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ASA (Acetylsalicylic Acid)
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Pharmacology
ASA interferes with the production of prostaglandins in various organs and tissues through acetylation and inactivation of the enzyme, cyclooxygenase. The main action of the drug is thought to be peripheral; however, it may have similar activity in the CNS. The reduction in tissue levels of prostaglandins may be responsible for the analgesic and anti-inflammatory effects of the drug. ASA is most effective in the management of pain of low to moderate intensity associated with inflammation.
ASA is also a potent antipyretic and lowers body temperature in patients with fever, mainly by inhibition of prostaglandin E 1 synthesis in the brain. Heat production is not affected but dissipation of heat is enhanced by increased blood flow through the skin and sweating.
ASA has antiplatelet activity through inhibition of thromboxane A 2 synthesis. Thromboxane A 2 plays an essential role in platelet aggregation. ASA prevents thromboxaneA 2 formation by acetylating cyclooxygenase, a catalytic enzyme involved in the early stages of the inflammatory cascade. ASA is a relatively selective inhibitor of cyclooxygenase-1 (COX-1). ASA's effect on the platelet is irreversible and persists for the life of the platelet (7to 10days). At higher doses, ASA prolongs bleeding time by altering the hepatic synthesis of certain blood coagulation factors. The increase in prothrombin time is dose dependent and rarely occurs with doses less than 6g/day.
Pharmacokinetics: Following oral administration, ASA is rapidly absorbed from the stomach and proximal small intestine, although there is some evidence that absorption may be substantially impaired during the febrile phase of Kawasaki syndrome (mucocutaneous lymph node syndrome). Absorption in the small intestine occurs at a significantly faster rate than in the stomach. Following oral administration, ASA is partially hydrolyzed to salicylate by esterases in the gastrointestinal mucosa. Once absorbed, further hydrolysis by esterases takes place, mainly in the liver but also in plasma, erythrocytes and synovial fluid.
Optimum absorption of salicylate occurs in the pH range of 2.15to 4.1. Enteric-coated tablets resist disintegration at a pH less than 3.5 for a period of at least 2 hours, but can disintegrate in 10 to 30 minutes at a pH of greater than 5.5. Absorption of enteric-coated tablets takes place primarily in the duodenum.
Rectal absorption of ASA is slow, variable and usually incomplete and may be associated with rectal mucosal irritation.
Peak blood levels occur approximately 2 hours after ingestion of regular tablets and 6 to 8 hours after the ingestion of enteric-coated tablets.
ASA is widely distributed in most body tissues and fluids. The protein binding of salicylate is concentration dependent. The bound fraction decreases as the plasma concentration of salicylate increases; at low concentrations of less than 0.75mmol/L about 90% of the drug is bound and at concentrations between 0.76 and 2.9mmol/L, approximately 70 to 85% is bound. Because of capacity-limited metabolism, serum concentrations of salicylate increase more than proportionally with an increase in dose.
The elimination half-life of ASA is 14 to 20 minutes. The half-life of salicylate is 2 to 3hours after low doses of ASA and up to 15to 30 hours after anti-inflammatory doses of ASA. Salicylate undergoes hepatic metabolism. Salicylate and its metabolites are rapidly and almost completely excreted in the urine. Only about 1% of ASA is excreted in the urine unchanged. This proportion is extremely variable and depends on dose and urinary pH.
ASA interferes with the production of prostaglandins in various organs and tissues through acetylation and inactivation of the enzyme, cyclooxygenase. The main action of the drug is thought to be peripheral; however, it may have similar activity in the CNS. The reduction in tissue levels of prostaglandins may be responsible for the analgesic and anti-inflammatory effects of the drug. ASA is most effective in the management of pain of low to moderate intensity associated with inflammation.
ASA is also a potent antipyretic and lowers body temperature in patients with fever, mainly by inhibition of prostaglandin E 1 synthesis in the brain. Heat production is not affected but dissipation of heat is enhanced by increased blood flow through the skin and sweating.
ASA has antiplatelet activity through inhibition of thromboxane A 2 synthesis. Thromboxane A 2 plays an essential role in platelet aggregation. ASA prevents thromboxaneA 2 formation by acetylating cyclooxygenase, a catalytic enzyme involved in the early stages of the inflammatory cascade. ASA is a relatively selective inhibitor of cyclooxygenase-1 (COX-1). ASA's effect on the platelet is irreversible and persists for the life of the platelet (7to 10days). At higher doses, ASA prolongs bleeding time by altering the hepatic synthesis of certain blood coagulation factors. The increase in prothrombin time is dose dependent and rarely occurs with doses less than 6g/day.
Pharmacokinetics: Following oral administration, ASA is rapidly absorbed from the stomach and proximal small intestine, although there is some evidence that absorption may be substantially impaired during the febrile phase of Kawasaki syndrome (mucocutaneous lymph node syndrome). Absorption in the small intestine occurs at a significantly faster rate than in the stomach. Following oral administration, ASA is partially hydrolyzed to salicylate by esterases in the gastrointestinal mucosa. Once absorbed, further hydrolysis by esterases takes place, mainly in the liver but also in plasma, erythrocytes and synovial fluid.
Optimum absorption of salicylate occurs in the pH range of 2.15to 4.1. Enteric-coated tablets resist disintegration at a pH less than 3.5 for a period of at least 2 hours, but can disintegrate in 10 to 30 minutes at a pH of greater than 5.5. Absorption of enteric-coated tablets takes place primarily in the duodenum.
Rectal absorption of ASA is slow, variable and usually incomplete and may be associated with rectal mucosal irritation.
Peak blood levels occur approximately 2 hours after ingestion of regular tablets and 6 to 8 hours after the ingestion of enteric-coated tablets.
ASA is widely distributed in most body tissues and fluids. The protein binding of salicylate is concentration dependent. The bound fraction decreases as the plasma concentration of salicylate increases; at low concentrations of less than 0.75mmol/L about 90% of the drug is bound and at concentrations between 0.76 and 2.9mmol/L, approximately 70 to 85% is bound. Because of capacity-limited metabolism, serum concentrations of salicylate increase more than proportionally with an increase in dose.
The elimination half-life of ASA is 14 to 20 minutes. The half-life of salicylate is 2 to 3hours after low doses of ASA and up to 15to 30 hours after anti-inflammatory doses of ASA. Salicylate undergoes hepatic metabolism. Salicylate and its metabolites are rapidly and almost completely excreted in the urine. Only about 1% of ASA is excreted in the urine unchanged. This proportion is extremely variable and depends on dose and urinary pH.
Indications
ASA Interferes With The Production Of Prostaglandins In Various Organs And Tissues Through Acetylation And Inactivation Of The Enzyme, Cyclooxygenase. The Main Action Of The Drug Is Thought To Be Peripheral; However, It May Have Similar Activity In The CNS. The Reduction In Tissue Levels Of Prostaglandins May Be Responsible For The Analgesic And Anti-inflammatory Effects Of The Drug. ASA Is Most Effective In The Management Of Pain Of Low To Moderate Intensity Associated With Inflammation.
ASA Is Also A Potent Antipyretic And Lowers Body Temperature In Patients With Fever, Mainly By Inhibition Of Prostaglandin E 1 Synthesis In The Brain. Heat Production Is Not Affected But Dissipation Of Heat Is Enhanced By Increased Blood Flow Through The Skin And Sweating.
ASA Has Antiplatelet Activity Through Inhibition Of Thromboxane A 2 Synthesis. Thromboxane A 2 Plays An Essential Role In Platelet Aggregation. ASA Prevents ThromboxaneA 2 Formation By Acetylating Cyclooxygenase, A Catalytic Enzyme Involved In The Early Stages Of The Inflammatory Cascade. ASA Is A Relatively Selective Inhibitor Of Cyclooxygenase-1 (COX-1). ASA's Effect On The Platelet Is Irreversible And Persists For The Life Of The Platelet (7to 10days). At Higher Doses, ASA Prolongs Bleeding Time By Altering The Hepatic Synthesis Of Certain Blood Coagulation Factors. The Increase In Prothrombin Time Is Dose Dependent And Rarely Occurs With Doses Less Than 6g/day.
Pharmacokinetics: Following Oral Administration, ASA Is Rapidly Absorbed From The Stomach And Proximal Small Intestine, Although There Is Some Evidence That Absorption May Be Substantially Impaired During The Febrile Phase Of Kawasaki Syndrome (mucocutaneous Lymph Node Syndrome). Absorption In The Small Intestine Occurs At A Significantly Faster Rate Than In The Stomach. Following Oral Administration, ASA Is Partially Hydrolyzed To Salicylate By Esterases In The Gastrointestinal Mucosa. Once Absorbed, Further Hydrolysis By Esterases Takes Place, Mainly In The Liver But Also In Plasma, Erythrocytes And Synovial Fluid.
Optimum Absorption Of Salicylate Occurs In The PH Range Of 2.15to 4.1. Enteric-coated Tablets Resist Disintegration At A PH Less Than 3.5 For A Period Of At Least 2 Hours, But Can Disintegrate In 10 To 30 Minutes At A PH Of Greater Than 5.5. Absorption Of Enteric-coated Tablets Takes Place Primarily In The Duodenum.
Rectal Absorption Of ASA Is Slow, Variable And Usually Incomplete And May Be Associated With Rectal Mucosal Irritation.
Peak Blood Levels Occur Approximately 2 Hours After Ingestion Of Regular Tablets And 6 To 8 Hours After The Ingestion Of Enteric-coated Tablets.
ASA Is Widely Distributed In Most Body Tissues And Fluids. The Protein Binding Of Salicylate Is Concentration Dependent. The Bound Fraction Decreases As The Plasma Concentration Of Salicylate Increases; At Low Concentrations Of Less Than 0.75mmol/L About 90% Of The Drug Is Bound And At Concentrations Between 0.76 And 2.9mmol/L, Approximately 70 To 85% Is Bound. Because Of Capacity-limited Metabolism, Serum Concentrations Of Salicylate Increase More Than Proportionally With An Increase In Dose.
The Elimination Half-life Of ASA Is 14 To 20 Minutes. The Half-life Of Salicylate Is 2 To 3hours After Low Doses Of ASA And Up To 15to 30 Hours After Anti-inflammatory Doses Of ASA. Salicylate Undergoes Hepatic Metabolism. Salicylate And Its Metabolites Are Rapidly And Almost Completely Excreted In The Urine. Only About 1% Of ASA Is Excreted In The Urine Unchanged. This Proportion Is Extremely Variable And Depends On Dose And Urinary PH.
ASA Interferes With The Production Of Prostaglandins In Various Organs And Tissues Through Acetylation And Inactivation Of The Enzyme, Cyclooxygenase. The Main Action Of The Drug Is Thought To Be Peripheral; However, It May Have Similar Activity In The CNS. The Reduction In Tissue Levels Of Prostaglandins May Be Responsible For The Analgesic And Anti-inflammatory Effects Of The Drug. ASA Is Most Effective In The Management Of Pain Of Low To Moderate Intensity Associated With Inflammation.
ASA Is Also A Potent Antipyretic And Lowers Body Temperature In Patients With Fever, Mainly By Inhibition Of Prostaglandin E 1 Synthesis In The Brain. Heat Production Is Not Affected But Dissipation Of Heat Is Enhanced By Increased Blood Flow Through The Skin And Sweating.
ASA Has Antiplatelet Activity Through Inhibition Of Thromboxane A 2 Synthesis. Thromboxane A 2 Plays An Essential Role In Platelet Aggregation. ASA Prevents ThromboxaneA 2 Formation By Acetylating Cyclooxygenase, A Catalytic Enzyme Involved In The Early Stages Of The Inflammatory Cascade. ASA Is A Relatively Selective Inhibitor Of Cyclooxygenase-1 (COX-1). ASA's Effect On The Platelet Is Irreversible And Persists For The Life Of The Platelet (7to 10days). At Higher Doses, ASA Prolongs Bleeding Time By Altering The Hepatic Synthesis Of Certain Blood Coagulation Factors. The Increase In Prothrombin Time Is Dose Dependent And Rarely Occurs With Doses Less Than 6g/day.
Pharmacokinetics: Following Oral Administration, ASA Is Rapidly Absorbed From The Stomach And Proximal Small Intestine, Although There Is Some Evidence That Absorption May Be Substantially Impaired During The Febrile Phase Of Kawasaki Syndrome (mucocutaneous Lymph Node Syndrome). Absorption In The Small Intestine Occurs At A Significantly Faster Rate Than In The Stomach. Following Oral Administration, ASA Is Partially Hydrolyzed To Salicylate By Esterases In The Gastrointestinal Mucosa. Once Absorbed, Further Hydrolysis By Esterases Takes Place, Mainly In The Liver But Also In Plasma, Erythrocytes And Synovial Fluid.
Optimum Absorption Of Salicylate Occurs In The PH Range Of 2.15to 4.1. Enteric-coated Tablets Resist Disintegration At A PH Less Than 3.5 For A Period Of At Least 2 Hours, But Can Disintegrate In 10 To 30 Minutes At A PH Of Greater Than 5.5. Absorption Of Enteric-coated Tablets Takes Place Primarily In The Duodenum.
Rectal Absorption Of ASA Is Slow, Variable And Usually Incomplete And May Be Associated With Rectal Mucosal Irritation.
Peak Blood Levels Occur Approximately 2 Hours After Ingestion Of Regular Tablets And 6 To 8 Hours After The Ingestion Of Enteric-coated Tablets.
ASA Is Widely Distributed In Most Body Tissues And Fluids. The Protein Binding Of Salicylate Is Concentration Dependent. The Bound Fraction Decreases As The Plasma Concentration Of Salicylate Increases; At Low Concentrations Of Less Than 0.75mmol/L About 90% Of The Drug Is Bound And At Concentrations Between 0.76 And 2.9mmol/L, Approximately 70 To 85% Is Bound. Because Of Capacity-limited Metabolism, Serum Concentrations Of Salicylate Increase More Than Proportionally With An Increase In Dose.
The Elimination Half-life Of ASA Is 14 To 20 Minutes. The Half-life Of Salicylate Is 2 To 3hours After Low Doses Of ASA And Up To 15to 30 Hours After Anti-inflammatory Doses Of ASA. Salicylate Undergoes Hepatic Metabolism. Salicylate And Its Metabolites Are Rapidly And Almost Completely Excreted In The Urine. Only About 1% Of ASA Is Excreted In The Urine Unchanged. This Proportion Is Extremely Variable And Depends On Dose And Urinary PH.
Contraindications
ASA is contraindicated in patients who have had a bronchospastic reaction, generalized urticaria, angioedema, severe rhinitis, laryngeal edema or shock precipitated by ASA or nonsteroidal anti-inflammatory drugs (see Precautions, Hypersensitivity).
ASA should not be used in patients with active peptic ulcer (see Warnings and Precautions).
ASA is contraindicated in patients who have had a bronchospastic reaction, generalized urticaria, angioedema, severe rhinitis, laryngeal edema or shock precipitated by ASA or nonsteroidal anti-inflammatory drugs (see Precautions, Hypersensitivity).
ASA should not be used in patients with active peptic ulcer (see Warnings and Precautions).
Safety Information / Warning
ASA is one of the most frequent causes of accidental poisoning in toddlers and infants. ASA-containing products should be kept well out of the reach of children.
Authorities advise that ASA not be used in children, teenagers or young adults with varicella or influenza. A strong association has been made between development of Reye's syndrome and ingestion of salicylates (almost exclusively ASA) for these illnesses, although a causal relationship has not been established. Reye's syndrome is characterized by the onset of protracted vomiting 3 to 7days following the onset of influenza or chickenpox, with subsequent development of progressive CNS symptoms such as lethargy, drowsiness, combative behavior, confusion, delerium, seizures and coma. The liver is also affected, with fatty infiltrations and elevation of AST (SGOT) and ALT (SGPT). Early recognition and treatment are crucial as this syndrome can be fatal or can leave permanent brain damage.
Most evidence to date, including a decline in the use of ASA in children and a continuing decline in reported cases of Reye's syndrome, supports an association between the two.
As with other nonsteroidal anti-inflammatory drugs, serious gastrointestinal toxicity, such as peptic ulceration, perforation and bleeding, sometimes severe and occasionally fatal, can occur at any time, with or without symptoms, in patients treated with ASA.
ASA is one of the most frequent causes of accidental poisoning in toddlers and infants. ASA-containing products should be kept well out of the reach of children.
Authorities advise that ASA not be used in children, teenagers or young adults with varicella or influenza. A strong association has been made between development of Reye's syndrome and ingestion of salicylates (almost exclusively ASA) for these illnesses, although a causal relationship has not been established. Reye's syndrome is characterized by the onset of protracted vomiting 3 to 7days following the onset of influenza or chickenpox, with subsequent development of progressive CNS symptoms such as lethargy, drowsiness, combative behavior, confusion, delerium, seizures and coma. The liver is also affected, with fatty infiltrations and elevation of AST (SGOT) and ALT (SGPT). Early recognition and treatment are crucial as this syndrome can be fatal or can leave permanent brain damage.
Most evidence to date, including a decline in the use of ASA in children and a continuing decline in reported cases of Reye's syndrome, supports an association between the two.
As with other nonsteroidal anti-inflammatory drugs, serious gastrointestinal toxicity, such as peptic ulceration, perforation and bleeding, sometimes severe and occasionally fatal, can occur at any time, with or without symptoms, in patients treated with ASA.
Precautions
ASA should be used with extreme caution in patients with decreased renal function, bleeding tendencies, significant anemia, hypoprothrombinemia, thrombocytopenia, vitaminK deficiency or severe hepatic disease.
Gastrointestinal: Gastrointestinal toxicity may occur with the use of ASA (see Warnings). No studies, to date, have identified any group of patients not at risk of ulceration and bleeding. A history of serious gastrointestinal events and other factors such as ASA dosage, excessive alcohol intake, smoking, advanced age, female gender and concomitant corticosteroid or anticoagulant use have been associated with increased risk. Patients should be informed about the signs and symptoms of serious gastrointestinal toxicity and advised to contact their physician immediately if they occur. Because serious events can occur without warning symptoms, patients on long-term therapy should have periodic hemoglobin determinations in conjunction with vigilant follow up.
Hypersensitivity: ASA sensitivity is rare, occurring in less that 1% of the general population. It usually involves bronchospasm, urticaria, angioedema and rarely, shock and death. ASA sensitivity occurs in a higher percentage (approximately 10%) of adults with asthma, more often in women than men, and rarely in children. The syndrome of ASA-induced asthma usually begins as chronic nasal congestion with subsequent development of nasal polyps. Asthma and ASA sensitivity follow, with disease progression despite avoidance of ASA and cross-reacting drugs. The mechanism is thought to involve inhibition of intracellular cyclooxygenase (COX) in respiratory cells. Patients with ASA-induced asthma should avoid other drugs that inhibit COX, such as NSAIDs, but the majority can safely take other salicylates that do not inhibit COX enzymes. Cross-sensitivity with acetaminophen has been reported with frequencies of up to 34%. It is recommended that patients with ASA-induced asthma use low initial doses of acetaminophen (less than 1000 mg) with monitoring for 3 hours after initial doses.
Some patients with ASA-induced asthma have been desensitized with small incremental oral doses of ASA over the course of 2 to 3 days until 400 to 650 mg is tolerated, followed by maintenance doses of 80 to 325mg daily. Cross-desensitization to other reacting drugs also occurs when patients are desensitized to ASA.
Salicylism: Chronic salicylate intoxication (also known as salicylism) can occur when repeated large doses (>100mg/kg/day) are used for 2or more days (see Overdose).
Surgery: ASA should be discontinued at least one week prior to elective surgery because of increased risk of bleeding.
Drug Interactions : Analgesics: Concurrent long-term use of ASA and other analgesic-antipyretic agents such as acetaminophen may be associated with analgesic nephropathy (papillary necrosis and tubulointerstitial inflammation).
Antacids: Chronic high-dose use of antacids may increase renal elimination of salicylates through alkalinization of the urine.
Anticoagulants: Concomitant use of ASA and anticoagulants increases the risk of bleeding. Large doses of ASA may enhance the hypoprothrombinemic response to warfarin; however, ASA is used in selected patients with prosthetic heart valves or coronary artery disease in conjunction with warfarin, with appropriate monitoring.
Anticonvulsants: Large doses of ASA may increase phenytoin serum levels by inhibition of phenytoin metabolism.
Valproic acid may cause hypoprothrombinemia and inhibit platelet aggregation. Concomitant use of ASA and valproic acid may cause increased valproic acid levels and may lead to an increased risk of bleeding.
Antihyperglycemic Agents: ASA increases the antihyperglycemic response to sulfonylureas, especially chlorpropamide. Large doses of ASA may cause a decrease in blood glucose, which may alter the insulin requirements of diabetic patients.
Corticosteroids: Corticosteroids may decrease the serum salicylate concentrations through increased excretion. Concomitant use may also increase the risk of gastrointestinal side effects.
Methotrexate: Concurrent use of ASA and methotrexate may lead to higher methotrexate serum levels, mainly through competition for renal excretion.
Nonsteroidal Anti inflammatory Drugs (NSAIDs): Concomitant use of ASA and NSAIDs increases the risk of gastrointestinal side effects while providing no additional therapeutic benefit.
Uricosuric agents: ASA may decrease the uricosuric effects of sulfinpyrazone and probenecid.
Vancomycin: Use of vancomycin with ASA may increase the risk of ototoxicity.
VitaminC: Large doses of vitaminC may decrease the excretion of ASA because of acidification of the urine.
Zidovudine: ASA may increase the risk of zidovudine toxicity by decreasing the hepatic metabolism of zidovudine.
Drug/Lab Test Interactions : Bleeding time: ASA may prolong bleeding time for 4to 7days due to its effects on platelet aggregation.
Copper sulfate urine sugar tests: Daily doses of ASA greater than 2.4g may cause false positive results.
Thyroid function tests: Large doses of salicylates may increase T 3 resin uptake and decrease serum concentrations of T 3 and T 4 when determined by radioimmunoassay. Salicylates may also affect TRH-induced TSH release determinations.
Pregnancy: The use of full-dose ASA during pregnancy should generally be avoided, particularly in the 3 rd trimester. ASA can affect hemostasis in both the mother and fetus, leading to higher risk of hemorrhage. Other possible effects include anemia and prolonged gestation and labor in the mother, and intrauterine growth retardation or premature closure of the ductus arteriosus in the fetus.
Low-dose ASA has been used therapeutically in very specific situations related to pregnancy, such as antiphospholipid syndrome and for prevention of pre-eclampsia; however more study is needed to establish the risk/benefit ratio of such therapy.
Lactation: ASA is excreted in breast milk in low concentrations. Because of the potential effects of ASA on nursing infants, caution is advised if ASA is used during lactation, particularly chronic high-dose therapy.
Geriatrics: Patients over 65years of age and frail or debilitated patients are more susceptible to many adverse effects of ASA, including gastrointestinal toxicity. Consideration should be given to using lower initial dosages in this patient group.
ASA should be used with extreme caution in patients with decreased renal function, bleeding tendencies, significant anemia, hypoprothrombinemia, thrombocytopenia, vitaminK deficiency or severe hepatic disease.
Gastrointestinal: Gastrointestinal toxicity may occur with the use of ASA (see Warnings). No studies, to date, have identified any group of patients not at risk of ulceration and bleeding. A history of serious gastrointestinal events and other factors such as ASA dosage, excessive alcohol intake, smoking, advanced age, female gender and concomitant corticosteroid or anticoagulant use have been associated with increased risk. Patients should be informed about the signs and symptoms of serious gastrointestinal toxicity and advised to contact their physician immediately if they occur. Because serious events can occur without warning symptoms, patients on long-term therapy should have periodic hemoglobin determinations in conjunction with vigilant follow up.
Hypersensitivity: ASA sensitivity is rare, occurring in less that 1% of the general population. It usually involves bronchospasm, urticaria, angioedema and rarely, shock and death. ASA sensitivity occurs in a higher percentage (approximately 10%) of adults with asthma, more often in women than men, and rarely in children. The syndrome of ASA-induced asthma usually begins as chronic nasal congestion with subsequent development of nasal polyps. Asthma and ASA sensitivity follow, with disease progression despite avoidance of ASA and cross-reacting drugs. The mechanism is thought to involve inhibition of intracellular cyclooxygenase (COX) in respiratory cells. Patients with ASA-induced asthma should avoid other drugs that inhibit COX, such as NSAIDs, but the majority can safely take other salicylates that do not inhibit COX enzymes. Cross-sensitivity with acetaminophen has been reported with frequencies of up to 34%. It is recommended that patients with ASA-induced asthma use low initial doses of acetaminophen (less than 1000 mg) with monitoring for 3 hours after initial doses.
Some patients with ASA-induced asthma have been desensitized with small incremental oral doses of ASA over the course of 2 to 3 days until 400 to 650 mg is tolerated, followed by maintenance doses of 80 to 325mg daily. Cross-desensitization to other reacting drugs also occurs when patients are desensitized to ASA.
Salicylism: Chronic salicylate intoxication (also known as salicylism) can occur when repeated large doses (>100mg/kg/day) are used for 2or more days (see Overdose).
Surgery: ASA should be discontinued at least one week prior to elective surgery because of increased risk of bleeding.
Drug Interactions : Analgesics: Concurrent long-term use of ASA and other analgesic-antipyretic agents such as acetaminophen may be associated with analgesic nephropathy (papillary necrosis and tubulointerstitial inflammation).
Antacids: Chronic high-dose use of antacids may increase renal elimination of salicylates through alkalinization of the urine.
Anticoagulants: Concomitant use of ASA and anticoagulants increases the risk of bleeding. Large doses of ASA may enhance the hypoprothrombinemic response to warfarin; however, ASA is used in selected patients with prosthetic heart valves or coronary artery disease in conjunction with warfarin, with appropriate monitoring.
Anticonvulsants: Large doses of ASA may increase phenytoin serum levels by inhibition of phenytoin metabolism.
Valproic acid may cause hypoprothrombinemia and inhibit platelet aggregation. Concomitant use of ASA and valproic acid may cause increased valproic acid levels and may lead to an increased risk of bleeding.
Antihyperglycemic Agents: ASA increases the antihyperglycemic response to sulfonylureas, especially chlorpropamide. Large doses of ASA may cause a decrease in blood glucose, which may alter the insulin requirements of diabetic patients.
Corticosteroids: Corticosteroids may decrease the serum salicylate concentrations through increased excretion. Concomitant use may also increase the risk of gastrointestinal side effects.
Methotrexate: Concurrent use of ASA and methotrexate may lead to higher methotrexate serum levels, mainly through competition for renal excretion.
Nonsteroidal Anti inflammatory Drugs (NSAIDs): Concomitant use of ASA and NSAIDs increases the risk of gastrointestinal side effects while providing no additional therapeutic benefit.
Uricosuric agents: ASA may decrease the uricosuric effects of sulfinpyrazone and probenecid.
Vancomycin: Use of vancomycin with ASA may increase the risk of ototoxicity.
VitaminC: Large doses of vitaminC may decrease the excretion of ASA because of acidification of the urine.
Zidovudine: ASA may increase the risk of zidovudine toxicity by decreasing the hepatic metabolism of zidovudine.
Drug/Lab Test Interactions : Bleeding time: ASA may prolong bleeding time for 4to 7days due to its effects on platelet aggregation.
Copper sulfate urine sugar tests: Daily doses of ASA greater than 2.4g may cause false positive results.
Thyroid function tests: Large doses of salicylates may increase T 3 resin uptake and decrease serum concentrations of T 3 and T 4 when determined by radioimmunoassay. Salicylates may also affect TRH-induced TSH release determinations.
Pregnancy: The use of full-dose ASA during pregnancy should generally be avoided, particularly in the 3 rd trimester. ASA can affect hemostasis in both the mother and fetus, leading to higher risk of hemorrhage. Other possible effects include anemia and prolonged gestation and labor in the mother, and intrauterine growth retardation or premature closure of the ductus arteriosus in the fetus.
Low-dose ASA has been used therapeutically in very specific situations related to pregnancy, such as antiphospholipid syndrome and for prevention of pre-eclampsia; however more study is needed to establish the risk/benefit ratio of such therapy.
Lactation: ASA is excreted in breast milk in low concentrations. Because of the potential effects of ASA on nursing infants, caution is advised if ASA is used during lactation, particularly chronic high-dose therapy.
Geriatrics: Patients over 65years of age and frail or debilitated patients are more susceptible to many adverse effects of ASA, including gastrointestinal toxicity. Consideration should be given to using lower initial dosages in this patient group.
Side Effects / Adverse Effects
Cardiovascular: Pulmonary edema may occur with chronic or acute ingestion of large doses.
Gastrointestinal: Ulcer, hemorrhage, dyspepsia, heartburn, epigastric distress, nausea, vomiting, diarrhea or abdominal pain may occur with increasing incidence at higher dosages (see Warnings, Precautions).
Hematologic: Leukopenia, thrombocytopenia, pancytopenia, agranulocytosis, aplastic anemia, purpura, eosinophilia associated with ASA-induced hepatoxicity have been reported rarely. Hematocrit and plasma iron concentration may be decreased with daily doses of3to 4g.
Hepatic: Reversible hepatoxicity, particularly in patients with juvenile rheumatoid arthritis and systemic lupus erythematosus, has been reported rarely.
Hypersensitivity: See Precautions, Hypersensitivity.
Otic: Tinnitus and hearing loss, usually completely reversible, may occur in patients receiving large doses of ASAor with long-term use and are dose related.
Dermatologic: Skin eruptions and lesions have been reported. Stevens-Johnson syndrome has rarely been associated with ASA.
Overdose: Acute ASA intoxication can result from single ingestions of 150 mg/kg or more. Chronic ASA intoxication, also known as salicylism, can occur during high-dose therapy, e.g., >100mg/kg/day for 2 or more days.
Symptoms:
Acute: The severity of symptoms depends on the size of the dose ingested. Mild to moderate toxicity usually results from ingestion of 150 to 300mg/kg; single doses of 300 to 500mg/kg can lead to severe intoxication and over 500mg/kg can be lethal. The main physiologic effects of ASA intoxication are: local gastrointestinal irritation; direct stimulation of respiratory centers leading to respiratory alkalosis; uncoupling of oxidative phosphorylation through interference with enzymes involved in the Krebs cycle, causing increased central and peripheral demand for glucose; metabolic acidosis; noncardiogenic pulmonary edema; confusion, delirium and seizures.
Chronic: Symptoms of chronic intoxication may include tinnitus, hearing loss, dizziness, confusion, drowsiness, hyperventilation, metabolic acidosis, respiratory alkalosis, tachycardia, nausea and vomiting.
Treatment: Acute: Treatment of acute ASA overdose consists of intensive symptomatic and supportive therapy aimed at removal of unabsorbed ASA from the gut, prevention of further ASA absorption, enhancement of ASA elimination and correction of fluid, electrolyte and acid-base disturbances. Specific recommendations regarding gut decontamination can vary considerably. Specialized references or a Poison Control Centre should be consulted for more information. Other measures may include: monitoring serum salicylate levels; correction of hypoglycemia, acidosis and hypokalemia with i.v. glucose, potassium and bicarbonate as required; management of seizures with i.v. diazepam; alkalinization of the urine; hemodialysis.
Chronic: Management of chronic ASA intoxication depends on the severity of the patient's clinical condition. Mild toxicity can usually be managed with reduction of the dose or discontinuation of ASA and symptomatic and supportive measures as required. Severe intoxication may require the same measures as for acute ingestions. Hemodialysis may be particularly beneficial, even in the absence of high serum salicylate levels.
Cardiovascular: Pulmonary edema may occur with chronic or acute ingestion of large doses.
Gastrointestinal: Ulcer, hemorrhage, dyspepsia, heartburn, epigastric distress, nausea, vomiting, diarrhea or abdominal pain may occur with increasing incidence at higher dosages (see Warnings, Precautions).
Hematologic: Leukopenia, thrombocytopenia, pancytopenia, agranulocytosis, aplastic anemia, purpura, eosinophilia associated with ASA-induced hepatoxicity have been reported rarely. Hematocrit and plasma iron concentration may be decreased with daily doses of3to 4g.
Hepatic: Reversible hepatoxicity, particularly in patients with juvenile rheumatoid arthritis and systemic lupus erythematosus, has been reported rarely.
Hypersensitivity: See Precautions, Hypersensitivity.
Otic: Tinnitus and hearing loss, usually completely reversible, may occur in patients receiving large doses of ASAor with long-term use and are dose related.
Dermatologic: Skin eruptions and lesions have been reported. Stevens-Johnson syndrome has rarely been associated with ASA.
Overdose: Acute ASA intoxication can result from single ingestions of 150 mg/kg or more. Chronic ASA intoxication, also known as salicylism, can occur during high-dose therapy, e.g., >100mg/kg/day for 2 or more days.
Symptoms:
Acute: The severity of symptoms depends on the size of the dose ingested. Mild to moderate toxicity usually results from ingestion of 150 to 300mg/kg; single doses of 300 to 500mg/kg can lead to severe intoxication and over 500mg/kg can be lethal. The main physiologic effects of ASA intoxication are: local gastrointestinal irritation; direct stimulation of respiratory centers leading to respiratory alkalosis; uncoupling of oxidative phosphorylation through interference with enzymes involved in the Krebs cycle, causing increased central and peripheral demand for glucose; metabolic acidosis; noncardiogenic pulmonary edema; confusion, delirium and seizures.
Chronic: Symptoms of chronic intoxication may include tinnitus, hearing loss, dizziness, confusion, drowsiness, hyperventilation, metabolic acidosis, respiratory alkalosis, tachycardia, nausea and vomiting.
Treatment: Acute: Treatment of acute ASA overdose consists of intensive symptomatic and supportive therapy aimed at removal of unabsorbed ASA from the gut, prevention of further ASA absorption, enhancement of ASA elimination and correction of fluid, electrolyte and acid-base disturbances. Specific recommendations regarding gut decontamination can vary considerably. Specialized references or a Poison Control Centre should be consulted for more information. Other measures may include: monitoring serum salicylate levels; correction of hypoglycemia, acidosis and hypokalemia with i.v. glucose, potassium and bicarbonate as required; management of seizures with i.v. diazepam; alkalinization of the urine; hemodialysis.
Chronic: Management of chronic ASA intoxication depends on the severity of the patient's clinical condition. Mild toxicity can usually be managed with reduction of the dose or discontinuation of ASA and symptomatic and supportive measures as required. Severe intoxication may require the same measures as for acute ingestions. Hemodialysis may be particularly beneficial, even in the absence of high serum salicylate levels.
Overdose
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Recommended Dosage
ASA should be taken with food or milk to minimize gastric irritation. Enteric-coated tablets may be used in patients with gastric intolerance to regular ASA tablets.
ASA should not be used 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.
ASA 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.
Enteric-coated preparations are not recommended for use in fever or in children under 2years.
Analgesic/Antipyretic: Oral: Adults: 325to 650mg 4to 6times daily as necessary.
Children: Authorities advise that ASA should not be used in children, teenagers and young adults with varicella or influenza. 10to 15mg/kg every 4to 6hours as needed up to a maximum of65mg/kg/day. Alternatively, TableI gives dosage recommendation for children.
Rectal: Adults: 650mg 4to 6times a day as required. Children: As for oral analgesic/antipyretic dose outlined above.
Anti-inflammatory: Dosage must be individualized according to the patient's response, tolerance and serum salicylate concentration.
Adults: Usual initial anti-inflammatory dose is 2.4to 3.6g daily in divided doses. Dosage may be increased gradually if necessary. The usual maintenance dose is 3.6 to 5.4 g daily in divided doses, but higher doses may be required.
Children (see Warnings): Usual initial anti-inflammatory dose is 60to 90mg/kg daily in divided doses, up to 100mg/kg daily.
Subsequently, adjust dosage slowly according to patient's tolerance to achieve optimal therapeutic response.
Serum salicylate concentration determinations are recommended if high dosage regimens are used, due to wide variations in pharmacokinetics. Usual serum salicylate concentrations for anti-inflammatory effect range from 1.1to 2.2mmol/L.
Platelet Antiaggregant: Doses of ASA ranging from 75 to 1300 mg daily have been used for prevention of ischemic events such as MI and stroke; there is no consensus in the current literature on the most appropriate dose for each indication. The following dosages represent the most commonly recommended regimens, based on the available evidence, and are expressed in accordance with available dosage forms. It has been suggested that in acute situations, regular ASA tablets, rather than enteric-coated ASA tablets, may be of greater benefit.
Acute MI: 160 to 325 mg daily, starting within 24 hours of onset of symptoms, for at least 30 days. Thereafter, ASA should be continued indefinitely at the recommended dose for secondary prevention (80 to 325 mg daily).
Secondary prevention following MI: 80 to 325 mg daily, continued indefinitely.
Primary prevention in patients with known coronary artery disease, chronic stable angina or unstable angina: 80 to 325 mg daily.
Secondary prevention in patients with a history of single or multiple TIAs or ischemic stroke: 325 mg daily. For patients who cannot tolerate 325 mg daily, one 81 mg enteric-coated tablet may be taken daily.
Vascular procedures: Recommendations vary according to procedure.
Prevention of thrombosis in patients with atrial fibrillation who cannot take warfarin: 325 mg daily.
Acute Pericarditis: 160 to 325 mg daily. Up to 650 mg every 4 to 6 hours may be required.
Kawasaki syndrome: Initial (febrile phase): 80to 100mg/kg per day in 4divided doses with serum level monitoring. Some patients may require higher doses to achieve thereapeutic levels because of impaired absorption during the febrile phase of the disease. When fever subsides, the dose should be reduced to 8to 10mg/kg once daily until 6to 10weeks after initial onset of illness. In patients with coronary involvement, ASA is often continued due to the potential benefit of its antithrombotic effects.
Acute Rheumatic Fever: Usual adult dose is 5to 8g daily and for children, 90to 130mg/kg/day administered in 4to 6divided doses for 1to 2weeks; then decreased to60to 70mg/kg/day for 1to 6weeks or until required; then gradually withdrawn over 1to 2weeks.
ASA should be taken with food or milk to minimize gastric irritation. Enteric-coated tablets may be used in patients with gastric intolerance to regular ASA tablets.
ASA should not be used 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.
ASA 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.
Enteric-coated preparations are not recommended for use in fever or in children under 2years.
Analgesic/Antipyretic: Oral: Adults: 325to 650mg 4to 6times daily as necessary.
Children: Authorities advise that ASA should not be used in children, teenagers and young adults with varicella or influenza. 10to 15mg/kg every 4to 6hours as needed up to a maximum of65mg/kg/day. Alternatively, TableI gives dosage recommendation for children.
Rectal: Adults: 650mg 4to 6times a day as required. Children: As for oral analgesic/antipyretic dose outlined above.
Anti-inflammatory: Dosage must be individualized according to the patient's response, tolerance and serum salicylate concentration.
Adults: Usual initial anti-inflammatory dose is 2.4to 3.6g daily in divided doses. Dosage may be increased gradually if necessary. The usual maintenance dose is 3.6 to 5.4 g daily in divided doses, but higher doses may be required.
Children (see Warnings): Usual initial anti-inflammatory dose is 60to 90mg/kg daily in divided doses, up to 100mg/kg daily.
Subsequently, adjust dosage slowly according to patient's tolerance to achieve optimal therapeutic response.
Serum salicylate concentration determinations are recommended if high dosage regimens are used, due to wide variations in pharmacokinetics. Usual serum salicylate concentrations for anti-inflammatory effect range from 1.1to 2.2mmol/L.
Platelet Antiaggregant: Doses of ASA ranging from 75 to 1300 mg daily have been used for prevention of ischemic events such as MI and stroke; there is no consensus in the current literature on the most appropriate dose for each indication. The following dosages represent the most commonly recommended regimens, based on the available evidence, and are expressed in accordance with available dosage forms. It has been suggested that in acute situations, regular ASA tablets, rather than enteric-coated ASA tablets, may be of greater benefit.
Acute MI: 160 to 325 mg daily, starting within 24 hours of onset of symptoms, for at least 30 days. Thereafter, ASA should be continued indefinitely at the recommended dose for secondary prevention (80 to 325 mg daily).
Secondary prevention following MI: 80 to 325 mg daily, continued indefinitely.
Primary prevention in patients with known coronary artery disease, chronic stable angina or unstable angina: 80 to 325 mg daily.
Secondary prevention in patients with a history of single or multiple TIAs or ischemic stroke: 325 mg daily. For patients who cannot tolerate 325 mg daily, one 81 mg enteric-coated tablet may be taken daily.
Vascular procedures: Recommendations vary according to procedure.
Prevention of thrombosis in patients with atrial fibrillation who cannot take warfarin: 325 mg daily.
Acute Pericarditis: 160 to 325 mg daily. Up to 650 mg every 4 to 6 hours may be required.
Kawasaki syndrome: Initial (febrile phase): 80to 100mg/kg per day in 4divided doses with serum level monitoring. Some patients may require higher doses to achieve thereapeutic levels because of impaired absorption during the febrile phase of the disease. When fever subsides, the dose should be reduced to 8to 10mg/kg once daily until 6to 10weeks after initial onset of illness. In patients with coronary involvement, ASA is often continued due to the potential benefit of its antithrombotic effects.
Acute Rheumatic Fever: Usual adult dose is 5to 8g daily and for children, 90to 130mg/kg/day administered in 4to 6divided doses for 1to 2weeks; then decreased to60to 70mg/kg/day for 1to 6weeks or until required; then gradually withdrawn over 1to 2weeks.
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Brand Name
ASA
ASA
Generic Name
Acetylsalicylic Acid
Acetylsalicylic Acid
General Indications
Analgesic Antipyretic Anti-inflammatory Platelet Aggregation
Analgesic Antipyretic Anti-inflammatory Platelet Aggregation
