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Acute Pericarditis Treatment & Management

  • Author: Sean Spangler, MD; Chief Editor: Richard A Lange, MD, MBA  more...
 
Updated: Oct 06, 2014
 

Approach Considerations

Oxygen and a cardiac monitor should be provided. Rule out other life-threatening causes of chest pain, such as myocardial infarction (MI) or aortic dissection. Evaluate for evidence of hemodynamic instability.

Consider whether further management is safe to continue on an outpatient basis. In one study, fever of more than 100.4°F (38°C), subacute onset, immunosuppression, trauma, oral anticoagulation therapy, aspirin or nonsteroidal anti-inflammatory drug (NSAID) treatment failure, myopericarditis, severe pericardial effusion, and cardiac tamponade were designated as poor prognostic predictors.[31] Patients without these factors were treated on an outpatient basis without serious complications after a mean follow-up of 38 months.[31]

Avoid NSAIDs and corticosteroids in acute MI pericarditis, because they may interfere with ventricular healing, remodeling, or both.

Patients may require transfer to a hospital setting in which hemodialysis and cardiothoracic surgery are available.

Form more information, see the Medscape Reference topics Constrictive Pericarditis, Constrictive-Effusive Pericarditis, and Pediatric Infective Pericarditis.

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Prehospital Care

Patients with chest pain, regardless of etiology, should routinely be treated with oxygen and cardiac monitor.

Patients suspected of having pericarditis should have routine care as for patients with acute cardiac conditions The initial prehospital care for suspected cardiac tamponade is the same as for any major trauma. The diagnosis may also be suspected based on the location of any penetrating wounds. The possibility of a tension pneumothorax should also be considered.

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Emergency Department Care

The emergency care of the patient centers on prompt diagnosis and treatment of potentially life-threatening entities. Thoracotomy and pericardiotomy may be required if the patient has rapid deterioration or cardiac arrest.

Pericarditis

Ideally, echocardiography should be readily available to determine the presence or absence of a pericardial effusion (see Echocardiography under Workup). If no pericardial effusion is noted, stable patients with presumptive viral pericarditis may be discharged with appropriate instructions and follow-up care.

If a small- to medium-sized effusion is present, the patient should be admitted for observation and serial echocardiography. If a large effusion is present, the stable patient may undergo an urgent pericardiocentesis or placement of a pericardial window (see Surgical Intervention).

Cardiac tamponade

Treatment for this condition depends on the patient’s stability. Unstable patients require immediate treatment of the increase in pericardial pressure with pericardiocentesis (see Surgical Intervention). Removing as little as 30-50 mL may produce dramatic hemodynamic improvement.

Patients may have subacute tamponade (intermittently decompressing) and may benefit from decompression in the operating room with cardiothoracic care available to treat cardiac injuries.

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Treatment of Specific Types of Pericarditis

The treatment for specific types of pericarditis are briefly discussed in this section.

Idiopathic pericarditis

Treatment for this condition is similar to viral pericarditis and includes anti-inflammatory drugs to control symptoms and inflammation.[32] Pericardiectomy should be considered in recurrent cases of chronic idiopathic pericarditis:, because it yields good long-term effects. However, high-dose prednisone may prevent recurrent pericarditis resistant to NSAIDs.

Infectious pericarditis

The treatment of viral pericarditis is based on the symptoms present, with observation for the development of tamponade. Treatment for bacterial pericarditis includes appropriate antibiotics for at least 4 weeks and drainage of pericardial fluid.

For fungal infection, the ESC 2004 guideline recommends fluconazole, ketoconazole, itraconazole, amphotericin B, liposomal amphotericin B, or amphotericin B lipid complex for treatment of fungal infection. Corticosteroids and NSAIDs can be used to support the antifungal drug treatment.[24]

Intrapericardial fibrinolysis can be a useful treatment to assist with drainage of thick, loculated fluid, but open surgical drainage is preferred. Occasionally, patients require partial to total pericardiectomy.

Tubercular infection is managed with the usual antituberculous chemotherapy.

Controversy exists regarding the use of steroids in the treatment of tuberculous pericarditis. The ESC 2004 guideline advises using corticosteroid therapy only in patients with secondary tuberculous pericarditis, and only as an adjunct to tuberculostatic treatment. A meta-analysis of patients with effusive and constrictive TBC pericarditis found that tuberculostatic treatment, combined with steroids, might be associated with fewer deaths, less frequent need for pericardiocentesis or pericardiectomy.[18] .

Use of adjunctive prednisolone in patients with acquired immunodeficiency syndrome (AIDS) may reduce mortality in this population.

Inflammatory pericarditis

Only symptomatic rheumatoid arthritis (RA) pericarditis should be treated. However, treat lupus pericarditis with anti-inflammatory agents and optimize systemic lupus erythematosus (SLE) treatment.

Rheumatic fever pericarditis resolves with anti-inflammatory treatment.

Metabolic pericarditis

The development of pericarditis in a patient with severe acute or chronic renal failure is an absolute indication for intensive dialysis. In most patients, relief of chest pain and reduction in the size of any effusion occurs within 1-2 weeks.

If no improvement is noted after 7-10 days or if the patient has hemodynamic instability, proceed with pericardiocentesis or pericardiectomy (see Surgical Intervention). The ESC 2004 guideline recommends pericardiocentesis for treating cardiac tamponade and large chronic effusions resistant to dialysis.[18] Intensive dialysis is beneficial to most patients with uremia who develop pericarditis before dialysis. Dialysis-induced pericarditis fails to respond to more intensive dialysis in 25-33% of patients.

Both hemodialysis and peritoneal dialysis are efficacious in the treatment of uremic pericarditis, though each technique has unique advantages and disadvantages. Hemodialysis may cause hypotension, which may be dangerous in the setting of tamponade. In addition, some physicians advocate heparin-free hemodialysis to reduce the risk of intrapericardial hemorrhage. Peritoneal dialysis may compromise respiratory function because of the effect of intraperitoneal fluid on the diaphragm.

In dialysis-associated pericarditis, an increased intensity of dialysis for 10-14 days is recommended. Close monitoring of fluid volume and electrolytes is mandatory to detect and correct hypophosphatemia and hypokalemia, which may occur with intensive dialysis. The response of dialysis-associated pericarditis is not predictable. In some instances, consider a switch to peritoneal dialysis if heparin-free dialysis cannot be performed.

NSAIDs and steroids may offer symptomatic relief but are not effective without dialysis. Indomethacin ameliorates fever, but it does not accelerate resolution of the effusion.

Early intervention with dialysis may prevent the development of uremic pericarditis. Maintenance of adequate dialysis therapy lessens the likelihood of a patient developing dialysis-associated pericarditis.

Treatment in hypothyroidism-associated pericarditis is hormone replacement.

The ESC 2004 guideline also recommends thyroid hormone therapy to decrease pericardial effusion.[24]

Cardiovascular pericarditis

Pericarditis does not contraindicate thrombolytic or anticoagulant therapy for an acute MI. However, anticoagulation should be discontinued if pericardial effusion develops or effusion size increases. Treatment is with aspirin.

In Dressler syndrome, anticoagulant therapy should be stopped because of the risk of hemorrhagic pericarditis. Treatment is with NSAIDs.

Miscellaneous conditions

With neoplasm-associated pericarditis, initial treatment includes relief of tamponade, confirmation of the diagnosis, and systemic treatment of the neoplasm. Further treatment options include sclerosis of the pericardial space, instillation of chemotherapeutic agents into the pericardial space, local radiation, or pericardiectomy.

The ESC 2004 guideline adds that prevention of recurrences of neoplastic pericarditis may be achieved via intrapericardial instillation of sclerosing, cytotoxic agents, or immunomodulators. Intrapericardial treatment tailored to the type of tumor shows that administration of cisplatin is most effective in secondary lung cancer and intrapericardial instillation of thiotepa was more effective in breast cancer or pericardial metastases.[33, 34]

The ESC 2004 guideline states that treatment of cardiac tamponade is a class I indication for pericardiocentesis in the presence of neoplastic pericarditis. In suspected neoplastic pericardial effusion without tamponade, the following are recommended:[24]

  • Systemic antineoplastic treatment as baseline therapy
  • Pericardiocentesis to relieve symptoms and to confirm diagnosis
  • Intrapericardial instillation of cytostatic/sclerosing agent

Drug-induced pericarditis treatment includes stopping the administration of the offending agent and anti-inflammatory therapy as needed. Treatment is with aspirin or NSAIDs.

Colchicine is effective in the prevention of postpericardiotomy syndrome and may halve the risk of developing this syndrome when used following cardiac surgery.[35]

Diet and activity

Patients on dialysis require a daily diet restricted to 1.2 g/kg of protein, 2 g of sodium, and 2 g of potassium. Patients on peritoneal dialysis may require less stringent protein restriction.

Activity should be limited to avoid strenuous activities or trauma, which may increase the risk of hypotension or arrhythmias.

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Pericardiectomy and Other Surgical Procedures

Surgical procedures for pericarditis include pericardiectomy, pericardiocentesis, pericardial window placement, and pericardiotomy.

Pericardiectomy

Pericardiectomy is the most effective surgical procedure for managing large effusions, because it has the lowest associated risk of recurrent effusions. This procedure is used for constrictive pericarditis, effusive pericarditis, or recurrent pericarditis with multiple attacks, steroid dependence, and/or intolerance to other medical management.

Pericardiectomy requires general anesthesia and a thoracotomy; therefore, pericardiectomy should be considered only if pericardiotomy cannot be performed or has been unsuccessful.[36]

Studies demonstrate that failure rates are proportional to the amount of pericardium removed (ie, the more pericardium removed, the less likely the procedure will fail). In effusive pericarditis, the higher failure rate associated with a pericardial window procedure or partial pericardiectomy is likely secondary to the continued fluid production from the remaining pericardium, with sealing of the remaining pericardium to the heart.

The operative mortality rate was 14% in one series, with a range of 1% for New York Heart Association (NYHA) class 1-2, 10% for class 3, and 46% for class 4. The 5-year survival rate was 80% for class 3-4 and approximately 95% for 1-2.

As with pericardiocentesis, studies involving pericardiectomy note a greatly improved diagnostic yield if pericardial biopsy is performed as part of a therapeutic procedure. Diagnostic biopsies yielded 5%, whereas therapeutic biopsies were at 22-54%.

A study by Thompson et al indicated that complete pericardiectomy can produce good outcomes in properly selected pediatric patients with pericarditis.[37] The report involved 27 pediatric patients (mean age, 16.7 y), including 16 patients with inflammatory pericarditis and 11 with constrictive pericarditis. The median presurgical period of symptom duration for these patients was 1 year. Before the pericardiectomies were performed, 10 patients had been hospitalized for treatment of symptoms, 15 had undergone pericardiocentesis, and 3 had already undergone a partial pericardiectomy.[37]

The procedures in the above study consisted of complete pericardiectomy (21 patients), biventricular pericardiectomy (3 patients), and completion pericardiectomy (3 patients). The postoperative course was, for most of the patients, uneventful, although one patient with radiation-induced heart disease died of acute hepatic failure 155 days after undergoing pericardiectomy.[37] At follow-up (median period, 1 y), 89% of the patients had experienced complete symptom resolution.

Pericardiocentesis

People with effusions larger than 250 mL, effusions in which size increases despite intensive dialysis for 10-14 days, or effusions with evidence of tamponade are candidates for pericardiocentesis (for the technique, see Pericardiocentesis under Workup).

The image below shows preprocedure and postprocedure images of a cardiac silhouette.

Chest radiographs revealing markedly enlarged card Chest radiographs revealing markedly enlarged cardiac silhouette and normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardiocentesis (B). Courtesy of Zhi Zhou, MD.

Pericardial window placement

In critically ill patients, a balloon catheter may be used to create a pericardial window, in which only 9 cm2 or less of pericardium is resected. This procedure is a modification of balloon valvuloplasty in which an uninflated balloon is passed inside the pericardial space, where it is opacified, inflated, and then pulled through the pericardium to create a window through which pericardial fluid drains into the peritoneal or pleural space.

Pericardial window placement is used for effusive pericarditis therapy. Some studies note the need for repeat operation in nearly 25% of patients who undergo the procedure at 2 years.

Pericardiotomy

Consider subxyphoidsubxiphoid pericardiotomy for large effusions that do not resolve. This procedure may be performed under local anesthesia and has a lower risk of complications compared with pericardiectomy.

The ESC 2004 guideline recommends percutaneous balloon pericardiotomy, which creates a pleuro-pericardial direct communication, allowing for drainage of fluid into the pleural space. In large malignant pericardial effusions and recurrent tamponade, it appears to be a safe and effective (90-97%) intervention.[24]

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Complications

The following conditions are possible complications of acute pericarditis itself or treatment used in its management:

  • Recurrence in 15-32% of patients
  • Cardiac tamponade
  • Constrictive pericarditis. In addition, liver disease has been reported in asymptomatic constrictive pericarditis
  • Combination of effusive and constrictive pericarditis
  • Noncompressive effusion
  • Cardiac perforation with pericardiocentesis

Bronchopericardial fistula has been reported as a complication of multi–drug-resistant tuberculosis in a patient with human immunodeficiency virus (HIV) infection.[38]

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Consultations and Long-Term Monitoring

Consult a cardiologist or internist for acute and idiopathic cases of pericarditis. In complicated cases (eg, tuberculous, traumatic pericardial injury, purulent uremic etiologies require multidisciplinary involvement) obtain consultations with a cardiologist, cardiac and/or trauma surgeon, and medical subspecialists (eg, infectious diseases specialist, nephrologist).

Consult with a cardiothoracic surgeon for all patients with large effusions. Development of tamponade is unpredictable, and it is important for the surgeon to be aware of the patient if an emergent procedure is necessary.

In patients with uremic or dialysis-associated pericarditis, carefully monitor the patient at follow-up hemodialysis visits for recurrence of signs or symptoms. Up to 15% of these patients may have recurrence of pericarditis.

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Contributor Information and Disclosures
Author

Sean Spangler, MD Cardiologist, William Beaumont Army Medical Center

Sean Spangler, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Philip J Gentlesk, MD Director, Cardiac Electrophysiology, Section of Cardiovascular Disease, Brooke Army Medical Center

Philip J Gentlesk, MD is a member of the following medical societies: American College of Cardiology, Christian Medical and Dental Associations

Disclosure: Nothing to disclose.

Chief Editor

Richard A Lange, MD, MBA President, Texas Tech University Health Sciences Center, Dean, Paul L Foster School of Medicine

Richard A Lange, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Acknowledgements

George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation

Disclosure: Nothing to disclose.

Vecihi Batuman, MD, FACP, FASN Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Christopher A Fly, MD Assistant Professor, Department of Emergency Medicine, Medical College of Georgia

Christopher A Fly, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Anupama Gowda, MBBS, MD Consulting Staff, Atlanta Nephrology Associates, PC

Disclosure: Nothing to disclose.

Eric L Legome, MD Chief, Department of Emergency Medicine, Kings County Hospital Center; Associate Professor, Department of Emergency Medicine, New York Medical College

Eric L Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

James W Lohr, MD Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Genzyme Honoraria Speaking and teaching

G Shawn Lynchard, MD Consulting Cardiologist, Medical Director of Cardiac Care Unit, Congestive Heart Failure Clinic, and ECG and Stress Testing Clinic, Brooke Army Medical Center

G Shawn Lynchard, MD is a member of the following medical societies: American College of Cardiology and American College of Physicians

Disclosure: Nothing to disclose.

Chike Magnus Nzerue, MD Associate Dean for Clinical Affairs, Vice-Chairman of Internal Medicine, Meharry Medical College

Chike Magnus Nzerue, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, and National Kidney Foundation

Disclosure: Nothing to disclose.

David A Peak, MD Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary

David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Verena T Valley, MD Associate Professor, Director of Ultrasound, Department of Emergency Medicine, University of Mississippi School of Medicine; Consulting Staff, Department of Emergency Medicine, Singing River Hospital System, Singing River Hospital, and Ocean Springs Hospital

Verena T Valley, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

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Stage 1 electrocardiograph changes in a patient with acute pericarditis.
Stage 4 electrocardiograph changes in the same patient as in the previous image, taken approximately 3 months after acute pericardial illness. The patient remained symptom free despite continued T-wave inversion.
Chest radiographs revealing markedly enlarged cardiac silhouette and normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardiocentesis (B). Courtesy of Zhi Zhou, MD.
Recording of aortic pressure showing pulsus paradoxus. During inspiration, systolic pressure declines 20 mm Hg. Courtesy of Zhi Zhou, MD.
This ultrasonogram demonstrates a normal subcostal 4-chamber view of the heart. The pericardium is brightly reflective (echogenic or white in appearance). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. Part B courtesy of Wikimedia Commons/Patrick J Lynch and C Carl Jaffe.
H&E stain, medium power magnification showing a rheumatoid nodule in rheumatoid pericarditis, composed of histiocytes and scattered multinucleated giant cells (lower right) surrounding necroinflammatory debris (upper left).
Pap stain, high power magnification of adenocarcinoma metastatic to the pericardium on pericardiocentesis with the red arrow showing a normal mesothelial cell and the black arrowhead showing adenocarcinoma.
 
 
 
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