Drug Interaction Report

Ibuprofen has a major potential interaction with Alcoholism.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with Alcoholism.

The use of ketorolac is contraindicated in patients with active peptic ulcers, recent gastrointestinal bleeding or perforation, or a history of peptic ulcer disease or gastrointestinal bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patients treated with ketorolac. Therapy with ketorolac should be considered and administered cautiously in patients with a history of GI inflammation or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of NSAIDs and seem to tolerate ulceration and bleeding less well than other individuals. Close monitoring for toxicity is recommended during ketorolac therapy, which should be limited to 5 days regardless of the route of administration.

Ibuprofen has a moderate potential interaction with Anemia.

Anemia has been reported in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). This may be due to fluid retention, occult/gross blood loss, or an incompletely described effect on erythropoiesis. Hemoglobin or hematocrit should be monitored in patients with any signs/symptoms of anemia or blood loss, especially during long-term therapy. NSAIDs may increase risk of bleeding events; comorbid conditions (e.g., coagulation disorders; concomitant use of warfarin/other anticoagulants, antiplatelet agents, serotonin/serotonin norepinephrine reuptake inhibitors) may increase this risk, and patients with these conditions should be monitored for signs of bleeding. Therapy with NSAIDs should be administered cautiously in patients with or predisposed to anemia. Clinical monitoring of hematopoietic function may be appropriate, particularly during chronic therapy.

The ketorolac in Toradol has a moderate potential interaction with Anemia.

Anemia has been reported in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). This may be due to fluid retention, occult/gross blood loss, or an incompletely described effect on erythropoiesis. Hemoglobin or hematocrit should be monitored in patients with any signs/symptoms of anemia or blood loss, especially during long-term therapy. NSAIDs may increase risk of bleeding events; comorbid conditions (e.g., coagulation disorders; concomitant use of warfarin/other anticoagulants, antiplatelet agents, serotonin/serotonin norepinephrine reuptake inhibitors) may increase this risk, and patients with these conditions should be monitored for signs of bleeding. Therapy with NSAIDs should be administered cautiously in patients with or predisposed to anemia. Clinical monitoring of hematopoietic function may be appropriate, particularly during chronic therapy.

Ibuprofen has a major potential interaction with Asthma.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are contraindicated in patients with history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs; severe, sometimes fatal, anaphylactic reactions to NSAIDs have been reported in such patients. A subpopulation of patients with asthma may have aspirin-sensitive asthma which may include chronic rhinosinusitis complicated by nasal polyps, severe potentially fatal bronchospasm, and/or intolerance to aspirin and other NSAIDs. Since cross-reactivity between aspirin and other NSAIDs has been reported in such aspirin-sensitive patients, therapy with any NSAID should be avoided in patients with this form of aspirin sensitivity. NSAIDs should be used with caution in patients with preexisting asthma (without known aspirin sensitivity), and these patients should be monitored for changes in the signs and symptoms of asthma.

The ketorolac in Toradol has a major potential interaction with Asthma.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are contraindicated in patients with history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs; severe, sometimes fatal, anaphylactic reactions to NSAIDs have been reported in such patients. A subpopulation of patients with asthma may have aspirin-sensitive asthma which may include chronic rhinosinusitis complicated by nasal polyps, severe potentially fatal bronchospasm, and/or intolerance to aspirin and other NSAIDs. Since cross-reactivity between aspirin and other NSAIDs has been reported in such aspirin-sensitive patients, therapy with any NSAID should be avoided in patients with this form of aspirin sensitivity. NSAIDs should be used with caution in patients with preexisting asthma (without known aspirin sensitivity), and these patients should be monitored for changes in the signs and symptoms of asthma.

The ketorolac in Toradol has a major potential interaction with Bleeding Disorder.

The use of ketorolac is considered by the manufacturer to be contraindicated in patients with suspected or confirmed cerebrovascular bleeding, hemorrhagic diathesis, incomplete hemostasis, or a high risk of bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in healthy individuals. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs, including ketorolac, should be administered cautiously in patients with significant active bleeding.

Ibuprofen has a moderate potential interaction with Bleeding Disorder.

Anemia has been reported in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). This may be due to fluid retention, occult/gross blood loss, or an incompletely described effect on erythropoiesis. Hemoglobin or hematocrit should be monitored in patients with any signs/symptoms of anemia or blood loss, especially during long-term therapy. NSAIDs may increase risk of bleeding events; comorbid conditions (e.g., coagulation disorders; concomitant use of warfarin/other anticoagulants, antiplatelet agents, serotonin/serotonin norepinephrine reuptake inhibitors) may increase this risk, and patients with these conditions should be monitored for signs of bleeding. Therapy with NSAIDs should be administered cautiously in patients with or predisposed to anemia. Clinical monitoring of hematopoietic function may be appropriate, particularly during chronic therapy.

Ibuprofen has a moderate potential interaction with Bleeding Disorder.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

The ketorolac in Toradol has a moderate potential interaction with Bleeding Disorder.

Anemia has been reported in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). This may be due to fluid retention, occult/gross blood loss, or an incompletely described effect on erythropoiesis. Hemoglobin or hematocrit should be monitored in patients with any signs/symptoms of anemia or blood loss, especially during long-term therapy. NSAIDs may increase risk of bleeding events; comorbid conditions (e.g., coagulation disorders; concomitant use of warfarin/other anticoagulants, antiplatelet agents, serotonin/serotonin norepinephrine reuptake inhibitors) may increase this risk, and patients with these conditions should be monitored for signs of bleeding. Therapy with NSAIDs should be administered cautiously in patients with or predisposed to anemia. Clinical monitoring of hematopoietic function may be appropriate, particularly during chronic therapy.

Ibuprofen has a major potential interaction with Cerebrovascular Insufficiency.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ketorolac in Toradol has a major potential interaction with Cerebrovascular Insufficiency.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ketorolac in Toradol has a major potential interaction with Coagulation Defects and Disorders.

The use of ketorolac is considered by the manufacturer to be contraindicated in patients with suspected or confirmed cerebrovascular bleeding, hemorrhagic diathesis, incomplete hemostasis, or a high risk of bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in healthy individuals. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs, including ketorolac, should be administered cautiously in patients with significant active bleeding.

Ibuprofen has a moderate potential interaction with Coagulation Defects and Disorders.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

Ibuprofen has a major potential interaction with Colonic Ulceration.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with Colonic Ulceration.

The use of ketorolac is contraindicated in patients with active peptic ulcers, recent gastrointestinal bleeding or perforation, or a history of peptic ulcer disease or gastrointestinal bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patients treated with ketorolac. Therapy with ketorolac should be considered and administered cautiously in patients with a history of GI inflammation or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of NSAIDs and seem to tolerate ulceration and bleeding less well than other individuals. Close monitoring for toxicity is recommended during ketorolac therapy, which should be limited to 5 days regardless of the route of administration.

Ibuprofen has a major potential interaction with Dehydration.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

The ketorolac in Toradol has a major potential interaction with Dehydration.

The use of ketorolac is contraindicated in patients with advanced renal impairment or increased risk for renal failure due to volume depletion. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). The use of NSAIDs may be associated with renal toxicities, including elevations in serum creatinine and BUN, tubular necrosis, glomerulitis, renal papillary necrosis, acute interstitial nephritis, nephrotic syndrome, and renal failure. In patients with prerenal conditions whose renal perfusion may be dependent on the function of renal prostaglandins, NSAIDs may precipitate overt renal decompensation via a dose-related inhibition of prostaglandin synthesis. Patients at greatest risk for this reaction include geriatric patients and those with impaired renal function, heart failure, liver dysfunction, or substantial volume and/or sodium depletion (e.g., due to diuretics). Therapy with ketorolac should be administered cautiously in such patients, and hypovolemia and hyponatremia should be corrected prior to initiating treatment. Clinical monitoring of renal function is recommended during therapy. If renal function declines or renal failure occurs, prompt discontinuation of ketorolac therapy will usually lead to recovery to the pretreatment state. Since ketorolac and its metabolites are eliminated by the kidney, a reduction to half the normal dosage with a maximum of 60 mg/day is recommended in patients with moderately impaired renal function to avoid drug accumulation.

Ibuprofen has a major potential interaction with Dermatitis, Drug-Induced.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious skin adverse reactions (e.g., Stevens-Johnson syndrome, toxic epidermal necrolysis, and exfoliative dermatitis), which can be fatal. NSAIDs can also cause fixed drug eruption, and may present as generalized bullous fixed drug eruption, which can be life-threatening. These serious events may occur without warning. Patients should be advised to discontinue the NSAID and seek medical attention promptly at the first sign of skin rash or any other sign of hypersensitivity. NSAIDs are contraindicated in patients with previous serious skin reactions to these drugs.

The ketorolac in Toradol has a major potential interaction with Dermatitis, Drug-Induced.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious skin adverse reactions (e.g., Stevens-Johnson syndrome, toxic epidermal necrolysis, and exfoliative dermatitis), which can be fatal. NSAIDs can also cause fixed drug eruption, and may present as generalized bullous fixed drug eruption, which can be life-threatening. These serious events may occur without warning. Patients should be advised to discontinue the NSAID and seek medical attention promptly at the first sign of skin rash or any other sign of hypersensitivity. NSAIDs are contraindicated in patients with previous serious skin reactions to these drugs.

Ibuprofen has a major potential interaction with Fluid Retention.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

The ketorolac in Toradol has a major potential interaction with Fluid Retention.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

Ibuprofen has a major potential interaction with Gastritis/Duodenitis.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with Gastritis/Duodenitis.

The use of ketorolac is contraindicated in patients with active peptic ulcers, recent gastrointestinal bleeding or perforation, or a history of peptic ulcer disease or gastrointestinal bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patients treated with ketorolac. Therapy with ketorolac should be considered and administered cautiously in patients with a history of GI inflammation or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of NSAIDs and seem to tolerate ulceration and bleeding less well than other individuals. Close monitoring for toxicity is recommended during ketorolac therapy, which should be limited to 5 days regardless of the route of administration.

Ibuprofen has a major potential interaction with Gastrointestinal Hemorrhage.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with Gastrointestinal Hemorrhage.

The use of ketorolac is contraindicated in patients with active peptic ulcers, recent gastrointestinal bleeding or perforation, or a history of peptic ulcer disease or gastrointestinal bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patients treated with ketorolac. Therapy with ketorolac should be considered and administered cautiously in patients with a history of GI inflammation or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of NSAIDs and seem to tolerate ulceration and bleeding less well than other individuals. Close monitoring for toxicity is recommended during ketorolac therapy, which should be limited to 5 days regardless of the route of administration.

Ibuprofen has a major potential interaction with Gastrointestinal Perforation.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with Gastrointestinal Perforation.

The use of ketorolac is contraindicated in patients with active peptic ulcers, recent gastrointestinal bleeding or perforation, or a history of peptic ulcer disease or gastrointestinal bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patients treated with ketorolac. Therapy with ketorolac should be considered and administered cautiously in patients with a history of GI inflammation or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of NSAIDs and seem to tolerate ulceration and bleeding less well than other individuals. Close monitoring for toxicity is recommended during ketorolac therapy, which should be limited to 5 days regardless of the route of administration.

Ibuprofen has a major potential interaction with Heart Failure.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

Ibuprofen has a major potential interaction with Heart Failure.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

The ketorolac in Toradol has a major potential interaction with Heart Failure.

The use of ketorolac is contraindicated in patients with advanced renal impairment or increased risk for renal failure due to volume depletion. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). The use of NSAIDs may be associated with renal toxicities, including elevations in serum creatinine and BUN, tubular necrosis, glomerulitis, renal papillary necrosis, acute interstitial nephritis, nephrotic syndrome, and renal failure. In patients with prerenal conditions whose renal perfusion may be dependent on the function of renal prostaglandins, NSAIDs may precipitate overt renal decompensation via a dose-related inhibition of prostaglandin synthesis. Patients at greatest risk for this reaction include geriatric patients and those with impaired renal function, heart failure, liver dysfunction, or substantial volume and/or sodium depletion (e.g., due to diuretics). Therapy with ketorolac should be administered cautiously in such patients, and hypovolemia and hyponatremia should be corrected prior to initiating treatment. Clinical monitoring of renal function is recommended during therapy. If renal function declines or renal failure occurs, prompt discontinuation of ketorolac therapy will usually lead to recovery to the pretreatment state. Since ketorolac and its metabolites are eliminated by the kidney, a reduction to half the normal dosage with a maximum of 60 mg/day is recommended in patients with moderately impaired renal function to avoid drug accumulation.

The ketorolac in Toradol has a major potential interaction with Heart Failure.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

Ibuprofen has a major potential interaction with High Blood Pressure.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

The ketorolac in Toradol has a major potential interaction with High Blood Pressure.

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs), including some topical formulations. NSAIDs (including topicals) can lead to new onset of hypertension or worsening of preexisting hypertension, either of which can contribute to the increased incidence of cardiovascular events. NSAIDs should be used with caution in patients with preexisting fluid retention, hypertension, or history of heart failure. NSAIDs should be avoided in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure; if an NSAID is used in such patients, they should be monitored for signs of worsening heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

Ibuprofen has a major potential interaction with History, Peptic Ulcer.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with History, Peptic Ulcer.

The use of ketorolac is contraindicated in patients with active peptic ulcers, recent gastrointestinal bleeding or perforation, or a history of peptic ulcer disease or gastrointestinal bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patients treated with ketorolac. Therapy with ketorolac should be considered and administered cautiously in patients with a history of GI inflammation or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of NSAIDs and seem to tolerate ulceration and bleeding less well than other individuals. Close monitoring for toxicity is recommended during ketorolac therapy, which should be limited to 5 days regardless of the route of administration.

Ibuprofen has a major potential interaction with History - Cerebrovascular Disease.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ketorolac in Toradol has a major potential interaction with History - Cerebrovascular Disease.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

Ibuprofen has a major potential interaction with History - Myocardial Infarction.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ketorolac in Toradol has a major potential interaction with History - Myocardial Infarction.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

Ibuprofen has a moderate potential interaction with Hyperkalemia.

Increases in serum potassium concentration (including hyperkalemia) have been reported with use of nonsteroidal anti-inflammatory drugs (NSAIDs), even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state. Caution is advised in patients with hyperkalemia.

The ketorolac in Toradol has a moderate potential interaction with Hyperkalemia.

Increases in serum potassium concentration (including hyperkalemia) have been reported with use of nonsteroidal anti-inflammatory drugs (NSAIDs), even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state. Caution is advised in patients with hyperkalemia.

Ibuprofen has a major potential interaction with Hyponatremia.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

The ketorolac in Toradol has a major potential interaction with Hyponatremia.

The use of ketorolac is contraindicated in patients with advanced renal impairment or increased risk for renal failure due to volume depletion. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). The use of NSAIDs may be associated with renal toxicities, including elevations in serum creatinine and BUN, tubular necrosis, glomerulitis, renal papillary necrosis, acute interstitial nephritis, nephrotic syndrome, and renal failure. In patients with prerenal conditions whose renal perfusion may be dependent on the function of renal prostaglandins, NSAIDs may precipitate overt renal decompensation via a dose-related inhibition of prostaglandin synthesis. Patients at greatest risk for this reaction include geriatric patients and those with impaired renal function, heart failure, liver dysfunction, or substantial volume and/or sodium depletion (e.g., due to diuretics). Therapy with ketorolac should be administered cautiously in such patients, and hypovolemia and hyponatremia should be corrected prior to initiating treatment. Clinical monitoring of renal function is recommended during therapy. If renal function declines or renal failure occurs, prompt discontinuation of ketorolac therapy will usually lead to recovery to the pretreatment state. Since ketorolac and its metabolites are eliminated by the kidney, a reduction to half the normal dosage with a maximum of 60 mg/day is recommended in patients with moderately impaired renal function to avoid drug accumulation.

Ibuprofen has a major potential interaction with Intestinal Anastomoses.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

Ibuprofen has a major potential interaction with Ischemic Heart Disease.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

The ketorolac in Toradol has a major potential interaction with Ischemic Heart Disease.

Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to 3 years duration have supported this increased risk. It is unclear from available data if the risk for cardiovascular thrombotic events is similar for all NSAIDs. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection; however, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious gastrointestinal events is increased. Physicians and patients should remain alert for the development of adverse cardiovascular events throughout the entire duration of therapy, even without prior cardiovascular symptoms. Patients should be advised to promptly seek medical attention if they experience symptoms of cardiovascular thrombotic events (including chest pain, shortness of breath, weakness, or slurring of speech).

NSAIDs are contraindicated in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

The use of NSAIDs should be avoided in patients with a recent myocardial infarction unless the benefits are expected to outweigh the risk of recurrent cardiovascular thrombotic events. If an NSAID is used in patients with a recent myocardial infarction, they should be monitored for signs of cardiac ischemia.

Ibuprofen has a major potential interaction with Liver Disease.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

Ibuprofen has a moderate potential interaction with Liver Disease.

Therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) should be administered cautiously in patients with preexisting liver disease. Periodic monitoring of liver function is recommended during prolonged therapy. NSAIDs are also highly protein-bound and some are extensively metabolized by the liver. Metabolic activity and/or plasma protein binding may be altered in patients with hepatic impairment. A dosage reduction may be required in some cases.

The ketorolac in Toradol has a moderate potential interaction with Liver Disease.

Therapy with nonsteroidal anti-inflammatory drugs (NSAIDs) should be administered cautiously in patients with preexisting liver disease. Periodic monitoring of liver function is recommended during prolonged therapy. NSAIDs are also highly protein-bound and some are extensively metabolized by the liver. Metabolic activity and/or plasma protein binding may be altered in patients with hepatic impairment. A dosage reduction may be required in some cases.

Ibuprofen has a major potential interaction with Noninfectious Colitis.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with Noninfectious Colitis.

The use of ketorolac is contraindicated in patients with active peptic ulcers, recent gastrointestinal bleeding or perforation, or a history of peptic ulcer disease or gastrointestinal bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patients treated with ketorolac. Therapy with ketorolac should be considered and administered cautiously in patients with a history of GI inflammation or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of NSAIDs and seem to tolerate ulceration and bleeding less well than other individuals. Close monitoring for toxicity is recommended during ketorolac therapy, which should be limited to 5 days regardless of the route of administration.

Ibuprofen has a major potential interaction with Peptic Ulcer.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with Peptic Ulcer.

The use of ketorolac is contraindicated in patients with active peptic ulcers, recent gastrointestinal bleeding or perforation, or a history of peptic ulcer disease or gastrointestinal bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can occur at any time, with or without warning symptoms, in patients treated with ketorolac. Therapy with ketorolac should be considered and administered cautiously in patients with a history of GI inflammation or alcoholism, particularly if they are elderly and/or debilitated, since such patients may be more susceptible to the GI toxicity of NSAIDs and seem to tolerate ulceration and bleeding less well than other individuals. Close monitoring for toxicity is recommended during ketorolac therapy, which should be limited to 5 days regardless of the route of administration.

Ibuprofen has a moderate potential interaction with Phenylketonuria.

Chewable products frequently may contain aspartame, which is metabolized in the gastrointestinal tract to phenylalanine. Motrin (brand of ibuprofen) chewable 50 mg and 100 mg tablets provide the equivalent of 3 mg and 6 mg of phenylalanine each, respectively. The aspartame/phenylalanine content should be considered when these and similar products are used in patients who must restrict their intake of phenylalanine (i.e. phenylketonurics).

Ibuprofen has a major potential interaction with Renal Dysfunction.

Long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) has resulted in renal papillary necrosis and other renal injury. Renal toxicity has been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion; in such patients, NSAIDs may cause a dose-dependent reduction in prostaglandin synthesis and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. Patients at greatest risk for this reaction include those with impaired renal function, dehydration, hypovolemia, heart failure, liver dysfunction; those taking diuretics, angiotensin-converting enzyme inhibitors, or angiotensin receptor blockers; and older adult patients. Discontinuation of NSAID therapy generally leads to recovery to the pretreatment state. No information is available regarding NSAID use in patients with advanced renal disease; the renal effects of NSAIDs may hasten the progression of renal dysfunction in patients with preexisting renal disease. Volume status should be corrected in dehydrated or hypovolemic patients prior to initiating treatment. Renal function should be monitored in patients with renal or liver dysfunction, heart failure, dehydration, or hypovolemia during therapy. NSAIDs should be avoided in patients with advanced renal disease unless the benefits are expected to outweigh the risk of worsening renal function; if an NSAID is used in such patients, they should be monitored for signs of worsening renal function.

The ketorolac in Toradol has a major potential interaction with Renal Dysfunction.

The use of ketorolac is contraindicated in patients with advanced renal impairment or increased risk for renal failure due to volume depletion. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). The use of NSAIDs may be associated with renal toxicities, including elevations in serum creatinine and BUN, tubular necrosis, glomerulitis, renal papillary necrosis, acute interstitial nephritis, nephrotic syndrome, and renal failure. In patients with prerenal conditions whose renal perfusion may be dependent on the function of renal prostaglandins, NSAIDs may precipitate overt renal decompensation via a dose-related inhibition of prostaglandin synthesis. Patients at greatest risk for this reaction include geriatric patients and those with impaired renal function, heart failure, liver dysfunction, or substantial volume and/or sodium depletion (e.g., due to diuretics). Therapy with ketorolac should be administered cautiously in such patients, and hypovolemia and hyponatremia should be corrected prior to initiating treatment. Clinical monitoring of renal function is recommended during therapy. If renal function declines or renal failure occurs, prompt discontinuation of ketorolac therapy will usually lead to recovery to the pretreatment state. Since ketorolac and its metabolites are eliminated by the kidney, a reduction to half the normal dosage with a maximum of 60 mg/day is recommended in patients with moderately impaired renal function to avoid drug accumulation.

Ibuprofen has a moderate potential interaction with Renal Dysfunction.

Increases in serum potassium concentration (including hyperkalemia) have been reported with use of nonsteroidal anti-inflammatory drugs (NSAIDs), even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state. Caution is advised in patients with hyperkalemia.

The ketorolac in Toradol has a moderate potential interaction with Renal Dysfunction.

Increases in serum potassium concentration (including hyperkalemia) have been reported with use of nonsteroidal anti-inflammatory drugs (NSAIDs), even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemic-hypoaldosteronism state. Caution is advised in patients with hyperkalemia.

Ibuprofen has a major potential interaction with Smoking.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can develop at any time, with or without warning symptoms. NSAIDs should be used with caution in patients with history of peptic ulcer disease and/or GI bleeding, as these patients had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other factors that increase risk of GI bleeding, such as: prolonged NSAID therapy; concomitant use of oral corticosteroids, antiplatelet agents (e.g., aspirin), anticoagulants, selective serotonin reuptake inhibitors; alcohol use; smoking; history of gastrointestinal surgery or anastomosis, older age; poor general health status; and advanced liver disease and/or coagulopathy. Particular vigilance is necessary when treating older adult or debilitated patients since most postmarketing reports of fatal GI events occurred in these patients.

The ketorolac in Toradol has a major potential interaction with Thrombocytopathy.

The use of ketorolac is considered by the manufacturer to be contraindicated in patients with suspected or confirmed cerebrovascular bleeding, hemorrhagic diathesis, incomplete hemostasis, or a high risk of bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in healthy individuals. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs, including ketorolac, should be administered cautiously in patients with significant active bleeding.

Ibuprofen has a moderate potential interaction with Thrombocytopathy.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

The ketorolac in Toradol has a major potential interaction with Thrombocytopenia.

The use of ketorolac is considered by the manufacturer to be contraindicated in patients with suspected or confirmed cerebrovascular bleeding, hemorrhagic diathesis, incomplete hemostasis, or a high risk of bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in healthy individuals. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs, including ketorolac, should be administered cautiously in patients with significant active bleeding.

Ibuprofen has a moderate potential interaction with Thrombocytopenia.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

The ketorolac in Toradol has a major potential interaction with Vitamin K Deficiency.

The use of ketorolac is considered by the manufacturer to be contraindicated in patients with suspected or confirmed cerebrovascular bleeding, hemorrhagic diathesis, incomplete hemostasis, or a high risk of bleeding. Ketorolac is a potent nonsteroidal anti-inflammatory drug (NSAID). NSAIDs reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in healthy individuals. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs, including ketorolac, should be administered cautiously in patients with significant active bleeding.

Ibuprofen has a moderate potential interaction with Vitamin K Deficiency.

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.