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Toradol (ketorolac) Disease Interactions

There are 10 disease interactions with Toradol (ketorolac):


Ketorolac (Includes Toradol) ↔ Gi Toxicity

Severe Potential Hazard, High plausibility

Applies to: Duodenitis/Gastritis, Gastrointestinal Hemorrhage, Gastrointestinal Perforation, History - Peptic Ulcer, Peptic Ulcer, Alcoholism, Colitis/Enteritis (Noninfectious), 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.


  1. Fuller DK, Kalekas PJ "Ketorolac and gastrointestinal ulceration." Ann Pharmacother 27 (1993): 978-9
  2. Estes LL, Fuhs DW, Heaton AH, Butwinick CS "Gastric ulcer perforation associated with the use of injectable ketorolac." Ann Pharmacother 27 (1993): 42-3
  3. Wiedrick JE, Friesen EG, Garton AM, Otten NH "Upper gastrointestinal bleeding associated with oral ketorolac therapy." Ann Pharmacother 28 (1994): 1109
View all 13 references

Ketorolac (Includes Toradol) ↔ Platelet Aggregation Inhibition

Severe Potential Hazard, Moderate plausibility

Applies to: Bleeding, Coagulation Defect, Thrombocytopathy, Thrombocytopenia, 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.


  1. "Product Information. Toradol (ketorolac)." Roche Laboratories, Nutley, NJ.
  2. Litvak KM, McEvoy GK "Ketorolac, an injectable nonnarcotic analgesic." Clin Pharm 9 (1990): 921-35
  3. Concannon MJ, Meng L, Welsh CF, Puckett CL "Inhibition of perioperative platelet aggregation using toradol (ketorolac)." Ann Plast Surg 30 (1993): 264-6
View all 5 references

Ketorolac (Includes Toradol) ↔ Renal Dysfunction

Severe Potential Hazard, Moderate plausibility

Applies to: Congestive Heart Failure, Dehydration, Renal Dysfunction, 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.


  1. Quan DJ, Kayser SR "Ketorolac induced acute renal failure following a single dose." J Toxicol Clin Toxicol 32 (1994): 305-9
  2. Brocks DR, Jamali F "Clinical pharmacokinetics of ketorolac tromethamine." Clin Pharmacokinet 23 (1992): 415-27
  3. Buller GK, Perazella MA "Acute renal failure and ketorolac." Ann Intern Med 127 (1997): 493
View all 22 references

Nsaids (Includes Toradol) ↔ Asthma

Severe Potential Hazard, High plausibility

Applies to: Asthma

Approximately 10% of patients with asthma may have aspirin-sensitive asthma, characterized by nasal polyposis, pansinusitis, eosinophilia, and precipitation of asthma and rhinitis attacks after ingestion of aspirin. The use of aspirin in these patients has been associated with severe bronchospasm and fatal anaphylactoid reactions. Since cross-sensitivity has been noted between aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), therapy with any NSAID should be avoided in asthmatic patients with a history of aspirin or other NSAID sensitivity, and administered cautiously in all patients with preexisting asthma. Prior to initiating therapy with NSAIDs, patients should be questioned about previous allergic-type reactions to these agents. Salicylate salts, salsalate, salicylamide, and acetaminophen may be appropriate alternatives in patients with a history of NSAID-induced bronchospasm, since cross-sensitivity to these agents appears to be low. However, cross-sensitivity has been demonstrated occasionally with high dosages of these agents (e.g., acetaminophen >= 1000 mg), thus it may be appropriate to initiate therapy with low dosages and increase gradually. There is some evidence suggesting that COX-2 inhibitors may be safely used in patients with aspirin-sensitive asthma, although the labeling for these products contraindicate such use. If necessary, aspirin desensitization may also be attempted in some patients under medical surveillance.


  1. "Product Information. Naprosyn (naproxen)." Syntex Laboratories Inc, Palo Alto, CA.
  2. Stevenson DD, Hougham AJ, Schrank PJ, Goldlust MB, Wilson RR "Salsalate cross-sensitivity in aspirin-sensitive patients with asthma." J Allergy Clin Immunol 86 (1990): 749-58
  3. "Product Information. Voltaren (diclofenac)." Novartis Pharmaceuticals, East Hanover, NJ.
View all 38 references

Nsaids (Includes Toradol) ↔ Fluid Retention

Severe Potential Hazard, Moderate plausibility

Applies to: Congestive Heart Failure, Hypertension, Fluid Retention

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Therapy with NSAIDs should be administered cautiously in patients with preexisting fluid retention, hypertension, or a history of heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.


  1. Heerdink ER, Leufkens HG, Herings RM, Ottervanger JP, Stricker BH, Bakker A "NSAIDs associated with increased risk of congestive heart failure in elderly patients taking diuretics." Arch Intern Med 158 (1998): 1108-12
  2. "Product Information. Orudis (ketoprofen)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  3. Lewis RV, Toner JM, Jackson PR, Ramsay LE "Effects of indomethacin and sulindac on blood pressure of hypertensive patients." Br Med J 292 (1986): 934-5
View all 29 references

Nsaids (Includes Toradol) ↔ Rash

Severe Potential Hazard, High plausibility

Applies to: Dermatitis - Drug-Induced

Severe, potentially fatal dermatologic reactions such as Stevens-Johnson syndrome, toxic epidermal necrolysis, and other exfoliative dermatitis have been associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs). These events may occur without warning. Patients should be advised to discontinue the NSAID and seek medical attention promptly at the first sign of rash, blisters, fever, itching, or any other sign of hypersensitivity.


  1. "Product Information. Indocin (indomethacin)." Merck & Co, Inc, West Point, PA.
  2. "Product Information. Tolectin (tolmetin)." McNeil Pharmaceutical, Raritan, NJ.
  3. "Product Information. Relafen (nabumetone)." SmithKline Beecham, Philadelphia, PA.
View all 16 references

Nsaids (Includes Toradol) ↔ Thrombosis

Severe Potential Hazard, High plausibility

Applies to: Cerebrovascular Insufficiency, History - Cerebrovascular Disease, History - Myocardial Infarction, Ischemic Heart Disease

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) may be associated with an increased risk of cardiovascular thrombotic events such as myocardial infarction and stroke, which can be fatal. The risk may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to three years duration have supported this association. Although not all NSAIDs have been studied, investigators believe it may be a class effect, and that the risk may be similar for all NSAIDs, both COX-2 selective and nonselective. 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 GI events is increased. Patients should be advised to promptly seek medical attention if they experience symptoms that could indicate a cardiovascular thrombotic event such as chest pain, shortness of breath, weakness, and slurring of speech.

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


  1. "Product Information. Vioxx (rofecoxib)." Merck & Co, Inc, West Point, PA.
  2. Fitzgerald GA, Patrono C "The coxibs, selective inhibitors of cyclooxsygenase-2." N Engl J Med 345 (2001): 433-42
  3. Marcus AJ, Broekman MJ, Pinsky DJ "COX inhibitors and thromboregulation." N Engl J Med 347 (2002): 1025-6
View all 6 references

Nsaids (Includes Toradol) ↔ Anemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Anemia, Bleeding

Dose-dependent decreases in serum hemoglobin and hematocrit have been observed in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). Anemia has been reported occasionally. The mechanism may involve NSAID-induced fluid retention or gastrointestinal blood loss, or an incompletely described effect on erythropoiesis. The decreases in hemoglobin concentration tend to be slight with average doses but may exceed 1 g/dL when large doses are given, such as those used to treat osteoarthritis or rheumatoid arthritis. Although these effects are generally not clinically important in otherwise healthy individuals, they may be relevant in patients with preexisting anemia or substantial blood loss. 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.


  1. "Product Information. Relafen (nabumetone)." SmithKline Beecham, Philadelphia, PA.
  2. Salom IL, Jacob G, Jallad N, Perdomo CA, Mullane JF, Weidler D "Gastrointestinal microbleeding associated with the use of etodolac, ibuprofen, indomethacin, and naproxen in normal males." J Clin Pharmacol 24 (1984): 240-6
  3. Squires JE, Mintz PD, Clark S "Tolmetin-induced hemolysis." Transfusion 25 (1985): 410-3
View all 49 references

Nsaids (Includes Toradol) ↔ Hepatotoxicity

Moderate Potential Hazard, Moderate plausibility

Applies to: Liver Disease

Borderline elevations of serum transaminases, LDH, and alkaline phosphatase have been reported in up to 15% of patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). These abnormalities may progress, remain unchanged, or regress with continuing therapy. Notable liver enzyme elevations exceeding 3 times the upper limit of normal have been reported in approximately 1% of patients in clinical trials. In addition, rare cases of severe hepatotoxicity, including liver necrosis, hepatic failure, jaundice and fatal fulminant hepatitis, have been reported. Therapy with 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.


  1. "Product Information. Orudis (ketoprofen)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  2. Dhand AK, LaBrecque DR, Metzger J "Sulindac (clinoril) hepatitis." Gastroenterology 80 (1981): 585-6
  3. Lockwood GF, Albert KS, Szpunar GJ, Wagner JG "Pharmacokinetics of ibuprofen in man III: plasma protein binding." J Pharmacokinet Biopharm 11 (1983): 469-82
View all 92 references

Nsaids (Includes Toradol) ↔ Hyperkalemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Hyperkalemia, Renal Dysfunction

Increase in serum potassium concentration, including hyperkalemia, have been reported with use of NSAIDs, even in some patients without renal impairment. In patients with normal renal function, these effects have been attributed to a hyporeninemic- hypoaldosteronism state.

Toradol (ketorolac) drug Interactions

There are 453 drug interactions with Toradol (ketorolac)

Toradol (ketorolac) alcohol/food Interactions

There are 2 alcohol/food interactions with Toradol (ketorolac)

Drug Interaction Classification

The classifications below are a general guideline only. It is difficult to determine the relevance of a particular drug interaction to any individual given the large number of variables.

Major Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.

Do not stop taking any medications without consulting your healthcare provider.

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