It has the following molecular formula C 22H 43N 5O 13 In addition, when administered intravenously, diuretics may enhance aminoglycoside toxicity by altering antibiotic concentrations in serum and tissue.Īmikacin sulfate is a semi-synthetic aminoglycoside antibiotic derived from kanamycin. The concurrent use of amikacin with potent diuretics (ethacrynic acid, or furosemide) should be avoided since diuretics by themselves may cause ototoxicity. Other factors that may increase risk of toxicity are advanced age and dehydration. Evidence of ototoxicity (dizziness, vertigo, tinnitus, roaring in the ears, and hearing loss) or nephrotoxicity requires discontinuation of the drug or dosage adjustment.Ĭoncurrent 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.
The death cure page 250 serial#
Serial audiograms should be obtained where feasible in patients old enough to be tested, particularly high risk patients. Blood urea nitrogen, serum creatinine, or creatinine clearance should be measured periodically. Urine should be examined for decreased specific gravity, increased excretion of proteins, and the presence of cells or casts. 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. 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. If blockage occurs, calcium salts may reverse these phenomena, but mechanical respiratory assistance may be necessary. 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. 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 risk of nephrotoxicity is greater in patients with impaired renal function and in those who receive high doses or prolonged therapy.
Aminoglycoside-induced ototoxicity is usually irreversible.Īminoglycosides are potentially nephrotoxic. 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. The risk of hearing loss due to aminoglycosides increases with the degree of exposure to either high peak or high trough serum concentrations.
The death cure page 250 skin#
Other manifestations of neurotoxicity may include numbness, skin tingling, muscle twitching, and convulsions. Vertigo may occur and may be evidence of vestibular injury. High frequency deafness usually occurs first and can be detected only by audiometric testing. The risk of aminoglycoside-induced ototoxicity is greater in patients with renal damage.
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.
Safety for treatment periods which are longer than 14 days has not been established. Patients treated with parenteral aminoglycosides should be under close clinical observation because of the potential ototoxicity and nephrotoxicity associated with their use.
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