Arikayce Disease Interactions

Aminoglycosides can cause dose-related neuromuscular blockade and muscle weakness, particularly in patients with neuromuscular disease or hypocalcemia and in patients receiving general anesthetics, neuromuscular blocking agents, or massive transfusions of citrate-anticoagulated blood. Although aminoglycoside- induced neuromuscular blockade is generally self-limiting, it may rarely result in respiratory paralysis. Neomycin is thought to be the most potent neuromuscular blocking agent in the class. However, the risk is greatest with intraperitoneal or intrapleural instillation of large doses or rapid intravenous administration of parenteral aminoglycosides. Therapy with aminoglycosides should be administered cautiously in patients with neuromuscular disorders (e.g., myasthenia gravis, parkinsonian syndrome, botulism) or hypocalcemia. If signs of respiratory paralysis occur during aminoglycoside therapy, the drug should be discontinued and mechanical respiratory assistance provided if necessary.

Aminoglycosides can cause eighth cranial nerve damage, resulting in vestibular and/or auditory toxicities. Symptoms include dizziness, nystagmus, vertigo, ataxia, tinnitus, and varying degrees of hearing impairment. Permanent hearing loss may occur, including, rarely, total or partial irreversible bilateral deafness after the drug has been discontinued. Therapy with aminoglycosides, particularly if prolonged (> 10 days), should be administered cautiously in patients with preexisting vestibular and/or auditory impairment, since it may delay the recognition or confound the diagnosis of a drug-induced ototoxic effect. To minimize the risk of toxicity, patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other ototoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be periodically determined and dosage adjusted to maintain desired levels. Serial audiograms should be obtained in patients old enough to be tested, since loss of high- frequency perception usually precedes clinical hearing loss. The dosage should be reduced or therapy withdrawn promptly if signs and symptoms of toxicity develop.

Aminoglycosides are potentially oto- and nephrotoxic. Eighth cranial nerve damage may manifest as vestibular and/or auditory toxicities, including dizziness, nystagmus, vertigo, ataxia, tinnitus, and varying degrees of hearing impairment. Nephrotoxicity is usually evidenced by tubular necrosis; increases in BUN, nonprotein nitrogen, and serum creatinine concentration; decreases in urine specific gravity and creatinine clearance; proteinuria; and cells or casts in the urine. Rarely, renal electrolyte wasting may occur, resulting in hypocalcemia, hypomagnesemia, and hypokalemia that may be associated with paresthesia, tetany, confusion, and positive Chvostek and Trousseau signs. Although aminoglycoside- induced nephrotoxicity is generally reversible following discontinuation of the drug, death from uremia has occurred rarely. Therapy with aminoglycosides should be administered cautiously at reduced dosages in patients with renal impairment, since they may be at increased risk for oto- and nephrotoxicity due to drug accumulation. To minimize the risk of toxicity, patients should be adequately hydrated, the usual aminoglycoside dosage should not be exceeded, use with other neuro- and nephrotoxic agents should be avoided, and peak and trough serum aminoglycoside concentrations should be periodically determined and dosage adjusted to maintain desired levels. Renal and eighth cranial nerve function should be closely monitored, and the dosage reduced or therapy withdrawn if toxicity develops.

Higher frequency of exacerbations of underlying pulmonary disease has been reported with amikacin liposome treatment. Monitor closely patients with pulmonary impairment and treat as medically appropriate if this occurs during treatment with amikacin liposome. Pre- treatment with short-acting selective beta- 2 agonists should be considered for patients with known hyperreactive airway disease, chronic obstructive pulmonary disease, asthma, or bronchospasm.