A 68-year-old septic ICU client receives IV tobramycin, IV vancomycin, IV furosemide drip, and recent IV contrast for CT. On day 4, creatinine has risen from 1.1 to 2.0 mg/dL and urine output has dropped to 0.3 mL/kg/h. The pharmacy reports a tobramycin trough of 3.8 mg/L. Which combined nursing and care-coordination action is most appropriate?

Aminoglycoside nephrotoxicity is markedly amplified by concurrent nephrotoxins, including loop diuretics (potassium and magnesium losses also potentiate ototoxicity), IV iodinated contrast (vasoconstriction and tubular injury), vancomycin (additive proximal tubule toxicity), NSAIDs, ACE inhibitors, and ARBs. The supratherapeutic trough (3.8 mg/L; goal less than 2 mg/L), the rising creatinine, and oliguria all confirm AKI from polypharmacy and possibly underlying sepsis. Standard nursing/care-coordination response: (1) hold the next tobramycin dose and notify prescriber and pharmacist immediately; (2) coordinated review of all nephrotoxins — hold or substitute the furosemide drip if possible (or address the volume status with thiazide combination/ultrafiltration), defer additional contrast, recalculate vancomycin dosing or change agents, review ACEi/ARBs, NSAIDs; (3) anticipate aminoglycoside hold or discontinuation, change to a non-aminoglycoside agent guided by culture; (4) strict intake and output, daily weight, electrolytes (K, Mg), and creatinine trend; (5) ototoxicity surveillance — hearing changes, tinnitus, vertigo, gait; (6) volume optimization — sufficient perfusion to avoid prerenal worsening but avoid overload; (7) consider nephrology and audiology consults; (8) fall precautions if vestibular involvement. Continuing all, increasing dose, and adding NSAID are all unsafe.

Polypharmacy nephrotoxicity in a septic patient. Hold tobramycin, coordinate stripping nephrotoxins, change to a non-aminoglycoside agent, monitor strict I/O and ototoxicity. NSAIDs and dose escalation are traps.