PT CASE: COPD EXACERBATION
(INSTRUCTOR VERSION)
By Dan Waldman, MD
Department of Family and Community Medicine
GOALS FOR SESSION
At the end of the session, the residents should:
1. Understand the initial approach to the urgent treatment of a patient with a
COPD Exacerbation.
2. Understand the different modalities typically utilized in the treatment of
COPD Exacerbations.
3. Recognize patients who may need more aggressive intervention, such as
Positive Pressure Ventilation, or Mechanical Intubation
4. Understand some basics of the magnitude of the societal burden of chronic
COPD and COPD exacerbations.
CASE PRESENTATION WITH QUESTIONS
A 65 year old Cuban male comes to the ED because of shortness of breath. He notes
that over the last 2-3 years he has had gradual worsening of his ability to exert himself
without feeling out of breath, and it has been acutely worse for the past week,
including a worsening productive cough. On questioning, he reveals that he coughs
almost every morning as well, and this has been going on for even longer, perhaps 4-5
years. The cough is now productive of yellowish-brownish sputum. He denies chest
pain, fevers, chills or night sweats. He has no history of lower extremity edema. The
rest of his review of systems is negative.
Other than an appendectomy when he was in his 20’s, the patient denies any
significant past medical history. He denies taking any medications, but does state that
a year ago he went to a walk-in clinic for cough and got some kind of inhaler, which he
used over the course of a month or two until it was gone. He lives in an apartment
with his wife, and has smoked a pack of cigarettes a day for 40 years.
On exam, his BP is 144/88 mmHg, HR is 98, respiratory rate is 28 breaths per minute.
His temp is 97.6. Oxygen saturation is documented as 93% on 4 L. You find him
sitting up in the ED bed, leaning forward. He appears uncomfortable with labored
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breathing and his lips are bluish. There is no cervical lymphadenopathy, JVD or
carotid bruits. Chest exam shows mild intercostal retractions seen around the
anterolateral costal margins. Wheezes and rhonchi are present bilaterally, without
crackles. Heart exam is unremarkable, though the heart sounds are distant. Lower
extremities show no cyanosis, clubbing or edema.

Q. What is the most likely diagnosis?
A. COPD with acute exacerbation.

Q. What is the most appropriate next diagnostic step?
A. Given the patient’s respiratory difficulty seen on exam and possible
hypoxia, an ABG would be helpful to measure adequacy of oxygenation
(PaO2) and ventilation (PCO2). In this case, the ABG was taken and found
to be 7.32/58/86/30. It was done while the patient was on room air.

Q. What is the interpretation of this ABG? (ABG values not given on
student version)
A. This ABG shows marked respiratory acidosis with a partial compensatory
metabolic alkalosis.
The patient’s room air saturation is subsequently found to be 84-86%. You vaguely
remember something about some kind of respiratory drive and suppressing it with too
much oxygen. You also remember that some people disputed this.

Q. What should your target O2 saturation be for this patient?
A. Target oxygen saturation should be 90-92%. Hypercapnia can
accompany the aggressive use of supplemental oxygen. While decreased
alveolar ventilation caused by suppression of the hypoxic drive does not
appear to play a major role by itself, this O2 target can help maximize
hemoglobin saturation, and lessen the likelihood of hypercapnia from
ventilation/perfusion mismatches. Placing patients with chronic COPD
and acute respiratory failure on 100% O2 has been shown to increase CO2
levels, by 23 +/- 5 mmHg in one study. (Ambier M, 1980)

Q. If this patient also had a history of heart failure, what test might be
helpful to exclude CHF as playing a role in the patients dyspnea?
A. B-type natriuretic peptide (BNP) can be used to help distinguish heart
failure from other causes of dyspnea. Use of BNP in the ED for patients
with dyspnea and a history of pulmonary disease can decrease the
likehood of admission (81% vs 91%; P = .034) and decrease time spent in
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the hospital (9 days vs 12 days; P = .001), as well as overall decreased
cost of care ($4841 US vs $5671 US; P = .008) (Mueller C, 2006).
In March of 2007, UNM adopted a new BNP test. This propeptide test is
listed as having a cutoff for a negative test as ≤125pg/mL for patients less
than 75, and ≤450 pg/mL for patients more than 75 years old. The “ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE)”
study evaluated this methodology and found the following results (
Januzzi JL Jr, Apr 2005) (note: this table appears at the end of the
student version as well):
Optimal Cut
Point
(pg/mL)
900
Sensitivity
(%)
90
Specificity
(%)
85
PPV (%)
76
NPV
(%)
94
<50 years old
450
93
95
67
99
≥ 50 years olf
900
91
80
77
92
300
99
68
62
99
RULE-IN Cut
Points
All Patients
RULE-OUT Cut
Point
All Patients
You obtain a BNP, and it’s 185. Additionally, a chest XRay shows only hyperinflation,
without acute infiltrates.

Q. What are the mainstays of treatment of acute COPD Exacerbations?
(answers to this question are also on the student version)
A. Routine treatment includes use of bronchodilators, systemic
corticosteroids and antibiotics. For patients sick enough to be
hospitalized, oxygen and possibly mechanical ventilation are often used.
1. Bronchodilators
a. Inhaled Beta Adrenergic Agonists

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Bronchodilators: the mainstay of therapy for acute exacerbations.
Rapid onset of action and efficacy in producing bronchodilation. Data
indicate similar efficacy with nebulizer or MDI, but MDI requires
patients to be more alert, and nebs still recommended by many
experts.

2.5 mg of albuterol is as efficacious in improvement of spirometry and
clinical outcomes, but 5mg still used often.(Nair, 2005).
b. Anticholinergic Bronchodilators

May be used in combination with beta adrenergic agonists to produce
bronchodilation in excess of that achieved with either agent alone.
2. Systemic Corticosteroids


Reduce 30 day treatment failure rate (23% vs 33%), 90 day treatment
failure rate (37-48%) and length of hospital stay (8 vs 10 days), while
improving lung function (Niewoehner, 1999).

Oral steroids have been shown to be effective for outpatient therapy,
while serious COPD exacerbations requiring hospitalization usually
call for starting with intravenous steroids, though data is limited.
Q. What about using steroids when the patient also has an underlying
infection, such as community acquired pneumonia?
A. This is an interesting question that often comes up and is difficult to
answer. We do know that COPD is a common co-morbidity in
hospitalized patients with CAP, and many of these patients receive
steroids. It seems that being on chronic steroids and subsequently
developing pneumonia increases mortality, as does just having the
diagnosis of COPD (Restrepo., 2006), but it is unclear what affect acute
administration of systemic steroids has on otherwise nonimmunosuppressed patients with CAP. Some preliminary studies have
actually shown improved outcomes with the administration of systemic
steroids in CAP, in patients without COPD (Confalonieri M, 2005). For
now we can only say that patients with the dual diagnosis of COPD and
CAP often receive system steroids, and the implications are not entirely
clear.

Q. What is the usual dose and time course of systemic corticosteroids in
this condition?
A. While there is no “correct” dose and taper, the usual starting dose for
admitted patients with COPD exacerbations is 1-2mg per kg of
methylprednisolone (Solu-Medrol) given every 6 to 12 hours. After 2-3
days of IV therapy, the patient can be switched to oral administration,
usually starting at 60mg prednisone daily, and tapered down for a total
course of 2 weeks of treatment. 8 weeks of steroids seems to offer no
benefit over 2 weeks (Niewoehner, 1999). Future directions may include
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studying which specific patient populations need to be tapered more
slowly, particularly older men with severe irreversible airway
obstruction (O'Brien A, 2001) .
3. Antibiotics

Antibiotics are recommended for acute exacerbations of COPD that
are characterized by “increased volume and purulence of secretions.”
They decrease mortality and treatment failure rates, while
accelerating improvement of peak expiratory flow rates (Ram, 2006).

Some advocate for the use of broad spectrum antibiotics in older
patients (over 65), patients with more frequent exacerbations or
patients with more severe exacerbations. There is no clear data to
support this position at present. Data on improvement with
antibiotics has been largely studied with doxycycline, trimethoprimsulfamethoxazole and amoxicillin (Anthonisen NR, 1987), usually
with a 10 day course. Some experts believe sicker hospitalized
patients should receive antipsuedomonal coverage, and recommend
treatment of the most serious exacerbations with a 3rd generation
cephalosporin or an augmented penicillin plus a fluorquinolone or
aminoglycoside for synergy. Examples of this coverage would be
ceftriaxone or unasyn plus levaquin or tobramycin (Hunter M, 2001).
4. Mucokinetic regimens

The use of mucolytic agents, chest physiotherapy, intermittent
positive pressure breathing and directed coughing have not been
shown to be effective.
5. Methylxanthines

Methylxanthines do not appear to significantly help in patients with
mild to moderate exacerbations of COPD. They may be of limited use
in patients with severe exacerbations, but they have a narrow
therapeutic index and high risk of toxicity.
6. Oxygen therapy

Venturi masks can provide precise FiO2 values, which can help
monitor oxygen status over time in patients where nasal cannula is
insufficient.
You admit the patient, write orders and then start seeing another admission. You are
called by the ED nurse who wants to let you know that your admitted patient with
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COPD looks worse, and is now somnolent and confused. You ask the nurse to draw
another ABG and go assess the patient.

Q. When should non-invasive positive pressure ventilation be
considered?
A. In situations where there is a need for ventilator assistance, as indicated
by hypercapnia associated with depressed mental status, profound acidemia,
worsening dyspnea and/or worsened oxygenation (e.g. ratio of PaO2 to FiO2
less than 200). It is possible that our patient’s hypercapnia is worsening and
causing somnolence and confusion. Benefits of positive pressure-ventilation
are lower rates of intubation, lower in-hospital mortality rates and shorter
hospital stays (Stoller, Mar 2002).

Q. Which patients are likely to need intubation?
A. Patients with respiratory arrest, medical instability (hypotensive shock,
cardiac ischemia), an inability to protect their airway, excessive
secretions, agitation or uncooperativeness (or those with a facial
structure that precludes proper mask fitting) are likely to need
intubation.
ADDITIONAL BACKGROUND INFORMATION (ALSO IN STUDENT VERSION)
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
The American Thoracic Society defines COPD as a disease process involving
progressive chronic airflow obstruction because of chronic bronchitis,
emphysema, or both. Chronic Bronchitis is defined clinically as excessive
cough and sputum production on most days for at least 3 months during at
least two consecutive years. Emphysema is characterized by chronic
dyspnea resulting from destruction of interalveolar septa. Emphysema
occurs in the distal or terminal airways and involves both airways and lung
parenchyma.

In the United States, age-standardized death rate amongst persons with
COPD doubled from 1970 to 2000 (Jemal A, 2005). COPD is now the 4th
leading cause of death in the U.S., and the only leading cause of death for
which the mortality rate is increasing.

Cigarette smoking is implicated in 90% of COPD cases.

The strongest predictors of mortality are older age and a decreased forced
expiratory volume per second (FEV1). 60 year old smokers with chronic
bronchitis have a 10 year mortality rate of 60 percent, which is four times
higher than the mortality rate for age-matched asthmatics (Hunter M, 2001).

Alpha1-antitrypsin deficiency should be suspected when COPD develops in a
patient younger than 45 years who does not have a history of chronic
bronchitis or tobacco use, or when multiple family members develop lung
disease at an early age.

Don’t forget to immunize patients with COPD (pneumococcal and influenza
vaccines)
BIBL I OGR AP H Y
Ambier M, M. D.-E. (1980). Effects of the administration of O2 on ventilation and blood gases in
patients with chronic obstructive pulmonary disease during acute respiratory failure. Am Rev Respir
Dis , 122:747-54.
Anthonisen NR, M. J. (1987). Antibiotic Therapy in Exacerbations of Chronic Obstructive Pulmonary
Disease. Ann Intern Med , 106:196-204.
Confalonieri M, U. R. (2005). Hydrocortisone infusion for severe community-acquired pneumonia: a
preliminary randomized study. Am J Respir Crit Care Med , 171:242–248.
Hunter M, K. D. (2001). COPD: Management of Acute Exacerbations and Chronic Stable Disease. Am
Fam Physician , 64:603-612.
Januzzi JL Jr, e. a. (Apr 2005). The N-terminal Pro-BNP investigation of dyspnea in the emergency
department (PRIDE) study. Am J Cardiol , 95(8): 948-54.
Jemal A, W. E. (2005). Trends in the leading causes of death in the United States, 1970-2002. JAMA ,
264:1255-9.
Mueller C, L.-K. K. (2006). Use of B-type natriuretic peptide in the management of acute dyspnea in
patients with pulmonary disease. Am Heart J , 151:471-77.
Nair, S. T. (2005). A randomized controlled trial to assess the optimal dose and effect of nebulized
albuterol in acute exacerbations of COPD. Chest , 128:48.
Niewoehner, D. E. (1999). Effect of systemic glucocorticoids on exacerbations of chronic obstructive
pulmonary disease. N Engl J Med , 340:1941.
O'Brien A, R.-M. P. (2001). Effects of withdrawal of inhaled steroids in men with severe irreversible
airflow obstruction. Am J Resp Crit Care Med , 164:365-371.
Ram, F. R.-R.-N. (2006). Antibiotics for exacerbations of chronic obstructive pulmonary disease.
Cochrane Database Syst Rev , CD004403.
Restrepo MI, M. E. (2006). COPD is associated with increased mortality in patients with communityacquired pneumonia. Eur Respir J , 28:346-35.
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Stoller, J. (Mar 2002). Acute Exacerbations of Chronic Obstructive Pulmonary Disease. NEJM , 988994.
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to Dr.
Wendy Gerstein, Department of Medicine, VAMC (111).
1) Topic of module:__________________________
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2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment
below:
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient
curriculum in general:
6) Please circle one:
Attending
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Resident (R2/R3)
Intern
Medical student