PERICARDITIS 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 common 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 (Launbjerg et al., 1996). However, pericarditis is associated with significant morbidity. Specifically, up to 50% of patients with acute idiopathic (viral) pericarditis (AIP) may experience recurrence of pericarditis within 18 months, which can lead to rehospitalization 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 decreased 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 admitted 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 procuring the necessary subjective and objective information that can be useful in identifying patients with a diagnosis of AIP in the ED. The 2015 European Society of Cardiology (ESC) Guidelines for the diagnosis and management 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 inspiration. 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 during 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 ascertaining 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 identify pericardial effusions by the appearance of the "water-bottle sign," the typical appearance 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 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 several 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 myopericarditis, 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 myocardial 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 infraction), 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 [degrees]C or 100.4 [degrees]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 receiving oral anticoagulation (Imazio et al., 2007).

Patients who present to the ED with at least one predictor of poor prognosis should be admitted to the hospital from the ED and would be classified as a "high-risk case." Cases considered "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 prognostic predictors and often yield a "good" response 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 therapy 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 discharged 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 patients 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 combination 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, 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 pericarditis. The principle mechanism behind colchicine's inhibition of the inflammatory process in AIP is through preventing leukocyte migration to the pericardium. Subsequently, colchicine, in combination with ASA/NSAID therapy, can improve symptoms related to pericarditis. Administration of attack 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 initially, followed by 0.5-1 mg daily. Although colchicine is available as a tablet or capsule 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 administration in the ED, with subsequent maintenance 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 adjustments are recommended not only in patients 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 facilitates the amelioration of disease progression, it is not considered as an analgesic agent. 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 symptoms in the ED. Most patients diagnosed with AIP will be treated with colchicine for a period of 3-6 months, in order to reduce the risk of future recurrences. Consequently, diligent 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 important role in improving adherence to pharmacotherapy. Although the adverse effects associated with colchicine rarely cause discontinuation of therapy, the most common adverse effects are gastrointestinal-related, specifically diarrhea (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; Schwier, 2015). Incessant diarrhea can cause more serious adverse effects, such as dehydration and subsequently acute kidney injury, 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 after the dose of colchicine, as GI-related adverse effects may limit patient's adherence upon admission into the hospital unit or after discharge. In many instances, clinicians can ameliorate the GI-related adverse effects 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, granulocytopenia, and pancytopenia) is an uncommon but serious adverse effect associated with colchicine toxicity, even at therapeutic doses (Schwier, 2015; Schwier et al., 2015). Although these hematological effects usually manifest within a few days of therapy, the nursing professional should proactively obtain or order a baseline complete blood cell count with differential in the ED. Rhabdomyolysis has also been documented in patients receiving therapeutic colchicine doses for AIP, especially in those who concomitantly 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 hepatic function (i.e., serum creatinine [SCr], and liver function tests, respectively) monitored 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 administered cautiously and with more frequent monitoring. Manufacturer package insert recommendations for the colchicine tablet formulation provide dosing recommendations for patients with hepatic and renal dysfunction-albeit extrapolated from other disease states (Colcrys (colchicine) Package Insert, 2012). Because many medications can also alter hepatic metabolism of colchicine, drug-drug interaction checks should be completed for every medication added to the patient's profile in the ED. Important drug-drug interactions for colchicine include statins, macrolide antibiotics (i.e., azithromycin, erythromycin, and clarithromycin), diltiazem, verapamil, and cyclosporine (Colcrys (colchicine) Package Insert, 2012). Such drug-drug interactions can increase the risk for myopathy and other adverse effects by inhibiting colchicine's metabolism, thereby increasing colchicine plasma concentrations. In the elderly 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 Administration in the United States, there has been some recent experience with safety 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) Package Insert, 2012).

Table 1. Colchicine for the management of acute idiopathic (viral) pericarditis in the emergency department

Aspirin and NSAIDs

Aspirin or NSAIDs are used for the symptomatic control of inflammation and pain experienced 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 recurrence 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 experience of the clinician (Schwier & Tran, 2016). Such patient factors include patient-preferred dosage forms/route of administration, cost, history of patients' efficacy and tolerability with using the agent, and evaluation for any drug-drug or drug-disease interactions (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 relatively higher doses required to produce anti-inflammatory properties, ASA should be administered 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 adequate anti-inflammatory effects. Most NSAIDs used in the treatment of AIP have comparable pharmacokinetic properties. Typically, the onset of analgesic effect for NSAIDs is within 30-60 min, and their duration of action 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 available in the United States as an over-the-counter oral medication (200 mg) or as a prescription 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 analgesia 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 capsule, suppository, intravenous formulation, and oral solution. Following multiple doses, indomethacin accumulates, resulting in a relatively longer half-life, accounting for the sustained 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. Ketorolac tromethamine's onset of action can be as swift as 30 min, when given orally, intravenously, or intramuscularly. Its duration of action is approximately 6-8 hr, which accounts for its 3-4 times a day dosing requirements. Compared with other NSAIDs, ketorolac tromethamine is a more potent analgesic; it is estimated that 30 mg of ketorolac tromethamine is equal to approximately 12 mg of morphine, with moderate 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 ketorolac tromethamine for pericarditis. Patients were administered 30-mg, 60-mg, or 90-mg injections of ketorolac tromethamine. All patients were symptom-free within 2 hr of receiving ketorolac tromethamine, with no patients requiring additional doses of ketorolac tromethamine after the first 36 hr of treatment. 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 adverse effects (Motov et al., 2017). Because 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 tolerability with using ASA or NSAIDs. This may provide guidance toward the most appropriate 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 requiring 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 dyspepsia, 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 bleeding. With this in mind, clinicians may be inclined to use ketorolac tromethamine for the short-term management of pain associated 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 professionals should also be mindful to not exceed 60 mg/day of ketorolac tromethamine in 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 idiopathic 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 pantoprazole 40 mg daily (Schwier et al., 2015). If a patient presents with contraindications or intolerances to PPIs, H₂ blockers (i.e., famotidine) are also available agents for use in patients receiving ASA/NSAID therapy. From a cardiovascular risk perspective, there are several considerations that the nursing professional 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 increase 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 (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 common CNS-related adverse effects associated with indomethacin use is headache (Lucas, 2016) and has been described as more common and severe in the morning. Moreover, indomethacin is also associated with other CNS-related adverse effects, including dizziness, drowsiness, and confusion (Schwier & Tran, 2016). If patients experience such adverse effects while receiving indomethacin, therapy should be discontinued and a different 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 Improving 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 conditions 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 altogether 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 setting of CKD. Ketorolac tromethamine, for example, should be dose adjusted in renal impairment and is contraindicated in progressive renal disease or patients at risk for renal failure due to hypovolemia ("Ketorolac Tromethamine Tablet [Prescribing Information]," 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 recommendations 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. Furthermore, patients should discontinue use of ketorolac tromethamine if clinical signs and symptoms of liver impairment develop ("Ketorolac Tromethamine Tablet [Prescribing 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. Moreover, the use of ASA is not recommended in pediatric patients (younger than 12 years) based on clinical concern for Reye syndrome.

Table 2. Anti-inflammatory therapies for the management of acute idiopathic (viral) pericarditis-related pain in the emergency department

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 favored as first-line therapy for AIP, primarily due to their increased rates of recurrence upon discontinuation, when compared with 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 pericardium (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), leading 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 inexpensive. 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 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 adverse 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 adverse effects associated with the short-term use of corticosteroids are most germane to this review. Moreover, because the most studied agent is prednisone, a glucocorticoid, this review will focus on glucocorticoids. Short-term adverse effects that are most commonly associated with glucocorticoids use include hyperglycemia, elevation in blood pressure, hypokalemic alkalosis, insomnia, increased appetite, weight gain, edema, and gastrointestinal disturbances (i.e., dyspepsia, GI bleed/ulceration; Imazio, 2012). It is recommended that the nursing professional advocate for prescription of lower doses of prednisone to facilitate preventing adverse effects in the ED. Relatively lower doses of prednisone (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 patients 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 corticosteroids, nursing professionals can draw inflammatory markers such as hs-CRP in the ED (Adler et al., 2015; Imazio, Brucato, Maestroni, et al., 2011). Because hs-CRP concentrations rise within 6 hr and peak within 48 hr in AIP (Imazio, Brucato, & Cemin, et al., 2011; Pepys & Hirschfield, 2003), the nursing professional would be the ideal health care professional to assess the timing of hs-CRP draw by extracting a detailed history of onset of pericarditis-related symptoms from patients during their assessment of the patients in the ED. They would also be able to consult 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 restrict physical activity to an ordinary sedentary 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 differential 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 recurrences 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 maintenance dosing thereafter. The ASA/NSAID attack dosing should be initiated and patient'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 contraindications and/or intolerances to ASA, NSAIDs, and/or colchicine, corticosteroids 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, relatively 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 optimizing 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, resolution 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 adverse 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 pharmacotherapy. Irrespective as to whether patients with AIP are discharged directly from the ED or transitioning to another unit within the institution, the nursing professional 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 responsible for the patients' care (i.e., cardiologist or primary care provider). Moreover, transitions of care will facilitate warranting the patients' necessity for close follow-up in monitoring to ensure efficacy and safety of pharmacotherapy (Schwier et al., 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.

REFERENCES