Pediatric Infective Pericarditis Medication
- Author: Poothirikovil Venugopalan, MBBS, MD, FRCPCH; Chief Editor: Stuart Berger, MD more...
Bed rest and use of anti-inflammatory agents are the mainstays of initial therapy. Aggressive pain control may be necessary in some patients; however, most cases respond to salicylates or nonsteroidal anti-inflammatory drugs (NSAIDs). Although corticosteroid therapy is rarely indicated, consider this course when NSAIDs are unsuccessful and when a bacterial etiology is clearly excluded.
Corticosteroids may dramatically reduce symptoms, but no convincing evidence suggests any long-term benefit. Anti-inflammatory therapy (eg, with aspirin, indomethacin) may continue for several months. After therapy is discontinued, 15-30% of patients may have a relapse. Management includes reinstitution of NSAIDs or corticosteroids. The use of immunosuppressive agents has been reported, and pericardiectomy should be reserved for patients with frequent recurrences. Colchicine has also been used in some patients, with a good response.
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 occur, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.
Ibuprofen is a propionic acid derivative that reduces formation of inflammatory mediators by enzyme inhibition.
Naproxen is a propionic acid derivative that reduces formation of inflammatory mediators by enzyme inhibition.
Diclofenac sodium possesses properties similar to propionic acid derivatives and reduces formation of inflammatory mediators by enzyme inhibition.
Indomethacin behaves like propionic acid derivatives and inhibits formation of inflammatory mediators. It is rapidly absorbed; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation; it inhibits prostaglandin synthesis.
These drugs have anti-inflammatory and immunosuppressive properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.
The use of prednisolone is restricted to resistant cases that do not respond to nonsteroidal medications. This agent decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
Prednisone is a corticosteroid that may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Until a definitive agent is identified, empiric therapy includes antibiotics to treat both S aureus and gram-negative bacilli. Initial empiric coverage requires a combination of a penicillinase-resistant penicillin and third-generation cephalosporin. In areas of high antibiotic resistance, substitute vancomycin for the penicillin antibiotic
Oxacillin is a bactericidal penicillin antibiotic that inhibits cell wall synthesis. It is used in the treatment of infections caused by penicillinase-producing staphylococci. It may be used to initiate therapy when a staphylococcal infection is suspected.
Nafcillin is a bactericidal penicillin antibiotic that inhibits cell wall synthesis. It is used in the treatment of infections caused by penicillinase-producing staphylococci. It may be used to initiate therapy when a staphylococcal infection is suspected.
Vancomycin is indicated for patients with suspected or known infection with resistant organisms. To avoid toxicity, assay vancomycin trough levels 30 min before the fourth dose. Use creatinine clearance to adjust the dose in patients diagnosed with renal impairment.
Cefotaxime arrests bacterial cell wall synthesis, which, in turn, inhibits bacterial growth. It is a third-generation cephalosporin with a gram-negative spectrum. It has lower efficacy against gram-positive organisms.
Ceftriaxone is a third-generation cephalosporin with broad-spectrum gram-negative activity; it has lower efficacy against gram-positive organisms; it has higher efficacy against resistant organisms. It arrests bacterial growth by binding to one or more penicillin binding proteins.
Gentamicin is an aminoglycoside antibiotic used to provide gram-negative coverage. Dosing regimens are numerous; adjust the dose on the basis of creatinine clearance and changes in the volume of distribution. To avoid toxicity, assay trough levels 30 min before the fourth dose and peak levels 30-60 min after.
Ceftazidime is a third-generation cephalosporin with broad-spectrum, gram-negative activity, including pseudomonas. It has lower efficacy against gram-positive organisms and higher efficacy against resistant organisms. It arrests bacterial growth by binding to one or more penicillin-binding proteins, which, in turn, inhibit the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall synthesis, thus inhibiting cell wall biosynthesis. The condition of the patient, severity of the infection, and susceptibility of the microorganism should determine the proper dose and route of administration.
Salicylates are commonly used for their anti-inflammatory and analgesic effects.
Aspirin irreversibly inhibits platelet aggregation by inhibiting platelet cyclooxygenase. This, in turn, inhibits the conversion of arachidonic acid to PGI2 (potent vasodilator and inhibitor of platelet activation) and thromboxane A2 (potent vasoconstrictor and platelet aggregate).
Anti-inflammatory agents such as colchicine have been used in patients with a first episode of acute pericarditis.
Colchicine is an alkaloid extract that inhibits microtubule formation. It has unique anti-inflammatory properties. It concentrates well in leukocytes and reduces neutrophilic chemotaxis and motility. It reduces release of lactic acid and proinflammatory enzymes. It inhibits release of histamine-containing granules from mast cells, which may be important in pathogenesis of elastic tissue changes found in anetoderma.
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