Drug Interactions between aspirin / carisoprodol / codeine and gentamicin

GENERALLY AVOID: Concomitant use of opioids with benzodiazepines or other central nervous system (CNS) depressants (e.g., nonbenzodiazepine sedatives/hypnotics, anxiolytics, muscle relaxants, general anesthetics, antipsychotics, other opioids, alcohol) may result in profound sedation, respiratory depression, coma, and death. The risk of hypotension may also be increased with some CNS depressants (e.g., alcohol, benzodiazepines, phenothiazines).

MANAGEMENT: The use of opioids in conjunction with benzodiazepines or other CNS depressants should generally be avoided unless alternative treatment options are inadequate. If coadministration is necessary, the dosage and duration of each drug should be limited to the minimum required to achieve desired clinical effect, with cautious titration and dosage adjustments when needed. Patients should be monitored closely for signs and symptoms of respiratory depression and sedation, and advised to avoid driving or operating hazardous machinery until they know how these medications affect them. Cough medications containing opioids (e.g., codeine, hydrocodone) should not be prescribed to patients using benzodiazepines or other CNS depressants including alcohol. For patients who have been receiving extended therapy with both an opioid and a benzodiazepine and require discontinuation of either medication, a gradual tapering of dose is advised, since abrupt withdrawal may lead to withdrawal symptoms. Severe cases of benzodiazepine withdrawal, primarily in patients who have received excessive doses over a prolonged period, may result in numbness and tingling of extremities, hypersensitivity to light and noise, hallucinations, and epileptic seizures.

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MONITOR: The nephrotoxic effect of aminoglycosides may be potentiated by nonsteroidal anti-inflammatory drugs (NSAIDs), particularly if the latter had been given in high dosages for prolonged periods. Four children with cystic fibrosis who had been receiving chronic ibuprofen developed acute renal insufficiency shortly after initiation of IV aminoglycoside therapy for pulmonary exacerbations. An adolescent with CF who received intermittent, standard-dose ibuprofen during treatment with IV gentamicin also developed renal failure in addition to severe vestibular toxicity. Animal models suggest that renal prostaglandins may play a role in maintaining normal renal blood flow and glomerular filtration rate during the development of aminoglycoside nephrotoxicity, thus inhibition of their production by NSAIDs may worsen the renal damage.

MANAGEMENT: Whenever feasible, NSAID use should preferably be discontinued prior to initiating IV aminoglycoside therapy. If concomitant administration is necessary, hydration status as well as renal and vestibular functions should be closely monitored.

MONITOR: In premature infants, NSAIDs may increase the plasma concentrations of aminoglycosides. The proposed mechanism is decreased aminoglycoside clearance due to NSAID reduction of glomerular filtration rate, which is already low in premature infants. In a study of 20 preterm infants who had been given at least three days of amikacin or gentamicin therapy, mean peak plasma concentration increased by 17% and 33%, and mean trough concentration increased by 29% and 48%, respectively, on day 1 following administration of IV indomethacin for patent ductus arteriosus. Serum creatinine increased by 17%, while urine output and serum sodium decreased. Six patients developed hyponatremia.

MANAGEMENT: It may be advisable to consider reducing the dosage of aminoglycoside prior to initiation of NSAID therapy in infants. During coadministration, plasma antibiotic concentrations and renal function should be closely monitored, and the antibiotic dosage further adjusted as necessary.

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