John, a 50-year-old Caucasian man, comes to the emergency department with worsening dyspnea, fever, cough, and increased purulent sputum production. He is accompanied by his sister, who says John has been experiencing shortness of breath, feeling fatigued and has not been thinking clearly.
His sister states that John has had a cold for the past three days, which he tried to manage with Tylenol.
According to past medical history, John has been a smoker for 30 years and has quit one year ago when he was diagnosed with stage II (moderate) chronic obstructive pulmonary disease. Since being diagnosed, John has been taking salbutamol PRN and tiotropium bromide (Spiriva) daily. He has no other medical conditions, and no known allergies.
Upon physical examination, the nurse notes John's vital signs are:
Blood pressure - 130/84
Respiratory rate - 28/min
Heart rate - 110/min
Oxygen saturation - 87%
Temperature - 38.1ºC
The client is using accessory muscles to breathe, has audible expiratory wheezing and inspiratory crackles, and diminished breath sounds in lower lobes upon auscultation.
Questions
- What is the potential cause for John coming to the ED?
- What are some of the medications that John is likely to be given specific to his admission diagnosis?
- John asks the nurse, "I quit a year ago, how come this happened to me?" What would be the nurse's response?
- What client-teaching can the nurse implement when John is ready to be discharged?
Answers
1. John came to ED with the symptoms of worsening dyspnea, fever, cough, and increased purulent sputum production. Taking into account his previous smoking history and the fact that he was diagnosed with stage II COPD one year ago, the healthcare practitioner will most likely suspect an acute exacerbation of COPD. According to Sahn (2012), the acute exacerbation of COPD (AECOPD) is characterized by such core symptoms as cough, sputum production and dyspnea. The patient is also experiencing fever (temperature of 38.1ºC), and has had a cold for the past three days, which is indicative of the presence of infection. Some scientists believe that lower respiratory tract infections cause the development of COPD exacerbation in 80% of cases (Xue-Jun, Qi, Liang-Yi & Qiao-Ying, 2011). Therefore, fever is another important sign facilitating the assumption of COPD exacerbation. The client has no other medical conditions, and that further simplifies the diagnostic process.
Sahn, S.A. (2012). Acute Exacerbation of Respiratory Diseases. London: Jaypee Brothers
Medical Publishers.
Xue-Jun, L., Qi, L., Liang-Yi, S., & Qiao-Ying, Y. (2011). Bacteriological Differences Between
COPD Exacerbation and Community-Acquired Pneumonia. Respiratory Care, 56(11),
1818-1824. doi:10.4187/respcare.00915.
Medical Publishers.
Xue-Jun, L., Qi, L., Liang-Yi, S., & Qiao-Ying, Y. (2011). Bacteriological Differences Between
COPD Exacerbation and Community-Acquired Pneumonia. Respiratory Care, 56(11),
1818-1824. doi:10.4187/respcare.00915.
2. John was diagnosed with the acute exacerbation of COPD. Treatment
of acute exacerbation of COPD includes:
i. Combined, increased
doses of inhaled bronchodilators , such as short-acting
beta2-agonist (SABA) and an
anticholinergic should be used to improve pulmonary function and
dyspnea.
ii. Oral or parenteral
corticosteroids are recommended in most patients with moderate to severe
AECOPD.
iii. Antibiotics are
beneficial to treat more severe purulent AECOPD.
iv. Long-term continuous oxygen (15
h/day or more to achieve an oxygen saturation of 90% or greater) to
patients with AECOPD with severe hypoxemia.
Pharmacotherapy of AECOPD (O'Donnell DE et al., 2008):
Long-acting anticholinergic + Inhaled corticosteroid/long-acting beta2-agonist (ICS/LABA) + Short-acting beta2-agonist - PRN; Persistent disability: Long-acting anticholinergic + Inhaled corticosteroid/long-acting beta2-agonist (ICS/LABA) + Short-acting beta2-agonist - PRN + Theophylline.
Long-acting anticholinergic + Inhaled corticosteroid/long-acting beta2-agonist (ICS/LABA) + Short-acting beta2-agonist - PRN; Persistent disability: Long-acting anticholinergic + Inhaled corticosteroid/long-acting beta2-agonist (ICS/LABA) + Short-acting beta2-agonist - PRN + Theophylline.
i.
Bronchodilators (Bostock-Cox, 2010; Higginson, 2010)
Long-acting
anticholinergics
(LAACs) (eg, tiotropium bromide (Spiriva): onset 30 mins and lasts 24 hours). Tiotropium provides improvements in lung
hyperinflation, exercise endurance, exacerbations and health resource
utilization in patients with moderate to severe COPD. Apart from occasional dry
mouth, inhaled anticholinergic drugs are generally well tolerated.
ICS/LABA combinations: Two combination ICS
and LABA, long-acting beta2-agonist, products are currently available in
Canada: fluticasone plus salmeterol (Advair), and budesonide plus formoterol
(Symbicort). The LABA/ICS combination seemed to have better anti-inflammatory
effect than either LABA or ICS by itself.
Short-acting
bronchodilators
(eg, Salbutamol /ventolin), both anticholinergics and beta2-agonists, have been
shown to improve pulmonary function, dyspnea and exercise performance in
patients with moderate to severe COPD. Inhalers:
(Albuterol/salbutamol) Ventolin, combivent. These medications provide relief
from COPD symptoms (wheezing, tightness in the chest, shortness of breath and
coughing). Relievers relax the muscle around the airways, making the airways
wider and breathing easier.
ii. Corticosteroids (Bostock-Cox, 2010; Hudd & Zaiken, 2011)
Oral corticosteroids: There is modest benefit of improvement with oral corticosteroids. Corticosteroids are beneficial during AECOPD, however, long-term use of low-dose oral steroids is not recommended in COPD due to serious adverse effects associated with maintenance use of systemic corticosteroids.
Tablets:
Singulair; Inhalers: Beclovent (Beclomethasone) , Flovent (Fluticasone), Advair
(combination of Servent and Flovent) and symbicort (newest on the market). Preventers reduce the redness and swelling
inside the airways and dry up the mucus. The medication containers are normally
autumn coloured (brown, orange, yellow or white). Rescue tablets or syrup: Prednisone,
Prednisolone.
Flovent is
an inhaled corticosteroid. It is not a rescue type medication and is not meant
to replace fast acting medications. Flovent is a preventative medication that
acts as an anti-inflammatory medication. Symbicort is a combination of an
anti-inflammatory corticosteroid and a rapid and long-lasting bronchodilator to
provide a simple, convenient and effective treatment.
Nursing teaching: It is important to rinse mouth with water after each steroid dose. This will help prevent hoarseness and throat irritation. This will also prevent unwanted side effects that may occur with inhaled steroid use. One of these side effects is oral thrush.
Oral theophyllines: Relatively weak bronchodilators that offer modest improvements in pulmonary function, dyspnea and exercise performance.
iii. Antibiotic during AECOPD
First choice:
Amoxicillin, cephalosporins, doxycycline, extended-spectrum macrolides,
trimethoprim/sulfamethoxazole (in alphabetical order). Patient
with complicated exacerbation: Fluoroquinolone, beta-lactam/beta-lactamase
Murinhibitor (in order of preference) (O'Donnell DE et al., 2008).
Bostock-Cox, B. (2010). Prescribing
inhaled therapies in the treatment of COPD. Nurse Prescribing, 8(12),
571-577.
O'Donnell DE, Hernandez P, Kaplan A,
Aaron S, Bourbeau J, Marciniuk D, Balter M, Ford G, Gervais A, Lacasse Y,
Maltais F, Road J, Rocker G, Sin D, Sinuff T, Voduc N. (2008). Canadian Thoracic
Society recommendations for management of chronic obstructive pulmonary disease.Can Respir ,15 Suppl A:1A-8A
Higginson, R. (2010). COPD:
Pathophysiology and treatment. Nurse Prescribing, 8(3), 102-110.
Hudd, T., R., & Zaiken, K.
(2011). Management of chronic obstructive pulmonary disease: An emphasis on
recently approved medications and products in the pipeline. Formulary, 46(9),
374-393.
3. The nurse would tell John that COPD is an irreversible disease, and smoking cessation does not stop lung inflammation and subsequent airflow limitation. This may be due to the lung not being able to remove some of the harmful components of cigarette smoke, or not being able to repair the damaged pulmonary tissues. Quitting cigarette smoke is however, the most effective means of slowing down the progression of this disease (Tashkin & Murray, 2009). Research has confirmed that there is an associated reduction in symptoms of wheeze, cough and sputum production in smokers who were able to quit. More than 80% of sustained quitters who had a chronic cough at baseline when still smoking, reported they no longer had a cough one year later (Pride, 2001).
In this situation, the nurse would also let John know how important it is to stay smoke-free, since it is considered the most important treatment for individuals with COPD.
Pride, N.B. (2001). Smoking cessaion: effects on symptoms, spirometry and future trends in
COPD. Thorax, 56, ii7-ii10.
Tashkin, D.P., & Murray, R.P. (2009). Smoking cessation in chronic obstructive pulmonary
disease. Respiratory Medicine, 103(7), 963-974.
In this situation, the nurse would also let John know how important it is to stay smoke-free, since it is considered the most important treatment for individuals with COPD.
Pride, N.B. (2001). Smoking cessaion: effects on symptoms, spirometry and future trends in
COPD. Thorax, 56, ii7-ii10.
Tashkin, D.P., & Murray, R.P. (2009). Smoking cessation in chronic obstructive pulmonary
disease. Respiratory Medicine, 103(7), 963-974.
4. After
the acute exacerbation of COPD has been stabilized, health education and
self-management are the important interventions to decrease the chance of being
re-admitted (Bourbeau et al., 2003).
- Encourage John to continue the smoking cessation. There is an associated reduction in symptoms of wheeze, cough and sputum production in smokers who were able to quit (Pride, 2001).
- In COPD, pulmonary rehabilitation has been proven to increase exercise capacity, reduce symptoms, and improve quality of life (Lacasse 2006).
- Health education also includes effective inhaler technique, early recognition and treatment of acute exacerbations, identification of community resources and end-of-life care issues. (O'Donnell et al., 2008)
- The self-treatment guideline (action plan) is a written plan produced for the purpose of patient self-management of COPD exacerbations. It informs patients about when and how to adjust and/or start medication in case of an exacerbation (Effing et al., 2007). The nurse should discuss the action plan with John together, which includes use of standby oral steroids and antibiotics.
- Give dietary advice if John’s BMI either over 25kg/m2 or less than 20kg/m2. Suggest John consult it with a dietitian.
- Suggest pneumococcal vaccination and annual influenza vaccination. The viral
infections and bacterial infections are the major causative factors for the
exacerbation of COPD (Papi, Luppi, Franco, & Fabbri, 2006).
Bourbeau J, Julien M, Maltais F, et al. (2003) Reduction of
hospital utilization in patients with chronic obstructive pulmonary disease: a
disease-specific self-management intervention. Arch Intern Med ; 163: 585–591
Effing
T, Monninkhof EM, van der Valk PD, et al. (2007) Self-management education for
patients with chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews 2007; 4:
Lacasse
Y, Goldstein R, Lasserson TJ, Martin S. (2006) Pulmorary rehabilitation for
chronic obstructive pulmonary disease. Cochrane
Database of Systematic Reviews 2006, Issue 4.
O'Donnell DE, Hernandez P and Kaplan A et al. (2008) Canadian Thoracic Society recommendations for management of chronic obstructive pulmonary disease-2008 update-highlights for primary care. Canadian Respiratory Journal: Journal of the Canadian Thoracic Society, 15(Suppl A), 1A-8A
O'Donnell DE, Hernandez P and Kaplan A et al. (2008) Canadian Thoracic Society recommendations for management of chronic obstructive pulmonary disease-2008 update-highlights for primary care. Canadian Respiratory Journal: Journal of the Canadian Thoracic Society, 15(Suppl A), 1A-8A
Pride,
N.B. (2001). Smoking cessaion: effects on symptoms, spirometry and future
trends in COPD.
Thorax, 56, ii7-ii10
