Maximum dosage: Do not exceed 5 mg/kg/day in patients with normal renal function.
Colistimethate sodium may cause nephrotoxicity, manifested as decreased urine output, increased serum concentrations of BUN and creatinine, proteinuria, hematuria, and casts in the urine. If these symptoms occur, dosing should be adjusted or the drug should be discontinued immediately.
Colistimethate sodium may cause transient nervous system effect, including circumoral or peripheral paresthesia or numbness, tingling or formication of the extremities or tongue, dizziness, vertigo, giddiness, ataxia, blurred vision, and slurred speech. These adverse nervous system effects generally appear within the first 4 days of therapy and disappear when the drug is discontinued. The patient should be monitored closely; some of these adverse nervous system effects may be alleviated by reducing dosage of the drug.
Treatment with Colistimethate sodium alters the normal flora in the gut leading to overgrowth of Clostridium difficile. C. difficile produces toxins which contribute to the development of CDAD that must be considered in all patients who present with diarrhea following Colistimethate sodium use. Mild cases of colitis may respond to discontinuance of the drug alone, but management of moderate to severe case should include treatment with fluid, electrolyte, protein supplementation, and appropriate anti-infective therapy.
Since nephrotoxic effects may additive, concurrent or sequential use of Colistimethate sodium with other drugs which have similar toxic potentials and with neuromuscular blocking agents should be avoided.
Patients who received Colistimethate sodium by oral inhalation via nebulization may cause bronchoconstriction. It has been suggested that premedication with bronchodilators may reduce the potentials for development of bronchoconstriction.
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