Pediatric Rheumatic Heart Disease Medication

  • Author: Thomas K Chin, MD; Chief Editor: Stuart Berger, MD   more...
 
Updated: Aug 4, 2010
 

Medication Summary

Medical therapy is directed at eliminating the group A streptococcal pharyngitis (if still present), suppressing inflammation from the autoimmune response, and providing supportive treatment for congestive heart failure. The treatment and prevention of group A streptococcal pharyngitis outlined here is based on the current recommendations of the Committee on Infectious Disease (American Academy of Pediatrics). See the eMedicine article Pharyngitis.

Penicillin V is the drug of choice for treatment of group A streptococcal pharyngitis. Ampicillin or amoxicillin may be used instead of penicillin V but have no microbiologic advantage. Tetracyclines and sulfonamides should not be used to treat group A streptococcal pharyngitis. For recurrent group A streptococcal pharyngitis, a second 10-day course of the same antibiotic can be repeated. Alternate drugs include narrow-spectrum cephalosporins, amoxicillin-clavulanate, dicloxacillin, erythromycin, or other macrolides for 10 d. As many as 15% of patients allergic to penicillin are also allergic to cephalosporins.

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Antibiotics

Class Summary

Antibiotics are used for the initial treatment of group A streptococcal pharyngitis to prevent the first attack of rheumatic fever (primary prophylaxis), for recurrent streptococcal pharyngitis, and for continuous therapy to prevent recurrent rheumatic fever and rheumatic heart disease (secondary prophylaxis).

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Penicillin VK (Beepen-VK, Betapen-VK, Pen-Vee K)

 

DOC for treatment of group A streptococcal pharyngitis. Inhibits the biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached, and most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.

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Penicillin G benzathine/penicillin G procaine (Bicillin L-A, Wycillin)

 

Used when PO administration of penicillin is not feasible or dependable. Discomfort of IM injection may be minimized if the penicillin G is brought to room temperature before injection or if a combination of benzathine penicillin G and procaine penicillin G (Bicillin CR) is used. Initial course of antibiotics given to eradicate the streptococcal infection also serves as the first course of prophylaxis. Benzathine penicillin G IM q4wk is recommended for secondary prevention for most United States patients. The same dosage should be used q3wk in areas where rheumatic fever is endemic, in patients with residual carditis, and in patients with high risk.

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Erythromycin ethylsuccinate (Ilosone, E.E.S, EryPed)

 

Used to treat patients allergic to penicillin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest.

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Anti-inflammatory agents

Class Summary

The manifestations of acute rheumatic fever (including carditis) typically respond rapidly to therapy with anti-inflammatory agents. Aspirin, in anti-inflammatory doses, is the drug of choice. Prednisone is added when evidence of worsening carditis and heart failure is noted.

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Aspirin (Anacin, Ascriptin, Bayer Aspirin)

 

Also called acetylsalicylic acid. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2. Start immediately after the diagnosis of rheumatic fever has been made. Initiation of therapy may mask manifestations of the disease.

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Prednisone (Deltasone, Orasone)

 

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. If moderate to severe carditis is indicated by cardiomegaly, congestive heart failure, or third-degree heart block, 2 mg/kg/d PO should be used in addition to, or in lieu of, salicylate therapy. Prednisone should be continued for 2-4 wk, depending on the severity of the carditis, and tapered during the last week of therapy. Adverse effects can be minimized by discontinuing prednisone therapy after 2 wk and adding or maintaining salicylates for an additional 2-4 wk.

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Angiotensin-converting enzyme (ACE) inhibitors

Class Summary

These agents are competitive inhibitors of ACE. They reduce angiotensin II levels and thus decrease aldosterone secretion.

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Enalapril (Vasotec)

 

Indicated for chronic aortic and/or mitral regurgitation. Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased plasma renin levels and a reduction in aldosterone secretion. Helps control blood pressure and proteinuria. Decreases pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance. Has favorable clinical effect when administered over a long period. Helps prevent potassium loss in distal tubules. Body conserves potassium; thus, less oral potassium supplementation needed. Goal is to decrease afterload to left ventricle (by reducing systemic blood pressure and by peripheral vasodilatation).

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Captopril (Capoten)

 

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Rapidly absorbed, but bioavailability is significantly reduced with food intake. It achieves a peak concentration in 1 h and has a short half-life. The drug is cleared by the kidneys.

Impaired renal function requires reduction of dosage. Absorbed well PO. Give at least 1 h before meals. If added to water, use within 15 min.

Can be started at low dose and titrated upward as needed and as patient tolerates.

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Contributor Information and Disclosures
Author

Thomas K Chin, MD  Professor of Pediatrics, Chief of Pediatric Cardiology and Medical Director of the Pediatric Heart Institute, University of Tennessee College of Medicine; Director of Cardiology and Endowed Chair for Excellence in Cardiology, St Jude Children's Research Hospital

Thomas K Chin, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Eric M Chin  California Institute of Technology

Disclosure: Nothing to disclose.

Tariq Siddiqui, MD  Staff Physician, Department of Anesthesiology, University of Louisville Medical Center

Disclosure: Nothing to disclose.

Ann-Kristin Sundell, MD  Staff Physician, Department of Pediatrics, East Tennessee State University

Ann-Kristin Sundell, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA  Professor, Departments of Pediatrics (Cardiology), Cardiovascular Sciences, and Molecular and Human Genetics, Baylor College of Medicine; Chief of Pediatric Cardiology, Foundation Chair in Pediatric Cardiac Research, Texas Children's Hospital

Jeffrey Allen Towbin, MD, MSc, FAAP, FACC, FAHA is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American College of Cardiology, American College of Sports Medicine, American Heart Association, American Medical Association, American Society of Human Genetics, Cardiac Electrophysiology Society, New York Academy of Sciences, Society for Pediatric Research, Texas Medical Association, and Texas Pediatric Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Hugh D Allen, MD  Professor, Department of Pediatrics, Division of Pediatric Cardiology and Department of Internal Medicine, Ohio State University College of Medicine

Hugh D Allen, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Pediatric Society, American Society of Echocardiography, Society for Pediatric Research, Society of Pediatric Echocardiography, and Western Society for Pediatric Research

Disclosure: Nothing to disclose.

Paul D Petry, DO, FACOP, FAAP  Consulting Staff, Freeman Pediatric Care, Freeman Health System

Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD  Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin

Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Clyde Worley, MD, to the development and writing of this article.

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Parasternal long-axis view demonstrating the typical systolic mitral insufficiency jet observed with rheumatic heart disease (blue jet extending from the left ventricle into the left atrium). The jet is typically directed to the lateral and posterior wall. (LV=left ventricle; LA=left atrium; Ao=aorta; RV=right ventricle).
Parasternal long-axis view demonstrating the typical diastolic aortic insufficiency jet observed with rheumatic heart disease (red jet extending from the aorta into the left ventricle). (LV=left ventricle; LA=left atrium; Ao=aorta; RV=right ventricle).
 
 
 
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