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Pericarditis

Author: Leilah J Dare / Editor: Jason Kendall / Codes: CAP7, HAP8 / Published: 17/06/2013 / Review Date: 17/12/2016

Jump to: Top | Introduction | Clinical assessment | Investigation Strategies | Management | Safety pearls and Pitfalls | MedicoLegal and other considerations | References

Introduction

Context

Acute Pericarditis is a well-recognised cause of chest pain. Patients with pericarditis are seen commonly in the Emergency Department (ED): it is reported that 5% of patients presenting to the ED with non-ischaemic chest pain have acute pericarditis [2]. It is therefore a condition that Emergency Physicians should be familiar with.

5% of patients presenting to the ED with non-ischaemic chest pain have acute pericarditis.

Definition

Acute pericarditis is defined as the presence of symptoms or signs resulting from pericardial inflammation of less than 1-2 weeks duration [3].

Aetiology

The causes of acute pericarditis are widespread and are listed in Table 1. Most cases are “idiopathic” (80-90%) [5]. Although labelled as idiopathic, the majority of these are likely to be viral in origin, but viral testing is not routinely done as it rarely alters the management and is not cost-effective.

acute_pericarditis_complications

The incidence of viral pericarditis is higher in young previously healthy adults and is lower in those patients who are subsequently found to need inpatient management. Patients with tuberculous pericarditis present with a less acute course. Patients with bacterial pericarditis present more acutely unwell and with other features of bacterial sepsis.

Most cases of “idiopathic” pericarditis are likely to be viral in origin

Pathophysiology

The pericardium is composed of 2 layers: (i) the outer thicker fibrous pericardium and (ii) the inner visceral or serosal pericardium which is made up of a thin layer of mesothelial cells. In a normal physiological state the pericardial sac between these 2 layers contains 15-50mls of fluid. The combined thickness of these 2 layers should measure less than 2mm [1]. Pericarditis is caused by inflammation of the pericardial layers associated with varying amounts of pericardial fluid collection which may result in a significant pericardial effusion.

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Clinical assessment

History

The clinical presentation is usually one of acute onset of chest pain; classically this is pleuritic in nature and eased by sitting up and leaning forward. The pain may be anywhere over the anterior chest wall, but it is usually retrosternal. It may radiate to the arm like ischaemic pain. A characteristic feature of the pain which is specific for pericarditis is radiation to the trapezius ridge [3]; the phrenic nerve traverses the pericardium and also innervates this muscle.

Learning bite

Pain radiating to the trapezius ridge has high degree of specificity for pericarditis

Examination

85% of patients have a pericardial friction rub at some time during the course of their disease [3]. This rub is often dynamic so repeated examination may be useful if it is not heard at the outset. It is heard maximally during expiration and is loudest at the lower left sternal edge. It can be distinguished from a pleural rub by the fact that it will still be heard when the patient holds their breath.

A diagnosis of acute pericarditis should be made when at least 2 out of 4 of the following criteria are met [3]:

  1. Characteristic chest pain
  2. Pericardial friction rub
  3. Suggestive ECG changes
  4. New or worsening pericardial effusion

Other clinical findings associated with the aetiology of the pericarditis

(a) Fever:

A temperature over 38 degrees centigrade is a high risk feature for pericarditis. It may be associated with the presence of a bacterial infection (eg. a coexistent pneumonia).

(b) Clinical features of HIV:

HIV is associated with acute pericarditis in a number of ways. It can cause a direct infective pericarditis or pericarditis can be associated with other opportunistic infections such as CMV. Kaposi’s sarcoma and lymphoma can cause a non-infective pericarditis.

(c) Clinical features associated with autoimmune disorders:

Patients with the cutaneous or musculoskeletal features of rheumatoid arthritis, SLE and systemic sclerosis may be at risk of acute pericarditis relating to these diseases.

(d) Patients presenting after a STEMI:

This can occur early (within days) or late (months).

(e) Clinical features of Uraemia:

Patients with a raised urea may have non-specific features of nausea, vomiting, anorexia and itching. Pericarditis may occur in association with chronic or acute kidney injury.

(f) Metastatic Disease:

Metastatic lung and breast cancer are the commonest malignancies to cause acute pericarditis. The primary lung lesion may be seen on CXR

Other clinical findings associated with the complications of pericarditis

(a) Cardiac Tamponade:

The classic triad of distended neck veins, muffled heart sounds and hypotension (Beck’s triad) may not be present. Patients can have an insidious onset of tamponade and the symptoms and signs may be very non-specific. They may have orthopnoea, dysphagia, cough and occasionally episodes of loss of conciousness [9]. Echocardiography is required in all cases of suspected pericarditis in order to complete risk stratification (see below).

(b) Recurrent Pericarditis:

Patients may give a history of previous resolved episodes of chest pain, or of ongoing chest pain which has required a prolonged course of NSAIDs.

(c) Chronic Pericarditis:

This is defined as pericarditis lasting for more than 3 months. Symptoms include chest pain, palpitations and fatigue.

Risk Stratification

In order to appropriately risk stratify a patient with pericarditis, the emergency physician needs to consider the possible aetiology of the pericarditis along with the presence of high risk features. These high risk features (see Table below) are associated with a poorer prognosis and may help guide the need for inpatient management [5].

highriskfeature

Learning bite

The presence of any high risk feature is associated with a poorer prognosis. These patients should be admitted for inpatient management.

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Investigation Strategies

To help establish the diagnosis and look for high risk features a number of simple investigations should be performed within the ED.

(i) Electrocardiography (ECG)

As well as looking for the characteristic features of pericarditis on the ECG it will also help to distinguish other potential causes of chest pain.

There are a number of ECG features which are characteristic of acute pericarditis (Fig 1):

(i) The changes seen are diffuse; this is because pericarditis may involve a large surface area of the heart and certainly does not follow the anatomical territory of a specific coronary artery.

(ii) ST elevation occurs in 90% of cases [6]. The most common pattern is ST elevation in leads, V5 and V6 (70%); more extensive involvement is indicated by additional ST elevation in leads , aVL, aVF and V 3-4.

(iii) The ST elevation is concave or saddle shaped

(iv) Associated ST depression in aVR and V1 is seen in 64% of cases [6].

(v) PR depression is another characteristic ECG finding which can be seen in any lead except aVR where PR elevation may occur. This may occur without the ST elevation.

Fig 1: ECG findings characteristic of pericarditis:

ecgFINDINGS

The above ECG changes are seen in the acute phase of pericarditis and are likely to be seen within the ED. As the disease progresses so may the ECG: there may be notched T waves, biphasic T waves or T wave inversion. These T wave changes may last for weeks or months but are of no clinical significance if the patient has recovered clinically.

Dysrhythmias are uncommon in pericarditis and if present may indicate myocardial involvement (Myopericarditis).

The ECG changes seen in pericarditis can be confused with Benign Early Repolarisation (BER). The most reliable ECG distinguishing feature is seen in lead V6. Specifically, when the ST elevation (mm) to T wave height (mm) ratio is greater than 0.25 acute pericarditis is more likely than BER (Figs 2 and 3) [7].

Learning bite

ST:T wave ratio in V6 can be used to help discriminate between BER and Acute Pericarditis [7]

Fig 2: (i) Benign Early Repolarisation:

benignEarly

Fig 3: (ii) Pericarditis:

pericarditis

(ii) Troponin

Troponin levels may be measured and are raised in 30-70% of patients with acute pericarditis. This does not offer any prognostic information [8]. A troponin rise is partially related to the extent of coexisting myocardial inflammation but, unlike in acute coronary syndromes, elevation in troponin is not associated with adverse outcome in pericarditis [13]. If there is elevation in troponin it is invariably associated with ST elevation. This creates a diagnostic dilemma and these cases may require additional specialist investigations to help make the correct diagnosis.

(iii) Haematology

A full blood count should be performed looking for an increase in the white cell count (WCC). A mild lymphocytosis is common. Significantly raised WCC is an indicator of poor prognosis and will therefore make inpatient management more likely.

(iv) Echocardiography (ECHO)

Echocardiography is a useful portable tool; it should be performed to look for the presence of adverse features. The views obtained may be limited in obese people and those with COPD [1]. When available, ECHO can be used for quantification of the size of a pericardial effusion (mild, moderate or large) and the presence of features of significant associated myocarditis (eg. poor ventricular function); there is some evidence that magnetic resonance imaging (MRI) may be more sensitive than ECHO for small effusions [1]. A large effusion or the presence of tamponade are both high risk features.

(v) Chest X-ray (CXR)

CXR is generally performed to look for alternative causes of chest pain. There may be radiological features of pneumonia if bacterial pericarditis is suspected or mass lesions indicative of neoplastic disease.

(vi) Computerised tomography of the chest (CT)

CT of the chest may be performed to look for alternative diagnoses such as acute aortic dissection or pulmonary embolism.

Myopericarditis vs Pericarditis

Acute pericarditis may be accompanied by some myocardial involvement. Once the diagnosis of acute pericarditis has been made one should consider whether there is any myocardial involvement. Troponin cannot be used to discriminate alone [9], however new onset of focal or depressed LV function on echocardiography would indicate inflammatory involvement and damage to the myocardium. A diagnosis of myopericarditis requires full clinical assessment including ECG, troponin and Echocardiography.

Troponin levels are elevated in 30-70% of patients with “pericarditis”; they offer no prognostic information [8].

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Management

In 70-90% of patients with acute pericarditis the cause is thought to be “idiopathic” . In these cases, where there are no identified high risk features, pericarditis is a self limiting disease [5,7] and treatment is primarily symptomatic (ie with non-steroidal anti-inflammatory medication (NSAIDs).

NSAIDs can be discontinued if symptoms have resolved within two weeks; if pain persists for longer, if there is uncertainty about the aetiology, or there are high risk features present at initial presentation, then patients should be admitted for further investigation and management.

Drug treatments

Any obvious underlying cause for acute pericarditis should be treated (eg. pneumonia, tuberculosis, uraemia, etc.).

NSAIDS are the mainstay of treatment for pericarditis (e.g. aspirin, ibuprofen, indomethacin, etc.). Aspirin is used preferentially if pericarditis is a complication of acute myocardial infarction.

Colchicine can be used as an alternative to NSAIDs and there is some evidence that it reduces recurrence rate [8]. It is considered in patients who do not respond initially to NSAIDs. The main reason that colchicine is not used as a first line agent is that it has significant side effects (nausea, vomiting, abdominal pain and diarrhoea).

Steroids are not indicated for acute pericarditis in the early phase as they are associated with an increased risk of relapsing pericarditis. Steroids should only be considered as first line treatment when the underlying cause is thought to be immune-mediated, due to a connective tissue disorder, or in uraemic pericarditis [9].

Learning bite

First line drug treatment for uncomplicated acute idiopathic pericarditis is NSAIDs

Complications

Studies evaluating the aetiology of acute pericarditis reported that a specific cause was found in 17% of patients and that most complications were seen in these patients [10]. Complications included acute cardiac tamponade (3.1%) and chronic constrictive pericarditis (1.5%).

Purulent pericarditis associated with tamponade is potentially fatal and requires urgent drainage and intravenous antibiotics; it carries a mortality rate of 40%.

Relapsing pericarditis occurs in 15-30% of patients with a presumed idiopathic aetiology, a small proportion of whom go on to suffer chronic relapsing pain.

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Safety pearls and Pitfalls

The main pitfall for the emergency physician is not carrying out a full risk stratification (including an echocardiogram) before declaring the patient suitable for discharge.

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MedicoLegal and other considerations

Key Learning points

  • 5% of patients presenting to the ED with non-ischaemic chest pain have acute pericarditis. Level of Evidence B
  • Pain radiating to the trapezius ridge is specific for acute pericarditis
  • 80-90% of acute pericarditis is viral in origin and often labelled as “idiopathic”. Level of Evidence B
  • The presence of any one of the high risk features is associated with a poorer prognosis. These patients should be admitted for inpatient management. Level of Evidence B
  • ST:T wave ratio in V6 can be used to help discriminate between benign early repolarisation and acute pericarditis [7].Level of evidence B
  • Troponin levels are elevated in 30-70% of patients. They offer no prognostic information[8].Level of evidence B
  • NSAIDs are the mainstay of treatment for acute idiopathic pericarditis.Level of Evidence B

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references

  1. Misselt AJ et al: MR Imaging of the pericardium. Magn Reson Imaging Clin N Am 16(2008) 185-199
  2. P. Fruergaard, J. Launbjerg et al The diagnoses of patients admitted with acute chest pain but without myocardial infarction. Eur Heart J, Vol. 17, July 1996
  3. Le Winter M, Tischler M: Pericardial Diseases Chapter 75 In Bonow: Braunwald’s Heart Disease – A Textbook of Cardiovascular Medicine, 9th ed.
  4. Khandaker MH, et al: Pericardial Diseases; diagnosis and Management. Mayo Clin Proc. June 2010; 85(6): 572-593
  5. Lange RA, Hills D : Acute Pericarditis N Engl J Med 2004;351: 2195-202
  6. Demangone D: ECG manifestations in Non coronary heart disease. Emerg Med Clin N Am 24(2006) 113-131
  7. Ginzon LE Laks MM: The differential diagnosis of acute pericarditis from the normal variant; new electrocardiographic criteria. Circulation 1982;65 : 1004-9
  8. Body R, Ferguson C: Should we be measuring troponins in patients with acute pericarditis? Emerg Med J 2008 25:253-524
  9. Maisch B et al on behalf of ESC : Guidelines on the diagnosis and management of pericardial diseases. Executive Summary European Heart Journal (2004) 25; 587-610
  10. Imazio M, Cecchi E, Demichelis B, et al: Indicators of poor prognosis of acute pericarditis. Circulation 115:2739, 2007
  11. Eppert A, Baombe J :Colchicine as an adjunct to non steroidal anti-inflammatory drugs for the treatment of acute pericarditis. Emerg Med J 2011 :244-245
  12. Imazio M, Cecchi E et al: Day hospital treatment of acute pericarditis. J Am Coll Cardiol. 2004; 43: 1042 1046.
  13. Imazio M, Trinchero R : Triage and Management of acute pericarditis International Journal of Cardiology 2007; 118: 286-294

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