Description #
This unit is designed to help health care professionals develop a better understanding of the goals and treament options for Acute Exacerbation of Chronic Obstructive Pulmonary Disease (AECOPD).
Learning Objectives #
By the end of this unit, you should be able to:
1. Explain the goals of treatment of AECOPD
2. Describe how to assess the severity of AECOPD
3. Describe the treatment options for AECOPD, including in-hospital management.
Definition #
Chronic Obstructive Pulmonary Disease (COPD) is a progressive respiratory disease that is characterized by episodes of worsening of symptoms. These episodes tend to occur with increasing frequency and severity throughout the natural course of the disease. Most COPD patients will experience from one to four exacerbations per year.
Exacerbations are also known as flare-ups or “lung attacks”. They are acute in onset and are defined as a change in symptoms, lasting longer than 48 hours, sufficient to cause a change in therapy. Acute Exacerbation of COPD (AECOPD) is the biggest cause of medical visits, hospitalizations and mortality among patients with COPD.
AECOPD results in an accelerated lung function decline and patients often do not return to their baseline functional ability following an exacerbation. Many patients hospitalized for AECOPD are readmitted because of persistent symptoms. It is therefore very important that management of stable COPD involves the prevention of exacerbations and reducing severity.
- “10% of patients admitted with an exacerbation of COPD die during that admission
- 50% of those that survive will be readmitted in the next six months
- A third will die within 6 months of their initial admission “
Symptoms of AECOPD :
Some of the common symptoms of AECOPD include:
- Worsening dyspnea
- Worsening cough
- Increased sputum volume
- Increased sputum purulence.
Classification of AECOPD:
Exacerbations of COPD may be classified as “purulent” (infectious) or “non-purulent” (non-infectious) based on the change in sputum colour. Classifying AECOP this way will help to determine the need for antibiotic therapy.
The next 2 pages of this unit address the assessment and management of AECOPD.
Causes #
Causes of AECOPD:
Exacerbations of COPD occur most often in winter. Half of all exacerbations are caused by infection (viral or bacterial).
Non-infectious causes include heart failure, and exposure to allergens or irritants (eg. air pollution, cigarette smoke).
AECOPD are commonly triggered by upper respiratory tract viral infections, especially in the winter. The role of bacteria in AECOPD is less clear. The bacteria present in exacerbations are the same as those that colonise the airways of patients with COPD.
AECOPD are also associated with episodes of atmospheric pollution and with changes in the weather.
Whatever the cause, AECOPD are important events that occur more frequently and become more severe as the disease progresses.
Enquiry about the frequency of exacerbations needs to be included in the routine review of COPD patients and such questions should ideally be included in the practice template.
Potential Causes of Exacerbations:
Pulmonary: Pneumonia, viral infection, pulmonary hypertension, pneumothorax, lung cancer
Non-pulmonary: cardiovascular disease, diastolic dysfunction, any form of cardiovascular disease that results in impaired heart function, dysrhythmias, cardiac medications, gastrointestinal disease ( gastroesophageal reflux, esophageal cancer)
Environmental: Pollutants, Nitrogen dioxide, Particulates (PM10), Sulphur dioxide, Ozone, Cold dry weather
Interruption of regular treatment
Anxiety
Medications (respiratory depressants)
Both ciliary dysfunction (in smokers) and a malnutrition-related decline in immune status may blunt airway defenses. These effects can contribute to undesirable clinical sequelae that include hypercapnic respiratory failure, difficulty with weaning from mechanical ventilation, and nosocomial lung infections.
Pathogens in COPD:
Viruses:
Influenza1,2
Parainfluenza1,3
Respiratory syncytial virus (RSV)1,2
Human metapneumonia virus1
Picornaviruses1,3
Coronavirus3
Bacteria:
Common1
Haemophilus influenzae
Moraxella catarrhalis
Streptococcus pneumoniae
Staphylococcus aureus
Common in Severe Exacerbations1
Pseudomonas aeruginosa
Gram-negative bacilli
Atypical3
Chlamydia pneumoniae
Mycoplasma pneumoniae
Legionella spp
Assessment #
The diagnosis of an exacerbation is made based on clinical presentation and does not depend on tests. A complete history and physical examination will reveal that the patient is experiencing an acute change of symptoms that is beyond normal day-to-day variation.
However, in certain situations, investigations may assist in ensuring appropriate treatment is given.
Tests performed in the assessment of AECOPD:
– Exacerbations tend to be characterized as “purulent” or “non-purulent”. This is helpful in determining the need for antibiotic therapy.
– Arterial blood gas measurements (in hospital): SpO2 < 92% if usually normal or a falling SpO2 PaO2 < 8.0 kPa with or without PaCO2 > 6.7 kPa when breathing room air indicates respiratory failure and need for ABGs
– Chest radiographs: useful to exclude alternative diagnoses.
– ECG: may aid in the diagnosis of coexisting cardiac problems.
– Whole blood count: identify polycythemia, anemia or bleeding.
– Purulent sputum during an exacerbation: indication to begin empirical antibiotic treatment.
– Biochemical tests: detect electrolyte disturbances, diabetes, and poor nutrition.
– Spirometry (FEV1): not recommended during an exacerbation; unreliable for detecting changes during an exacerbation; should be done following recovery
The Primary signs and symptoms of acute exacerbation are:
- Increased dyspnea
- Increased cough
- Increased sputum volume/ change in colour/ tenacity
- Increased sputum purulence
- reduction of physical activity beyond what is normal or confined to bed
Secondary Symptoms:
Wheezing
Tightness of chest
Chest pain
Tachycardia
Tachypnoea
pursed lip breathing
Malaise
Insomnia
Sleepiness
Fatigue
Depression
Confusion
Patients who present with an acute chest illness report increased cough, purulent sputum, wheezing, and dyspnea that occur intermittently, with or without fever. Diagnosis can be problematic in such patients. The complaint of wheezing plus dyspnea often leads to an incorrect diagnosis of asthma. Conversely, other illnesses with similar manifestations are often incorrectly diagnosed as a COPD exacerbation (eg, heart failure, bronchiectasis, bronchiolitis) (table 2). The interval between exacerbations decreases as the severity of the COPD increases.
On auscultation:
- Diminished breath sounds or expiratory wheezes
ABGs:hypoxemia, hypercapnia
Physical examination:
- Increased respiratory rate, accessory muscle use/ tripodding
- New onset lower extremity edema or other signs of heart failure
- Cyanosis (new onset)
- paradoxical breathing
- Acute Altered mental status/confusion
Patients with AECOPD may also complain of:
- Chest tightness
- Increase fatigue and weakness
- Insomnia
- Cold or sore throat
- Severe AECOPD complicated by acute respiratory failure is a medical emergency.
- Fever if pneumonia s present
- hemodynamic instability
Physical assessment:
- Assess respiratory status – rate, depth and character of respirations. Can the patient carry on a conversation without shortness of breath? Auscultate lung sounds—assess for crackles, wheezes, prolonged expiration and diminished breath sounds. Are accessory muscles being used? What is the oxygen saturation via pulse oximeter? Impaired oxygenation leads to hypoxia.
- Determine cardiovascular status—what is the patient’s heart rate? The heart rate can increase during a constant state of hypoxia.
- Assess for cyanosis—look at the patient’s lips, nailbeds—do they appear bluish?
- Assess for cough—is it productive/nonproductive? If productive what is the colour of the sputum? Also assess the type of cough (harsh, croupy etc).
- Look for clubbing of the fingernails—this is a sign of chronic hypoxia. In clubbing, the end bone of each finger is round and bulbous, the nail plate is convex (the angle between the plate and the nail fold increases to 180 degrees or more), and the nail fold feels spongy when palpated.
Management #
Exacerbations may be managed at home or, when severe, may require admission to hospital. Some indications for admission to hospital for AECOPD are listed in Table 1. Management of AECOPD involves an intensification of therapy. This requires identifying the precipitating factor or condition and reversing or ameliorating it while optimizing gas exchange and improving the patient’s symptoms.
Escalation of maintenance therapies and addition of supplemental medications (an increase in the use of maintenance medications and/or supplementation with additional medications.)
Goals of AECOPD management:
- Minimize the impact of the exacerbation in terms of need for hospitalization, morbidity and mortality
- Return the patient to baseline: symptoms, lung function, quality of life
- Prevent a replase and the development of future exacerbations
Usual therapy includes bronchodilators, corticosteroids, oxygen and sometimes antibiotics. In more severe exacerbations, non-invasive ventilations or intubation and mechanical ventilation may be necessary.
Home Management
Bronchodilator therapy
Corticosteroids: inhaled combination (Advair) or oral prednisone
Antibiotics
prevent deterioration and hospitalization
Hospital Management: ; AECOPD is typically treated in-hospital
Bronchodilatory therapy
Antibiotics: 50% infectious in nature, always prescibed on admission
Oral or intravenous glucocorticosteroids: always prescibed on admission eg. prednisone (7-14 days)
Noninvasive mechanical ventilation
Closely monitor patient’s overall condition, including comorbidities
Management Strategies:
Hospital admission
Assess need for Oxygen
Assess need for NPPV, intubation ICU
Education, self-managementaction plan and follow up are all essential
Develop an exacerbation plan with the patient on discharge
Medications and education to help prevent future exacerbations should be considered as part of follow-up, as exacerbations affect the quality of life and prognosis of
Medications #
an increase in the use of maintenance medications and/or supplementation with additional medications. #
nhaled bronchodilators (particularly inhaled ß2-agonists with or without anticholinergics) and oral glucocorticosteroids are effective treatments for exacerbations of COPD (Evidence A). #
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Oxygen Therapy #
The role of oxygen therapy is to correct the hypoxemia that usually accompanies the AECOPD. The end point is to maintain oxygen tension at approximately 60 to 65 mm Hg, thereby assuring near-maximal hemoglobin saturation while minimizing the potential for deleterious hypercapnia. Hypercapnia complicating supplemental oxygen is mainly a result of ventilation-perfusion mismatch, with generally smaller contributions of depression of the respiratory drive and the Haldane effect.
Oxygen: titrate to improve the patient’s hypoxemia with a target saturation of 88-92%.
The aim of supplemental oxygen therapy in exacerbations of COPD is to maintain adequate levels of oxygenation (SaO2 greater than 90%), without precipitating respiratory acidosis or worsening hypercapnia.
Bronchodilators #
therapy with short-acting beta2 agonists and anticholinergic bronchodilators
Short-acting inhaled beta2-agonists with or without short-acting anticholinergics are usually the preferred bronchodilators for treatment of an exacerbation.
Bronchodilators are widely used in AECOPD, and β-adrenergic agonists and anticholinergics are first-line therapies. As in stable COPD, both can improve airflow in AECOPD, and although recommendations vary, combined therapy is often recommended. β-Adrenergic agonists have a quicker onset of action, whereas anticholinergics have a more favorable side-effect profile. Because of their potential side effects, as well as their limited benefit, methylxanthines are used mostly as second-line therapy.
This is usually managed by taking increased doses of short acting bronchodilators and these drugs may be given using different delivery systems.
-Both nebulisers and hand-held inhalers can be used to administer inhaled therapy during exacerbations of COPD.
-The choice of delivery system should reflect the dose of drug required, the ability of the patient to use the device and the resources available to supervise the administration of the therapy.
Bronchodilators: Short-acting inhaled beta2-agonists with or without short-acting anticholinergics are preferred.
Antibiotics
Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased sputum purulence) may benefit from antibiotic treatment (Evidence B).
Antibiotics play a favorable role in treating AECOPD, especially in the setting of increased volume and purulence of phlegm.64-66 A narrow-spectrum antibiotic (e.g., amoxicillin, trimethoprim-sulfamethoxazole, doxycycline) is often recommended as first-line therapy, although use of a beta-lactam/beta-lactamase combination has been recommended in patients with severe AECOPD, and fluoroquinolones have been used in patients suspected to be colonized with Pseudomonas aeruginosa.8 The optimal duration of treatment is still unclear, although most guidelines recommend treating for between 7 and 14 days.
Antibiotics should be used to treat exacerbations of COPD associated with a history of more purulent sputum.
-Patients with exacerbations without more purulent sputum do not need antibiotic therapy unless there is consolidation on a chest radiograph or clinical signs of pneumonia.
-Initial empirical treatment should be an aminopenicillin, a macrolide, or a tetracycline.
Antibiotics should be given to patients with: Three cardinal symptoms: increased dyspnea, increased sputum volume, and increased sputum purulence. And who require mechanical ventilation.
antibiotic use is based on risk factors (see Appendix E Antibiotic Treatment Recommendations for Acute Exacerbations of COPD (AECOPD)).
Corticosteroids #
Randomized clinical trials generally support the use of systemic corticosteroids to enhance airflow and to lessen treatment failure in AECOPD. Prolonged therapy beyond 2 weeks confers no additional benefits, with 5 to 10 days being the likeliest optimal duration.
In the absence of significant contraindications, oral corticosteroids should be considered in patients managed in the community who have an exacerbation with a significant increase in breathlessness which interferes with daily activities.
-Patients requiring corticosteroid therapy should be encouraged to present early to get maximum benefits
-Prednisolone 30 mg orally should be prescribed for 7 to 14 days
-It is recommended that a course of corticosteroid treatment should not be longer than 14 days as there is no advantage in prolonged therapy.
Systemic Corticosteroids: 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. A dose of 30-40 mg prednisolone per day for 10-14 days is recommended.
oral corticosteroids (e.g. prednisone 25-50 mg/day) for less than two weeks in most moderate to severe COPD patients. A dose of 30 – 40 mg of prednisone equivalent per day has been used in practice.2
Ventilation #
Noninvasive positive pressure ventilation
Noninvasive positive pressure ventilation (NPPV) refers to ventilation delivered through a noninvasive interface (nasal mask, full facemask, or nasal pillows), rather than an invasive interface (endotracheal tube or tracheostomy tube).
NPPV is used to treat acute respiratory failure of many causes, including AECOPD. When used with appropriately selected patients, NPPV can improve respiratory acidosis, and reduce work of breathing and shortness of breath. NPPV has fewer complications than invasive positive pressure ventilation, and has been shown to decrease hospital length stay, mortality and need for intubation.
Patient Selection: NPPV is recommended in the treatment of more severe COPD exacerbations (PaCO2 >45 mmHg, pH <7.30, RR >25breaths/min, accessory muscle use). Patients with milder exacerbations do not show as much benefit from NPPV.
NPPV might also be considered in patients with advanced COPD who have been designated as Do Not Resuscitate or Do Not Intubate, but are experiencing acute respiratory distress. Cardiogenic pulmonary edema, a common comorbid condition of COPD, is also often treated with NPPV.
NPPV should only be provided in a setting that allows close monitoring of cardiopulmonary status.
Benefits of NPPV:
- Improves respiratory acidosis
- Reduces respiratory rate, severity of dyspnea
- Length of hospital stay
- Decreases mortality and need for intubation
Contraindications:
- Emergent need for intubation
- Cardiac or respiratory arrest
- Hemodynamic instability
- Aspiration risk, including inability to protect the airway or clear secretions
- Altered mental status with inability to cooperate or agitation
- Distorted facial anatomy, facial trauma, or recent facial surgery
- Recent gastroesophageal surgery
Considerations: The most common complication of NPPV is local skin damage caused by tight fitting masks. Other complications include eye irritation, sinus pain and gastric distention. Some patients do not tolerate NPPV because the phases of ventilator breath do not match that of the patient. This is known as asynchrony and is often caused by air leaks around the mask. Changing the mask or the ventilator settings can improve asynchrony. Patients may feel anxious or claustrophobic when NPPV is initiated and should be provided with reassurance and encouragement.
Invasive positive pressure ventilation
Patients with AECOPD who have one or more contraindications to NPPV, or who fail to stabilize with NPPV should be promptly intubated, if eligible, and mechanically ventilated.
Indications:
Unable to tolerate NIV or NIV failure
Severe dyspnoea with use of accessory muscles and paradoxical abdominal motion
Respiratory frequency >35 breaths per minute
Life-threatening hypoxaemia
Severe acidosis (pH <7.25) and/or hypercapnia (PaCO2 >8.0 kPa, 60 mm Hg)
Respiratory arrest
Somnolence, impaired mental status
Cardiovascular complications (hypotension, shock)
Other complications (metabolic abnormalities, sepsis, pneumonia, pulmonary embolism, barotrauma, massive pleural effusion)
Ventilate patients to normal pH
Invasive positive pressure ventilation carries more risks and complications than NPPV, including ventilator-associated pneumonia, barotrauma and hemodynamic instability. Every effort should be taken to minimize its duration.
Discharge Home #
Transition to MDI’s, ensure technique is adequate
Transition to maintenance ICS
CTS:
All patients should be encouraged to maintain an active lifestyle, including patients with advanced COPD or those who experience frequent exacerbations. Referral of COPD patients to pulmonary rehabilitation following an acute exacerbation (within ONE month following AECOPD) has shown to be effective in reducing the future risk of hospitalization, and improving dyspnea, quality of life and excercise capacity.
Patients should be made aware of the optimum duration of treatment and the adverse effects of prolonged therapy.
-Patients, particularly those discharged from hospital, should be given clear instructions about why, when and how to stop their corticosteroid treatment.
– COPD exacerbations can often be prevented.
home oxygen assessment
Education, self-managementaction plan and follow up are all essential
Develop an exacerbation plan with the patient on discharge
Medications and education to help prevent future exacerbations should be considered as part of follow-up, as exacerbations affect the quality of life and prognosis of
Prevent readmissions
Better discharge transition to home and follow-up using community health services or telehealth initiatives may reduce this readmission rate.
Involvement of the individual and family in all aspects of care is essential to improve health outcomes. Programs and services such as home care, home oxygen, supportive housing and pulmonary rehabilitation, provided in a supportive community environment, can meet the complex needs of individuals with COPD and their families.
– need to ensure the appropriate referrals have been made: these include:…..
Data is now emerging to demonstrate the benefit of a self-management plan for patients who exacerbate frequently. The earlier treatment is started during an exacerbation, the better. Patients need to be advised to take action promptly. All patients need clear, written information about what to do and how to contact medical help.
The key elements of a self-management plan are
- How to recognise an exacerbation
- What to do about it
- When and how to call for medical help
Some patients benefit from a self-management plan that includes stand-by courses of antibiotics and oral corticosteroids, so that they can initiate therapy. They should be advised to contact their doctor as well so that the use of these drugs can be effectively monitored and further advice given, as necessary.