Advanced Emergency Nursing Journal

Vol. 42, No. 1, pp. 17–29

Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.

A P P L I E D

Pharmacology
Column Editor: Kyle A. Weant, PharmD, BCPS, FCCP

Management of Acute Idiopathic

(Viral) Pericarditis in the Emergency
Downloaded from http://journals.lww.com/aenjournal by BhDMf5ePHKbH4TTImqenVErHeFes2idEAjvet/zdjrDcteCBrjjeFGxLH/ns2RMp on 03/01/2020

Department
A Review for the Nursing Professional
Nicholas C. Schwier, PharmD, BCPS-AQ Cardiology
J. Jacob Cannedy, PharmD
Grant H. Skrepnek, PhD, RPh

Abstract
Acute pericarditis is an inflammatory disorder that contributes to chest pain admissions in the emer-
gency department (ED). Nursing professionals can play a vital role in the differential, triage and
management of acute pericarditis in the ED. First-line pharmacotherapy to specifically treat acute
pericarditis of viral or idiopathic origin is paramount in improving patients’ quality of life and reduc-
ing the risk of further recurrences of pericarditis and consists of combination therapy with aspirin
(acetylsalicylic acid [ASA]) or a nonsteroidal anti-inflammatory drug (NSAID), in combination with
colchicine. Corticosteroids should not be initiated as first-line therapy in idiopathic (viral) pericarditis,
as they increase the risk of recurrences. Nursing professionals are also pivotal in monitoring pharma-
cotherapy with respect to safety and efficacy. Overall, the nursing professional can facilitate timely
administration and monitoring of medications, provide patient education, promote adherence, and
assist in transitions of care for patients diagnosed with acute idiopathic (viral) pericarditis in the ED.
Key words: emergency department, idiopathic, nursing, pericarditis, viral

Author Affiliations: Department of Pharmacy, Clini-
cal and Administrative Sciences, College of Pharmacy,
The University of Oklahoma Health Sciences Center,
Oklahoma City, Oklahoma (Drs Schwier and Skrep-
nek); and INTEGRIS Baptist Medical Center, Oklahoma
City, Oklahoma (Dr Cannedy).
Disclosure: The authors report no conflicts of interest.
Corresponding Author: Nicholas C. Schwier, PharmD,
BCPS-AQ Cardiology, Department of Pharmacy, Clini-
cal and Administrative Sciences, College of Pharmacy,
The University of Oklahoma Health Sciences Center,
1110 N Stonewall Ave, CPB 217, Oklahoma City, OK
73117 (Nicholas-Schwier@ouhsc.edu).
DOI: 10.1097/TME.0000000000000284
P
ERICARDITIS is a cardiovascular-
related disorder in which the parietal
and visceral layers of the pericardium
rub against one other, causing inflammatory
sequela (Adler et al., 2015). In the Western
hemisphere of the world, the most com-
mon etiology of pericarditis is idiopathic,
presumed to be of viral origin (Adler et al.,
2015). Pericarditis is considered to be a
relatively uncommon etiology of cardiac
chest pain in the emergency department
(ED), responsible for 5% of ED admissions

17

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 18
(Launbjerg et al., 1996). However, pericardi-
tis is associated with significant morbidity.
Specifically, up to 50% of patients with acute
idiopathic (viral) pericarditis (AIP) may ex-
perience recurrence of pericarditis within
18 months, which can lead to rehospitaliza-
tion and may also lead to steroid-dependent
pericarditis and/or constrictive pericarditis
in rare circumstances (Adler et al., 2015).
The incidence of recurrence can be de-
creased by utilizing the most appropriate
pharmacotherapy regimen when patients
present with AIP (Imazio, Bobbio, Cecchi,
Demarie, Demichelis, et al., 2005; Imazio
et al., 2013). Extensive reviews have been
published regarding the management of AIP,
especially among patients who have been ad-
mitted to the hospital and for those patients
who are discharged. Nevertheless, much less
literature is available regarding the care and
management of AIP in the ED, specifically for
health care professionals within the practice
of nursing. The purpose of this review is to
facilitate the ED nursing professionals’ ability
to provide a profound impact in identifying
the signs and symptoms of acute pericarditis
in patients who present to the ED, triage
patients with AIP in the ED, identify the most
appropriate pharmacotherapy used to treat
symptoms of AIP, and monitor disease and
pharmacotherapy associated with treating
AIP in the ED.
DIFFERENTIATING AIP FROM OTHER
ETIOLOGIES OF CHEST PAIN IN THE ED
Acute idiopathic (viral) pericarditis can
present similarly to other causes of chest
pain in the ED, including acute coronary
syndromes, aortic dissection, pulmonary
embolism, pneumonia, costochondritis, and
gastroesophageal reflux disease, wherein the
nursing professional can play a vital role in
the differential (LeWinter & Hopkins, 2015).
Nursing professionals can assist in procur-
ing the necessary subjective and objective
information that can be useful in identifying
patients with a diagnosis of AIP in the ED.
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Advanced Emergency Nursing Journal
The 2015 European Society of Cardiology
(ESC) Guidelines for the diagnosis and man-
agement of pericardial diseases describe the
general diagnosis of pericarditis as a “clinical
diagnosis,” one that can be made using two
of the four following criteria (Adler et al.,
2015): pericarditic chest pain, ST-segment
elevation or PR-segment depressions on
electrocardiogram (ECG), new or worsening
pericardial effusions, or a pericardial friction
rub. Pericarditic chest pain is described as
pleuritic: sharp and worsened upon inspi-
ration. The chest pain is usually improved
by having the patients sit up in bed, or lean
forward; leaning forward will help improve
the patient’s pleuritic chest pain by reducing
pressure on the parietal membrane of the
pericardium during inspiration (Adler et al.,
2015). The chest pain may radiate to the
trapezius ridge of the patients’ shoulders.
The ECG changes are normally present dur-
ing the acute phase of pericarditis and can
often make differentiation between a an ST-
segment elevation myocardial infarction and
pericarditis challenging. The ECG changes
associated with pericarditis primarily consist
of new widespread, ST-segment elevation
or PR-segment depressions. A transthoracic
echocardiogram (TTE) can facilitate ascer-
taining the severity of the pericardial effusion
(small, moderate, or large) and can also help
determine whether the patient is in clinical
tamponade; chest radiography can also iden-
tify pericardial effusions by the appearance
of the “water-bottle sign,” the typical ap-
pearance of the cardiac silhouette, indicating
the presence of a moderate-large pericardial
effusion. The pericardial friction rub can best
be auscultated by placing the diaphragm of
the stethoscope over the left sternal border.
The classic teaching is that the friction rub
is reminiscent of footsteps over fresh, fallen,
snow, upon auscultation.
Inflammatory surrogates, such as fever,
leukocytosis, and markers of inflammation
(i.e., high sensitivity (hs)-C-reactive protein
[CRP] and antinuclear antibodies) may also
be useful in the diagnosis of AIP (Adler
 January–March 2020 r Vol. 42, No. 1
et al., 2015). Patients with a viral etiology of
pericarditis often present with a history
of viral prodrome, which precedes typical
signs and symptoms of pericarditis by sev-
eral weeks. Such prodrome consists of upper
respiratory tract infection–like symptoms,
as well as gastroenteritis (Rey, Delhumeau-
Cartier, Meyer, & Genne, 2015). Troponin
may be elevated, which may be suggestive of
myocardial injury, specifically myopericardi-
tis, otherwise defined as pericarditis with
known or clinically suspected concomitant
myocardial involvement (Adler et al., 2015).
Overall, the 2015 ESC guidelines recommend
an ECG, TTE, and chest radiography in all
patients with suspected acute pericarditis.
Evaluation of inflammatory markers and my-
ocardial injury is also recommended in all
patients with suspected acute pericarditis
(Adler et al., 2015).
TRIAGING AIP IN THE ED
Because the majority of patients with AIP
will present with signs and symptoms that
may be misconstrued from more terminal
cardiovascular issues (i.e., myocardial infrac-
tion), the ED nursing professional should be
cognizant in triaging patients who present
with acute pericarditis, according to severity
and prognosis. Triaging patients with AIP
can be performed by identifying whether
the patient presents to the ED with certain
high-risk features. These high-risk features
are subsequently associated with a higher
risk of pericarditis-related adverse events
and, thusly, a poor prognosis; they include
(Imazio et al., 2007): fever (greater than 38
°C or 100.4 °F); subacute course (symptoms
over several days without a clear-cut acute
onset); large pericardial effusion (diastolic
echo-free space greater than 20 mm); cardiac
tamponade; and/or failure to respond within
7 days to nonsteroidal anti-inflammatory
drugs (NSAIDs) or acetylsalicylic acid (ASA).
The presence of the following risk factors
for poor prognosis should also proliferate
the clinician’s concern: myopericarditis,
immunosuppression, trauma, and those
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Management of Pericarditis in the Emergency Department 19
receiving oral anticoagulation (Imazio et al.,
2007).
Patients who present to the ED with at least
one predictor of poor prognosis should be ad-
mitted to the hospital from the ED and would
be classified as a “high-risk case.” Cases con-
sidered “moderate risk” are those patients
without negative prognostic predictors, who
have an incomplete or lack of response to
anti-inflammatory therapy. “Low-risk cases”
include patients without negative prognos-
tic predictors and often yield a “good” re-
sponse to anti-inflammatory therapy; “low-
risk cases” can be discharged directly from
the ED with close outpatient follow-up (Adler
et al., 2015). Empiric anti-inflammatory ther-
apy may be prescribed to “low risk cases,”
and short-term follow-up within a week is
warranted to ascertain outcomes associated
with treatment in such patients (Adler et al.,
2015).
INITIATING AND MONITORING TREATMENT OF
AIP IN THE ED
Although patients with AIP may be dis-
charged from the ED or admitted within the
hospital, many patients may be considered
boarded—remain in the ED after admission
or placed into observation status but not yet
transported to an inpatient or observation
unit. Therefore, it is imperative that an ED
nursing professional have more of an intimate
understanding, with respect to managing pa-
tients with AIP. First-line management of
AIP should consist of pharmacotherapy,
aimed at reducing the inflammatory response
(Adler et al., 2015; Imazio & Gaita, 2017).
First-line pharmacotherapy (pending no
intolerances or contraindications) should
consist of combination therapy with anti-
inflammatory therapy (NSAID or ASA) plus
colchicine (Adler et al., 2015). The combina-
tion of ASA/NSAIDs plus colchicine improves
time to remission and decreases time to
symptom relief, compared with ASA/NSAIDs
alone (Imazio et al., 2014; Imazio, Bobbio,
Cecchi, Demarie, Demichelis, et al., 2005;
Imazio, Bobbio, Cecchi, Demarie, Pomari,
 20
et al., 2005; Imazio, Brucato, Cemin, et al.,
2011; Imazio et al., 2013). It should be noted
that although none of the medications being
discussed in this review have Food and Drug
Administration–approved indications for the
treatment of AIP, multiple landmark studies
have vetted the benefit of certain agents on
the morbidity that is associated with AIP
(Imazio et al., 2014; Imazio, Bobbio, Cecchi,
Demarie, Demichelis, et al., 2005; Imazio,
Bobbio, Cecchi, Demarie, Pomari, et al.,
2005; Imazio, Brucato, Cemin, et al., 2011;
Imazio et al., 2013). Combination therapy
consisting of ASA/NSAIDs plus colchicine
should be administered early in the patients’
treatment (i.e., the ED) to provide faster
symptom control and to ensure adherence
and tolerability to pharmacotherapy aimed at
reducing the incidence of future recurrences
(Imazio & Gaita, 2015). In addition, various
forms of monitoring should be implemented
while patients receive pharmacotherapy to
treat AIP in the ED, in order to ensure efficacy
and safety of pharmacotherapy used.
Colchicine
Colchicine should be initiated as part of first-
line therapy, in order to aid in quelling the
inflammatory cascade associated with peri-
carditis. The principle mechanism behind
colchicine’s inhibition of the inflammatory
process in AIP is through preventing leuko-
cyte migration to the pericardium. Subse-
quently, colchicine, in combination with
ASA/NSAID therapy, can improve symptoms
Table 1. Colchicine for the management of acute idiopathic (viral) pericarditis in the
emergency department
Dosinga (Schwier, 2015)
Attack dosing: 1.2–1.8 mg
Maintenance dosing: 0.3–1.2 mg/day;
single dose or every 12 hr
a Dosing is based on available U.S.-scored tablet formulation and is extrapolated from European landmark studies; dosing
to be used only in patients who do not present with any drug–drug or drug–disease interactions.
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Advanced Emergency Nursing Journal
related to pericarditis. Administration of at-
tack doses of colchicine in the ED may be
useful to ensure clinical utility of the drug
throughout the day (Schwier, Coons, & Rao,
2015). Dosing within the landmark studies
consisted of an attack dose of 1–2 mg ini-
tially, followed by 0.5–1 mg daily. Although
colchicine is available as a tablet or cap-
sule formulation in the United States, it is
recommended to utilize the single-strength
0.6 mg scored tablet formulation in the ED.
The tablet formulation can be split, if needed,
in order to dose adjust for drug–drug and
drug–disease interactions, as well as patient’s
tolerability (Schwier, 2015). Using the 0.6-mg
tablet formulation available in the United
States, an initial attack dose of 1.2 mg of
colchicine may be appropriate for initial ad-
ministration in the ED, with subsequent main-
tenance doses of 0.6 mg twice daily (see
Table 1). If the patient experiences adverse
effects to colchicine (discussed later), or if
the patient’s actual body weight is less than
70 kg, the dose should be reduced to 0.3
mg twice daily due to an increased risk for
adverse effects. Colchicine is metabolized
hepatically and eliminated renally. Dose ad-
justments are recommended not only in pa-
tients with renal and/or hepatic dysfunction
but also in the elderly (i.e., older than 70
years). Patients older than 70 years should
have their colchicine dose reduced by 50%
(Colcrys (colchicine) Package Insert, 2012;
Schwier, 2015). Although colchicine facili-
tates the amelioration of disease progression,
it is not considered as an analgesic agent.
Pearls (Schwier, 2015)
Dose adjust by 50% in patients older than 70 years
Dose adjust in renal and/or hepatic impairment
Adjust initial attack (1.2 mg) and/or maintenance dose
(0.6 mg/day) in patients:
Less than 70 kg or experience adverse effects
 January–March 2020 r Vol. 42, No. 1
Therefore, the addition of ASA/NSAIDs to
colchicine should be part of the mainstay
management of AIP in the ED, in order to
reduce patients’ pain and associated symp-
toms in the ED. Most patients diagnosed with
AIP will be treated with colchicine for a pe-
riod of 3–6 months, in order to reduce the
risk of future recurrences. Consequently, dili-
gent monitoring should be imparted early in
the care of patients with AIP, especially in
the ED, which may help decrease the risk
for future adverse effects and play an impor-
tant role in improving adherence to phar-
macotherapy. Although the adverse effects
associated with colchicine rarely cause dis-
continuation of therapy, the most common
adverse effects are gastrointestinal-related,
specifically diarrhea (Imazio et al., 2014;
Imazio, Bobbio, Cecchi, Demarie, Demiche-
lis, et al., 2005; Imazio, Bobbio, Cecchi, De-
marie, Pomari, et al., 2005; Imazio, Brucato,
Cemin, et al., 2011; Imazio et al., 2013;
Schwier, 2015). Incessant diarrhea can cause
more serious adverse effects, such as dehy-
dration and subsequently acute kidney in-
jury, resulting in serious toxic adverse effects,
caused by an accumulation of colchicine
plasma concentrations. Nursing professionals
should assess for gastrointestinal (GI)-related
adverse effects in the ED several hours af-
ter the dose of colchicine, as GI-related ad-
verse effects may limit patient’s adherence
upon admission into the hospital unit or af-
ter discharge. In many instances, clinicians
can ameliorate the GI-related adverse ef-
fects by decreasing the dose of colchicine,
changing the frequency to once daily, and/or
instructing the patient to take colchicine
with food (Schwier, 2015). Myelosuppression
(i.e., thrombocytopenia, leucopenia, granu-
locytopenia, and pancytopenia) is an un-
common but serious adverse effect associ-
ated with colchicine toxicity, even at thera-
peutic doses (Schwier, 2015; Schwier et al.,
2015). Although these hematological effects
usually manifest within a few days of ther-
apy, the nursing professional should proac-
tively obtain or order a baseline complete
blood cell count with differential in the ED.
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Management of Pericarditis in the Emergency Department 21
Rhabdomyolysis has also been documented
in patients receiving therapeutic colchicine
doses for AIP, especially in those who con-
comitantly take medications that may cause
myopathy (i.e., statins; Colcrys (colchicine)
Package Insert, 2012). In these instances,
colchicine doses may be lowered empirically.
All patients should also have renal and hep-
atic function (i.e., serum creatinine [SCr],
and liver function tests, respectively) moni-
tored while in the ED to determine whether
dose adjustment of colchicine is required, or
whether use should be avoided. In patients
with renal and/or hepatic dysfunction renal
impairment, colchicine should be adminis-
tered cautiously and with more frequent mon-
itoring. Manufacturer package insert recom-
mendations for the colchicine tablet formula-
tion provide dosing recommendations for pa-
tients with hepatic and renal dysfunction—
albeit extrapolated from other disease states
(Colcrys (colchicine) Package Insert, 2012).
Because many medications can also alter hep-
atic metabolism of colchicine, drug–drug in-
teraction checks should be completed for
every medication added to the patient’s pro-
file in the ED. Important drug–drug interac-
tions for colchicine include statins, macrolide
antibiotics (i.e., azithromycin, erythromycin,
and clarithromycin), diltiazem, verapamil,
and cyclosporine (Colcrys (colchicine) Pack-
age Insert, 2012). Such drug–drug inter-
actions can increase the risk for myopa-
thy and other adverse effects by inhibiting
colchicine’s metabolism, thereby increasing
colchicine plasma concentrations. In the el-
derly patient population, polypharmacy can
also create a cumbersome environment in
which drug–drug interactions may be more
common, due to the relatively high number
of medications that may potentially interact
with colchicine. Specific emphasis should be
made on ensuring medication adherence as
well as appropriate dosing of medications
prior to discharge. Although colchicine is
considered pregnancy category C (i.e., “risk
not ruled out”) by the Food and Drug Ad-
ministration in the United States, there has
been some recent experience with safety
 22
associated with using colchicine to treat AIP
in pregnant patients (Brucato et al., 2019).
Colchicine is also known to be excreted in
breast milk, which should be considered in
nursing women (Colcrys (colchicine) Pack-
age Insert, 2012).
Aspirin and NSAIDs
Aspirin or NSAIDs are used for the symp-
tomatic control of inflammation and pain ex-
perienced by the patients with AIP. However,
compared with ASA/NSAIDs as monotherapy,
the addition of colchicine has been shown
to result in less time to remission, faster
time to symptom control, and decreased re-
currence rates within 18 months (Imazio et
al., 2014; Imazio, Bobbio, Cecchi, Demarie,
Demichelis, et al., 2005; Imazio, Brucato,
Cemin, et al., 2011; Imazio et al., 2013).
The decision as to which agent to use for
treatment should be based on a variety of
patient-specific factors as well as personal ex-
perience of the clinician (Schwier & Tran,
2016). Such patient factors include patient-
preferred dosage forms/route of administra-
tion, cost, history of patients’ efficacy and
tolerability with using the agent, and evalua-
tion for any drug–drug or drug–disease inter-
actions (Schwier & Tran, 2016). In the United
States, ASA is available as an over-the-counter
oral medication (chewable or enteric coated)
and a rectal suppository. Because of rela-
tively higher doses required to produce anti-
inflammatory properties, ASA should be ad-
ministered every 6–8 hr to ensure around the
clock analgesia for patients (Schwier & Tran,
2016). Higher doses, or “attack doses” (see
Table 1), should be utilized with the intention
of achieving optimal pain control and ade-
quate anti-inflammatory effects. Most NSAIDs
used in the treatment of AIP have compa-
rable pharmacokinetic properties. Typically,
the onset of analgesic effect for NSAIDs is
within 30–60 min, and their duration of ac-
tion can range from 6 to 12 hr, depending
on the half-life (Schwier & Tran, 2016). One
of the most common NSAIDs used in the
treatment of AIP is ibuprofen. Ibuprofen is
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Advanced Emergency Nursing Journal
available in the United States as an over-the-
counter oral medication (200 mg) or as a pre-
scription oral (400–800 mg) and intravenous
preparation. Similar to ASA, relatively higher
doses (attack doses) of ibuprofen should be
used. Oral ibuprofen’s onset of analgesia is
within 20–60 min but has a short half-life,
requiring frequent dosing to maintain anal-
gesia in patients with AIP (Davies, 1998). In
patients with AIP, ibuprofen is usually dosed
600 mg orally every 8 hr. Indomethacin is
accessible only as a prescription formulation
in the United States. It is available as a cap-
sule, suppository, intravenous formulation,
and oral solution. Following multiple doses,
indomethacin accumulates, resulting in a rel-
atively longer half-life, accounting for the sus-
tained relief of pain seen in many patients
(Lucas, 2016). Ketorolac tromethamine is a
prescription NSAID in the United States and is
formulated as both a parenteral (intravenous/
intramuscular) and an oral preparation. Ke-
torolac tromethamine’s onset of action can
be as swift as 30 min, when given orally, in-
travenously, or intramuscularly. Its duration
of action is approximately 6–8 hr, which ac-
counts for its 3–4 times a day dosing re-
quirements. Compared with other NSAIDs,
ketorolac tromethamine is a more potent
analgesic; it is estimated that 30 mg of ke-
torolac tromethamine is equal to approxi-
mately 12 mg of morphine, with moder-
ate anti-inflammatory effects (Vadivelu et al.,
2017) but has been scarcely documented
in the management of AIP. A pilot study
by Arunasalam and Siegel (1993) reported
22 patients who were administered ketoro-
lac tromethamine for pericarditis. Patients
were administered 30-mg, 60-mg, or 90-mg
injections of ketorolac tromethamine. All pa-
tients were symptom-free within 2 hr of
receiving ketorolac tromethamine, with no
patients requiring additional doses of ketoro-
lac tromethamine after the first 36 hr of treat-
ment. It should be noted that there is limited
evidence to support using doses greater than
10 mg of ketorolac tromethamine, due to a
ceiling effect and associated with higher ad-
verse effects (Motov et al., 2017). Because
 January–March 2020 r Vol. 42, No. 1
relatively higher doses have been used in
practice, dosing of ketorolac tromethamine
should be based on clinical discretion.
Prior to initiating therapy, the ED nursing
professional should inquire regarding the
patients’ current/past medical history, as well
as the patients’ history of efficacy and toler-
ability with using ASA or NSAIDs. This may
provide guidance toward the most appropri-
ate anti-inflammatory agent to initiate. Many
of the adverse effects associated with ASA or
NSAIDs can potentially have a fast onset and
are relatively common. This is especially true
with use of high dose of anti-inflammatory
therapies (i.e., ASA or NSAIDs, which are
associated with an increased risk of adverse
effects. However, most of the adverse effects
are easily controlled by reducing the dose of
the agent(s) during the course of treatment,
and the risk of such adverse effects increases
in patients older than 70 years, those re-
quiring use of ASA or NSAIDs for extended
periods of time, or patients requiring larger
doses (Fardman, Charron, Imazio, & Adler,
2016). One of the most common adverse
effects associated with ASA or NSAID use is
injury to the upper GI tract, such as dyspep-
sia, ulcers, or GI bleeding (Day & Graham,
2013). For some NSAIDs, the incidence of
GI-related issues, such as GI bleeding, may be
more prevalent with certain agents compared
with others within the class. For example,
when using ketorolac tromethamine, the
nursing professional should be aware that the
maximum combined duration of treatment
with ketorolac tromethamine (for parenteral
and oral use) should not be greater than
5 days, due to increased risk for GI bleed-
ing. With this in mind, clinicians may be
inclined to use ketorolac tromethamine for
the short-term management of pain asso-
ciated with AIP (“Ketorolac Tromethamine
Tablet [Prescribing Information],” 2015). The
maximum total daily oral dose of ketorolac
tromethamine is 40 mg, compared with
the total daily dose of parenteral ketorolac
tromethamine being 120 mg. Nursing profes-
sionals should also be mindful to not exceed
60 mg/day of ketorolac tromethamine in
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Management of Pericarditis in the Emergency Department 23
patients 65 years of age and older, weight of
50 kg or less, or those patients presenting
with moderately elevated SCr; such patients
are at an increased risk for GI bleeding if the
60 mg/day dose of ketorolac tromethamine
is exceeded (“Ketorolac Tromethamine
Tablet [Prescribing Information],” 2015).
The GI-related adverse effects of ASA or
NSAIDs can be mitigated or reduced by use
of gastroprotection or GI prophylaxis (Adler
et al., 2015). The GI prophylaxis, consisting
of proton pump inhibitors (PPIs), namely,
omeprazole 20 mg daily, was provided to
all patients in the landmark studies for id-
iopathic pericarditis, in order to reduce the
rates of NSAID-/ASA-induced adverse GI
effects (Imazio et al., 2014; Imazio, Bobbio,
Cecchi, Demarie, Demichelis, et al., 2005;
Imazio, Bobbio, Cecchi, Demarie, Pomari,
et al., 2005; Imazio, Brucato, Cemin, et al.,
2011; Imazio et al., 2013). Clinicians should
use a PPI such as omeprazole 20 mg or panto-
prazole 40 mg daily (Schwier et al., 2015). If
a patient presents with contraindications or
intolerances to PPIs, H2 blockers (i.e., famo-
tidine) are also available agents for use in
patients receiving ASA/NSAID therapy. From
a cardiovascular risk perspective, there are
several considerations that the nursing pro-
fessional should be cognizant of, especially
with use of high doses of ASA or NSAID. In
patients with coronary artery disease (CAD),
NSAIDs should be avoided as they may in-
crease the potential for vasoconstriction of
the coronary arteries, increase myocardial
oxygen consumption, and can interfere with
myocardial scar formation (Pacold et al.,
1986; Schwier et al., 2015). Therefore, ASA
should be the anti-inflammatory of choice in
patients with CAD, as almost all patients will
need to be continued on ASA, lifelong for
CAD. Given the associated increased risk of
cardiovascular events including myocardial
infarction and stroke, the selective COX-2
inhibitors should be avoided in patients with
AIP and concomitant cardiovascular disease
(Schwier & Tran, 2016). The use of NSAIDs
or ASA at relatively high doses may also cause
a dose-dependent increase in blood pressure
 24
(mean increase in systolic blood pressure of
approximately 2–3 mm Hg). Subsequently,
nursing professionals should be monitoring
blood pressure in patients at risk or those
who have uncontrolled hypertension, while
receiving ASA or NSAID therapy. Central
nervous system (CNS)-related adverse effects
are uncommon and associated with the use
of relatively high doses of ASA/NSAID—
namely, indomethacin (Auriel, Regev, &
Korczyn, 2014). The lipophilic nature of
indomethacin, compared with other NSAIDs
in its class, is thought to be responsible for
the CNS-related effects. One of the most com-
mon CNS-related adverse effects associated
with indomethacin use is headache (Lucas,
2016) and has been described as more com-
mon and severe in the morning. Moreover,
indomethacin is also associated with other
CNS-related adverse effects, including dizzi-
ness, drowsiness, and confusion (Schwier &
Tran, 2016). If patients experience such ad-
verse effects while receiving indomethacin,
therapy should be discontinued and a differ-
ent agent should be initiated.
Nursing professionals should not only be
cognizant of adverse effects when initiating
high doses of ASA or NSAIDs but also dose
adjustments for organ dysfunction. Overall,
for the use of NSAIDs in chronic kidney
disease (CKD), the Kidney Disease Improv-
ing Global Outcomes (KDIGO) guidelines
recommend avoiding NSAIDs in patients
with an estimated glomerular filtration rate
(eGFR) between 30 and 59 ml/min/1.73 m2 ,
who also present with comorbid condi-
tions that can increase the risk of further
kidney injury (i.e., hypertension, diabetes
mellitus, and atherosclerosis; CKD Work
Group, 2013). The KDIGO guidelines also
recommend avoiding use of NSAIDs alto-
gether in patients with an eGFR of less than
30 ml/min/1.73 m2 (Auriel et al., 2014).
In addition, clinicians should also consult
the labeling of certain NSAIDs, as there be
more specific guidance for use in the set-
ting of CKD. Ketorolac tromethamine, for
example, should be dose adjusted in renal
impairment and is contraindicated in pro-
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Advanced Emergency Nursing Journal
gressive renal disease or patients at risk for
renal failure due to hypovolemia (“Ketorolac
Tromethamine Tablet [Prescribing Informa-
tion],” 2015). Because ASA is metabolized by
various esterases, it is common to prescribe
ASA for the treatment of AIP in patients with
renal impairment (Schwier & Tran, 2016).
Nonsteroidal anti-inflammatory drugs are
also metabolized by the liver and should
also be used with caution in patients with
hepatic impairment. Although formal rec-
ommendations regarding dose adjustment
in patients with hepatic impairment are
lacking, the manufacturer package insert
advises that clinicians should use ketorolac
tromethamine with caution in patients with
hepatic impairment; ketorolac tromethamine
may cause elevation of liver enzymes. Fur-
thermore, patients should discontinue use
of ketorolac tromethamine if clinical signs
and symptoms of liver impairment develop
(“Ketorolac Tromethamine Tablet [Prescrib-
ing Information],” 2015). In instances in
which patients are pregnant, NSAIDs may
be used safely during the first and second
trimesters. After gestational Week 20, all
NSAIDs (except ASA ≤100 mg/day) can
cause constriction of the ductus arteriosus
and impair fetal renal function. At gestational
Week 32, all NSAIDs including ASA should be
withdrawn from therapy. Treatment of AIP
in the pediatric population consists of anti-
inflammatory therapies, such as NSAIDs (see
Table 2). The dosing of NSAIDs in pediatric
patients, however, should be dose-adjusted
according to patients’ body weight. More-
over, the use of ASA is not recommended in
pediatric patients (younger than 12 years)
based on clinical concern for Reye syndrome.
Corticosteroids
Historically, corticosteroids have long been
used in the treatment of pericarditis due
to their rapid induction of symptom relief.
However, corticosteroids are no longer fa-
vored as first-line therapy for AIP, primarily
due to their increased rates of recurrence
upon discontinuation, when compared with
 January–March 2020 r Vol. 42, No. 1 Management of Pericarditis in the Emergency Department 25

Table 2. Anti-inflammatory therapies for the management of acute idiopathic (viral)

pericarditis–related pain in the emergency department

Agent (Schwier Dosing Clinical Pearls

& Tran, 2016) (Schwier & Tran, 2016) (Schwier & Tran, 2016)

Aspirin (ASA) 750—1,000 mg by mouth Can be used safely in patients with renal or
every 6–8 hr hepatic impairment.
Preferred in patients with HF, HTN, and/or
CAD.
Half-life increases with relatively higher
doses.
Ibuprofen 600–800 mg by mouth Use with caution in patients with renal
every 8 hr and/or hepatic impairment.
Not recommended in patients with HF,
HTN, and/or CAD.
Indomethacin 50 mg by mouth three Use with caution in patients with renal
times daily and/or hepatic impairment.
Not recommended in patients with HF,
HTN, and/or CAD.
Relatively increased risk of CNS-related
adverse effects.
Ketorolac Intramuscularly: 30–60 mg, Can be used only for a maximum of 5 days.
tromethamine once Not recommended in patients with HF,
Intramuscularly or HTN, and/or CAD.
intravenously: 15–30 mg Dose adjust in patients with mild to
every 6 hr (MDD: moderate renal impairment;
120 mg) contraindicated in patients with
advanced renal impairment.
Use with caution in patients with hepatic
impairment.

Note. CAD = coronary artery disease; CNS = central nervous system; HF = heart failure; HTN = hypertension; MDD
= maximum daily dose.

ASA/NSAIDs plus colchicine therapy (Imazio,
Bobbio, Cecchi, Demarie, Demichelis, et al.,
2005). The mechanism behind the increased
risk of recurrence is thought to be due to
impaired viral clearance and potentiation
of viral nucleic acid replication in the peri-
cardium (Schwier et al., 2015). Moreover,
corticosteroids have also been implicated
in diminishing the effects of colchicine for
pericarditis (Artom et al., 2005). Because of
increased rates of recurrences, as well as the
adverse effects associated with long-term use
of corticosteroids, they are recommended
only in patients with contraindications or
intolerances to ASA/NSAIDs and colchicine
therapy (Adler et al., 2015). Patients who may
benefit from corticosteroids in the treatment
of AIP include pediatric patients, pregnant
patients, and patients who fail combination
therapy (ASA/NSAID plus colchicine), lead-
ing to successive recurrence of pericarditis
(Adler et al., 2015). Historically, prednisone is
most commonly used for the treatment of AIP,
as it is dosed once daily and is relatively in-
expensive. Patients receiving prednisone for
the treatment of AIP should be initiated with
0.25–0.50 mg/kg/day (Imazio et al., 2010).
In addition to corticosteroids increasing the
number of relapses, they are also associated
with inducing dependence due to their
adverse effect profile (Pepys & Hirschfield,
2003). Although the nursing professional

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 26
in the ED will most likely be involved in
the relatively short-term management of AIP,
one needs to be cognizant of the types of
monitoring and adverse effects associated
with corticosteroid use, as well as which
patient populations should not be prescribed
corticosteroids. In general, the risk for ad-
verse effects from corticosteroid therapy is
related to the dose and duration of therapy,
as well as the specific type of corticosteroid
prescribed. As the nursing professional might
be more likely to manage only the patients
while they are treated in the ED, the ad-
verse effects associated with the short-term
use of corticosteroids are most germane to
this review. Moreover, because the most stud-
ied agent is prednisone, a glucocorticoid,
this review will focus on glucocorticoids.
Short-term adverse effects that are most com-
monly associated with glucocorticoids use
include hyperglycemia, elevation in blood
pressure, hypokalemic alkalosis, insomnia,
increased appetite, weight gain, edema, and
gastrointestinal disturbances (i.e., dyspep-
sia, GI bleed/ulceration; Imazio, 2012). It is
recommended that the nursing professional
advocate for prescription of lower doses of
prednisone to facilitate preventing adverse ef-
fects in the ED. Relatively lower doses of pred-
nisone (0.25–0.5 mg/kg/day) are associated
with less adverse effects than higher doses
in patients with pericarditis (Williams, 2018).
Specific patient populations should avoid
corticosteroid use, including patients with
osteopenia or osteoporosis and those with
a presumed or confirmed infection. In pa-
tients with hepatic impairment, prednisolone
should be initiated rather than prednisone, as
prednisone requires hepatic activation to its
active metabolite, prednisolone.
To assess and monitor the efficacy anti-
inflammatory response of therapies such as
ASA, NSAIDs, colchicine, and/or corticos-
teroids, nursing professionals can draw in-
flammatory markers such as hs-CRP in the
ED (Adler et al., 2015; Imazio, Brucato, Mae-
stroni, et al., 2011). Because hs-CRP concen-
trations rise within 6 hr and peak within 48
hr in AIP (Imazio, Brucato, & Cemin, et al.,
2011; Pepys & Hirschfield, 2003), the nursing
Copyright © 2020 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Advanced Emergency Nursing Journal
professional would be the ideal health care
professional to assess the timing of hs-CRP
draw by extracting a detailed history of on-
set of pericarditis-related symptoms from pa-
tients during their assessment of the patients
in the ED. They would also be able to con-
sult with other ED clinicians before drawing
an hs-CRP level, as certain factors (i.e., renal
impairment, autoimmune diseases, statins)
could confound the interpretation of hs-CRP-
level response to anti-inflammatory therapies
(Pepys & Hirschfield, 2003). Restriction of
exercise/physical activity may also improve
the patient’s morbidity. If patients are being
discharged directly from the ED, the nursing
professional can instruct the patient to re-
strict physical activity to an ordinary seden-
tary lifestyle for upward of 3 months, until the
patient follows up with the provider in clinic
(Adler et al., 2015; Imazio et al., 2008).
CONCLUSION
Idiopathic or viral etiologies of pericarditis
are the most common form of pericardial
diseases in the Western hemisphere (Adler
et al., 2015). Nursing professionals in the
ED can provide a pivotal part in the differ-
ential diagnosis and triage of patients with
AIP. Once the diagnosis of AIP has been
made, the combination of ASA/NSAIDs plus
colchicine is considered first-line therapy for
the treatment of AIP and should be initiated
in the ED as soon as possible, as it leads to
faster onset of pain control and remission
of symptoms, and also prevent future recur-
rences of pericarditis (Imazio et al., 2005;
Imazio et al., 2013). Attack doses should be
used for both colchicine and ASA/NSAIDs to
provide a more rapid onset of pain control
(Schwier et al., 2015). Colchicine attack
dosing should be incorporated as the first
dose and then the clinician can initiate main-
tenance dosing thereafter. The ASA/NSAID
attack dosing should be initiated and pa-
tient’s response should be assessed often, as
incomplete or partial response to ASA/NSAID
therapy is associated with a poorer prognosis
(Adler et al., 2015; Schwier, 2015; Schwier
& Tran, 2016). If patients present with
 January–March 2020 r Vol. 42, No. 1
contraindications and/or intolerances to
ASA, NSAIDs, and/or colchicine, corticos-
teroids are considered the last-line therapy
for AIP, as they are associated with increased
risk of future recurrences, compared with
ASA/NSAIDs plus colchicine (Adler et al.,
2015). If corticosteroids are chosen, rela-
tively lower doses should be initiated (Adler
et al., 2015; Williams, 2018). Overall, nursing
professionals have the opportunity to initiate
pharmacotherapy for AIP in the ED, helping
ensure patient’s tolerance to combination
therapy, which can ultimately facilitate op-
timizing pain control, as well as decreasing
the risk of recurrence. Nursing professionals
can also play a vital role in procuring drug
therapy, ensure timely administration of
medications, and encourage adherence to
pharmacotherapy initiated in the ED. The
nursing professional can also monitor the
efficacy of anti-inflammatory therapies by
patient-reported improvement of symptoms,
as well as signs of pericarditis to include a
decrease in hs-CRP concentrations, resolu-
tion of ECG changes, and/or amelioration of
pericardial friction rub. Nursing professionals
can also appropriately monitor patients prior
to admission into a unit or discharge from
the ED, in order to decrease incidence of ad-
verse drug effects associated with colchicine,
ASA/NSAIDs, and/or corticosteroids. If the
nursing professional can employ diligent
monitoring in the ED, the patient may be
more likely to respond to and tolerate phar-
macotherapy. Irrespective as to whether
patients with AIP are discharged directly
from the ED or transitioning to another unit
within the institution, the nursing profes-
sional can be vital to ensuring transitions
of care. The nursing professional’s ability to
practice diligent care transitions is paramount
in ensuring effective communication among
the patient and the health care team respon-
sible for the patients’ care (i.e., cardiologist
or primary care provider). Moreover, tran-
sitions of care will facilitate warranting
the patients’ necessity for close follow-
up in monitoring to ensure efficacy and
safety of pharmacotherapy (Schwier et al.,
Copyright © 2020 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Management of Pericarditis in the Emergency Department 27
2015). Overall, nursing professionals in the
ED have the opportunity to impact patient
outcomes along the entire continuum of care
associated with the management of AIP.
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