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Acetaminophen (Paracetamol)
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Pharmacology
Acetaminophen is a synthetic derivative of -aminophenol. It is also an active metabolite of two other -aminophenol derivatives, phenacetin and acetanilid, which were withdrawn from the market because of unacceptable nephrotoxicity.
Acetaminophen is an analgesic and antipyretic agent, similar in potency and efficacy to the salicylates. Acetaminophen does not, however, share the anti-inflammatory or uricosuric effects of ASA and does not cause gastrointestinal ulceration or inhibit platelet aggregation.
The mechanism of acetaminophen's antipyretic action is believed to be a direct effect on the heat-regulating centres in the hypothalamus, leading to increased heat dissipation through vasodilation and sweating.
The proposed mechanism of acetaminophen's analgesic action, while not well understood, is through inhibition of prostaglandin synthetase in the CNS. Acetaminophen has minimal effect on peripheral prostaglandin synthesis, which may explain its relative lack of anti-inflammatory effect compared to ASA.
Pharmacokinetics: Acetaminophen is rapidly and completely absorbed from the gastrointestinal tract. A mean peak plasma concentration of 100µmol/L is reached approximately 0.8hours following a 1000mg dose of immediate-release acetaminophen tablets. Acetaminophen is conjugated in the liver, mainly with glucuronic acid, and excreted in the urine. A small amount is excreted unchanged. The plasma half-life ranges from 1to 4hours but may be prolonged in acute overdose or liver disease.
Extended-release bilayer caplets contain a total of 650mg acetaminophen, with 325mg in an immediate-release layer and 325mg in a slow-release matrix. Following a 1300mg oral dose, a mean peak concentration of 60µmol/L is reached in approximately 1.5hours. The half-life is similar to that of immediate-release formulations.
A small percentage of acetaminophen is converted by the cytochrome P450 system to a toxic metabolite that is subsequently conjugated by glutathione and excreted by the kidney. However, when glutathione is depleted following a high dose of acetaminophen, the toxic metabolite accumulates and is thought to be the cause of acetaminophen-induced liver necrosis
Acetaminophen is a synthetic derivative of -aminophenol. It is also an active metabolite of two other -aminophenol derivatives, phenacetin and acetanilid, which were withdrawn from the market because of unacceptable nephrotoxicity.
Acetaminophen is an analgesic and antipyretic agent, similar in potency and efficacy to the salicylates. Acetaminophen does not, however, share the anti-inflammatory or uricosuric effects of ASA and does not cause gastrointestinal ulceration or inhibit platelet aggregation.
The mechanism of acetaminophen's antipyretic action is believed to be a direct effect on the heat-regulating centres in the hypothalamus, leading to increased heat dissipation through vasodilation and sweating.
The proposed mechanism of acetaminophen's analgesic action, while not well understood, is through inhibition of prostaglandin synthetase in the CNS. Acetaminophen has minimal effect on peripheral prostaglandin synthesis, which may explain its relative lack of anti-inflammatory effect compared to ASA.
Pharmacokinetics: Acetaminophen is rapidly and completely absorbed from the gastrointestinal tract. A mean peak plasma concentration of 100µmol/L is reached approximately 0.8hours following a 1000mg dose of immediate-release acetaminophen tablets. Acetaminophen is conjugated in the liver, mainly with glucuronic acid, and excreted in the urine. A small amount is excreted unchanged. The plasma half-life ranges from 1to 4hours but may be prolonged in acute overdose or liver disease.
Extended-release bilayer caplets contain a total of 650mg acetaminophen, with 325mg in an immediate-release layer and 325mg in a slow-release matrix. Following a 1300mg oral dose, a mean peak concentration of 60µmol/L is reached in approximately 1.5hours. The half-life is similar to that of immediate-release formulations.
A small percentage of acetaminophen is converted by the cytochrome P450 system to a toxic metabolite that is subsequently conjugated by glutathione and excreted by the kidney. However, when glutathione is depleted following a high dose of acetaminophen, the toxic metabolite accumulates and is thought to be the cause of acetaminophen-induced liver necrosis
Indications
Acetaminophen Is A Synthetic Derivative Of -aminophenol. It Is Also An Active Metabolite Of Two Other -aminophenol Derivatives, Phenacetin And Acetanilid, Which Were Withdrawn From The Market Because Of Unacceptable Nephrotoxicity.
Acetaminophen Is An Analgesic And Antipyretic Agent, Similar In Potency And Efficacy To The Salicylates. Acetaminophen Does Not, However, Share The Anti-inflammatory Or Uricosuric Effects Of ASA And Does Not Cause Gastrointestinal Ulceration Or Inhibit Platelet Aggregation.
The Mechanism Of Acetaminophen's Antipyretic Action Is Believed To Be A Direct Effect On The Heat-regulating Centres In The Hypothalamus, Leading To Increased Heat Dissipation Through Vasodilation And Sweating.
The Proposed Mechanism Of Acetaminophen's Analgesic Action, While Not Well Understood, Is Through Inhibition Of Prostaglandin Synthetase In The CNS. Acetaminophen Has Minimal Effect On Peripheral Prostaglandin Synthesis, Which May Explain Its Relative Lack Of Anti-inflammatory Effect Compared To ASA.
Pharmacokinetics: Acetaminophen Is Rapidly And Completely Absorbed From The Gastrointestinal Tract. A Mean Peak Plasma Concentration Of 100µmol/L Is Reached Approximately 0.8hours Following A 1000mg Dose Of Immediate-release Acetaminophen Tablets. Acetaminophen Is Conjugated In The Liver, Mainly With Glucuronic Acid, And Excreted In The Urine. A Small Amount Is Excreted Unchanged. The Plasma Half-life Ranges From 1to 4hours But May Be Prolonged In Acute Overdose Or Liver Disease.
Extended-release Bilayer Caplets Contain A Total Of 650mg Acetaminophen, With 325mg In An Immediate-release Layer And 325mg In A Slow-release Matrix. Following A 1300mg Oral Dose, A Mean Peak Concentration Of 60µmol/L Is Reached In Approximately 1.5hours. The Half-life Is Similar To That Of Immediate-release Formulations.
A Small Percentage Of Acetaminophen Is Converted By The Cytochrome P450 System To A Toxic Metabolite That Is Subsequently Conjugated By Glutathione And Excreted By The Kidney. However, When Glutathione Is Depleted Following A High Dose Of Acetaminophen, The Toxic Metabolite Accumulates And Is Thought To Be The Cause Of Acetaminophen-induced Liver Necrosis
Acetaminophen Is A Synthetic Derivative Of -aminophenol. It Is Also An Active Metabolite Of Two Other -aminophenol Derivatives, Phenacetin And Acetanilid, Which Were Withdrawn From The Market Because Of Unacceptable Nephrotoxicity.
Acetaminophen Is An Analgesic And Antipyretic Agent, Similar In Potency And Efficacy To The Salicylates. Acetaminophen Does Not, However, Share The Anti-inflammatory Or Uricosuric Effects Of ASA And Does Not Cause Gastrointestinal Ulceration Or Inhibit Platelet Aggregation.
The Mechanism Of Acetaminophen's Antipyretic Action Is Believed To Be A Direct Effect On The Heat-regulating Centres In The Hypothalamus, Leading To Increased Heat Dissipation Through Vasodilation And Sweating.
The Proposed Mechanism Of Acetaminophen's Analgesic Action, While Not Well Understood, Is Through Inhibition Of Prostaglandin Synthetase In The CNS. Acetaminophen Has Minimal Effect On Peripheral Prostaglandin Synthesis, Which May Explain Its Relative Lack Of Anti-inflammatory Effect Compared To ASA.
Pharmacokinetics: Acetaminophen Is Rapidly And Completely Absorbed From The Gastrointestinal Tract. A Mean Peak Plasma Concentration Of 100µmol/L Is Reached Approximately 0.8hours Following A 1000mg Dose Of Immediate-release Acetaminophen Tablets. Acetaminophen Is Conjugated In The Liver, Mainly With Glucuronic Acid, And Excreted In The Urine. A Small Amount Is Excreted Unchanged. The Plasma Half-life Ranges From 1to 4hours But May Be Prolonged In Acute Overdose Or Liver Disease.
Extended-release Bilayer Caplets Contain A Total Of 650mg Acetaminophen, With 325mg In An Immediate-release Layer And 325mg In A Slow-release Matrix. Following A 1300mg Oral Dose, A Mean Peak Concentration Of 60µmol/L Is Reached In Approximately 1.5hours. The Half-life Is Similar To That Of Immediate-release Formulations.
A Small Percentage Of Acetaminophen Is Converted By The Cytochrome P450 System To A Toxic Metabolite That Is Subsequently Conjugated By Glutathione And Excreted By The Kidney. However, When Glutathione Is Depleted Following A High Dose Of Acetaminophen, The Toxic Metabolite Accumulates And Is Thought To Be The Cause Of Acetaminophen-induced Liver Necrosis
Contraindications
Hypersensitivity to acetaminophen.
Hypersensitivity to acetaminophen.
Safety Information / Warning
Information not available
Information not available
Precautions
Precautions: Potentially fatal hepatotoxicity can result from acetaminophen overdose (see Overdose). However, hepatotoxicity has occurred in patients receiving high or excessive doses with therapeutic intent. Certain patients may be more susceptible to acetaminophen hepatotoxicity, e.g., chronic alcoholics, patients with liver disease or those who are malnourished or taking other drugs that induce hepatic enzymes (see also Children and Drug Interactions).
Because of the risk of hepatotoxicity, patients should be cautioned against the inadvertent administration of excessive doses of acetaminophen by using multiple acetaminophen-containing products at once, such as cough and cold remedies, analgesic or arthritis formulations, antipyretics or products for relief of menstrual symptoms or muscle spasm. This is especially important when administering acetaminophen to children. To avoid dosing errors, all product labels should be checked carefully to ensure accurate calculation of the amount of acetaminophen to be given.
Drug Interactions : Anticoagulants, Oral: Chronic, high-dose administration of acetaminophen may potentiate the anticoagulant effect of warfarin. Patients stabilized on oral anticoagulants should be advised to limit their intake of acetaminophen to not more than 2g daily for no more than a few days at a time. When higher doses of acetaminophen are required, additional monitoring of INR is recommended.
ASA: Concurrent long-term use of analgesic-antipyretic agents with ASA may be associated with analgesic nephropathy (papillary necrosis and tubulointerstitial inflammation).
Cholestyramine: Cholestyramine reduces the absorption of acetaminophen. Oral doses of cholestyramine and acetaminophen should be given at least 1hour apart.
Enzyme Inducers: Barbiturates and other enzyme inducers such as carbamazepine, phenytoin or rifampin, may enhance the metabolism of acetaminophen. The combination of enzyme inducers with excessive doses of acetaminophen may accelerate the production of hepatotoxic metabolites of acetaminophen.
Lactation: Acetaminophen passes into breast milk but is not likely to have an adverse effect on the infant at therapeutic doses. Peak concentrations in the milk occur 1to 2hours after a dose.
Pregnancy: Acetaminophen crosses the placenta and is considered safe for short-term use when therapeutic doses are used.
Children: Dosages of acetaminophen for children should be calculated on a mg/kg basis. Liquid dosage forms should be measured with a calibrated measuring device, as household spoons vary significantly with respect to the volume of liquid they hold.
No more than 5 doses of acetaminophen should be given to a child in a 24-hour period. Children under two years old who are acutely malnourished and dehydrated may be at higher risk for hepatotoxicity from high therapeutic doses of acetaminophen even for short periods of time.
The Canadian Paediatric Society recommends consulting with a physician before administering acetaminophen to infants under 6 months of age.
Precautions: Potentially fatal hepatotoxicity can result from acetaminophen overdose (see Overdose). However, hepatotoxicity has occurred in patients receiving high or excessive doses with therapeutic intent. Certain patients may be more susceptible to acetaminophen hepatotoxicity, e.g., chronic alcoholics, patients with liver disease or those who are malnourished or taking other drugs that induce hepatic enzymes (see also Children and Drug Interactions).
Because of the risk of hepatotoxicity, patients should be cautioned against the inadvertent administration of excessive doses of acetaminophen by using multiple acetaminophen-containing products at once, such as cough and cold remedies, analgesic or arthritis formulations, antipyretics or products for relief of menstrual symptoms or muscle spasm. This is especially important when administering acetaminophen to children. To avoid dosing errors, all product labels should be checked carefully to ensure accurate calculation of the amount of acetaminophen to be given.
Drug Interactions : Anticoagulants, Oral: Chronic, high-dose administration of acetaminophen may potentiate the anticoagulant effect of warfarin. Patients stabilized on oral anticoagulants should be advised to limit their intake of acetaminophen to not more than 2g daily for no more than a few days at a time. When higher doses of acetaminophen are required, additional monitoring of INR is recommended.
ASA: Concurrent long-term use of analgesic-antipyretic agents with ASA may be associated with analgesic nephropathy (papillary necrosis and tubulointerstitial inflammation).
Cholestyramine: Cholestyramine reduces the absorption of acetaminophen. Oral doses of cholestyramine and acetaminophen should be given at least 1hour apart.
Enzyme Inducers: Barbiturates and other enzyme inducers such as carbamazepine, phenytoin or rifampin, may enhance the metabolism of acetaminophen. The combination of enzyme inducers with excessive doses of acetaminophen may accelerate the production of hepatotoxic metabolites of acetaminophen.
Lactation: Acetaminophen passes into breast milk but is not likely to have an adverse effect on the infant at therapeutic doses. Peak concentrations in the milk occur 1to 2hours after a dose.
Pregnancy: Acetaminophen crosses the placenta and is considered safe for short-term use when therapeutic doses are used.
Children: Dosages of acetaminophen for children should be calculated on a mg/kg basis. Liquid dosage forms should be measured with a calibrated measuring device, as household spoons vary significantly with respect to the volume of liquid they hold.
No more than 5 doses of acetaminophen should be given to a child in a 24-hour period. Children under two years old who are acutely malnourished and dehydrated may be at higher risk for hepatotoxicity from high therapeutic doses of acetaminophen even for short periods of time.
The Canadian Paediatric Society recommends consulting with a physician before administering acetaminophen to infants under 6 months of age.
Side Effects / Adverse Effects
Chronic use of large doses of acetaminophen may produce significant toxicity (see Precautions).
Hematologic: Neutropenia and thrombocytopenia purpura have been reported and rarely agranulocytosis.
Hepatic: See Precautions.
Hypersensitivity: Reactions including laryngeal edema, angioedema, bronchospasm and/or anaphylaxis have occurred rarely. A small percentage of ASA-sensitive asthmatics have been reported to be cross-sensitive to acetaminophen. Low initial doses of acetaminophen (less than 1000mg) are recommended in these patients, with monitoring for about 3hours following initial doses.
Renal: Nephropathy, including papillary renal failure has been reported following consumption of large amounts of acetaminophen. Renal tubular necrosis has been associated occasionally with hepatic injury produced by acetaminophen overdose.
Chronic use of large doses of acetaminophen may produce significant toxicity (see Precautions).
Hematologic: Neutropenia and thrombocytopenia purpura have been reported and rarely agranulocytosis.
Hepatic: See Precautions.
Hypersensitivity: Reactions including laryngeal edema, angioedema, bronchospasm and/or anaphylaxis have occurred rarely. A small percentage of ASA-sensitive asthmatics have been reported to be cross-sensitive to acetaminophen. Low initial doses of acetaminophen (less than 1000mg) are recommended in these patients, with monitoring for about 3hours following initial doses.
Renal: Nephropathy, including papillary renal failure has been reported following consumption of large amounts of acetaminophen. Renal tubular necrosis has been associated occasionally with hepatic injury produced by acetaminophen overdose.
Overdose
In adults, hepatotoxicity may occur after ingestion of a single dose of more than 7.5g (adults) or 150mg/kg (children) of acetaminophen; a dose of10g or more is potentially fatal. However, reports have indicated hepatic necrosis with a single dose of6g and death occurring with a single dose of13g. Nonfatal overdoses of12.5to 31.5g have also been reported (see also Precautions).
Symptoms:
Early symptoms (nausea, vomiting, weakness, diaphoresis) usually occur after acute ingestion of an acetaminophen overdose large enough to cause hepatic toxicity. However, since some patients may exhibit few or none of these early signs, in cases of suspected acetaminophen overdose, antidotal therapy should begin as soon as possible. A latent period of 24to 36hours exists between ingestion and the onset of symptoms of hepatic injury. Laboratory evidence usually appears within 24 to 48hours if severe hepatotoxicity is to occur. In mild cases, clinical evidence of hepatotoxicity may be delayed for as long as 5days. Consequently, liver function should be monitored for several days following overdose. Following the latent period, vomiting, pain in the upper right quadrant and manifestations of hepatic failure including the onset of coma, may ensue. Maximum hepatic necrosis appears 2to 5days following overdose. Signs include gross elevation of ALT, AST, increased bilirubin, hypoglycemia and increased prothrombin time.
In addition to hepatic damage, clotting defects, and myocardial damage with ST segment abnormalities, Twave flattening and pericarditis have been reported.
Treatment: Treatment of acute acetaminophen overdose includes supportive measures, such as control of respiration and fluid and electrolyte balance, as well as decontamination of the gastrointestinal tract and prompt administration of acetylcysteine as an antidote. Laboratory determinations include plasma acetaminophen levels, AST, ALT, prothrombin time, bilirubin, creatinine, urea, blood glucose and electrolyte concentrations.
A single dose of activated charcoal is recommended, ideally within one hour of ingestion of overdose, and may be of benefit if given up to 4hours postingestion.
Properly timed plasma acetaminophen levels are key prognosticators in determining a patient's risk of hepatotoxicity. The first level should be drawn at least 4hours postingestion as peak concentrations may not be reached before this time. The Matthew-Rumack Nomogram for Acetaminophen Poisoning (see FigureI) should be used when acetaminophen levels are drawn between 4and 24hours postingestion, to determine the probability of hepatotoxicity and need for acetylcysteine therapy. For immediate-release acetaminophen formulations, when serum levels are above the lower treatment line (above 990µmol/L at 4hours, above 460µmol/L at 8hours or above 260µmol/L at 12hours postingestion), acetylcysteine therapy should be instituted to minimize hepatic toxicity. In the case of extended-release caplets, if the serum level at 4hours postingestion is below 990µmol/L, a second level should be drawn at 8to 10hours postingestion. If either level is above the lower treatment line on the nomogram, acetylcysteine should be given.
Even in the absence of acetaminophen serum level determinations, therapy with acetylcysteine should be promptly instituted if a massive acetaminophen overdose is suspected (i.e., >7.5g in adults or >150mg/kg in children) and 24hours or less have elapsed since ingestion. In the case of overdose with immediate-release formulations, maintenance doses of acetylcysteine may be discontinued if the initial acetaminophen serum level is nontoxic. Subsequent levels are not predictive of toxicity and should not be used as criteria for acetylcysteine discontinuation.
Antidotal therapy with acetylcysteine is most effective if initiated within 10hours following acetaminophen overdose. However, acetylcysteine therapy may improve outcomes even in patients presenting more than 24hours postingestion with or without severe hepatic injury including fulminant hepatic failure.
Acetylcysteine Dosing in Acetaminophen Overdose: Oral: Loading dose: 140mg/kg. Maintenance dose: 70mg/kg every 4hours for a total of 17doses. Each oral dose should be diluted to a final concentration of 5% acetylcysteine (i.e., 3mL of soft drinks, fruit juice or water added for each mL of 20% acetylcysteine solution) and consumed within 1hour of preparation. If vomiting occurs within 1hour following any oral dose, the entire dose should be repeated.
I.V.: Acetylcysteine may be given by the i.v. route if necessary. Loading dose: 150mg/kg in 5% dextrose over 15minutes. Maintenance infusion: 12.5mg/kg/hour for 4hours, followed by 6.25mg/kg/hour for 16hours
Conditions for the use of this chart:
)Serum levels drawn before 4hours may not represent peak levels.
2)The nomogram was designed for management of single acute ingestion of immediate-release dosage forms. See Overdose, Treatment for information on using this chart for overdose involving extended-release caplets.
3)The lower treatment line represents plasma acetaminophen levels 25% below corresponding levels on the standard nomogram treatment line and is included to allow for possible errors in acetaminophen plasma assays and estimated time from ingestion of an overdose.
Adapted with permission from: Pediatrics 1975;55:871-6 (Copyright 1975, American Academy of Pediatrics) and Arch Intern Med 1981; 141: 380-5
In adults, hepatotoxicity may occur after ingestion of a single dose of more than 7.5g (adults) or 150mg/kg (children) of acetaminophen; a dose of10g or more is potentially fatal. However, reports have indicated hepatic necrosis with a single dose of6g and death occurring with a single dose of13g. Nonfatal overdoses of12.5to 31.5g have also been reported (see also Precautions).
Symptoms:
Early symptoms (nausea, vomiting, weakness, diaphoresis) usually occur after acute ingestion of an acetaminophen overdose large enough to cause hepatic toxicity. However, since some patients may exhibit few or none of these early signs, in cases of suspected acetaminophen overdose, antidotal therapy should begin as soon as possible. A latent period of 24to 36hours exists between ingestion and the onset of symptoms of hepatic injury. Laboratory evidence usually appears within 24 to 48hours if severe hepatotoxicity is to occur. In mild cases, clinical evidence of hepatotoxicity may be delayed for as long as 5days. Consequently, liver function should be monitored for several days following overdose. Following the latent period, vomiting, pain in the upper right quadrant and manifestations of hepatic failure including the onset of coma, may ensue. Maximum hepatic necrosis appears 2to 5days following overdose. Signs include gross elevation of ALT, AST, increased bilirubin, hypoglycemia and increased prothrombin time.
In addition to hepatic damage, clotting defects, and myocardial damage with ST segment abnormalities, Twave flattening and pericarditis have been reported.
Treatment: Treatment of acute acetaminophen overdose includes supportive measures, such as control of respiration and fluid and electrolyte balance, as well as decontamination of the gastrointestinal tract and prompt administration of acetylcysteine as an antidote. Laboratory determinations include plasma acetaminophen levels, AST, ALT, prothrombin time, bilirubin, creatinine, urea, blood glucose and electrolyte concentrations.
A single dose of activated charcoal is recommended, ideally within one hour of ingestion of overdose, and may be of benefit if given up to 4hours postingestion.
Properly timed plasma acetaminophen levels are key prognosticators in determining a patient's risk of hepatotoxicity. The first level should be drawn at least 4hours postingestion as peak concentrations may not be reached before this time. The Matthew-Rumack Nomogram for Acetaminophen Poisoning (see FigureI) should be used when acetaminophen levels are drawn between 4and 24hours postingestion, to determine the probability of hepatotoxicity and need for acetylcysteine therapy. For immediate-release acetaminophen formulations, when serum levels are above the lower treatment line (above 990µmol/L at 4hours, above 460µmol/L at 8hours or above 260µmol/L at 12hours postingestion), acetylcysteine therapy should be instituted to minimize hepatic toxicity. In the case of extended-release caplets, if the serum level at 4hours postingestion is below 990µmol/L, a second level should be drawn at 8to 10hours postingestion. If either level is above the lower treatment line on the nomogram, acetylcysteine should be given.
Even in the absence of acetaminophen serum level determinations, therapy with acetylcysteine should be promptly instituted if a massive acetaminophen overdose is suspected (i.e., >7.5g in adults or >150mg/kg in children) and 24hours or less have elapsed since ingestion. In the case of overdose with immediate-release formulations, maintenance doses of acetylcysteine may be discontinued if the initial acetaminophen serum level is nontoxic. Subsequent levels are not predictive of toxicity and should not be used as criteria for acetylcysteine discontinuation.
Antidotal therapy with acetylcysteine is most effective if initiated within 10hours following acetaminophen overdose. However, acetylcysteine therapy may improve outcomes even in patients presenting more than 24hours postingestion with or without severe hepatic injury including fulminant hepatic failure.
Acetylcysteine Dosing in Acetaminophen Overdose: Oral: Loading dose: 140mg/kg. Maintenance dose: 70mg/kg every 4hours for a total of 17doses. Each oral dose should be diluted to a final concentration of 5% acetylcysteine (i.e., 3mL of soft drinks, fruit juice or water added for each mL of 20% acetylcysteine solution) and consumed within 1hour of preparation. If vomiting occurs within 1hour following any oral dose, the entire dose should be repeated.
I.V.: Acetylcysteine may be given by the i.v. route if necessary. Loading dose: 150mg/kg in 5% dextrose over 15minutes. Maintenance infusion: 12.5mg/kg/hour for 4hours, followed by 6.25mg/kg/hour for 16hours
Conditions for the use of this chart:
)Serum levels drawn before 4hours may not represent peak levels.
2)The nomogram was designed for management of single acute ingestion of immediate-release dosage forms. See Overdose, Treatment for information on using this chart for overdose involving extended-release caplets.
3)The lower treatment line represents plasma acetaminophen levels 25% below corresponding levels on the standard nomogram treatment line and is included to allow for possible errors in acetaminophen plasma assays and estimated time from ingestion of an overdose.
Adapted with permission from: Pediatrics 1975;55:871-6 (Copyright 1975, American Academy of Pediatrics) and Arch Intern Med 1981; 141: 380-5
Recommended Dosage
Acetaminophen should not be used in adults or children for self-medication of marked fever (greater than 39.5°C), fever persisting longer than 3days, or recurrent fever, unless directed by a physician, since such fevers may indicate serious illness requiring prompt medical attention.
Acetaminophen should not be used for self-medication of pain for longer than 10days in adults or 5days in children, unless directed by a physician, since pain of such intensity and duration may indicate a pathological condition requiring medical evaluation.
Immediate-release dosage forms (oral or rectal): Adults: 325to 650mg every 4to 6hours, not to exceed 4000mg/24hours.
*The Canadian Paediatric Society recommends consultation with a physician for infants under 6months.
Dosing for children must not exceed 5 doses in 24hours unless under the advice of a physician, because of the risk of toxicity.
Extended-release caplets: Adults and children over 12years: 1300mg every 8 hours, to a maximum of 4000mg daily. Caplets should be swallowed whole and taken with water on an empty stomach.
Note: Acetaminophen in liquid drop formulations tends to be approximately 2.5 to 5times more concentrated than the elixir or syrup formulations. Careful attention must be paid to acetaminophen concentration when dosage volumes are calculated for liquid preparations.
Acetaminophen should not be used in adults or children for self-medication of marked fever (greater than 39.5°C), fever persisting longer than 3days, or recurrent fever, unless directed by a physician, since such fevers may indicate serious illness requiring prompt medical attention.
Acetaminophen should not be used for self-medication of pain for longer than 10days in adults or 5days in children, unless directed by a physician, since pain of such intensity and duration may indicate a pathological condition requiring medical evaluation.
Immediate-release dosage forms (oral or rectal): Adults: 325to 650mg every 4to 6hours, not to exceed 4000mg/24hours.
*The Canadian Paediatric Society recommends consultation with a physician for infants under 6months.
Dosing for children must not exceed 5 doses in 24hours unless under the advice of a physician, because of the risk of toxicity.
Extended-release caplets: Adults and children over 12years: 1300mg every 8 hours, to a maximum of 4000mg daily. Caplets should be swallowed whole and taken with water on an empty stomach.
Note: Acetaminophen in liquid drop formulations tends to be approximately 2.5 to 5times more concentrated than the elixir or syrup formulations. Careful attention must be paid to acetaminophen concentration when dosage volumes are calculated for liquid preparations.
Supplied / Packaging
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Brand Name
Acetaminophen
Acetaminophen
Generic Name
Paracetamol
Paracetamol
General Indications
Analgesic Antipyretic
Analgesic Antipyretic
