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Amikin®
(amikacin)
Also see: Amoxicillin
Prevacid
Amikacin
Amoxil Augmentin
Augmentin ES
Augmentin XR Biaxin
Prevpac
Trimox
Amikacin is an antibiotic. It fights bacteria in
the body.
Amikacin is used to treat severe or serious bacterial infections.
Amikacin may also be used for purposes
Amikacin sulfate is a semi-synthetic
aminoglycoside antibiotic derived from kanamycin. D-Streptamine,
O-3-amino-3-deoxy-a-b-glucopyranosyl)1>6)-O-[6-amino-6-deoxy-a-D-glucopyranosyl(1>4)]-N1-(4-amino-2-hydroxy-1-oxobutyl)-2-deoxy-(S)-,sulfate
(1:2)(salt).
It has the following molecular formula C22H43N5O13 •2H2SO4 with a molecular
weight of 781.75.
The dosage form is supplied as asterile, colorless to lightstraw colored
solution for IM or IV use. The 100 mg per 2 mL vial, each mL contains: 50 mg
Amikacin(as the sulfate), 0.13% Sodium Metabisulfite, 0.5% Sodium Citrate
Dihydrate, Water for Injections, Air replaced with Nitrogen. pH is adjusted with
Sulfuric Acid and/or if necessary Sodium Hydroxide. pH 3.5-5.5. The 500 mg per 2
mL vial and the 1 gram per 4 mL vial, each mL contains: 250 mg Amikacin(as the
sulfate), 0.66% Sodium Metabisulfite, 2.5% Sodium Citrate Dihydrate, Water for
Injection qs, Air replaced with Nitrogen. pH is adjusted with Sulfuric Acid
and/or if necessary Sodium Hydroxide. pH 3.5-5.5.
WARNINGS
Patients treated with parenteral
aminoglycosides should be under close clinical observation because of the
potential ototoxicity and nephrotoxicity associated with their use. Safety for
treatment periods which are longer than 14 days has not been established.
Neurotoxicity, manifested as vestibular and permanent bilateral auditory
ototoxicity, can occur in patients with preexisting renal damage and in patients
with normal renal function treated at higher doses and/or for periods longer
than those recommended. The risk of aminoglycoside-induced ototoxicity is
greater in patients with renal damage. High frequency deafness usually occurs
first and can be detected only by audiometric testing. Vertigo may occur and may
be evidence of vestibular injury. Other manifestations of neurotoxicity may
include numbness, skin tingling, muscle twitching, and convulsions. The risk of
hearing loss due to aminoglycosides increases with the degree of exposure to
either high peak or high trough serum concentrations. Patients developing
cochlear damage may not have symptoms during therapy to warn them of developing
eighth-nerve toxicity, and total or partial irreversible bilateral deafness may
occur after the drug has been discontinued. Aminoglycoside-induced ototoxicity
is usually irreversible.
Aminoglycosides are potentially nephrotoxic. The risk of nephrotoxicity is
greater in patients with impaired renal function and in those who receive high
doses or prolonged therapy.
Neuromuscular blockade and respiratory paralysis have been reported following
parenteral injection, topical instillation (as in orthopedic and abdominal
irrigation or in local treatment of empyema), and following oral use of
aminoglycosides. The possibility of these phenomena should be considered if
aminoglycosides are administered by any route, especially in patients receiving
anesthetics, neuromuscular blocking agents such as tubocurarine, succinylcholine,
decamethonium, or in patients receiving massive transfusions of citrate-anticoagulated
blood. If blockage occurs, calcium salts may reverse these phenomena, but
mechanical respiratory assistance may be necessary.
Renal and eighth-nerve function should be closely monitored especially in
patients with known or suspected renal impairment at the onset of therapy and
also in those whose renal function is initially normal but who develop signs of
renal dysfunction during therapy. Serum concentrations of amikacin should be
monitored when feasible to assure adequate levels and to avoid potentially toxic
levels and prolonged peak concentrations above 35 micrograms per mL. Urine
should be examined for decreased specific gravity, increased excretion of
proteins, and the presence of cells or casts. Blood urea nitrogen, serum
creatinine, or creatinine clearance should be measured periodically. Serial
audiograms should be obtained where feasible in patients old enough to be
tested, particularly high risk patients. Evidence of ototoxicity (dizziness,
vertigo, tinnitus, roaring in the ears, and hearing loss) or nephrotoxicity
requires discontinuation of the drug or dosage adjustment.
Concurrent and/or sequential systemic oral, or topical use of other neurotoxic
or nephrotoxic products, particularly bacitracin, cisplatin, amphotericin B,
cephaloridine, paromomycin, viomycin, polymyxin B, colistin, vancomycin, or
other aminoglycosides should be avoided. Other factors that may increase risk of
toxicity are advanced age and dehydration.
The concurrent use of amikacin with potent diuretics (ethacrynic acid , or
furosemide) should be avoided since diuretics by themselves may cause
ototoxicity. In addition, when administered intravenously, diuretics may enhance
aminoglycoside toxicity by altering antibiotic concentrations in serum and
tissue.
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