The manufacturer provides a Dosage Guide and Preparation Chart in relation to body weight in the product label. If administered via a gastric tube, water may be used as the diluent.ĭilution of 10% solution: 1 mL of diluent for every 1 mL of solution.ĭilution of 20% solution: 3 mL of diluent for every 1 mL of solution. The 20% solution is usually preferable to the 10% solution because a lower volume of drug is needed in the dilution, thereby increasing palatability. May administer with a straw to limit contact in mouth. It is recommended that the 10% or 20% solution be diluted to a 5% solution with diet cola or other diet soda to increase palatability and minimize the likelihood of vomiting. Not FDA approved for parenteral injection Patients also received 0.9% Sodium Chloride hydration at a rate of 1 mL/kg/hour for 12 hours after angioplasty if the patients had overt heart failure, a lower rate of 0.5 mL/kg/hour for 12 hours was used. Furthermore, the incidence of death, acute renal failure requiring temporary renal replacement therapy, and the need for mechanical ventilation was also reduced vs. The incidence of acute renal failure was 8% in the high-dose acetylcysteine group, 15% in the low-dose acetylcysteine group, and 33% in patients receiving placebo (p less than 0.001). In 354 patients with acute myocardial infarction undergoing angioplasty, a dose of 1,200 mg IV bolus before angioplasty followed by 1,200 mg PO twice daily for the 48 hours following angioplasty significantly reduced the incidence of contrast-induced nephropathy (defined as a 25% increase in creatinine over baseline within 72 hours after angioplasty) compared to a lower dose of acetylcysteine (600 mg IV bolus prior to angioplasty followed by 600 mg PO twice daily for 48 hours after angioplasty) or placebo. Assistance may be obtained by contacting your regional poison control center at 1-800-222-1222 or the acetaminophen overdose center at 1-800-525-6115. In these patients, treatment should be guided by information obtained from laboratory tests, including: acetaminophen serum concentrations, liver function tests (LFTs), serum creatinine, BUN, electrolytes, bilirubin, blood glucose, and INR. NOTE: The Rumack-Matthew nomogram is ineffective at predicting hepatotoxicity in patients who have ingested repeated supratherapeutic doses of acetaminophen over an extended period of time. If greater than 24 hours has elapsed since the APAP ingestion, the clinician should determine the appropriateness of acetylcysteine administration based on the patients liver status and clinical presentation. If the time of ingestion is unknown, or the serum APAP concentration is not available, cannot be interpreted, or is not available within 8 hours of APAP ingestion, acetylcysteine should be administered immediately regardless of the quantity reported to have been ingested. Beginning treatment 15 to 24 hours post-ingestion results in limited efficacy however, it does not appear to worsen the condition and should not be withheld since the reported time of ingestion may not be correct. The efficacy of acetylcysteine diminishes progressively after 8 hours post-ingestion. For extended-release APAP overdoses, if the initial APAP serum concentration was below the possible toxicity line, obtain a second concentration 8 to 10 hours post-ingestion. For regular-release APAP overdoses, obtain serum drug concentration at least 4 hours post-ingestion concentrations obtained earlier than 4 hours may not represent maximum APAP concentrations. Give activated charcoal as soon as possible after ingestion to prevent APAP absorption. For patients whose serum APAP concentrations fall above the "possible" toxicity line on the nomogram, initiate treatment within 8 hours of suspected APAP ingestion for maximal protection against hepatic injury. NOTE: The Rumack-Matthew nomogram should be used to estimate the hepatotoxicity potential from an acute acetaminophen (APAP) overdose in patients with a known APAP concentration, a known APAP ingestion time, and who present within 8 hours of the overdose. For the prevention of hepatotoxicity after an acute acetaminophen overdose or repeated ingestion of supratherapeutic doses.
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