eMedicine Specialties > Cardiology > Pericardial Disease

Pericardial Effusion: Treatment & Medication

Author: William J Strimel, DO, Fellow, Cardiovascular Disease, Scott and White Memorial Hospital
Coauthor(s): Ramin Assadi, MD, Staff Physician, Department of Internal Medicine, Loma Linda University; Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA); Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Contributor Information and Disclosures

Updated: Sep 9, 2008

Treatment

Medical Care

Initially, medical care of pericardial effusion is focused on determination of the underlying etiology.

  • Aspirin/nonsteroidal anti-inflammatory agents (NSAIDs)
    • Most acute idiopathic or viral pericarditis occurrences are self-limited and respond to treatment with aspirin (650 mg q6h) or another NSAID.
    • Aspirin may be the preferred nonsteroidal agent to treat pericarditis after myocardial infarction because other NSAIDs may interfere with myocardial healing.
    • Indomethacin should be avoided in patients who may have coronary artery disease.
  • Colchicine
    • The routine use of colchicine is supported by results from the COlchicine for acute PEricarditis (COPE) trial. In this trial, 120 patients with a first episode of acute pericarditis (idiopathic, acute, postpericardiotomy syndrome, and connective tissue disease) entered a randomized, open-label trial comparing aspirin treatment alone with aspirin plus colchicine (1-2 mg for the first day followed by 0.5-1 mg/d for 3 mo). Colchicine reduced symptoms at 72 hours (11.7% vs 36.7%; P =0.03) and reduced recurrence at 18 months (10.7% vs 36.7%; P =0.004; 5 needed treatment). Colchicine was discontinued in 5 patients because of diarrhea. No other adverse events were noted. Importantly, none of the 120 patients developed cardiac tamponade or progressed to pericardial constriction.10
  • Steroids
    • Steroid administration early in the course of acute pericarditis appears to be associated with an increased incidence of relapse after tapering the steroids.
    • In the COPE trial, steroid use was an independent risk factor for recurrence (odds ratio=4.3). Also, an observational study strongly suggests that the use of steroids increases the probability of relapse in patients treated with colchicine.10
    • Systemic steroids should be considered only in patients with recurrent pericarditis unresponsive to NSAIDs and colchicine or as needed for treatment of an underlying inflammatory disease. If steroids are to be used, an effective dose (1-1.5 mg/kg of prednisone) should be given, and it should be continued for at least 1 month before slow tapering.
    • The intrapericardial administration of steroids has been reported to be effective in acute pericarditis without producing the frequent reoccurrence of pericarditis that complicates the use of systemic steroids, but the invasive nature of this procedure limits its use.
  • Hemodynamic support
    • Patients who have effusions with actual or threatened tamponade should be considered to have a true or potential emergency. Most patients require pericardiocentesis to treat or prevent tamponade. However, treatment should be carefully individualized.
    • Hemodynamic monitoring with a balloon flotation pulmonary artery catheter is useful, especially in those with threatened or mild tamponade in whom a decision is made to defer pericardiocentesis. Hemodynamic monitoring is also helpful after pericardiocentesis to assess both reaccumulation and the presence of underlying constrictive disease. However, insertion of a pulmonary artery catheter should not be allowed to delay definitive therapy in critically ill patients.
    • Intravenous fluid resuscitation may be helpful in cases of hemodynamic compromise.
    • In patients with tamponade who are critically ill, intravenous positive inotropes (dobutamine, dopamine) can be used but are of limited use and should not be allowed to substitute for or delay pericardiocentesis.
  • Antibiotics
    • In patients with purulent pericarditis, urgent pericardial drainage combined with intravenous antibacterial therapy (eg, vancomycin 1 g bid, ceftriaxone 1-2 g bid, and ciprofloxacin 400 mg/d) is mandatory. Irrigation with urokinase or streptokinase, using large catheters, may liquify the purulent exudate, but open surgical drainage is preferable.
    • The initial treatment of tuberculous pericarditis should include isoniazid 300 mg/day, rifampin 600 mg/day, pyrazinamide 15-30 mg/kg/day, and ethambutol 15-25 mg/kg/day. Prednisone 1-2 mg/kg/day is given for 5-7 days and progressively reduced to discontinuation in 6-8 weeks. Drug sensitivity testing is essential. Uncertainty remains whether adjunctive corticosteroids are effective in reducing mortality or progression to constriction. Surgical resection of the pericardium remains the appropriate treatment for constrictive pericarditis. The timing of surgical intervention is controversial, but many experts recommend a trial of medical therapy for noncalcific pericardial constriction and pericardiectomy in nonresponders after 4-8 weeks of antituberculosis chemotherapy.
  • Antineoplastic therapy (eg, systemic chemotherapy, radiation) in conjunction with pericardiocentesis has been shown to be effective in reducing recurrences of malignant effusions.
  • Corticosteroids and NSAIDs are helpful in patients with autoimmune conditions.

Surgical Care

Surgical care of pericardial effusion includes the following:

  • Subxiphoid pericardial window with pericardiostomy
    • This procedure is associated with low morbidity, mortality, and recurrence rates.
    • It can be performed under local anesthesia.
    • It may be less effective when effusion is loculated.
    • It may replace pericardiocentesis as initial treatment for stable pericardial effusions.
    • A recent study suggests that this may be safer and more effective at reducing recurrence rates than pericardiocentesis. However, only patients who were hemodynamically unstable underwent pericardiocentesis, and no change in overall survival rate was observed.
  • Thoracotomy
    • This should be reserved for patients in whom conservative approaches have failed.
    • Thoracotomy allows for creation of a pleuropericardial window, which provides greater visualization of pericardium.
    • Thoracotomy requires general anesthesia and thus has higher morbidity and mortality rates than the subxiphoid approach.
  • Video-assisted thoracic surgery
    • Video-assisted thoracic surgery (VATS) enables resection of a wider area of pericardium than the subxiphoid approach without the morbidity of thoracotomy.
    • The surgeon is able to create a pleuropericardial window and address concomitant pleural pathology, which is especially common in patients with malignant effusions.
    • One disadvantage of VATS is that it requires general anesthesia with single lung ventilation, which may be difficult in otherwise seriously ill patients.
  • Median sternotomy
    • This procedure is reserved for patients with constrictive pericarditis.
    • Operative mortality rate is high (5-15%).

Consultations

  • A cardiologist should be involved in the care of patients with pericardial effusion.
  • Cardiothoracic surgery may be required for recurrent or complicated cases (see Surgical Care).

Medication

Autoimmune pericardial effusions may respond to treatment with anti-inflammatory medications. In general, selection of an agent depends on the severity of the patient's symptoms and the tolerability and adverse effect profiles of the medications.

Nonsteroidal anti-inflammatory drugs

Are used mostly for patients with active, nonhemorrhagic pericarditis with or without pericardial effusion. NSAIDS have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action in pericarditis is not known, but NSAIDS may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.


Indomethacin (Indocin, Indometh)

Drug of choice in this class, although other NSAIDs (ie, ibuprofen, naproxen, aspirin) possess some efficacy. Used as initial therapy for mild-to–moderately severe inflammatory pericardial effusions.

Adult

25-50 mg PO bid/tid
75 mg SR PO bid; titrate to effectiveness; not to exceed 200 mg/d

Pediatric

1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; may increase phenytoin levels

Documented hypersensitivity; GI bleeding; renal insufficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia)
May mask signs and symptoms of infection

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.


Prednisone (Deltasone, Orasone, Sterapred)

Used for patients with severe inflammatory pericardial effusions or for those in whom initial treatment with NSAIDs has failed. Other agents may be used if adverse effect profile warrants; dosages should be determined by prednisone equivalents.

Adult

5-60 mg/d PO qd or divided bid/qid; taper over 2 wk, as symptoms resolve, to 5-10 mg PO qd

Pediatric

4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk, as symptoms resolve

Estrogens may decrease clearance; may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); diuretics require monitoring for hypokalemia

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation may cause adrenal crisis; adverse effects may include hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections

Anti-inflammatory Agent

These agents inhibit key factors involved in inflammatory reactions.


Colchicine

Alkaloid extract that inhibits microtubule formation. Has unique anti-inflammatory properties. Concentrates well in leukocytes and reduces neutrophilic chemotaxis and motility. Reduces release of lactic acid and proinflammatory enzymes. Inhibits release of histamine-containing granules from mast cells, which may be important in pathogenesis of elastic tissue changes found in anetoderma.

Use in autoimmune disease is primarily empiric, and mechanism of action in decreasing inflammation is not clear, nor is it truly an immunomodulating agent.

Adult

1-2 mg PO to start, then 0.5- 1 mg PO qd

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Sympathomimetic agent toxicity and effect of CNS depressants are significantly increased with colchicine

Documented hypersensitivity; severe renal, hepatic, GI, or cardiac disorders; blood dyscrasias

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Risk of renal failure, hepatic failure, permanent hair loss, bone marrow suppression, numbness or tingling in hands and feet, disseminated intravascular coagulopathy, and decreased sperm count; dose-dependent GI upset is common

More on Pericardial Effusion

Overview: Pericardial Effusion
Differential Diagnoses & Workup: Pericardial Effusion
Treatment & Medication: Pericardial Effusion
Follow-up: Pericardial Effusion
Multimedia: Pericardial Effusion
References
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Further Reading

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Keywords

pericardial effusion, pericardial sac, dropsy of pericardium, pericarditis, pericardial tamponade, pericardiocentesis, pericardioscopy, malignant pericardial effusion, leukemia, lymphoma, idiopathic effusions, Beck triad of pericardial tamponade, hypotension, muffled heart sounds, jugular venous distension

pulsus paradoxus, pericardial friction rub, hepatojugular reflux, Ewart sign, hepatosplenomegaly, cyanosis, hydropericardium, congestive heart failure, valvular disease, mediastinal lymphoma, Hodgkin disease, metastatic breast cancer, bacterial pericardial effusion, viral pericardial effusion, tuberculous pericardial effusion, parasitic pericardial effusion, HIV-related pericardial effusion, fungal pericardial effusion, systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, vasculitides, uremia, postpericardiotomy syndrome, chylopericardium, myxedema, radiation-induced pericardial effusion

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Contributor Information and Disclosures

Author

William J Strimel, DO, Fellow, Cardiovascular Disease, Scott and White Memorial Hospital
William J Strimel, DO is a member of the following medical societies: American College of Cardiology, American College of Physicians, and Society of Hospital Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Ramin Assadi, MD, Staff Physician, Department of Internal Medicine, Loma Linda University
Ramin Assadi, MD is a member of the following medical societies: American College of Physicians and American Medical Association
Disclosure: Nothing to disclose.

Ali A Sovari, MD, Research Fellow, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles (UCLA)
Ali A Sovari, MD is a member of the following medical societies: American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Abraham G Kocheril, MD, FACC, FACP, Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago
Abraham G Kocheril, MD, FACC, FACP is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, Cardiac Electrophysiology Society, Central Society for Clinical Research, Heart Failure Society of America, Heart Rhythm Society, and Illinois State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Justin D Pearlman, MD, PhD, ME, MA, Director of Dartmouth Advanced Imaging Center, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center
Justin D Pearlman, MD, PhD, ME, MA is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Federation for Medical Research, International Society for Magnetic Resonance in Medicine, and Radiological Society of North America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Ronald J Oudiz, MD, Director of Pulmonary Hypertension, Associate Professor, Department of Medicine, Division of Cardiology, Harbor-UCLA Medical Center, David Geffen School of Medicine at UCLA
Ronald J Oudiz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, and American Heart Association
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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