Pericarditis, Viral

INTRODUCTION

Background: Both viral and bacterial infections may involve the pericardium (pericarditis), although viral pericarditis is more common in both children and adults. Awareness of this disease has increased since introduction of noninvasive diagnostic techniques such as echocardiography (ECHO) and CT scanning. Usually benign, the disease can be severe and even fatal, especially in children who are immunosuppressed. The infection may also involve the myocardium (myopericarditis).

 

Pathophysiology: The pericardium consists of 2 layers: the visceral pericardium (epicardium) and the parietal pericardium, which enclose the pericardial cavity (a potential space) between them. This cavity is lubricated by a small volume of serous fluid (<30 cm3 in adults). Inflammation of the pericardium secondary to a viral infection causes an increase in serous fluid (pericardial effusion). Studies show that persistent pericarditis triggers an autoimmune reaction to the myopericardial cells.

Pathogenesis of clinical manifestations

In a healthy individual, the pericardium does not limit filling of the cardiac chambers during rest or exercise. Pericardial effusion may reduce chamber capacity and may severely limit venous return and, therefore, cardiac output. Capacity of the pericardial space is influenced by its natural stiffness. Rapid accumulation of fluid is tolerated poorly, whereas slow accumulation may allow large amounts of pericardial fluid to collect without producing symptoms. Increased pressure within the pericardial space elevates filling pressure in all chambers of the heart. In advanced stages, right and left atrial mean pressures and right and left ventricular end-diastolic pressures are virtually identical to the intrapericardial pressure. The clinical features, therefore, result from limited cardiac output and elevated venous pressures.

Pericardial pain is related to pericardial inflammation and acute distension.

 

Frequency:

  • In the US: Frequency is unknown.
  • Internationally: Various studies indicate frequency ranges from 12.5-60% of all pericarditis.

Mortality/Morbidity:

  • The vast majority of patients recover with no sequelae.
  • Causes of death include cardiac tamponade and systemic involvement by the viral infection or the underlying disease.

Sex: Both sexes are affected.

Age: People of all ages are affected.

CLINICAL

History:

  • Fever and chest pain (usual presenting symptoms)
    • Low-to-moderate fever usually occurs but may be absent when the patient presents.
    • Pain in the chest or left shoulder is often aggravated or relieved by changes in physical position. Patients usually feel better in a sitting position.
    • Pain usually is substernal, accompanied by a sensation of chest constriction.
    • Pain is increased by any movement of the chest, including respiratory motion.
    • Pain may be reduced by sitting up and leaning forward. A child, therefore, may refuse to lie down for examination.
    • Palm pressure applied to the sternum markedly increases the pain.
  • A hacking cough (occasional presenting symptom)
    • The cough varies with position.

       

    • Sitting up and leaning forward improves the cough.
  • Preceding symptoms of viral illness (present in 40-75% of patients)
    • Fever
    • Runny nose
    • Cough
    • Diarrhea
    • Rash

Physical:

  • Patients with viral pericarditis generally appear less toxemic than those with bacterial pericarditis. However, some patients may appear quite ill, especially if the accompanying myocarditis is significant.

     

  • Physical signs in the absence of tamponade or significant myocarditis are minimal and may be limited to a pericardial friction rub audible in 80% of patients.
    • Rub sounds are best heard with the stethoscope's diaphragm. Sounds may occur in 3 phases of the cardiac cycle. Ventricular contraction is the first phase and occurs during systole. Ventricular filling and atrial contraction are the second and third phases and occur during diastole. The sounds may seem quite close to the ear. They are caused by the inflamed pericardial surfaces rubbing against each other. This rubbing sound may be misinterpreted as movement of the stethoscope on the chest surface. Pericardial friction rub may sound like 2 leather surfaces being rubbed together or like hair being rubbed between the fingers.

       

    • Loudness of a rub may decrease or even disappear with a large effusion because the pericardial surfaces separate.
  • With rapid accumulation of fluid, the patient may develop the clinical syndrome of cardiac tamponade. Physical signs, such as elevated nonpulsatile jugular venous pulse and tachycardia, mimic those of congestive heart failure (CHF). However, do not misinterpret this event as heart failure because drugs often used to treat heart failure may cause vascular collapse in a patient with pericarditis. Similarly, avoid administering diuretics because intravascular depletion can cause greater cardiac compression.
  • Cardiac tamponade refers to sudden accumulation of pericardial fluid sufficient to inhibit cardiac output. Rapidly accumulating effusion may cause cardiovascular collapse and death.
    • With cardiac tamponade, heart sounds seem distant, peripheral pulses are weak, and blood pressure (BP) is low. Pulse pressure also is low. Extremities may be cool and clammy.
    • Pulsus paradoxus may be documented by observing a more than 10–mm Hg inspiratory drop in BP.

       

    • In healthy individuals, inspiration causes systolic BP to fall slightly as a result of the greater volume of blood accommodated by the pulmonary vascular bed. This occurs despite inspiratory increase in venous return to the right heart. In cardiac tamponade, right ventricular filling is maintained at the expense of restricted left ventricular filling, and systolic BP falls further (>10 mm Hg). This exaggerated fall in systolic BP with inspiration is referred to as pulsus paradoxus, an important sign of cardiac tamponade. Occasionally, severe respiratory distress of any cause (eg, asthma, emphysema, pleural effusion) may cause this sign.
    • Distended neck veins may be present.
    • Hepatomegaly can develop, and the patient may report abdominal pain due to acute hepatic distension.
  • Chronic large pericardial effusion may cause ascites and peripheral edema.
  • Pulmonary edema is unusual because pericardial effusion limits the amount of blood that can enter the heart. No rales are heard in the lungs, and the patient does not demonstrate dyspnea or tachypnea. With myocarditis, in contrast, evidence of left heart failure may occur.
  • Recognize that signs and symptoms of viral pericarditis can mimic those of systemic lupus erythematosus.

Causes:

  • Coxsackievirus B (most common cause)
  • Echovirus
  • Adenovirus
  • Influenza virus
  • Mumps virus
  • Varicella virus
  • Epstein-Barr virus
  • Cytomegalovirus
  • Viral hepatitis B
  • Human immunodeficiency virus
  • Human herpesvirus 6
  • Parvovirus B19

DIFFERENTIALS

Esophagitis
Hypothyroidism
Nephrotic Syndrome
Pericarditis, Bacterial
Pericarditis, Constrictive
Pneumonia
Pneumothorax
Rheumatic Fever
Systemic Lupus Erythematosus
Thalassemia


Other Problems to be Considered:

Effusion, pleurodynia
Erythematosus
Esophageal, foreign body
Lymphedema
Other causes of chest pain
Other collagen vascular disease
Pulmonary causes, pleural
Postpericardiotomy effusion
Radiation pericarditis
Renal failure, chronic, with dialysis
Trauma, hemopericardium, cocaine use
Tuberculous pericarditis
Tumors, invasive and noninvasive
Uremia

WORKUP

Lab Studies:

  • Complete blood cell count
    • CBC usually is within reference ranges but may show a relative lymphocytosis.

       

    • Obtain a blood culture to help exclude bacterial infection.
    • Obtain a nasopharyngeal aspirate and stool for virus isolation and blood samples for viral titers (acute and convalescent).
    • Other blood tests (eg, electrolytes, BUN, glucose, blood gas analysis) may be required for acute-stage management.

Imaging Studies:

  • Chest radiography
    • Radiography demonstrates cardiomegaly, depending on the amount of fluid and presence of underlying myocarditis.

       

    • A typical saclike appearance of the cardiac silhouette is characteristic of large effusions.

       

    • Chamber enlargement is not observed.

       

    • Pulmonary venous congestion is not a feature of pericarditis, although coexistent myocarditis and heart failure may cause such congestion.
  • Two-dimensional ECHO
    • ECHO is the definitive test to demonstrate pericardial fluid and to establish the diagnosis.
    • Thickness of the pericardium and the amount of fluid can be quantified, and the effect of fluid on cardiac hemodynamics can be assessed.

Other Tests:

  • Electrocardiography
    • Generalized elevation of the ST segment in leads with an upright T wave is the typical pattern of pericarditis, although this finding may not be apparent.
    • Low-voltage complexes may occur in the presence of a large effusion.

Procedures:

  • Pericardiocentesis: This procedure is required for all patients who have clinical evidence of cardiac tamponade or suspected bacterial pericarditis and for some patients who are immunocompromised. Pericardiocentesis is also used as a diagnostic test in patients with a pericardial effusion of unknown cause. Caution: The volume of fluid present should be sufficient to allow removal of a reasonable portion for diagnostic purposes.
    • Place the child in a half-sitting position (roughly 45°) with sedation or anesthesia as needed. If anesthesia is used, avoid agents that precipitously drop systemic pressure because circulatory collapse can ensue.
    • Have ECHO available to monitor needle position.

       

    • Insert a short, beveled, and sharp needle beneath the xiphoid, angling up and left toward the left shoulder. Sometimes a pop is felt as the needle is passed into the pericardium.

       

    • Attempt to withdraw fluid with each advance of the needle. If fluid is obtained, remove enough to alleviate tamponade. A small amount (as little as 20 mL in an adult) provides significant benefit.

       

    • If the fluid is grossly bloody, consider the possibility that the needle is in a cardiac chamber. A few drops on a towel sometimes immediately prove whether the problem is bloodstained fluid and not pure blood. If debatable, centrifuge the fluid because it may show a hematocrit much lower than that of blood.

       

    • Once certain that the fluid obtained is from the pericardium, drain all easily removable fluid. Older patients may report relief from symptoms at this point.

       

    • The decision whether to leave a drain in the pericardium depends upon the probable diagnosis. If evidence of bacterial infection is found, pass a guide wire into the pericardium and confirm its position by ECHO or fluoroscopy. Then pass a catheter over the guide wire into the pericardium as a drain. Leave the drain in place.

       

    • Definitive therapy can begin when a precise diagnosis is established, often only after detailed examination of the fluid.
  • Pericardioscopy and epicardial biopsy: This new diagnostic procedure seldom applies to an episode of viral pericarditis but instead is used to macroscopically visualize alterations of both the epicardium and the pericardium. Macropathology of the epicarditis and pericarditis can be observed in vivo.
    • The prerequisite is documentation of a larger pericardial effusion (>150 mL by the cubic model) with an echocardiographically documented effusion of type C. This procedure requires at least a 5-mm separation between the epicardial and pericardial layers in diastole at the anterior side of the heart when echocardiographic imaging is performed from the subxiphoidal or third intercostal space.

       

    • After puncture of the pericardial effusion, introduce a 9-ft sheath by use of a guide wire under echocardiographic or fluoroscopic control.

       

    • Remove the fluid by aspiration and infuse 100-150 mL of body temperature warmed saline in the pericardial sac.

       

    • Use a flexible 8-ft fiberglass instrument (eg, Vantec, Baxter, Storz) and a rigid 110°, 8-ft endoscope (Storz) to visualize the pericardium and epicardium and for videotape documentation.

       

    • After endoscopic inspection of the macropathology, fibrinous strands or increased vascular injection can be observed in viral, autoimmune, or idiopathic pericarditis or perimyocarditis. In the latter 3 forms of pericardial effusion, only inflammatory cells can be observed when the pericardial fluid is analyzed.
  • Cardiac catheterization: This is not indicated for diagnosis of viral pericarditis.
Histologic Findings: Pericardial fluid is either serous or serosanguineous, with a predominance of lymphocytes, although neutrophils may also be present.

 

TREATMENT

Medical Care: Management is conservative (expectant) and symptomatic.

  • Bed rest and anti-inflammatory agents are mainstays of initial therapy.
  • Aggressive pain control may be necessary in some patients, although most respond to salicylates or nonsteroidal anti-inflammatory drugs (NSAIDs).
  • Steroid therapy is rarely indicated. Consider this option only when nonsteroidal agents are unsuccessful or a bacterial etiology has clearly been excluded. While steroid therapy might reduce symptoms dramatically, no convincing evidence exists of any long-term benefits.
  • Resolution of effusion may occur within several days to weeks after initiating anti-inflammatory drugs; however, initially observe patients closely for the development of pericardial tamponade.
  • Pericardiocentesis is indicated when the etiology is doubtful and is essential in suspected tamponade.

Surgical Care:

  • Place a pericardial drainage catheter.
  • Pericardiectomy, the surgical creation of a pericardial window needed in refractory cases to facilitate open drainage, is only rarely required for chronic recurrent cases.

Consultations:

  • Pediatric cardiologist
  • Radiologist
  • Family physician
  • Psychologist
  • School teacher
  • Specialist nurse

     

  • Pharmacist

     

  • Dietitian

Diet: Viral pericarditis requires no special diet.

Activity: Reduce activity to the level tolerated by patients with the condition.

MEDICATION

Bed rest and anti-inflammatory agents are the mainstays of initial therapy. Aggressive pain control may be necessary in some patients; however, most respond to salicylates or NSAIDs. Although corticosteroid therapy is rarely indicated, consider such a course when NSAIDs are unsuccessful and a bacterial etiology has clearly been excluded.

Corticosteroids may reduce symptoms dramatically, but no convincing evidence exists of any long-term benefit. Anti-inflammatory therapy (eg, aspirin, indomethacin) may continue for several months. After therapy is discontinued, 15-30% of patients may relapse. The optimal method for prevention is not fully established, but accepted modalities include NSAIDs, corticosteroids, immunosuppressive agents, and pericardiectomy. Colchicine has also been tried in some patients with good response.

Drug Category: Nonsteroidal anti-inflammatory drugs (NSAIDs) -- Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action inhibits cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may also exist, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.
Drug Name
Ibuprofen (Motrin, Ibuprin) -- Propionic acid derivative that reduces formation of inflammatory mediators by enzyme inhibition.
Adult Dose 1.6-2.4 g/d PO divided qid
Pediatric Dose 10 mg/kg PO qid
Contraindications Documented hypersensitivity; aspirin hypersensitivity; breastfeeding; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
Interactions Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; may decrease effects of beta-blockers, hydralazine, and captopril; may decrease effects of loop diuretics with coadministration; coadministration with anticoagulants may increase PT (monitor and watch for signs of bleeding); may increase serum lithium levels and risk of methotrexate and phenytoin toxicity; probenecid may increase toxicity of NSAIDs
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Pregnancy category D (ie, unsafe in pregnancy) in third trimester; use with care in renal, cardiac, and hepatic impairment
Drug Name
Naproxen (Aleve, Anaprox, Naprosyn) -- Propionic acid derivative that reduces formation of inflammatory mediators by enzyme inhibition.
Adult Dose 0.5-1 g/d PO qd or divided bid
Pediatric Dose <2 years: Not established
>2 years: 10 mg/kg/d PO divided bid
Contraindications Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; aspirin hypersensitivity; breastfeeding; coagulation defects
Interactions Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; may decrease effects of beta-blockers, hydralazine, and captopril; may decrease effects of loop diuretics with coadministration; coadministration with anticoagulants may increase PT (monitor and watch for signs of bleeding); may increase serum lithium levels and risk of methotrexate and phenytoin toxicity; probenecid may increase toxicity of NSAIDs
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Pregnancy category D (ie, unsafe in pregnancy) in third trimester; use with care in renal, cardiac, and hepatic impairment
Drug Name
Diclofenac sodium (Cataflam, Voltaren) -- Possesses properties similar to propionic acid derivatives and reduces formation of inflammatory mediators by enzyme inhibition.
Adult Dose 75-150 mg/d PO divided bid/tid
Pediatric Dose 1-3 mg/kg/d PO divided bid/tid
Contraindications Documented hypersensitivity; aspirin hypersensitivity; breastfeeding; coagulation defects; peptic ulcer disease
Interactions Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; may decrease effects of beta-blockers, hydralazine, and captopril; may decrease effects of loop diuretics with coadministration; coadministration with anticoagulants may increase PT (monitor and watch for signs of bleeding); may increase serum lithium levels and risk of methotrexate and phenytoin toxicity; probenecid may increase toxicity of NSAIDs
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Pregnancy category D (ie, unsafe in pregnancy) in third trimester; use with care in renal, cardiac, and hepatic impairment
Drug Name
Indomethacin (Indocin) -- Behaves like propionic acid derivatives and inhibits formation of inflammatory mediators.
Adult Dose 50-200 mg/d PO divided tid/qid
Pediatric Dose 0.3-3 mg/kg/d PO divided tid/qid
Contraindications Documented hypersensitivity; aspirin hypersensitivity; breastfeeding; coagulation defects; peptic ulcer disease
Interactions Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; may decrease effects of beta-blockers, hydralazine, and captopril; may decrease diuretic effects of furosemide and thiazides; coadministration with anticoagulants may prolong PT (monitor and watch for signs of bleeding); may increase risk of methotrexate toxicity, which can manifest as stomatitis, bone marrow suppression, or nephrotoxicity; coadministration may increase phenytoin levels; probenecid may increase toxicity of NSAIDS
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Pregnancy category D (ie, unsafe in pregnancy) if used >48 h or after 34 weeks’ gestation; use with care in renal, cardiac, and hepatic impairment; has more anti-inflammatory action but more adverse effects; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia exists)
Drug Category: Corticosteroids -- Elicit anti-inflammatory and immunosuppressive properties and cause profound and varied metabolic effects. They modify the body’s immune response to diverse stimuli.
Drug Name
Prednisolone (Pediapred, Orapred, Econopred) -- Use restricted to resistant cases not responding to nonsteroidal medications. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Adult Dose 10-60 mg PO every am
Pediatric Dose 1-2 mg/kg/d PO every am
Contraindications Documented hypersensitivity; viral, fungal, or tubercular skin lesions
Interactions Increases risk of GI bleeding with analgesics; decreases effects of salicylates and toxoids (for immunizations); phenytoin, carbamazepine, barbiturates, and rifampin decrease effects of corticosteroids
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Only essential use suggested; caution in hyperthyroidism, osteoporosis, cirrhosis, nonspecific ulcerative colitis, peptic ulcer, diabetes mellitus, and myasthenia gravis; do not stop abruptly if used for >1 wk; may cause GI upset, peptic ulcer disease, acute pancreatitis, candidiasis, myopathy, psychosis, hypertension, hyperglycemia, osteoporosis, growth delay, and cataracts

FOLLOW-UP

Further Inpatient Care:

  • Reevaluate recurrent cases
  • Pericardial biopsy
  • Pericardiectomy

Further Outpatient Care:

  • Continue anti-inflammatory therapy, such as aspirin or indomethacin, for at least several months to monitor progress.

Complications:

  • Severe tamponade may cause cardiac arrest due to electromechanical dissociation.
    • Less severe cases may cause tachycardia, tachypnea, fall in arterial BP, rise in central venous pressure, and paradoxical pulse. The patient reports dyspnea and chest pain.

       

    • Cardiac tamponade may develop from any cause of acute fluid accumulation in the pericardial sac.

       

    • Therapy for cardiac tamponade consists of removing the pericardial fluid by means of pericardiocentesis, pericardiotomy, or pericardiectomy.

       

    • Caution: Do not confuse tamponade with CHF. Medications used to treat heart failure (eg, digoxin) may slow the heart rate. Because tachycardia represents the only effective compensatory mechanism available to the patient for maintaining cardiac output, slowing the rate may cause acute cardiovascular collapse. Administration of diuretics or afterload-reducing agents can also lead to cardiovascular collapse.
  • After therapy is discontinued, 15-30% of patients may experience relapse. The optimal method for prevention is not fully established. Accepted modalities include NSAIDs, corticosteroids, immunosuppressive agents, and pericardiectomy. Colchicine has also been tried in some patients with good response.

Prognosis:

  • Almost all patients recover completely if no serious acute complication occurs.
  • Constrictive pericarditis rarely occurs following viral pericarditis.

Patient Education:

  • Educate the patient on the chances of recurrence and, as needed, on continuing medications and the need for follow-up.
 

MISCELLANEOUS

Medical/Legal Pitfalls:

  • Failure to diagnose bacterial pericarditis
  • Failure to diagnose tamponade
  • Failure to suspect effusion in chest infections or other systemic diseases
  • Failure to attribute symptoms to tamponade, especially in patients with underlying malignancy or in posttransplant patients
  • Failure to follow up for recurrence
  • Failure to distinguish between tamponade and CHF

Special Concerns:

  • Early identification of bacterial effusion is important because it requires antibiotic therapy and open drainage.
  • Any underlying collagen vascular disease must be recognized.
  • Discontinue aspirin administration to patients in cases of contact with chicken pox infection.

PICTURES

 

Caption: Picture 1. Pericarditis, viral. Two-dimensional echocardiogram showing a large pericardial effusion.
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Picture Type: Image
Caption: Picture 2. Pericarditis, viral. M-mode echocardiogram showing moderate pericardial effusion.
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Picture Type: Image
Caption: Picture 3. Pericarditis, viral. Plain chest radiograph of a 2-year-old boy with viral pericarditis and massive pericardial effusion.
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Picture Type: X-RAY