It is rarely used alone.It is often used in the following situations:
Bronchiectasis
Bone and joint infections
Granulocytopenia, when combined with ticarcillin, in people with cancer
Intra-abdominal infections (such as peritonitis) as an adjunct to other medicines, like clindamycin, metronidazole, piperacillin/tazobactam, or ampicillin/sulbactam
Meningitis:
for meningitis by E. coli, as an adjunct to imipenem
for meningitis caused by Pseudomonas, as an adjunct to meropenem
for meningitis caused by Acetobacter, as an adjunct to imipenem or colistin
for neonatal meningitis caused by Streptococcus agalactiae or Listeria monocytogenes, as an adjunct to ampicillin
for neonatal meningitis caused by Gram negative bacteria such as E. coli, as adjunct to a 3rd-generation cephalosporin
Mycobacterial infections, including as a second-line agent for active tuberculosis. It is also used for infections by Mycobacterium avium, M. abcessus, M. chelonae, and M. fortuitum. Rhodococcus equi, which causes an infection resembling tuberculosis
Respiratory tract infections, including as an adjunct to beta-lactams or carbapenem for hospital-acquired pneumonia
Sepsis, including that in neonates, as an adjunct to beta-lactams or carbapenem
Skin and suture-site infections
Urinary tract infections that are caused by bacteria resistant to less toxic drugs (often by Enterobacteriaceae or P. aeruginosa)Amikacin may be combined with a beta-lactam antibiotic for empiric therapy for people with neutropenia and fever. Available forms
Amikacin may be administered once or twice a day and is usually given by the intravenous or intramuscular route, though it can be given via nebulization. There is no oral form available, as amikacin is not absorbed orally. In people with kidney failure, dosage must be adjusted according to the creatinine clearance, usually by reducing the dosing frequency.
Pharmacology
Mechanism of action
Amikacin irreversibly binds to 16S rRNA and the RNA-binding S12 protein of the 30S subunit of prokaryotic ribosome and inhibits protein synthesis by changing the ribosomes shape so that it cannot read the mRNA codons correctly. It also interferes with the region that interacts with the wobble base of the tRNA anticodon. It works in a concentration-dependent manner, and has better action in an alkaline environment.At normal doses, amikacin-sensitive bacteria respond within 24–48 hours. Resistance
Amikacin evades attacks by all antibiotic-inactivating enzymes that are responsible for antibiotic resistance in bacteria, except for aminoacetyltransferase and nucleotidyltransferase. This is accomplished by the L-hydroxyaminobuteroyl amide (L-HABA) moiety attached to N-1 (compare to kanamycin, which simply has a hydrogen), which blocks the access and decreases the affinity of aminoglycoside-inactivating enzymes. Amikacin ends up with only one site where these enzymes can attack, while gentamicin and tobramycin have six.Bacteria that are resistant to streptomycin and capreomycin are still susceptible to amikacin; bacteria that are resistant to kanamycin have varying susceptibility to amikacin. Resistance to amikacin also confers resistance to kanamycin and capreomycin.Resistance to amikacin and kanamycin in Mycobacterium, the causative agent of tuberculosis, is due to a mutation in the rrs gene, which codes for the 16S rRNA. Mutations such as these reduce the binding affinity of amikacin to the bacterias ribosome.