percent predicted postbronchodilator FEV1 when the FEV1/FVC is < 70%) are as follows:

• Stage I (mild) - FEV 1 80% or greater of predicted

• Stage II (moderate) - FEV 1 50-79% of predicted

• Stage III (severe) - FEV 1 30-49% of predicted

• Stage IV (very severe) - FEV 1 less than 30% of predicted or FEV 1 less than 50% and chronic respiratory failure

STAGING

Management

Once the diagnosis of COPD is established, it is important to educate the patient about the disease and to encourage his or her active participation in therapy.

• Smoking cessation continues to be the most important therapeutic intervention for COPD

• Smoking cessation continues to be the most important therapeutic intervention for COPD

• Studies have shown that brief (3 mins) counseling to urge a smoker to quit results in smoking quit rate of 5 – 10%.

• Smoking cessation continues to be the most important therapeutic intervention for COPD

• Studies have shown that brief (3 mins) counseling to urge a smoker to quit results in smoking quit rate of 5 – 10%.

• Nicotine replacement therapy (nicotine gum, nasal spray, transdermal patch, sublingual tablet) as well as pharmacotherapy with Bupropion or nortriptyline reliably increases long term smoking abstinence rate.

Bronchodilators (Inhalers):• SABA: Salbutamol , Terbutaline• SAMA: Ipratropium: 2-4 puffs 6-8 hourly• LABA: Salmeterol: 2 puff B.D, Formoterol: 2 puff B.D, Indacaterol: 2 puff O.D,• LAMA: Tiotropium 2 puff O.D

Inhaled Corticosteroids: Fluticasone, Budesonide

Bronchodilators (ORAL):• Xanthine derivatives (ie, theophylline) • Phosphodiesterase-4 Inhibitors (ie, roflumilast)

Oral Corticosteroids: Prednisone

Other Therapy

• Mucolytics: Acetylcysteine

• Antibiotic: If Infection

• Diuretics

Oxygen therapy for COPD• Oxygen is usually given via a facemask or nasal cannulae.

• Titrate the amount guided by the SaO2 (aim for 94–98% (or 88–92% if, or at risk of hypercapnia)

• Humidification is only required for longer-term delivery of O2 at high flow rates and tracheostomies.

Nasal cannulae: preferred by patients, but O2 delivery is relatively imprecise and may cause nasal soreness. The flow rate (1–4L/min) roughly defines the concentration of O2 (24–40%). May be used to maintain SaO2 when nebulizers need to be run using air.

Venturi mask: provides a precise percentage of O2 (FiO2) at high flow rates. Colour codes: 24% BLUE 28% WHITE 35% YELLOW 40% RED 60% GREEN Start at 24–28% in COPD

Indication of Long term Oxygen Therapy in COPD

When PaO2 is <55mmHg or SaO2 <88% irrespective of PaCO2.

When PaO2 is 55-60 mmHg associated with• Pulmonary Hypertension• Peripheral Edema suggesting CCF• Nocturnal Hypoxemia• Secondary Polycythemia (Hematocrit > 55%)

• Carboxyhemoglobin <3% (in patient who have stopped smoking)

Acute Exacerbation of COPD

An exacerbation of COPD is:

“an acute event characterized by a worsening of the patient’s respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication.”

The most common causes of COPD exacerbations are viral upper respiratory tract infections and infection of the tracheobronchial tree.

Diagnosis relies exclusively on the clinical presentation of the patient complaining of an acute change of symptoms that is beyond normal day-to-day variation.

The goal of treatment is to minimize the impact of the current exacerbation and to prevent the development of subsequent exacerbations.

Manage Exacerbations: keypoints

Short-acting inhaled beta2-agonists with or without short-acting anticholinergics are usually the preferred bronchodilators for treatment of an exacerbation.

Systemic corticosteroids and antibiotics can shorten recovery time, improve lung function (FEV1) and arterial hypoxemia (PaO2), and reduce the risk of early relapse, treatment failure, and length of hospital stay.

COPD exacerbations can often be prevented.

Manage Exacerbations: keypoints

Short-acting inhaled beta2-agonists with or without short-acting anticholinergics are usually the preferred bronchodilators for treatment of an exacerbation.

Systemic corticosteroids and antibiotics can shorten recovery time, improve lung function (FEV1) and arterial hypoxemia (PaO2), and reduce the risk of early relapse, treatment failure, and length of hospital stay.

COPD exacerbations can often be prevented.

Manage Exacerbations: keypoints

MANAGEMENT

Indications of Hospitalization

Marked increase in the symptoms.

Severe underlying COPD

Failure to respond to initial Outpatient management

Presence of serious comorbidities

Older age

Insufficient home support

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