and administration , and adverse reactions ). patients should be switched to alternative analgesics as soon as possible, but ketorolac tromethamine therapy is not to exceed 5 days.

stinal problems, such as dyspepsia, are common and may also occur at any time during nsaid therapy. the incidence and severity of gastrointestinal complications increases with increasing dose of, and duration of treatment with ketorolac tromethamine. do not use ketorolac tromethamine for more than five days. however, even short-term therapy is not without risk. in addition to past history of ulcer disease, other factors that increase the risk for gi bleeding in patients treated with nsaids include concomitant use of oral corticosteroids, or anticoagulants, longer duration of nsaid therapy, smoking, use of alcohol, older age, and poor general health status. most spontaneous reports of fatal gi events are in elderly or debilitated patients and therefore, special care should be taken in treating this population. to minimize the potential risk for an adverse gi event, the lowest effective dose should be used for the shortest possible duration. patients and physicians should remain alert for signs and symptoms of gi ulceration and bleeding during nsaid therapy and promptly initiate additional evaluation and treatment if a serious gi adverse event is suspected. this should include discontinuation of ketorolac tromethamine until a serious gi adverse event is ruled out. for high risk patients, alternate therapies that do not involve nsaids should be considered. nsaids should be given with care to patients with a history of inflammatory bowel disease (ulcerative colitis, crohn's disease) as their condition may be exacerbated. hemorrhage because prostaglandins play an important role in hemostasis and nsaids affect platelet aggregation as well, use of ketorolac tromethamine in patients who have coagulation disorders should be undertaken very cautiously, and those patients should be carefully monitored. patients on therapeutic doses of anticoagulants (e.g., heparin or dicumarol derivatives) have an increased risk of bleeding complications if given ketorolac tromethamine concurrently; therefore, physicians should administer such concomitant therapy only extremely cautiously. the concurrent use of ketorolac tromethamine and therapy that affects hemostasis, including prophylactic low-dose heparin (2500 to 5000 units every 12 hours), warfarin and dextrans have not been studied extensively, but may also be associated with an increased risk of bleeding. until data from such studies are available, physicians should carefully weigh the benefits against the risks, and use such concomitant therapy in these patients only extremely cautiously. patients receiving therapy that affects hemostasis should be monitored closely. in postmarketing experience, postoperative hematomas and other signs of wound bleeding have been reported in association with the peri-operative use of intravenous or intramuscular dosing of ketorolac tromethamine. therefore, peri-operative use of ketorolac tromethamine should be avoided and postoperative use be undertaken with caution when hemostasis is critical (see precautions ). renal effects long-term administration of nsaids has resulted in renal papillary necrosis and other renal injury. renal toxicity has also been seen in patients in whom renal prostaglandins have a compensatory role in the maintenance of renal perfusion. in these patients, administration of a nsaid may cause a dose-dependent reduction in prostaglandin formation and, secondarily, in renal blood flow, which may precipitate overt renal decompensation. patients at greatest risk of this reaction are those with impaired renal function, heart failure, liver dysfunction, those taking diuretics and ace inhibitors, and the elderly. discontinuation of nsaid therapy is usually followed by recovery to the pretreatment state. ketorolac tromethamine and its metabolites are eliminated primarily by the kidneys, which, in patients with reduced creatinine clearance, will result in diminished clearance of the drug (see clinical pharmacology ). therefore, ketorolac tromethamine should be used with caution in patients with impaired renal function (see dosage and administration ) and such patients should be followed closely. with the use of ketorolac tromethamine, there have been reports of acute renal failure, interstitial nephritis and nephrotic syndrome. impaired renal function ketorolac tromethamine is contraindicated in patients with serum creatinine concentrations indicating advanced renal impairment (see contraindications ). ketorolac tromethamine should be used with caution in patients with impaired renal function or a history of kidney disease because it is a potent inhibitor of prostaglandin synthesis. because patients with underlying renal insufficiency are at increased risk of developing acute renal decompensation or failure, the risks and benefits should be assessed prior to giving ketorolac tromethamine to these patients. anaphylactoid reactions as with other nsaids, anaphylactoid reactions may occur in patients without known prior exposure to ketorolac tromethamine. ketorolac tromethamine should not be given to patients with the aspirin triad. this symptom complex typically occurs in asthmatic patients who experience rhinitis with or without nasal polyps, or who exhibit severe, potentially fatal bronchospasm after taking aspirin or other nsaids (see contraindications and precautions - pre-existing asthma ). emergency help should be sought in cases where an anaphylactoid reaction occurs. cardiovascular effects cardiovascular thrombotic events clinical trials of several cox-2 selective and nonselective nsaids of up to three years duration have shown an increased risk of serious cardiovascular (cv) thrombotic events, including myocardial infarction (mi) and stroke, which can be fatal. based on available data, it is unclear that the risk for cv thrombotic events is similar for all nsaids. the relative increase in serious cv thrombotic events over baseline conferred by nsaid use appears to be similar in those with and without known cv disease or risk factors for cv disease. however, patients with known cv disease or risk factors had a higher absolute incidence of excess serious cv thrombotic events, due to their increased baseline rate. some observational studies found that this increased risk of serious cv thrombotic events began as early as the first few weeks of treatment. the increase in cv thrombotic risk has been observed most consistently at higher doses. to minimize the potential risk for an adverse cv event in nsaid-treated patients, use the lowest effective dose for the shortest duration possible. physicians and patients should remain alert for the development of such events, throughout the entire treatment course, even in the absence of previous cv symptoms. patients should be informed about the symptoms of serious cv events and the steps to take if they occur. there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cv thrombotic events associated with nsaid use. the concurrent use of aspirin and an nsaid, such as ketorolac tromethamine, increases the risk of serious gastrointestinal (gi) events (see warnings ). status post coronary artery bypass graft (cabg) surgery two large, controlled 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. nsaids are contraindicated in the setting of cabg surgery (see contraindications ). post-mi patients observational studies conducted in the danish national registry have demonstrated that patients treated with nsaids in the post-mi period were at increased risk of reinfarction, cv-related death, and all-cause mortality beginning in the first week of treatment. in this same cohort, the incidence of death in the first year post mi was 20 per 100 person years in nsaid-treated patients compared to 12 per 100 person years in non-nsaid exposed patients. although the absolute rate of death declined somewhat after the first year post-mi, the increased relative risk of death in nsaid users persisted over at least the next four years follow-up. avoid the use of ketorolac tromethamine in patients with a recent mi unless the benefits are expected to outweigh the risk of recurrent cv thrombotic events. if ketorolac tromethamine is used in patients with a recent mi, monitor patients for signs of cardiac ischemia. hypertension nsaids, including ketorolac tromethamine, can lead to onset of new hypertension or worsening of pre-existing hypertension, either of which may contribute to the increased incidence of cv events. patients taking thiazides or loop diuretics may have impaired response to these therapies when taking nsaids. nsaids, including ketorolac tromethamine, should be used with caution in patients with hypertension. blood pressure (bp) should be monitored closely during the initiation of nsaid treatment and throughout the course of therapy. heart failure and edema the coxib and traditional nsaid trialists' collaboration meta-analysis of randomized controlled trials demonstrated an approximately two-fold increase in hospitalizations for heart failure in cox-2 selective‑treated patients and nonselective nsaid-treated patients compared to placebo-treated patients. in a danish national registry study of patients with heart failure, nsaid use increased the risk of mi, hospitalization for heart failure, and death. additionally, fluid retention and edema have been observed in some patients treated with nsaids. use of ketorolac tromethamine may blunt the cv effects of several therapeutic agents used to treat these medical conditions (e.g., diuretics, ace inhibitors, or angiotensin receptor blockers (arbs) (see precautions – drug interactions ). avoid the use of ketorolac tromethamine in patients with severe heart failure unless the benefits are expected to outweigh the risk of worsening heart failure. if ketorolac tromethamine is used in patients with severe heart failure, monitor patients for signs of worsening heart failure. skin reactions nsaids, including ketorolac tromethamine, can cause serious skin adverse events such as exfoliative dermatitis, stevens-johnson syndrome (sjs), and toxic epidermal necrolysis (ten), which can be fatal. these serious events may occur without warning. patients should be informed about the signs and symptoms of serious skin manifestations and use of the drug should be discontinued at the first appearance of skin rash or any other sign of hypersensitivity. drug reaction with eosinophilia and systemic symptoms (dress) drug reaction with eosinophilia and systemic symptoms (dress) has been reported in patients taking nsaids such as ketorolac tromethamine. some of these events have been fatal or life-threatening. dress typically, although not exclusively, presents with fever, rash, lymphadenopathy, and/or facial swelling. other clinical manifestations may include hepatitis, nephritis, hematological abnormalities, myocarditis, or myositis. sometimes symptoms of dress may resemble an acute viral infection. eosinophilia is often present. because this disorder is variable in its presentation, other organ systems not noted here may be involved. it is important to note that early manifestations of hypersensitivity, such as fever or lymphadenopathy, may be present even though rash is not evident. if such signs or symptoms are present, discontinue ketorolac tromethamine and evaluate the patient immediately. fetal toxicity premature closure of fetal ductus arteriosus: avoid use of nsaids, including ketorolac tromethamine, in pregnant women at about 30 weeks gestation and later. nsaids including ketorolac tromethamine, increase the risk of premature closure of the fetal ductus arteriosus at approximately this gestational age. oligohydramnios/neonatal renal impairment: use of nsaids, including ketorolac tromethamine, at about 20 weeks gestation or later in pregnancy may cause fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. these adverse outcomes are seen, on average, after days to weeks of treatment, although oligohydramnios has been infrequently reported as soon as 48 hours after nsaid initiation. oligohydramnios is often, but not always, reversible with treatment discontinuation. complications of prolonged oligohydramnios may, for example, include limb contractures and delayed lung maturation. in some postmarketing cases of impaired neonatal renal function, invasive procedures such as exchange transfusion or dialysis were required. if nsaid treatment is necessary between about 20 weeks and 30 weeks gestation, limit ketorolac tromethamine use to the lowest effective dose and shortest duration possible. consider ultrasound monitoring of amniotic fluid if ketorolac tromethamine treatment extends beyond 48 hours. discontinue ketorolac tromethamine if oligohydramnios occurs and follow up according to clinical practice (see precautions; pregnancy ) .

on of use of intravenous or intramuscular dosing of ketorolac tromethamine and oral ketorolac tromethamine is not to exceed 5 days. ketorolac tromethamine injection ketorolac tromethamine injection may be used as a single or multiple dose on a regular or "as needed" schedule for the management of moderately severe, acute pain that requires analgesia at the opioid level, usually in a postoperative setting. hypovolemia should be corrected prior to the administration of ketorolac tromethamine (see warnings – renal effects ). patients should be switched to alternative analgesics as soon as possible, but ketorolac tromethamine therapy is not to exceed 5 days. when administering ketorolac tromethamine injection, the intravenous bolus must be given over no less than 15 seconds. the intramuscular administration should be given slowly and deeply into the muscle. the analgesic effect begins in ~30 minutes with maximum effect in 1 to 2 hours after dosing intravenous or intramuscular. duration of analgesic effect is usually 4 to 6 hours. single-dose treatment: the following regimen should be limited to single administration use only intramuscular dosing • patients <65 years of age: one dose of 60 mg. • patients ≥65 years of age, renally impaired and/or less than 50 kg (110 lbs) of body weight: one dose of 30 mg. intravenous dosing • patients <65 years of age: one dose of 30 mg. • patients ≥65 years of age, renally impaired and/or less than 50 kg (110 lbs) of body weight: one dose of 15 mg. multiple-dose treatment ( intravenous or intramuscular) • patients <65 years of age: the recommended dose is 30 mg ketorolac tromethamine injection every 6 hours. the maximum daily dose for these populations should not exceed 120 mg. • for patients ≥65 years of age, renally impaired patients (see warnings ), and patients less than 50 kg (110 lbs): the recommended dose is 15 mg ketorolac tromethamine injection every 6 hours. the maximum daily dose for these populations should not exceed 60 mg. for breakthrough pain, do not increase the dose or the frequency of ketorolac tromethamine. consideration should be given to supplementing these regimens with low doses of opioids "as needed" unless otherwise contraindicated. pharmaceutical information for ketorolac tromethamine injection ketorolac tromethamine injection should not be mixed in a small volume (e.g., in a syringe) with morphine sulfate, meperidine hydrochloride, promethazine hydrochloride or hydroxyzine hydrochloride; this will result in precipitation of ketorolac from solution. note: parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit.

other experiences: abnormal renal function anemia dizziness drowsiness edema elevated liver enzymes headaches hypertension increased bleeding time injection site pain pruritus purpura rashes tinnitus sweating additional adverse experiences reported occasionally (<1% in patients taking ketorolac tromethamine or other nsaids in clinical trials) include: body as a whole: fever, infections, sepsis cardiovascular: congestive heart failure, palpitation, pallor, tachycardia, syncope dermatologic: alopecia, photosensitivity, urticaria gastrointestinal: anorexia, dry mouth, eructation, esophagitis, excessive thirst, gastritis, glossitis, hematemesis, hepatitis, increased appetite, jaundice, melena, rectal bleeding hemic and lymphatic: ecchymosis, eosinophilia, epistaxis, leukopenia, thrombocytopenia metabolic and nutritional: weight change nervous system: abnormal dreams, abnormal thinking, anxiety, asthenia, confusion, depression, euphoria, extrapyramidal symptoms, hallucinations, hyperkinesis, inability to concentrate, insomnia, nervousness, paresthesia, somnolence, stupor, tremors, vertigo, malaise reproductive, female: infertility respiratory: asthma, cough, dyspnea, pulmonary edema, rhinitis special senses: abnormal taste, abnormal vision, blurred vision, hearing loss urogenital: cystitis, dysuria, hematuria, increased urinary frequency, interstitial nephritis, oliguria/polyuria, proteinuria, renal failure, urinary retention other rarely observed reactions (reported from postmarketing experience in patients taking ketorolac tromethamine or other nsaids) are: body as a whole: angioedema, death, hypersensitivity reactions such as anaphylaxis, anaphylactoid reaction, laryngeal edema, tongue edema (see warnings ), myalgia cardiovascular: arrhythmia, bradycardia, chest pain, flushing, hypotension, myocardial infarction, vasculitis dermatologic: exfoliative dermatitis, erythema multiforme, lyell's syndrome, bullous reactions including stevens-johnson syndrome and toxic epidermal necrolysis gastrointestinal: acute pancreatitis, liver failure, ulcerative stomatitis, exacerbation of inflammatory bowel disease (ulcerative colitis, crohn's disease) hemic and lymphatic: agranulocytosis, aplastic anemia, hemolytic anemia, lymphadenopathy, pancytopenia, post operative wound hemorrhage (rarely requiring blood transfusion — see boxed warning , warnings , and precautions ) metabolic and nutritional: hyperglycemia, hyperkalemia, hyponatremia nervous system: aseptic meningitis, convulsions, coma, psychosis respiratory: bronchospasm, respiratory depression, pneumonia special senses: conjunctivitis urogenital: flank pain with or without hematuria and/or azotemia, hemolytic uremic syndrome postmarketing surveillance study a large postmarketing observational, nonrandomized study, involving approximately 10,000 patients receiving ketorolac tromethamine, demonstrated that the risk of clinically serious gastrointestinal (gi) bleeding was dose-dependent (see tables 3a and 3b ). this was particularly true in elderly patients who received an average daily dose greater than 60 mg/day of ketorolac tromethamine (see table 3a ). table 3: incidence of clinically serious g.i. bleeding as related to age, total daily dose, and history of g.i. perforation, ulcer, bleeding (pub) after up to 5 days of treatment with ketorolac tromethamine injection a. adult patients without history of pub age of patients total daily dose of ketorolac tromethamine injection ≤60 mg >60 to 90 mg >90 to 120 mg >120 mg <65 years of age 0.4% 0.4% 0.9% 4.6% ≥65 years of age 1.2% 2.8% 2.2% 7.7% b. adult patients with history of pub age of patients total daily dose of ketorolac tromethamine injection ≤60 mg >60 to 90 mg >90 to 120 mg >120 mg <65 years of age 2.1% 4.6% 7.8% 15.4% ≥65 years of age 4.7% 3.7% 2.8% 25.0%

he pharmacokinetics of ketorolac tromethamine, following intravenous, intramuscular, and oral doses of ketorolac tromethamine are compared in table 1 . in adults, the extent of bioavailability following administration of the oral and intramuscular forms of ketorolac tromethamine was equal to that following an intravenous bolus. table 1: table of approximate average pharmacokinetic parameters (mean±sd) following oral, intramuscular and intravenous doses of ketorolac tromethamine oral † intramuscular* intravenous bolus ‡ pharmacokinetic parameters (units) 10 mg 15 mg 30 mg 60 mg 15 mg 30 mg bioavailability (extent) 100% t max 1 (min) 44±34 33±21** 44±29 33±21** 1.1±0.7** 2.9±1.8 c max 2 (mcg/ml) [single-dose] 0.87±0.22 1.14±0.32** 2.42±0.68 4.55±1.27** 2.47±0.51** 4.65±0.96 c max (mcg/ml) [steady state qid] 1.05±0.26** 1.56±0.44** 3.11±0.87** n/a †† 3.09±1.17** 6.85±2.61 c min 3 (mcg/ml) [steady state qid] 0.29±0.07** 0.47±0.13** 0.93±0.26** n/a 0.61±0.21** 1.04±0.35 c avg 4 (mcg/ml) [steady state qid] 0.59±0.2** 0.94±0.29** 1.88±0.59** n/a 1.09±0.3** 2.17±0.59 v β 5 (l/kg) ———— 0.175±0.039 ———— 0.210±0.044 % dose metabolized = <50 % dose excreted in urine = 91 % dose excreted in feces = 6 % plasma protein binding = 99 1 time-to-peak plasma concentration 2 peak plasma concentration 3 trough plasma concentration 4 average plasma concentration 5 volume of distribution † derived from oral pharmacokinetic studies in 77 normal fasted volunteers * derived from intramuscular pharmacokinetic studies in 54 normal volunteers ‡ derived from intravenous pharmacokinetic studies in 24 normal volunteers †† not applicable because 60 mg is only recommended as a single dose ** mean value was simulated from observed plasma concentration data and standard deviation was simulated from percent coefficient of variation for observed c max and t max data linear kinetics in adults, following administration of single oral, intramuscular or intravenous doses of ketorolac tromethamine in the recommended dosage ranges, the clearance of the racemate does not change. this implies that the pharmacokinetics of ketorolac tromethamine in adults, following single or multiple intramuscular, intravenous, or recommended oral doses of ketorolac tromethamine, are linear. at the higher recommended doses, there is a proportional increase in the concentrations of free and bound racemate. distribution the mean apparent volume (v β ) of ketorolac tromethamine following complete distribution was approximately 13 liters. this parameter was determined from single-dose data. the ketorolac tromethamine racemate has been shown to be highly protein bound (99%). nevertheless, plasma concentrations as high as 10 mcg/ml will only occupy approximately 5% of the albumin binding sites. thus, the unbound fraction for each enantiomer will be constant over the therapeutic range. a decrease in serum albumin, however, will result in increased free drug concentrations. ketorolac tromethamine is excreted in human milk (see precautions – nursing mothers ). metabolism ketorolac tromethamine is largely metabolized in the liver. the metabolic products are hydroxylated and conjugated forms of the parent drug. the products of metabolism, and some unchanged drug, are excreted in the urine. excretion the principal route of elimination of ketorolac and its metabolites is renal. about 92% of a given dose is found in the urine, approximately 40% as metabolites and 60% as unchanged ketorolac. approximately 6% of a dose is excreted in the feces. a single-dose study with 10 mg ketorolac tromethamine (n = 9) demonstrated that the s-enantiomer is cleared approximately two times faster than the r-enantiomer and that the clearance was independent of the route of administration. this means that the ratio of s/r plasma concentrations decreases with time after each dose. there is little or no inversion of the r- to s- form in humans. the clearance of the racemate in normal subjects, elderly individuals and in hepatically and renally impaired patients is outlined in table 2 (see clinical pharmacology – kinetics in special populations ). the half-life of the ketorolac tromethamine s-enantiomer was approximately 2.5 hours (sd ± 0.4) compared with 5 hours (sd ± 1.7) for the r-enantiomer. in other studies, the half-life for the racemate has been reported to lie within the range of 5 to 6 hours. accumulation ketorolac tromethamine administered as an intravenous bolus, every 6 hours, for 5 days, to healthy subjects (n = 13), showed no significant difference in c max on day 1 and day 5. trough levels averaged 0.29 mcg/ml (sd ± 0.13) on day 1 and 0.55 mcg/ml (sd ± 0.23) on day 6. steady state was approached after the fourth dose. accumulation of ketorolac tromethamine has not been studied in special populations (geriatric, pediatric, renal failure patients, or hepatic disease patients). kinetics in special populations geriatric patients based on single-dose data only, the half-life of the ketorolac tromethamine racemate increased from 5 to 7 hours in the elderly (65 to 78 years) compared with young healthy volunteers (24 to 35 years) (see table 2 ). there was little difference in the c max for the two groups (elderly, 2.52 mcg/ml ± 0.77; young, 2.99 mcg/ml ± 1.03) (see precautions – geriatric use ). pediatric patients limited information is available regarding the pharmacokinetics of dosing of ketorolac tromethamine in the pediatric population. following a single intravenous bolus dose of 0.5 mg/kg in 10 children 4 to 8 years old, the half-life was 5.8 ± 1.6 hours, the average clearance was 0.042 ± 0.01 l/hr/kg, the volume of distribution during the terminal phase (v β ) was 0.34 ± 0.12 l/kg and the volume of distribution at steady state (v ss ) was 0.26 ± 0.08 l/kg. the volume of distribution and clearance of ketorolac in pediatric patients was higher than those observed in adult subjects (see table 1 ). there are no pharmacokinetic data available for administration of ketorolac tromethamine by the intramuscular route in pediatric patients. renal insufficiency based on single-dose data only, the mean half-life of ketorolac tromethamine in renally impaired patients is between 6 and 19 hours and is dependent on the extent of the impairment. there is poor correlation between creatinine clearance and total ketorolac tromethamine clearance in the elderly and populations with renal impairment (r = 0.5). in patients with renal disease, the auc ∞ of each enantiomer increased by approximately 100% compared with healthy volunteers. the volume of distribution doubles for the s-enantiomer and increases by 1/5th for the r-enantiomer. the increase in volume of distribution of ketorolac tromethamine implies an increase in unbound fraction. the auc ∞ -ratio of the ketorolac tromethamine enantiomers in healthy subjects and patients remained similar, indicating there was no selective excretion of either enantiomer in patients compared to healthy subjects (see warnings – renal effects ). hepatic insufficiency there was no significant difference in estimates of half-life, auc ∞ and c max , in 7 patients with liver disease compared to healthy volunteers (see precautions – hepatic effects and table 2 ). race pharmacokinetic differences due to race have not been identified. table 2: the influence of age, liver and kidney function, on the clearance and terminal half-life of ketorolac tromethamine (intramuscular 1 and oral 2 ) in adult populations 1 estimated from 30 mg single intramuscular doses of ketorolac tromethamine 2 estimated from 10 mg single oral doses of ketorolac tromethamine 3 liters/hour/kilogram total clearance [in l/h/kg] 3 terminal half-life [in hours] type of subjects intramuscular mean (range) oral mean (range) intramuscular mean (range) oral mean (range) normal subjects intramuscular (n = 54) mean age = 32, range = 18-60 oral (n = 77) mean age = 32, range = 20-60 0.023 (0.010- 0.046) 0.025 (0.013- 0.050) 5.3 (3.5-9.2) 5.3 (2.4-9) healthy elderly subjects intramuscular (n = 13), oral (n = 12) mean age = 72, range = 65-78 0.019 (0.013- 0.034) 0.024 (0.018- 0.034) 7 (4.7-8.6) 6.1 (4.3-7.6) patients with hepatic dysfunction intramuscular and oral (n = 7) mean age = 51, range = 43-64 0.029 (0.013- 0.066) 0.033 (0.019- 0.051) 5.4 (2.2-6.9) 4.5 (1.6-7.6) patients with renal impairment intramuscular (n = 25), oral (n = 9) serum creatinine = 1.9-5.0 mg/dl, mean age (intramuscular) = 54, range = 35-71 mean age (oral) = 57, range = 39‑70 0.015 (0.005- 0.043) 0.016 (0.007- 0.052) 10.3 (5.9-19.2) 10.8 (3.4-18.9) renal dialysis patients intramuscular and oral (n = 9) mean age = 40, range = 27-63 0.016 (0.003- 0.036) – 13.6 (8.0-39.1) – intravenous-administration: in normal subjects (n=37), the total clearance of 30 mg intravenous‑administered ketorolac tromethamine was 0.030 (0.017-0.051) l/h/kg. the terminal half-life was 5.6 (4.0‑7.9) hours. (see kinetics in special populations for use of intravenous dosing of ketorolac tromethamine in pediatric patients.)