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which reduces myocytoplasmic calcium concentration thereby causing bronchial smooth muscle relaxation.
15
Three doses, 2.5–5 mg each, administered
every 20 minutes in the ED is a safe initial strategy.
Sixty to seventy percent of patients will respond well
enough to the initial three doses to be discharged
home.
16
Further treatments for patients that have a
response that is not sufficient to allow discharge
home can be given in the OU if it is felt that the
patient will require more than 1–2 hours more of
treatment and less than the time constraints of the
unit, usually < 24 hours. Patients anticipated to
require more prolonged treatment should be admitted to the hospital directly from the ED.
The primary anticholinergic agent used for
asthma is ipratropium bromide. Ipratropium bromide is a synthetic quaternary derivative of atropine. It
has virtually replaced atropine, as the inhaled anticholinergic of choice, due to its improved side effect
profile. Anticholinergic medications competitively
antagonize acetylcholine at the post ganglionicjunction of the parasympathetic nerve terminal.
15
This
results in bronchodilation of the larger airways,
which compliments the dilation of smaller airways
caused by beta2 agonists.
15
The combination of an inhaled beta2 agonist
and an inhaled anticholinergic agent has been
shown to decrease hospitalizations in patients
with severe airway obstruction.
17,18
The exact mechanism of systemic corticosteroids has not been fully elucidated, but the effect is
felt to be due to increasing responsiveness to beta2
agonists and decreasing inflammation. Onset of
action is 4 to 8 hours after administration. Use of
systemic corticosteroids administered within an
hour of admission results in a decreased need for
hospitalization.
15
The usual dose is oral prednisone
40–80 mg daily or methylprednisolone 1 mg/kg.
15
Supplemental oxygen should be administered to
patients to maintain an oxygen saturation of greater
than 90%. Magnesium, usually used in moderate to
severe asthma is generally administered in the ED.
The dose is 1–2 grams IV over 30 min.
Heliox and ketamine are used for severe
asthma and, thus, are not appropriate for OU
patients. Leukotriene modifiers, mast cell modifiers, and theophylline are maintenance medications and are not used during an acute asthma
attack. Aminophylline has virtually disappeared
from the pharmacologic armamentarium due to
its side effects profile. Generally patients sick
enough to require positive pressure ventilation
are sick enough to be admitted to the hospital.
Disposition
Patients who fail to respond or become worse
during treatment should be hospitalized. Some
patients may become worse to the point of
requiring intubation. The OU should have staff,
equipment, and expertise to manage acutely
decompensating asthma patients. Certain patients
are at increased risk for death during an asthma
exacerbation. Those who have had repeated ED
visits, repeated hospitalizations, ICU stays or prior
intubations with asthma warrant close monitoring
of their respiratory status. Medical conditions that
Table 27.2 Inclusion and Exclusion Criteria for Adult
Asthma Patients in an Observation Unit
Inclusion Exclusion
Improved clinical
course in ED
(measured PEFR or
FEV1) but patient not
well enough to go
home
Systolic BP < 80 or > 200
Expected discharge
within time parameters
of the observation unit
Respiratory Rate > 40
No new symptoms
suspicious for ACS, CHF
Pulse > 140
No pneumothorax Hypoxia (or changed
from patient’s baseline if
on home O
2
)
Unit has capabilities to
perform respiratory
treatments and
assessments
Unable to speak due to
SOB
Unit has capability to
intervene if patient
decompensates
Indecision between ICU
vs. medical floor
Pulse Oximetry < 80 on
room air, pH < 7.3 or >
7.5, pO
2
< 60, pCO2> 50
ECG changes consistent
with ACS
ED = emergency department
PEFR = peak expiratory flow rate
FEV1 = forced expiratory volume one second
ACS = acute coronary syndrome
CHF = congestive heart failure
ICU = intensive care unit
SOB = shortness of breath
ECG = electrocardiogram
Asthma
030
20:58:41
complicate asthma care include congestive heart
failure, pneumonia, psychiatric conditions, and
substance abuse. Other risk factors that increase
the risk of death in asthma are listed in Table 27.3.
Patients who respond to treatment and are
deemed fit for discharge should have discharge
instructions reviewed with them prior to discharge. There should be an asthma treatment plan
if symptoms become worse, in the follow-up
instructions. Patients with asthma severe enough
to place them in an OU will generally require oral
corticosteroids for 3–10 days after discharge.
15, 16
Those who have returned for the second time or
whose symptoms persisted for several weeks prior
to presentation may require a longer oral treatment course and a slow taper over a longer period
of time. A Canadian study showed that patients at
risk for relapse and return visit to the ED include
those with the following characteristics: ethnicity
(white), gender (female), prior ED visits and hospital admissions, and recent treatment with oral
corticosteroids.
19
Discharge instructions should
include with whom (person or clinic) and when
the patient should follow up. The patient should
have prescriptions for needed medications: oral
corticosteroids, meter dose inhalers for beta adrenergic medications and anticholinergic medications. Prescriptions for maintenance meter dose
inhalers for long acting beta2 adrenoreceptor
agonist and inhaled steroids should be written
if patient is on these medications and has run
out. The patient should be educated in the use of
a spacer device. If the patient does not have one,
a prescription for a spacer device should be
provided. The patient can use the inhaled corticosteroid while on the tapering dose of oral
corticosteroids.
16
Conclusion
Treatment of appropriate patients with asthma in
an OU is an efficient and safe utilization of
limited health care resources. These patients
should be expected to be discharged from the
OU after a period of treatment that is expected
to be within the time parameters of the OU. The
OU should have the capability to perform serial
evaluations and treatments of asthma patients.
The personnel in the OU should have the ability
to intervene if the patient becomes unexpectedly
worse during the treatment period. Use of an OU
can free up hospital beds for sicker patients. OU
treatment can be done at less cost than hospitalization.
20,21
Treatment time in the OU is less than
treatment time in the hospital.
20
References
1. Fanta CH, Fletcher SW. An
overview of asthma
management. Up to date. 2012
www.uptodate.com/contents/
an-overview-of-asthmamanagement?source=see_link
2. Ginde AA, Espinola JA,
Camargo CA. Improved overall
trends but persistent racial
disparities in emergency
department visits for acute
asthma, 1993–2005. J Aller
Clin Immunol 2008;122:
313–318.
3. Rowe BH, Voaklander DC,
Wang D, et al. Asthma
presentations by adults to
emergency departments
in Alberta Canada a
large population based
study. Chest 2009;135:
57–65.
Table 27.3 Risk Factors for Death in Asthma
Asthma History
Pervious ICU admit or intubation for asthma
Two or more hospitalizations with asthma in the last
year
Three or more ED visits for asthma in the last year
Hospitalization or ED visit for asthma in the past
month
Using > 2 canisters of SABA per month
Difficulty perceiving severity of asthma
Social History
Low socioeconomic status or inner city residence
Illicit drug use
Comorbidities
Cardiovascular disease
Other chronic lung disease
Chronic psychiatric disease
Physician Factors
Failure to evaluate severity
Failure to disposition appropriately
Failure to prescribe appropriate therapy
Failure to address comorbidities
ICU = intensive care unit
ED = emergency department
SABA = short acting beta2 agonist
Adapted from References:
13,16
Eric Anderson
030
20:58:41
4. Tsai CL, Sullivan AF, Gordon
JA. Quality of care for acute
asthma in 63 US emergency
departments. J Allergy clin
Immunol 2009;123:354–361.
5. Manfreda J, Becklake MR,
Sears MR, et al. Prevalence of
asthma symptoms among
adults aged 20–44 yrs in
Canada. Can Med Assoc J 2001;
164:995–1001.
6. Moorman JE, Rudd RA,
Johnson CA, et al. National
surveillance for asthma: United
States, 1980–2004. MMWR
Surveill Summ 2007;56:1–54.
7. Sly RM. Decreases in asthma
mortality in the United States.
Ann Allergy Asthma Immunol
2000;85:121–127.
8. Sly RM. Continuing decreases
in asthma mortality in the
United States. Ann Allergy
Asthma Immunol 2004;92:
313–318.
9. Agency for healthcare research
and quality, Rockville, MD
HCUP statistical brief # 58.
Hospital stays related to
asthma for children. 2006,
2008. www.hcup-us.ahrq.gov/
reports/statbriefs/sb58.jsp
10. Hodder R, Lougheed MD,
Fitzgerald JM, et al.
Management of acute asthma
in adults in the emergency
department: assisted
ventilation. CMAJ 2010;182(3):
265–272.
11. Akinbani L. Asthma
prevalence, healthcare use and
mortality: United States,
2003–5. www.cdc.gov/nchs/
product/pubs/pubd/hestats/
asthma03-05/asthma03-
05.htm.
12. Crane S, Sailer D, Patch SC.
Improving asthma care in
emergency departments:
Results of a multihospital
collaborative quality initiative
in rural western North
Carolina. NCMJ 2011;72
(2):111–117.
13. Mace SE. Asthma therapy in
the observation unit. Emerg
Med Clin of N America 2001;
19(1):1–16.
14. Tapp S, Lasserson TJ, Rowe
BH. Education interventions
for adults who attend the
emergency room for acute
asthma (Review). The Cochrane
Collaboration. The Cochrane
Library 2010 issue 10. Pub John
Wiley & Sons Ltd. 1–60.
15. Cydulka RK. Acute Asthma in
Adults. Emergency Medicine:
A Comprehensive Study Guide.
Tintinalli JE, Ma J, Cline DM,
et al. (eds.) 7th ed 2011;
504–511.
16. Camargo CA, Rachelefsky G,
Schatz. Managing asthma
exacerbations in the emergency
department: summary of the
national asthma education and
prevention program expert
panel report 3 guidelines for
the management of asthma
exacerbations. J Em Med
2009;37:2S:S6–S17.
17. Plotnick LH, Ducharme FM.
Combined inhaled
anticholinergics and beta2agonists for initial treatment of
acute asthma in children.
Cochrane Database Syst Rev
2000; (4):CD000060.
18. Rodrigo GJ, Castro-Rodriguez
JA. Anticholinergics in the
treatment of children and
adults with acute asthma: a
systematic review with metaanalysis. Thorax 2005;60:
740–746.
19. Rowe BH, Villa-Roel C,
Sivilotte LA, et al. Relapse after
emergency department
discharge for acute asthma.
SAEM 2008;15(8):709–17.
20. Leykum LK, Huerta V,
Mortensen. Implementation
of a hospitalist-run observation
unit and impact on length
of stay (LOS): a brief
report. J of Hosp Med 2010;5:
E2–E5.
21. Rydman RJ, Isola ML, Roberts
R et al. Emergency department
observation unit versus
hospital inpatient care for a
chronic asthmatic population:
a randomized trial of
health status outcome and
cost. Med Care 1998;36(4):
599–609.
Asthma
030
20:58:41
Subpart IVB
Chapter
28
Clinical – Respiratory
Acute Exacerbation of Chronic Obstructive
Pulmonary Disease and Bronchitis
Eric Anderson, MD, MBA, FACEP, FAAEM
Introduction
Chronic obstructive pulmonary disease (COPD) is
commonly encountered in the emergency department (ED). COPD is the term used to describe
a spectrum of pulmonary disease that includes a
reversible component of airway obstruction, a
chronic cough with sputum component (bronchitis) and an emphysematous component where
there is irreversible destruction of terminal
airways. There are 1.5 million ED visits in the
United States due to COPD.
1
COPD is the third
most common cause for hospital admissions, with
an estimated 726,000 admissions in 2000.
2
COPD
is the fourth leading cause of death in the United
States.
2,3
According to the World Health Organization, COPD is projected to be the third leading
cause of death and the fifth leading cause of disability worldwide by the year 2020.
4
The mortality
of COPD is significant with a greater than 50%
mortality rate within 10 years of diagnosis.
5
The
World Health Organization estimates that 80 million people worldwide suffer from moderate
COPD and that there were 3 million deaths worldwide due to COPD.
4
ThecostofCOPDtosociety
is significant. In 2007, the total estimated expenditure for COPD in the United States was $42.6
billion with direct medical costs accounting for
26.7 billion.
6
COPD was listed as the primary or
secondary diagnosis in 8.5% of all U.S. admissions
for patients > 25 years old and 11.5–15.1% of all
hospitalizations in patients > 65 years old.
7
Pathophysiology
COPD is characterized by airway obstruction and
inflammation. Unlike asthma, the obstruction is not
fully reversible. There is an inflammatory component and a component due to destruction of elastic
recoil of the smaller airways as well as narrowing of
theairwaysduetomucosaledema,bronchospasm
and bronchoconstriction.
8
COPD has two main
types, chronic bronchitis and emphysema.
Emphysema, which represents approximately
15% of patients with COPD, is characterized
by a progressive destruction of lung tissue as a
result of a cellular and chemotactic response to
chronic irritants in the terminal airways.
9
The
most common irritants are cigarette smoke and
recurrent industrial exposures. A similar response
is seen in alpha 1-protease deficiency where the
enzyme elastase, elaborated by polymorphonucleocytes, destroys the alveolar septum, which
provides support for the bronchial walls. Without
the alveolar septal support, the bronchioles collapse
early during expiration resulting in airway obstruction. Alpha 1-protease (and alpha 2-macroglobulin)
inactivate elastase and provide protection against
alveolar septal destruction.
9
Emphysema is a pathological diagnosis based
on lung tissue findings. The small airways collapse
prematurely on exhalation. These patients compensate for the diminishing lung function by
expanding the chest cavity to increase the available lung capacity. These patients do not ventilate
well and will increase the work of breathing to
compensate. The rate and depth of breathing will
be increased in order to maintain adequate ventilation. This increased work of breathing causes
increased metabolic energy demands. The problem
is ventilation not oxygenation.
9
Clinical findings
that typify the emphysematous patient include
tendency to be thin, have a barrel chest, use pursed
lipped breathing, and maintain oxygenation.
This presentation has come to be known as the
“pink puffer.”
Chronic bronchitis is characterized by the
hypersecretion of mucus and airway inflammation and obstruction with decreased airflow.
There is a loss of surfactant and protease inhibitor
producing pulmonary epithelial cells, which are
replaced by mucus producing cells.
8
There is
recruitment of inflammatory cells, which leads
to chronic inflammation and narrowing of the
airways. This results in fibrosis and narrowing
031
20:58:47
resulting in chronic bronchitis.5These patients
will have a chronic cough. Chronic hypoxia and
decreased cardiac output secondary to pulmonary
hypertension and cor pulmonale gives these
patients the appearance of mild cyanosis and peripheral edema.
9
The underlying problem is one of
poor oxygenation. The classic appearance of these
patients is that they will tend to retain CO
2
,
appear somewhat edematous and cyanotic, the
“blue bloater.” Chronic Bronchitis is a diagnosis
based on clinical findings: cough producing
sputum for 3 months out of the year for 2 consecutive years not attributable to another cause.
Most COPD patients present with a combination of chronic bronchitis and emphysema symptoms. It is the rare patient that will be purely one or
the other.
5
A dominant risk factor for the development
of COPD is cigarette smoking. Fifteen percent
of chronic smokers develop COPD. Why some
smokers develop COPD and others do not is not
clearly understood. Five to ten percent of COPD
patients have never smoked.
10
Alpha 1 anti-
trypsin deficiency is present in 1–2% of COPD
patients.
5
Other factors that predispose for the
development of COPD include indoor and outdoor air pollution from fuel burning and oc cupational ex posures.
4,11
The Global initiative for chronic obstructive
lung disease (GOLD) has adopted a definition
for COPD that recogn izes airflow limitation as
often being progressive and associated with an
abnormal inflammatory response of the lungs
to noxious particles and gases.
4,12
The GOLD
classification of COPD has four stages of severity. With Stage I Mild COPD, the FEV1 is 80%
of predicted, with or without chronic symptoms
(cough, sputum production). Stage II Moderate
COPD is FEV1 between 50% and 79% of predicted and the patient may have dyspnea on
exertion and cough. Stage III Severe COPD is
FEV1 between 30% and 40% of predicted, and
reduced exercise capacity. Stage IV very severe
COPD is FEV1 < 30% predicted or < 50% predicted with chronic respiratory failure. In all
stages the FEV1/FVC ratio is < 0.70. Since most
EDs do not have formal pulmonary function
testing, clinicians evaluate the severity of the
exacerbation clinically.
The Anthonisen criteria are historical factors
used to grade the acute exacerbation of COPD.
Three symptoms are used to evaluate the patient.
Increased sputum production, increased sputum
purulence and the presence of dyspnea are
used in the Anthonisen criteria. Type III patients
have three symptoms, Type II patients have two
of the three symptoms an d Type I have one
symptom.
13
Since patients presenting to the
ED usually have at least dyspnea, most are
Type I or II. Guidelines recommend antibiotics
at discharge for Type I and II.
13
The Anthonisen
criteria have a high clinical utility in the ED
setting.
Clinical Presentation
The typical COPD patient will present to the ED
complaining of shortness of breath (SOB) and
cough productive of phlegm. There may be
wheezing and minimal or no response to medications. In many cases the patient will know their
diagnosis. In other cases the patient will report
only a breathing problem, lung problem or frequent use of inhalers. Key elements of the history
include onset and duration of symptoms, presence of SOB, fever, chest pain, cough, production
of phlegm, change in phlegm amount or purulence and recent respiratory infection. Other
historical keys include smoking, prior similar presentations to EDs and prior intubations or ICU
stays for shortness of breath.
Differential diagnosis includes cardiovascular
disease (CVD) where chest pain may or may
not be a prominent complaint. CVD may present
with SOB only. Differentiating COPD from
CVD may be difficult on clinical grounds alone
as many patients have both conditions and both
conditions have symptoms and physical examination eleme nts that overlap. Patients with CVD
and COPD have more frequent COPD exacerbations and incur higher costs than patients with
COPD alone.
14
Cardiac enzymes will help only if
positive. Congestive heart failure (CHF) can be
difficult to distinguish from chronic bronchitis
as both conditions may present with SOB, edema
and CO
2
retention. Patient history and B type
naturetic peptide (BNP) level will help in these
situations. Some patients will have both conditions. Pneumonia may be distinguished by focal
infiltrates on chest radiograph, though a gain
there is overlap in the symptoms and physical
examination findings. Other conditi ons with
similar presentations to COPD are listed in
Table 28.1.
Acute Exacerbation of COPD and Bronchitis
031
20:58:47
Emergency Department
Management
This chapter focuses on the observation unit (OU)
management of COPD exacerbations so ED management will only be covered briefly here. Patients
are treated with beta adrenergic agonists, anticholinergics, corticosteroids, supplemental oxygen as
needed and hydration as needed. Antibiotics will
be used on most acute exacerbations of COPD.
Evaluations to rule out confounding conditions
include: a good history and physical examination,
chest radiography, electrocardiogram, BNP, and
cardiac enzymes. A decision about disposition
must be made during the emergency evaluation
and treatment period. Clinical factors associated
with poor outcome, death or need for invasive
mechanical ventilation include: advanced age, high
respiratory rate, high pulse rate, low body mass
index, neurologic impairment, number of previous
COPD exacerbation admissions, smoking, number
of Anthonisen criteria, poor performance status,
SpO
2
, APACHE II Score (Acute Physiology and
Chronic Health Evaluation II), and blood gas
values: low pH, low oxygen saturation, and high
pCO
2
. (See Table 28.2.)
15
Treatment of decompensated comorbid conditions such as CHF, diabetes, hypertension and
others should be initiated in the ED. As mentioned
earlier, patients with comorbid conditions will tend
to have more COPD exacerbations and require
more resources than patients with COPD alone.
14
A relatively high percentage of patients, up to
59% in one study, with acute exacerbation of
COPD are admitted from the ED.
13
Approximately
15% of patients discharged from the ED returned
within 2 weeks for readmission.
5
Patients suitable
for the OU include those who demonstrated some
clinical improvement of their symptoms during
the ED stay. OU patients should be those where
it is expected that their symptoms are expected to
improve during the period in the OU. Patients who
are expected to require a longer period of treatment should be admitted to the hospital from
the ED.
Observation Unit Management
Treatment should be continued in the OU at intervals that facilitate clinical improvement. Therapeutic
Table 28.1 Differential Diagnosis of Chronic Obstructive
Pulmonary Disease (COPD) Exacerbation
Cardiac
Acute Coronary syndrome
Congestive heart failure
Pulmonary
Pneumonia
Asthma
Pulmonary embolus
Pneumothorax
Other
Carbon monoxide
Hemoglobinopathy
Severe anemia
Table 28.2 Predictors of Poor Outcome in Chronic
Obstructive Pulmonary Disease (COPD) Exacerbations
(Death, Prolonged Hospitalization, Mechanical Ventilation)
Patient
Characteristics
Male sex
Age > 70 years
Continued smoking
Poor functional performance
status
Historical
Characteristics
Prior hospitalizations for
COPD within the last 6
months
Maintenance corticosteroids
Maintenance oxygen
Physical
Examination
Findings
Increased heart rate
Increased respiratory rate
Cyanosis
Low body mass index
Neurologic impairment
Asterixis
Accessory muscle use on
inspiration
Abdominal muscle use on
expiration
Labs Blood gas results: low pH, low
oxygen, high pCO
2
Adapted from Roche et al.
15
Eric Anderson
031
20:58:47
modalities include: bronchodilators, anticholinergic agents, co rticosteroids, supplemental oxygen,
antibiotics, and stabilization and treatment of
other medical conditions that may have been
exacerbated. (See Table 28.3.)
Short-acting beta adrenergic agonists administered via nebulizer device or metered dose inhaler
are first-line agents to treat the reversible component of COPD. Albuterol and levalbuterol are
the primary short-acting beta adrenergic agents
used in COPD. Salmeterol a long-acting beta
adrenergic agent is used as maintenance therapy
and is not used as treatment in the acute exacerbation of COPD. The pharmacology of these agents
is detailed in Chapter 27 on Asthma.
The anticholinergic agent ipratropium bromide
is a synthetic quaternary derivative of atropine.
This agent works to competitively antagonize
acetylcholine at the post ganglionic junction of
the parasympathetic nerve terminal.
16
This results
in dilation of the larger airways which compliments the dilation of the smaller airways caused
by beta 2 agonists.
16
Short acting beta agonists and anticholinergics
are complimentary agents used to treat the
bronchospasm component of COPD. Albuterol
2.5–5 mg with atrovent 0.5 mg given via nebulizer
every 2–4 hours while in the OU will work to
improve pulmonary function.
As described in Chapter 27 on asthma, the
exact mechanism of action of corticosteroids in
not fully understood. Onset of action is 4–8 hours
after administration. The typical dose is prednisone 60 mg orally daily or methylprednisolone 1
mg/kg IV every 6 hours.
16
Supplemental oxygen should be administered
to patients on home oxygen therapy and others as
needed to keep the saturation greater than 92%.
Caution must be used in COPD patients who are
chronically hypoxic and have adapted to hypoxia
not to provide too much oxygen and suppress the
hypoxic respiratory drive. These patients will tolerate some degree of hypoxia with saturations in
the high 80s or low 90s. Review of the medical
record with particular attention to prior arterial
blood gas results (to determine if the patient is a
Table 28.3 Treatment for Chronic Obstructive Pulmonary Disease (COPD)
Medication Dosage Therapeutic Effect Common Side Effect
Short-acting beta
adrenergic
agonists Albuterol,
Levalbuterol
Albuterol 2.5–5 mg neb every 2 to
4 hrs.
Levalbuterol 0.63–1.25 mg neb
every 4 hrs.
Bronchodilation of
small airways
Tremulousness,
anxiety, nausea, some
decrease in serum
potassium
Anticholinergics
Ipratropium
0.5 mg neb every 4 hrs. Bronchodilation of
large airways
Tachycardia,
palpitations, nausea
Antibiotics First-line: amoxicillin, trimethoprim-
sulfamethoxazole, doxycycline
Second-line: Advanced generation
quinolones, 2nd or 3rd generation
cephalosporins, amoxicillin/
clavulanate
Treat infections that
may be contributing
to the acute attack
Per the antibiotic
chosen
Corticosteroids Prednisone 40–60 mg po or
Methyprednisolone 125 mg IV
Decreases
inflammatory
response
Hyperglycemia, fluid
retention, weight gain,
adrenal suppression
Oxygen As needed to keep O
2
saturation
above 92%, between 88 and 92%
in known CO
2
retainers
Improve
oxygenation
Respiratory depression
in CO
2
retainers
Treatment of
comorbid
conditions
Neb = nebulizer
Acute Exacerbation of COPD and Bronchitis
031
20:58:47
CO2retainer) and discussions with knowledgeable patients about their baseline respiratory
status will help to determine the patient’s oxygen
requirement.
The bronchitis component of COPD is treated
with antibiotics. Antibiotics are recommended
for Anthonisen Type I and II exacerbation of
COPD.
13
Typical bacteria in the sputum of COPD
patients include: Streptococcus pneumonia, Hae-
mophilus influenzae, Moraxella catarrhalis and
Pseudomonas aeruginosa. Typical viruses include:
rhinovirus, influenza, parainfluenza, respiratory
syncytial virus, coronavirus and adenovirus.
5
P. aeruginosa should be considered in more severe
cases and in patients who have recently been
hospitalized or had several courses of antibiotics
in the last year.
13
Antibacterial coverage should
take into consideration the local bacterial sensitivity and prevalence patterns of the typical bacterial
species listed above. Typical (first-line) antibiotics
include: trimethoprim-sulfamethoxazole, ampicillin and doxycycline. However, some authors recommend amoxicillin/clavulanate, second- and
third-generation cephalosporins or advanced generation quinolones (moxifloxacin, levofloxacin) as
superior to the first-line antibiotics.
5
Treatment
with antibiotics decreases short-term mortality,
treatment failures and sputum purulence.
13
Corticosteroids are used in the acute exacerbation of COPD to treat the inflammatory component of COPD. Corticosteroids have been shown to
reduce admission rates, decrease the length of hospital stay and decrease treatment failures defined as
relapse or hospitalization within 30 days.
13,17,18
Corticosteroids are effective when given orally or
parenterally. Typical treatments are Prednisone 4060 mg orally per day. There has been no benefit to
taking more than 60 mg of Prednisone daily.
8
Methylprednisolone 125 mg IV may be given to
patients who cannot take oral medications.
5
Noninvasive positive pressure ventilation
(NIPPV) is typically initiated in the ED when
the patient is not responding to treatment or
initiated on ED arrival and discontinued after
the patient improves. In general, patients that
require continual NIPPV should be admitted
to the hospital and not to the OU while on
NIPPV, as they require a higher level of monitoring and care.
Disposition
Patients who fail to respond to treatment will
need to be admitted to the hospital. Some patients
will unexpectedly decompensate to the point of
needing NIPPV or intubation and mechanical
ventilation. Personnel who staff the OU need to
be able to recognize respiratory decompensation
and have the skills and equipment needed to
intervene. Predictors of poor outcome are listed
in Table 28.2.
Patients deemed well enough to go home
should have discharge instructions reviewed with
them prior to discharge. Recommendation of
smoking cessation should be made for those
that continue to smoke. Discharge instructions
should be time and person (or clinic) specific as
to when and whom the patient is to follow up.
Instructions about COPD, bronchitis and other
comorbid conditions and medications should be
provided. Warning of signs of reasons to return
sooner than their scheduled follow-up time
should be part of the COPD instructions. Prescriptions for prednisone, inhalers, antibiotics
and refills of maintenance medications should
be provided.
Conclusion
COPD is a chronic condition that has several components: inflammatory and obstructive. Chronic
Bronchitis can be exacerbated by bacterial or viral
infection. These conditions are worsened by cigarette smoking. Of COPD patients that seek care in
EDs, 50–60% require admission to hospital from
the ED and 20–30% will relapse within 4 weeks.
13
There are no specific data on relapse rates or
admission rates for COPD patients seen in OUs
and research can be done in this area. Treatment of
appropriate COPD patients in the OU can save
inpatient beds for sicker patients.
References
1. Tsai, CL, Rowe BH, Cydulka
RK, et al. ED visit volume and
quality of care in acute
exacerbations of chronic
obstructive pulmonary disease.
Am J of Emerg Med
2009;27:1040–1049.
2. Mannino DM, Homa DM,
Akimbami LJ, et al. Chronic
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1–16.
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3. Mannino DM, Braman S. The
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GM, Cendon SP, et al. Urban
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9. Anderson E. Chronic
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10. Barnes PJ. New therapies for
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NL, et al. Outdoor and indoor
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income countries. Int J Tuberc
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12. Pauwels RA, Buist AS,
Calverley PM, et al. Global
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initiative for chronic
obstructive lung disease
(GOLD). Workshop summary.
Am J Resp Crit Care Med
2001;163:1256–1276.
13. Bhutani M, Cydulka R, Rowe
B, et al. Assessment and
management of chronic
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in the emergency department
and beyond. Expert Review of
Respiratory Medicine 2011
(Aug);5.4:549–565.
14. Dalal AA, Shah M, Lunacsek O,
et al. Clinical and economic
burden of patients diagnosed
with COPD with comorbid
cardiovascular disease.
Respir Med 2011;105:
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15. Roche N, Rabbat A, Zureik M,
et al. Chronic obstructive
pulmonary disease
exacerbations in emergency
departments: predictors of
outcome. Curr Opin in Pul
Med 2010;16:112–117.
16. Cydulka RK. Acute Asthma in
Adults. Emergency Medicine:
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Tintinalli JE et al. (eds.) 7th
edition 2011;504–511.
17. Bullard MJ, Liaw SJ, Tsai YH,
et al. Early corticosteroid use in
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airflow obstruction. Am
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18. Neiwoehner DE, Erbland ML,
Deupree RH, et al. Effect of
systemic glucocorticoids in
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Acute Exacerbation of COPD and Bronchitis
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Subpart IVB
Chapter
29
Clinical – Respiratory
Community Acquired Pneumonia
Eric Anderson, MD, MBA, FACEP, FAAEM
Introduction
Pneumonia is a common complaint treated daily
in emergency departments (EDs). There are
approximately 5–6 million patients diagnosed with
community acquired pneumonia (CAP) annually.
1
There are approximately 1.5 million ED visits
annually due to pneumonia.
2
CAP causes approximately 4 million episodes of illness and results in
more than 1 million hospital admissions in the
United States each year.
3,4
CAP is the leading cause of death due to
infectious diseases in Western countries.
5
CAP is
a leading cause of intensive care unit (ICU) death
internationally.
5,6
The average mortality rate for hospitalized
patients is 13%, however the range is from 8%
mortality in nonhospitalized to 36.5% in patients
admitted to the ICU.
7,8,9
Approximately 10% of
hospitalized CAP patients are admitted to the
ICU.
10
In the United States, CAP is the seventh
leading cause of death with an annual estimated
economic cost of 9 billion dollars.
11
Definitions
12
1. Health care associated pneumonia (HCAP)
occurs in patients who: have been hospitalized
for more than 2 days within the last 90 days,
reside in a nursing home or long-term care
facility, are hemodialysis patients, are on
immunosuppressive therapy or wound care
within the last 30 days.
2. Hospital acquired pneumonia (HAP): occurs
after 48 hours of hospital admission.
3. Ventilator associated pneumonia (VAP):
occurs after the first 48 to 72 hours post
intubation.
4. Community acquired pneumonia (CAP):
occurs in patients who do not meet the criteria
for HCAP, HAP, and VAP.
Presentation and Disposition of
Patients Presenting to the ED
with CAP
Patients will present to the ED in various states of
illness ranging from nonspecific symptoms to
septic. The very young and the very old may not
present with respiratory symptoms at all. The
elderly or very young may simply present with a
fever or malaise or alteration of baseline mental
status. Classic symptoms for pneumonia include:
cough productive of phlegm, fever, pleuritic chest
pain, and general malaise with or without shortness of breath. The patient may have all or any
combination of the symptoms slowly increasing
over several days. There may also be loss of appetite or unexplained general fatigue.
Risk factors for CAP include: chronic conditions such as diabetes, chronic renal failure, liver
disease, congestive heart failure (CHF), chronic
obstructive pulmonary disease (COPD), valvular
heart disease, muscular dystrophies, nasogastric
tubes, stroke, chronic alcoholism, and neoplasia.
See Table 29.1.
Emergency Department
Initial ED management of CAP includes identification of the illness and initiation of treatment.
Intravenous (IV) fluids and supplemental oxygen
are administered as needed and antibiotic treatment is initiated (see later in chapter). The disposition is based on the patient’s hemodynamic
stability and the physician’s impression of the
likelihood that the patient will recover on oral
antibiotics at home.
There are several clinical grading scales to help
with this decision. confusion, urea concentration,
respiratory rate, blood pressure (CURB) and
pneumonia severity index (PSI) are two of the
commonly used clinical tools used to assess the
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