Tobramycin, Serum, Peak

Serum or plasma

1 mL

0.3 mL

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.

Tobramycin is administered 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.

Tobramycin frequently is the aminoglycoside of choice for infections caused by P aeruginosa because of its greater in vitro activity against this organism; however, superior clinical efficacy is unproven. It usually is given in combination with an antipseudomonal penicillin for severe, systemic P aeruginosa infections.

Some infectious disease experts have preferred the more costly tobramycin to gentamicin for general use in hospitals where resistance is not a problem because it appears to be less nephrotoxic; however, this does not appear to be warranted when all of the available data are evaluated. Amikacin is the aminoglycoside of choice in hospitals where gentamicin and tobramycin resistance is a problem.

Immunoassay

Therapeutic: peak: 6.0−10.0 μg/mL, trough: 0.5−1.5 μg/mL

Tobramycin 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 this serves as a useful 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 tobramycin 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 eliminated 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 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.