This aminoglycoside is used to treat serious infections caused by aerobic gram-negative bacilli (eg, a number of the Enterobacteriaceae, P aeruginosa). These include lower respiratory tract, intra-abdominal, soft tissue, bone or joint, wound, and complicated urinary tract infections; bacteremias; and meningitis (by intrathecal administration). Gentamicin often is the preferred aminoglycoside for general use in hospitals where the prevalence of bacterial resistance to this agent is low (based on locally generated antimicrobial susceptibility profiles). Its major advantage over tobramycin, amikacin, and netilmicin is lower cost. The empiric use of gentamicin or tobramycin is not justified in hospitals where gentamicin resistance is common; amikacin is the aminoglycoside of choice in these locales. The combination of gentamicin plus penicillin G (or ampicillin) exhibits synergistic activity against enterococci (eg, Enterococcus faecalis) and viridans streptococci and frequently is the regimen of choice for the treatment of endocarditis caused by these organisms. Streptomycin is an alternative to gentamicin for streptomycin-susceptible strains of enterococci. Enterococcal clinical isolates with high-level resistance to gentamicin and other aminoglycosides (minimum inhibitory concentrations, >2000 μg/mL) have been reported. Therapy for endocarditis caused by these gentamicin-resistant enterococci is not established, but some isolates do remain susceptible to streptomycin, which may be given with penicillin to treat this infection. Gentamicin is recommended by the American Heart Association for parenteral prophylactic use with ampicillin or vancomycin in patients who are at high risk of developing bacterial endocarditis but are unable to take the standard oral regimen prior to undergoing invasive procedures involving the oral cavity and upper respiratory, gastrointestinal, or genitourinary tract.
Gentamicin is cleared by the kidney and accumulates in renal tubular cells. Nephrotoxicity is most closely related to the length of time that trough levels are >2 μg/mL. Creatinine levels should be monitored every two to three days as an indicator of impending renal toxicity. The initial toxic result is nonoliguric renal failure that is usually reversible if the drug is discontinued. Continued administration of gentamicin may produce oliguric renal failure. Nephrotoxicity may occur in as many as 10% to 25% of patients receiving aminoglycosides; most of this toxicity can be avoided by monitoring levels and adjusting dosing schedules accordingly. Aminoglycosides may also cause irreversible ototoxicity that manifests itself clinically as hearing loss. Aminoglycoside ototoxicity is relatively uncommon and clinical trials where levels were carefully monitored and dosing adjusted failed to show a correlation between auditory toxicity and plasma aminoglycoside levels. In situations where dosing is not monitored and adjusted, however, sustained high levels may be associated with ototoxicity. This association is far from clear cut, and new once-daily dosing regimens (and associated high peak serum concentrations) that fail to enhance toxicity further complicate this issue.
Serum or plasma
Red-top tube or green-top (heparin) tube. Do not use a gel-barrier tube. The use of gel-barrier tubes is not recommended due to slow absorption of the drug by the gel. Depending on the specimen volume and storage time, the decrease in drug level due to absorption may be clinically significant.
Transfer separated serum or plasma to a plastic transport tube. Both peak and trough concentrations should be monitored. The trough sample is drawn immediately prior to the next dose. Peak samples should be drawn 45 to 60 minutes after an IM injection, 30 minutes after the end of a 30-minute IV infusion, or immediately after a 60-minute IV infusion.
Gel-barrier tube; hemolysis; lipemia