Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease characterised by persistent airflow limitation that is usually progressive, and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.
COPD includes:
(1) Chronic Bronchitis (cough and sputum on most days for at least 3 months, in each of 2 consecutive years)
(2) Emphysema ( (abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis).
Risk Factors of COPD:
1. Environmenal:
• Tobacco smoke accounts for 95% of cases in UK
• Indoor air pollution; cooking with biomass fuels in confined
areas in developing countries
• Occupational exposures, such as coal dust, silica and
cadmium
• Low birth weight may reduce maximally attained lung
function in young adult life
• Lung growth: childhood infections or maternal smoking may
affect growth of lung during childhood, resulting in a lower
maximally attained lung function in adult life
• Infections: recurrent infection may accelerate decline in FEV1;
persistence of adenovirus in lung tissue may alter local
inflammatory response, predisposing to lung damage; HIV
infection is associated with emphysema
• Low socioeconomic status
• Cannabis smoking
2. Host
• Genetic factors: α1-antiproteinase deficiency; other COPD
susceptibility genes are likely to be identified
• Airway hyper-reactivity
Clinical Presentation of COPD:
History:
Patients with chronic obstructive pulmonary disease (COPD) present with a combination of signs and symptoms of chronic bronchitis, emphysema, and asthma. Symptoms include worsening dyspnea, progressive exercise intolerance, and alteration in mental status. In addition, some important clinical and historical differences can exist between the types of COPD.
In the Chronic bronchitis group, classic symptoms include the following:
•Productive cough, with progression over time to intermittent dyspnea
•Frequent and recurrent pulmonary infections
•Progressive cardiac/respiratory failure over time, with edema and weight gain
In the Emphysema group, the history is somewhat different and may include the following set of classic symptoms:
•A long history of progressive dyspnea with late onset of nonproductive cough
•Occasional mucopurulent relapses
•Eventual cachexia and respiratory failure
Physical Examination of COPD:
Chronic bronchitis (blue bloaters) findings may be as follows:
•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.
•Because they share many of the same physical signs, COPD may be difficult to distinguish from congestive heart failure (CHF). One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation.
Emphysema (pink puffers) findings may be as follows:
•Patients may be very thin with a barrel chest.
•They typically have little or no cough or expectoration.
•Breathing may be assisted by pursed lips and use of accessory respiratory muscles; they may adopt the tripod sitting position. In this manner, the patient is trying to maintain a certain amount of positive end-expiratory pressure (PEEP) at the end of expiration, to help keep their lungs open, owing to the loss of lung structure from the disease.
•The chest may be hyperresonant, and wheezing may be heard; heart sounds are very distant.
•Overall appearance is more like classic COPD exacerbation.
Investigations for COPD:
1:Pulmonary Function Test (PFT):
Forced expiratory volume in 1 second (FEV1) is decreased, with concomitant reduction in FEV1/forced vital capacity (FVC) ratio. Patients have poor/absent reversibility with bronchodilators. FVC is normal or reduced. Total lung capacity (TLC) is normal or increased. Residual volume (RV) is increased. Diffusing capacity is normal or reduced.
2:Arterial Blood Gas (ABG's):
Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity. In general, renal compensation occurs even in chronic CO2 retainers (ie, bronchitics); thus, pH usually is near normal. Generally, consider any pH below 7.3 a sign of acute respiratory compromise.
3:CBC
CBC may reveal polycythemia.
4:Chest Radiology
Chronic bronchitis is associated with increased bronchovascular markings and cardiomegaly.
Emphysema is associated with a small heart, hyperinflation, flat hemidiaphragms, and possible bullous changes. Typical findings are shown in the radiographs below.
Chronic obstructive pulmonary disease (COPD). A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragms on posteroanterior chest radiograph.
Spirometric classification of COPD severity based on post-bronchodilator FEV1
Stage Severity FEV1
I Mild* FEV1/FVC < 0.70
FEV1 ≥ 80% predicted
II Moderate FEV1/FVC < 0.70
FEV1 50–79% predicted
III Severe FEV1/FVC < 0.70
FEV1 30–49% predicted
IV Very severe FEV1/FVC < 0.70
FEV1 < 30% predicted or FEV1 < 50%
predicted if respiratory failure present
Management:
Prevention and maintenance therapy recommendations are as follows:
Smoking cessation is key. Pharmacotherapy and nicotine replacement increase long-term smoking abstinence rates, as do legislative bans on smoking. The effectiveness and safety of e-cigarettes as a smoking cessation aid is uncertain.
Pharmacologic therapy can reduce the symptoms of COPD, can reduce the severity and frequency of exacerbations, and can improve exercise tolerance and health status.
Pharmacologic treatment regimens should be individualized. They should be guided by symptom severity; exacerbation risk; adverse effects; comorbidities; drug availability and cost; and patient response, preference, and ability to utilize the various drug delivery devices.
Inhaler technique should be assessed regularly.
Pneumococcal and influenza vaccinations decrease the incidence of lower respiratory tract infections.
Pulmonary rehabilitation improves symptoms, physical and emotional participation in everyday activities, and quality of life.
Patients with severe resting chronic hypoxemia have improved survival with long-term oxygen therapy.
In patients with stable COPD and resting or exercise-induced moderate desaturation, routine long-term oxygen treatment is not recommended; however, consider individual patient factors regarding the need for supplemental oxygen.
With severe chronic hypercapnia and a history of hospitalization for acute respiratory failure, long-term noninvasive ventilation may prevent rehospitalization and decrease mortality.
Select patients with advanced emphysema refractory to optimized medical care may benefit from surgical or bronchoscopic interventional treatments.
In advanced COPD, palliative approaches are effective in controlling symptoms.
Exacerbation recommendations are as follows:
A COPD exacerbation is defined as acute respiratory symptom worsening with the need for additional therapy. Several factors can lead to an exacerbation, the most common being respiratory tract infections.
The recommended initial bronchodilators to treat an exacerbation are short-acting beta2-agonists, with or without short-acting anticholinergics.
As soon as possible before hospital discharge, initiate maintenance therapy with a long-acting bronchodilator.
Systemic corticosteroids can improve lung function and oxygenation. They also shorten recovery time and hospital duration. The duration of systemic corticosteroid therapy should not exceed 5-7 days.
If indicated, antibiotic therapy can shorten recovery time, reduce the risk of early relapse and treatment failure, and reduce hospitalization duration. The duration of antibiotic therapy should not exceed 5-7 days.
Owing to increased adverse effect profiles, methylxanthines are not recommended.
The first mode of ventilation used in COPD with acute respiratory failure and without contraindications is noninvasive mechanical ventilation. It improves gas exchange, reduces the work of breathing, decreases the need for intubation, decreases hospitalization duration, and improves survival.
GOLD patient grouping:
The GOLD patient group-based management recommendations include the following
Group A-D: Reduction of risk factors (influenza and pneumococcal vaccine); smoking cessation; physical activity; short-acting anticholinergic or short-acting beta-adrenergic agonists as needed
Group B: Long-acting anticholinergics or long-acting beta-adrenergic agonists; cardiopulmonary rehabilitation
Group C: Inhaled corticosteroid and long-acting beta-adrenergic agonists or long-acting anticholinergics; cardiopulmonary rehabilitation
Group D: Inhaled corticosteroid and long-acting beta-adrenergic agonists and/or long-acting anticholinergics; cardiopulmonary rehabilitation; long-term oxygen therapy (if criteria met); consider surgical options such as lung volume reduction surgery (LVRS)
Differential Diagnosis:
Acute Respiratory Distress Syndrome (ARDS)
Aspiration Pneumonitis and Pneumonia
Bacterial Pneumonia
Emergent Management of Pleural Effusion
Empyema and Abscess Pneumonia
Heart Failure
Mycoplasmal Pneumonia
Myocardial Infarction
Panic Disorder
Pneumonia in Immunocompromised Patients
Pneumothorax
Pulmonary Embolism (PE)
Viral Pneumoniae
Complications:
Incidence of pneumothorax due to bleb formation is relatively high; consider pneumothorax in all patients with COPD who have increased shortness of breath.
In patients who require long-term steroid use, the possibility of adrenal crisis is very real; at a minimum, patients with steroid-dependent COPD should receive stress dosing in the event of an exacerbation or any other stressor.
Infection (common)
Cor pulmonale
Secondary polycythemia
Bullous lung disease
Acute or chronic respiratory failure
Pulmonary hypertension
Malnutrition
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