Drug Monograph

Amikacin

amikacin sulfate — aminoglycoside antibacterial
Aminoglycoside·IV / IM·Narrow Therapeutic Index
Pharmacokinetic Profile
Half-Life
2–3 h (normal renal function)
Metabolism
None — excreted unchanged
Protein Binding
Low (~0–11%)
Bioavailability
100% (IV/IM); negligible oral
Volume of Distribution
~0.25 L/kg (extracellular fluid)
Clinical Information
Drug Class
Aminoglycoside (kanamycin derivative)
Available Forms
250 mg/mL vials (500 mg, 1 g)
Route
IV (30–60 min infusion) or IM
Renal Adjustment
Required — dose/interval by CrCl & levels
Hepatic Adjustment
None required
Pregnancy
May cause fetal harm — congenital deafness reported with aminoglycosides
Lactation
Unknown if excreted in human milk; use caution
Schedule
Prescription only (not scheduled)
Generic Available
Yes
Therapeutic Index
Narrow — TDM mandatory
Black Box Warning
Yes — Nephrotoxicity, Ototoxicity, Neuromuscular Blockade, Fetal Harm
Rx

Indications

IndicationApproved PopulationTherapy TypeStatus
Bacterial septicaemia (incl. neonatal sepsis)Adults, paediatrics, neonatesMonotherapy or combinationFDA Approved
Serious respiratory tract infectionsAdults & paediatricsCombinationFDA Approved
Bone and joint infectionsAdults & paediatricsCombinationFDA Approved
CNS infections (meningitis)Adults & paediatricsCombinationFDA Approved
Skin and soft tissue infections (incl. burns)Adults & paediatricsMonotherapy or combinationFDA Approved
Intra-abdominal infections (peritonitis)Adults & paediatricsCombinationFDA Approved
Complicated urinary tract infectionsAdults & paediatricsMonotherapyFDA Approved

Amikacin is a semi-synthetic aminoglycoside derived from kanamycin with a uniquely broad resistance profile. The L-hydroxyaminobutyryl amide (L-HABA) modification at the N-1 position protects amikacin from most aminoglycoside-inactivating enzymes that confer resistance to gentamicin and tobramycin, making it the aminoglycoside of choice when resistance to other agents in the class is suspected. Its FDA-approved spectrum includes Pseudomonas species, E. coli, Proteus species, Providencia, Klebsiella-Enterobacter-Serratia species, and notably Acinetobacter species. Like other aminoglycosides, amikacin lacks reliable activity against streptococci, most enterococci (alone), and anaerobes.

Off-Label Uses

Non-tuberculous mycobacterial (NTM) infections: Amikacin is a cornerstone of multi-drug regimens for M. avium complex (MAC), M. abscessus, M. fortuitum, and M. chelonae infections. Liposomal inhaled amikacin (ARIKAYCE) is FDA-approved for MAC lung disease. Parenteral amikacin is used per ATS/IDSA NTM guidelines. Evidence quality: High.

Multi-drug resistant tuberculosis (MDR-TB): Second-line injectable agent in MDR-TB regimens when the isolate is susceptible. Used per WHO guidelines. Evidence quality: High.

Extended-interval (once-daily) dosing for serious gram-negative infections: 15 mg/kg IV q24h; widely adopted in clinical practice and supported by meta-analyses. Evidence quality: High.

Dose

Dosing

Adult Dosing by Clinical Scenario

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
Serious gram-negative infection — traditional dosing7.5 mg/kg IV/IM q12hAdjusted by TDM15 mg/kg/day (max 1.5 g/day)FDA PI: 15 mg/kg/day in 2 or 3 equal doses (7.5 mg/kg q12h or 5 mg/kg q8h). Infuse IV over 30–60 min
Peak (30–90 min post-dose): avoid >35 µg/mL. Trough: avoid >10 µg/mL
Serious gram-negative infection — extended-interval (once-daily) dosing15 mg/kg IV q24hGuided by levels / nomogram15 mg/kg/dose (max 1.5 g)Widely used in clinical practice; Cmax:MIC ≥8–10 target
Extended-interval trough target <2.5 µg/mL. Not for endocarditis, burns, pregnancy, ascites, or CrCl <20 mL/min
Uncomplicated urinary tract infection250 mg IV/IM q12h250 mg q12h500 mg/dayFDA PI: 250 mg BID for uncomplicated UTI
Reserve for resistant organisms only; aminoglycosides not first-line for UTI
MDR-TB or NTM infection — parenteral component15 mg/kg IV/IM q24hGuided by levels1–1.5 g/dayPart of multi-drug regimen; duration often months
ATS/IDSA: consider 3×/week dosing after initial daily phase to reduce toxicity in prolonged courses
Renal impairment — any indicationLoading dose 7.5 mg/kgReduce dose or extend interval per CrCl and levelsPer TDMInterval (h) ≈ serum creatinine (mg/dL) × 9 (FDA PI). Removed by haemodialysis and peritoneal dialysis
Half-life ~50 h in ESRD; supplement after dialysis
Obesity (BMI ≥30)Use adjusted body weight: ABW = IBW + 0.4 × (TBW − IBW). Amikacin distributes in extracellular fluid and does not penetrate adipose tissue proportionally
Do not exceed 1.5 g/day regardless of weight

Paediatric & Neonatal Dosing

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
Newborns — serious infectionLoading dose 10 mg/kg7.5 mg/kg IV q12h15 mg/kg/dayFDA PI dosing. Neonates have larger Vd and prolonged t½
Extended-interval (15 mg/kg q24–48h) used in clinical practice; guided by GA, postnatal age, and levels
Children and older infants — serious infection15 mg/kg/day in 2–3 divided dosesAdjusted by levels15 mg/kg/dayFDA PI: 7.5 mg/kg q12h or 5 mg/kg q8h; same as adult dosing
Duration 7–10 days; infants receive 1–2 hour infusion
Clinical Pearl: Amikacin TDM — Different Targets from Gentamicin/Tobramycin

Amikacin is dosed at approximately 3× higher mg/kg than gentamicin or tobramycin, and its TDM targets are proportionally higher. For traditional dosing: peak 20–35 µg/mL (drawn 30–90 min post-dose; avoid >35 µg/mL per FDA PI), trough <10 µg/mL (avoid >10 per FDA PI). For extended-interval dosing: trough <2.5 µg/mL. These targets are NOT interchangeable with gentamicin/tobramycin targets (peak <12, trough <2). The clinical efficacy target is Cmax:MIC ≥8–10. The FDA PI recommends measuring levels intermittently during therapy and adjusting dosage accordingly. Safety beyond 14 days of treatment has not been established.

PK

Pharmacology

Mechanism of Action

Amikacin is a semi-synthetic aminoglycoside derived from kanamycin A by acylation of the 1-amino group with L-4-amino-2-hydroxybutyryl. Like other aminoglycosides, it irreversibly binds to the 16S rRNA of the 30S ribosomal subunit, causing misreading of the genetic code and inhibiting protein synthesis. This produces aberrant proteins that are inserted into the bacterial cell membrane, increasing permeability and triggering rapid cell death. The L-HABA side chain at N-1 sterically protects amikacin from the majority of aminoglycoside-modifying enzymes (acetyltransferases, phosphotransferases, and nucleotidyltransferases) that inactivate gentamicin and tobramycin, explaining its wider resistance profile. Amikacin exhibits concentration-dependent bactericidal activity with a Cmax:MIC ratio of 8–10 as the primary pharmacodynamic predictor of efficacy, and a post-antibiotic effect (PAE) of 1–3 hours against susceptible gram-negatives.

ADME Profile

ParameterValueClinical Implication
AbsorptionNegligible oral; 100% via IV/IM; Tmax 0.5–2 h (IM); peak ~20 µg/mL after 7.5 mg/kg IM doseMust be given parenterally for systemic infections; no oral formulation
DistributionVd ~0.25 L/kg; ECF distribution; renal cortex concentrations ~10× plasma; distributes to heart, gallbladder, lungs, bone; poor CSF penetration (10–20% plasma in infants; up to 50% with meningitis); crosses placentaVd increased in burns, sepsis, ascites; low CSF levels may require intrathecal dosing; avoid intraocular use (macular infarction reported)
MetabolismNot metabolised; excreted as unchanged drugNo hepatic dose adjustment; no CYP450 interactions
Eliminationt½ 2–3 h (normal renal function); ~50 h in ESRD; 95–99% excreted unchanged in urine via glomerular filtration within 24 h; 1–2% biliary; removed by haemodialysis and peritoneal dialysisHalf-life directly proportional to renal impairment; renal cortex retention for weeks (basis for nephrotoxicity); removable by both haemodialysis and peritoneal dialysis (unlike gentamicin which is poorly removed by PD)
SE

Side Effects

1–10%Common
Adverse EffectIncidenceClinical Note
Nephrotoxicity (rising BUN/SCr, proteinuria, oliguria, electrolyte wasting)1–10% (clinically significant); BUN/Cr elevations in 5–25%Proximal tubular necrosis; risk factors: trough >10 µg/mL, cumulative dose, concurrent nephrotoxins, dehydration. Generally reversible with early detection (FDA PI). BUN/Cr laboratory increases are common but not all represent clinical nephrotoxicity
Ototoxicity (auditory — high-frequency hearing loss)4–6%Primarily auditory (cochlear) damage; usually irreversible. Risk with high doses, prolonged therapy, renal impairment, concurrent ototoxins (StatPearls)
Vestibulotoxicity (dizziness, vertigo, ataxia)~3–5%Can occur independently of auditory damage; may be permanent
EosinophiliaReportedHaematological change noted in FDA PI adverse reactions section
HypomagnesaemiaReportedRenal tubular magnesium wasting; may cause tetany and arrhythmias (FDA PI)
SeriousSerious Adverse Effects (Regardless of Frequency)
Adverse EffectEstimated FrequencyTypical OnsetRequired Action
Irreversible sensorineural hearing loss4–6%Days to weeks; may manifest after therapy endsBaseline and serial audiometry; discontinue at first sign of hearing changes. Pre-existing renal damage is the strongest risk factor (FDA PI)
Acute kidney injury / renal failure1–10%Days into therapyMonitor SCr daily; reduce dose or discontinue if rising; ensure hydration; generally reversible (FDA PI)
Neuromuscular blockade / respiratory paralysisRareDuring or shortly after administration; also after topical irrigationIV calcium salts for reversal; mechanical ventilation if needed. Irreversible deafness, renal failure, and death have been reported following surgical irrigation (FDA PI)
Macular infarction / permanent vision lossReportedPost-intravitreous injectionAmikacin injection is NOT approved for intraocular use (FDA PI)
DiscontinuationDiscontinuation Rates
Duration Guideline
7–10 days
FDA PI: Safety beyond 14 days has not been established. Discontinuation is driven by rising creatinine, hearing changes, or completion of planned course.
Response Assessment
24–48 hours
FDA PI: Uncomplicated infections should respond within 24–48 hours. If no clinical response by 3–5 days, stop therapy and recheck susceptibility.
Managing Nephrotoxicity

Amikacin nephrotoxicity results from drug accumulation in proximal tubular lysosomes, causing phospholipidosis and cell death. Risk factors include trough levels above 10 µg/mL, cumulative dose, concurrent nephrotoxic drugs (vancomycin, amphotericin B, cisplatin, cephalosporins), dehydration, and advanced age. Maintaining adequate hydration and monitoring daily serum creatinine, electrolytes (Mg, Ca, K), and urinalysis during the first week are essential. Extended-interval dosing may reduce nephrotoxicity by saturating tubular uptake mechanisms and allowing a drug-free recovery interval.

Int

Drug Interactions

Amikacin is not metabolised and has low protein binding, so CYP450 or displacement interactions are absent. Clinically significant interactions are pharmacodynamic (additive toxicity) with other nephrotoxic, ototoxic, or neuromuscular blocking agents.

MajorOther Nephro-/Ototoxic Drugs (Vancomycin, Amphotericin B, Cisplatin, Other Aminoglycosides)
MechanismAdditive nephrotoxicity and/or ototoxicity via independent damage pathways
EffectSubstantially increased risk of AKI and irreversible hearing loss
ManagementAvoid concurrent or sequential use; if essential, monitor renal function daily, serum levels frequently, and consider serial audiometry (FDA PI)
FDA PI (Boxed Warning)
MajorLoop Diuretics (Furosemide, Ethacrynic Acid)
MechanismIndependent ototoxic potential; may alter aminoglycoside concentrations
EffectEnhanced irreversible ototoxicity risk
ManagementAvoid concurrent use when possible; monitor hearing closely (FDA PI)
FDA PI
MajorNeuromuscular Blocking Agents (Succinylcholine, Tubocurarine)
MechanismAminoglycosides have intrinsic curare-like NMB activity
EffectProlonged respiratory paralysis
ManagementUse with extreme caution; IV calcium for reversal; mechanical ventilation may be needed (FDA PI)
FDA PI
ModerateCephalosporins
MechanismAdditive nephrotoxic potential reported with concurrent parenteral use
EffectIncreased nephrotoxicity risk
ManagementMonitor renal function; combination frequently used clinically with acceptable safety when TDM and hydration maintained (FDA PI)
FDA PI
ModerateBeta-Lactam Antibiotics (in vitro inactivation)
MechanismIn vitro inactivation of amikacin by beta-lactam ring opening; clinically relevant mainly in severe renal impairment
EffectReduced amikacin levels, subtherapeutic concentrations
ManagementNever mix in same IV line; administer separately. Monitor levels more frequently in renal failure
FDA PI
ModerateNSAIDs (especially Indomethacin)
MechanismReduced renal prostaglandin synthesis may decrease amikacin clearance
EffectIncreased amikacin concentrations and nephrotoxicity risk
ManagementMonitor amikacin levels and renal function; consider alternative analgesic
Clinical Practice
Mon

Monitoring

  • Serum Drug Levels (TDM)Intermittently during therapy
    Routine
    Traditional: peak 20–35 µg/mL (30–90 min post-dose; avoid >35), trough <10 µg/mL (just before next dose; avoid >10). Extended-interval: trough <2.5 µg/mL. These targets differ from gentamicin/tobramycin. Measure after 2–3 doses and periodically thereafter (FDA PI).
  • Renal Function (BUN, SCr, CrCl)Baseline, daily first week, then twice weekly
    Routine
    FDA PI notes BUN is less reliable than SCr for monitoring. Monitor urinalysis (casts, protein, cells) as early markers. Rising SCr warrants dose adjustment or discontinuation.
  • Auditory FunctionBaseline audiometry; serial if therapy >7 days or high-risk
    Routine
    Pre-treatment audiogram recommended. High-frequency hearing loss occurs first and may initially be subclinical. Tinnitus is a sentinel symptom. Ototoxicity described as “permanent in a significant proportion of patients” in the FDA PI.
  • Vestibular FunctionThroughout therapy
    Routine
    Monitor for dizziness, vertigo, nystagmus, ataxia. May be independent of auditory damage.
  • Electrolytes (Mg, Ca, K)Baseline, then twice weekly
    Routine
    Renal tubular wasting of Mg, Ca, K reported. Hypomagnesaemia can cause tetany and arrhythmias (FDA PI).
  • Neuromuscular FunctionIn operative/ICU settings
    Trigger-based
    Particularly in patients receiving NMBAs, anaesthetics, or citrate-anticoagulated blood transfusions. Have IV calcium available (FDA PI).
CI

Contraindications & Cautions

Absolute Contraindications

  • Known hypersensitivity to amikacin or any aminoglycoside — cross-allergenicity exists across the class (FDA PI).

Relative Contraindications (Specialist Input Recommended)

  • Pre-existing significant renal impairment — intensified TDM and dose individualisation required.
  • Pre-existing auditory or vestibular impairment — baseline audiometry essential.
  • Pregnancy — aminoglycosides cross the placenta; irreversible congenital deafness reported. Use only if benefit clearly outweighs risk (FDA PI).
  • Myasthenia gravis — risk of neuromuscular blockade and respiratory failure.

Use with Caution

  • Elderly patients — reduced renal function may not be reflected by SCr alone; use CrCl-based dosing.
  • Premature and neonatal infants — renal immaturity prolongs half-life; use with caution (FDA PI).
  • Dehydration — ensure adequate hydration to reduce nephrotoxicity risk.
  • Concurrent nephro-/ototoxic agents — avoid concurrent or sequential use when possible.
  • Topical irrigation of surgical fields — aminoglycosides are almost completely absorbed; irreversible deafness, renal failure, and death from NMB have been reported (FDA PI).
  • Obesity — use adjusted body weight; max 1.5 g/day.
FDA Boxed Warning Nephrotoxicity, Ototoxicity, Neuromuscular Blockade, and Fetal Harm

Amikacin is potentially nephrotoxic, ototoxic, and neurotoxic. Neurotoxicity manifested as vestibular and permanent bilateral auditory ototoxicity can occur in patients with pre-existing renal damage and in those treated at higher doses or for periods longer than recommended. Safety beyond 14 days has not been established. Peak concentrations above 35 µg/mL and trough concentrations above 10 µg/mL should be avoided. Concurrent or serial use of other ototoxic or nephrotoxic agents should be avoided. Aminoglycosides can cause fetal harm when administered to a pregnant woman. Irreversible deafness, renal failure, and death from neuromuscular blockade have been reported following irrigation of surgical fields.

Pt

Patient Counselling

Purpose of Therapy

Amikacin is a powerful antibiotic used to treat serious bacterial infections, particularly those caused by organisms resistant to other antibiotics. It is given by injection or intravenous infusion in a hospital or supervised clinical setting. Regular blood tests are required to monitor drug levels and kidney function. It does not treat viral infections.

How to Take

Amikacin is administered by healthcare professionals. The typical treatment course is 7 to 10 days. Complete the full course as prescribed even if symptoms improve early. Skipping doses or stopping treatment prematurely may allow bacteria to develop resistance.

Hearing Changes
Tell patientAmikacin can cause hearing loss, which may be permanent. Hearing tests will be performed before and during treatment in some cases.
Call prescriberImmediately if you notice ringing in your ears, muffled hearing, or difficulty understanding speech.
Dizziness and Balance
Tell patientThis medication may affect the balance centres in your inner ear. You may experience dizziness, unsteadiness, or a spinning sensation.
Call prescriberIf you develop new dizziness, difficulty walking, or a sensation that the room is spinning.
Kidney Function
Tell patientAmikacin can affect the kidneys. Your care team will monitor kidney function with blood and urine tests. Staying well hydrated helps protect your kidneys.
Call prescriberIf you notice a decrease in urine output, swelling, or unusually dark urine.
Pregnancy
Tell patientAmikacin may harm an unborn baby, including causing permanent hearing loss. Inform your doctor if you are pregnant or planning pregnancy.
Call prescriberIf you become pregnant during treatment.
Diarrhoea
Tell patientDiarrhoea may occur during or after treatment. Most antibiotic-related diarrhoea resolves after therapy ends, but serious intestinal infections can develop up to two months later.
Call prescriberIf diarrhoea is watery, bloody, or accompanied by fever and cramping.
Ref

Sources

Regulatory (PI / SmPC)
  1. Amikacin Sulfate Injection, USP — Full Prescribing Information (Fresenius Kabi). DailyMed LabelPrimary FDA label source for all dosing, TDM targets, indications, boxed warnings, and adverse reactions.
  2. Amikacin Sulfate Injection, USP — Full Prescribing Information (Sagent Pharmaceuticals). DailyMed LabelAlternate FDA label providing additional clinical context and adverse reaction detail.
Key Clinical Trials / Meta-Analyses
  1. Hatala R, Dinh T, Cook DJ. Once-daily aminoglycoside dosing in immunocompetent adults: a meta-analysis. Ann Intern Med. 1996;124(8):717–725. doi:10.7326/0003-4819-124-8-199604150-00003Meta-analysis supporting extended-interval aminoglycoside dosing as at least as effective and no more toxic than traditional dosing.
  2. Barza M, Ioannidis JPA, Cappelleri JC, Lau J. Single or multiple daily doses of aminoglycosides: a meta-analysis. BMJ. 1996;312(7027):338–345. doi:10.1136/bmj.312.7027.338Independent meta-analysis confirming similar efficacy and possible reduced nephrotoxicity with once-daily aminoglycoside dosing.
  3. Smith CR, Lipsky JJ, Laskin OL, et al. Double-blind comparison of the nephrotoxicity and auditory toxicity of gentamicin and tobramycin. N Engl J Med. 1980;302(20):1106–1109. doi:10.1056/NEJM198005153022002Landmark aminoglycoside toxicity study establishing comparative nephro- and ototoxicity incidence data relevant to the entire class.
Guidelines
  1. Daley CL, Iaccarino JM, Lange C, et al. Treatment of nontuberculous mycobacterial pulmonary disease: an official ATS/ERS/ESCMID/IDSA clinical practice guideline. Clin Infect Dis. 2020;71(4):e1–e36. doi:10.1093/cid/ciaa241ATS/IDSA guideline positioning parenteral amikacin in multi-drug regimens for MAC, M. abscessus, and other NTM infections.
  2. WHO consolidated guidelines on tuberculosis. Module 4: treatment — drug-resistant tuberculosis treatment, 2022 update. Geneva: WHO; 2022. WHO PublicationWHO guideline positioning amikacin as a second-line injectable for MDR-TB when isolate susceptibility is confirmed.
  3. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the SIS and IDSA. Clin Infect Dis. 2010;50(2):133–164. doi:10.1086/649554SIS/IDSA guideline including aminoglycoside options for empiric combination therapy in cIAI.
Mechanistic / Basic Science
  1. Moore RD, Lietman PS, Smith CR. Clinical response to aminoglycoside therapy: importance of the ratio of peak concentration to minimal inhibitory concentration. J Infect Dis. 1987;155(1):93–99. doi:10.1093/infdis/155.1.93Established the Cmax:MIC ratio as the key PK/PD predictor of aminoglycoside clinical efficacy.
  2. Lacy MK, Nicolau DP, Nightingale CH, Quintiliani R. The pharmacodynamics of aminoglycosides. Clin Infect Dis. 1998;27(1):23–27. doi:10.1086/514620Key review of concentration-dependent killing and post-antibiotic effect principles supporting extended-interval dosing.
Pharmacokinetics / Special Populations
  1. Bauer LA, Blouin RA. Amikacin pharmacokinetics: wide interpatient variation in 98 patients. J Clin Pharmacol. 1983;23(2-3):123–130. doi:10.1002/j.1552-4604.1983.tb02713.xDemonstrated wide inter-patient variability in amikacin PK (Vd 0.08–0.48 L/kg, t½ 0.68–14.4 h), reinforcing the need for individualised TDM.
  2. Traynor AM, Nafziger AN, Bertino JS Jr. Aminoglycoside dosing weight correction factors for patients of various body sizes. Antimicrob Agents Chemother. 1995;39(2):545–548. doi:10.1128/AAC.39.2.545Established the 0.4 correction factor for adjusted body weight dosing in obese patients receiving aminoglycosides.
  3. Touw DJ, Westerman EM, Sprij AJ. Therapeutic drug monitoring of aminoglycosides in neonates. Clin Pharmacokinet. 2009;48(2):71–88. doi:10.2165/0003088-200948020-00001Comprehensive review of neonatal aminoglycoside PK and TDM strategies.
  4. Rybak MJ, Abate BJ, Kang SL, Ruffing MJ, Lerner SA, Drusano GL. Prospective evaluation of the effect of an aminoglycoside dosing regimen on rates of observed nephrotoxicity and ototoxicity. Antimicrob Agents Chemother. 1999;43(7):1549–1555. doi:10.1128/AAC.43.7.1549Prospective study comparing extended-interval vs traditional dosing for nephrotoxicity and ototoxicity outcomes.