Ketorolac Tromethamine (ketorolac tromethamine)

The lowest possible effective dosage and shortest duration of therapy consistent with treatment goals of the patient should be employed.

Current principles of pain management indicate that analgesics, including ketorolac tromethamine, preferably should be administered at regularly scheduled intervals, although the drug also has been administered on an as-needed basis (i.e., withholding subsequent doses until pain returns). The manufacturer states that clinicians should manage breakthrough pain in adults receiving ketorolac tromethamine therapy with supplemental low doses of opiate analgesics (unless contraindicated) as needed rather than considering higher or more frequent dosages of ketorolac tromethamine.

Because there is some evidence of dose-related adverse effects (e.g., GI bleeding), particularly in geriatric patients, the lowest possible effective ketorolac tromethamine dosage should be employed, and total duration of therapy with the drug (including parenteral, oral, and intranasal formulations) should not exceed 5 days. Particular caution and reduced dosage should be employed in geriatric patients, adults weighing less than 50 kg, and those with renal impairment (see Dosage in Renal and Hepatic Impairment under Dosage and Administration). Elimination of the drug generally is slower and sensitivity to adverse renal effects of NSAIAs generally is increased in geriatric patients.

The potential benefits and risks of ketorolac therapy as well as alternative therapies should be considered prior to initiating ketorolac therapy.

Ketorolac tromethamine is administered by IM or IV injection, orally, or intranasally.

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There are no contraindication interactions for this drug.

There are no severe interactions for this drug.

There are no moderate interactions for this drug.

There is no enhanced messaging for this drug.

There are no contraindication contraindications for this drug.

There are no severe contraindications for this drug.

There are no moderate contraindications for this drug.

There is no enhanced messaging for this drug.

There are no severe adverse reactions for this drug.

There are no less severe adverse reactions for this drug.

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Use of NSAIAs during pregnancy at about 30 weeks of gestation or later can cause premature closure of the fetal ductus arteriosus, and use at about 20 weeks of gestation or later has been associated with fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment. Because of these risks, use of NSAIAs should be avoided in pregnant women at about 30 weeks of gestation or later; if NSAIA therapy is necessary between about 20 and 30 weeks of gestation, the lowest effective dosage and shortest possible duration of treatment should be used. Monitoring of amniotic fluid volume via ultrasound examination should be considered if the duration of NSAIA treatment exceeds 48 hours; if oligohydramnios occurs, the drug should be discontinued and follow-up instituted according to clinical practice. Pregnant women should be advised to avoid use of NSAIAs beginning at 20 weeks' gestation unless otherwise advised by a clinician; they should be informed that NSAIAs should be avoided beginning at 30 weeks' gestation because of the risk of premature closure of the fetal ductus arteriosus and that monitoring for oligohydramnios may be necessary if NSAIA therapy is required for longer than 48 hours' duration between about 20 and 30 weeks of gestation.

Known effects of NSAIAs on the human fetus during the third trimester of pregnancy include prenatal constriction of the ductus arteriosus, tricuspid incompetence, and pulmonary hypertension; nonclosure of the ductus arteriosus during the postnatal period (which may be resistant to medical management); and myocardial degenerative changes, platelet dysfunction with resultant bleeding, intracranial bleeding, renal dysfunction or renal failure, renal injury or dysgenesis potentially resulting in prolonged or permanent renal failure, oligohydramnios, GI bleeding or perforation, and increased risk of necrotizing enterocolitis.

Fetal renal dysfunction resulting in oligohydramnios and, in some cases, neonatal renal impairment has been observed, on average, following days to weeks of maternal NSAIA use, although oligohydramnios has been observed infrequently as early as 48 hours after initiation of NSAIA therapy. Oligohydramnios is often, but not always, reversible (generally within 3-6 days) following discontinuance of NSAIA therapy. Complications of prolonged oligohydramnios may include limb contracture and delayed lung maturation. A limited number of case reports have described maternal NSAIA use and neonatal renal dysfunction, in some cases irreversible, without oligohydramnios. Some cases of neonatal renal dysfunction have required treatment with invasive procedures such as exchange transfusion or dialysis. Deaths associated with neonatal renal failure have been reported. Methodologic limitations of these postmarketing studies and case reports include lack of a control group; limited information regarding dosage, duration, and timing of drug exposure; and concomitant use of other drugs. These limitations preclude establishing a reliable estimate of the risk of adverse fetal and neonatal outcomes with maternal NSAIA use. Available data on neonatal outcomes generally involved preterm infants, and the extent to which certain reported risks can be generalized to full-term infants is uncertain.

Animal data indicate that prostaglandins have an important role in endometrial vascular permeability, blastocyst implantation, and decidualization. In animal studies, inhibitors of prostaglandin synthesis, such as ketorolac, were associated with increased pre- and post-implantation losses. Prostaglandins also have an important role in fetal kidney development. In animal studies, inhibitors of prostaglandin synthesis impaired kidney development at clinically relevant doses.

Reproduction studies in rabbits and rats receiving oral ketorolac tromethamine dosages of 3.6 and 10 mg/kg daily, respectively (about 1.8 and 5 times the maximum recommended human parenteral dosage, respectively), during the period of organogenesis have not revealed evidence of harm to the fetus; however, oral dosages exceeding the maximum recommended human parenteral dosage in rats produced delayed parturition and dystocia, probably secondary to inhibition of prostaglandin synthesis.

Use of ketorolac during labor and delivery is contraindicated, since its inhibitory effect on prostaglandin synthesis may adversely affect fetal circulation and inhibit uterine contractions, thus increasing the risk of uterine hemorrhage. In animal studies, NSAIAs, including ketorolac, delayed parturition and increased the incidence of stillbirths.

Ketorolac may be distributed into milk in small amounts. (See Distribution under Pharmacokinetics.) The developmental and health benefits of breast-feeding should be considered along with the mother's clinical need for ketorolac and any potential adverse effects on the breast-fed infant from the drug or from the underlying maternal condition.

Caution should be exercised when ketorolac is used in nursing women; although available information has not revealed any specific adverse events in nursing infants, women who are breast-feeding should be advised to contact their infant's clinician if they observe any adverse events.

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