Renal Insufficiency Associated with Intramuscular Administration of Ketorolac Tromethamine

1993 ◽  
Vol 27 (9) ◽  
pp. 1055-1057 ◽  
Author(s):  
Robin L. Corelli ◽  
Kristin R. Gericke
Keyword(s):  
Renal Insufficiency ◽  
Renal Toxicity ◽  
Adverse Drug Reaction Reporting ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Ketorolac Tromethamine ◽  
Antiinflammatory Drugs ◽  
Narcotic Analgesics ◽  
Term Administration ◽  
The Mean ◽  
Peak Value

OBJECTIVE: To evaluate reports of renal toxicity associated with intramuscular ketorolac tromethamine. Medical charts were reviewed for all cases of renal toxicity associated with ketorolac therapy. METHODS: Patients with possible ketorolac-associated nephrotoxicity were identified through our institution's adverse drug reaction reporting program. Patients were included in this report if: (1) renal insufficiency was temporally related to ketorolac administration; (2) resolution of renal insufficiency occurred after discontinuation of ketorolac; and (3) no other causes of renal insufficiency, including other medications, could be identified. RESULTS: Six patients had renal insufficiency secondary to ketorolac administration. The mean age of the patients was 58 years and cardiovascular disease was present in five. Serum creatinine values increased from a mean of 106 ± 26 μmol/L (1.2 ± 0.3 mg/dL) to a mean peak value of 256 ± 195 μmol/L (2.9 ± 2.2 mg/dL). Recovery of renal function was observed after a mean of 2.3 ± 0.5 days. CONCLUSIONS: Short-term administration of ketorolac can be associated with reversible oliguric renal insufficiency. Indiscriminate use of ketorolac for pain management in place of narcotic analgesics should be avoided, especially in patients at high risk for toxicity induced by nonsteroidal antiinflammatory drugs.

scholarly journals Recent Trends in Medication Usage for the Treatment of Juvenile Idiopathic Arthritis and the Influence of Tumor Necrosis Factor Inhibitors

2014 ◽  
Vol 41 (10) ◽  
pp. 2078-2084 ◽  
Author(s):  
Melissa L. Mannion ◽  
Fenglong Xie ◽  
Jeffrey R. Curtis ◽  
Timothy Beukelman
Keyword(s):  
Juvenile Idiopathic Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Temporal Trends ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Tumor Necrosis Factor Inhibitors ◽  
Antiinflammatory Drugs ◽  
Medication Usage ◽  
The Mean ◽  
Necrosis Factor

Objective.Using administrative data from a large commercial US health insurer, we investigated temporal trends in medication use among children diagnosed with juvenile idiopathic arthritis (JIA).Methods.Children with ≥ 1 physician diagnosis code for JIA in the calendar years 2005 through 2012 were included. Use of tumor necrosis factor inhibitors (TNFi), methotrexate (MTX), nonsteroidal antiinflammatory drugs (NSAID), and oral glucocorticoids (GC) was determined. Temporal changes in medication usage were evaluated with the Cochran-Armitage test for trend. We used paired t-tests to evaluate the use of NSAID and GC in the 6 months before and after new TNFi use.Results.We identified 4261 unique individuals with JIA. The proportion of patients receiving TNFi increased from 8.7% in 2005 to 22.4% in 2012 (p < 0.0001). MTX use increased from 18.4% to 23.2% (p = 0.02). NSAID use decreased from 49% to 40% (p = 0.02). GC use was relatively unchanged. Following new TNFi use, the mean number of NSAID prescriptions (among prevalent users) decreased from 2.8 to 2.0 (p < 0.0001), and the mean daily GC dose (among prevalent users) decreased from 7.3 mg/day to 3.9 mg/day (p < 0.0001). Many new TNFi users (57%) had not used MTX in the previous 6 months, and only 37% had any concurrent MTX use in the 6 months following new TNFi use.Conclusion.TNFi use in the treatment of JIA increased 2- to 3-fold over the last 8 years. New TNFi use was associated with decreased NSAID and GC use. TNFi may be replacing, rather than complementing, MTX in the treatment of many patients.

Blood Pressure in Native Americans Switched from Celecoxib to Rofecoxib

2005 ◽  
Vol 39 (5) ◽  
pp. 797-802 ◽  
Author(s):  
Jefferson Fredy ◽  
Daniel A Diggins ◽  
Gregory B Morrill
Keyword(s):  
Blood Pressure ◽  
Native American ◽  
Native Americans ◽  
Index Date ◽  
Medical Center ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Cardiovascular Safety ◽  
Antiinflammatory Drugs ◽  
The Mean ◽  
Cox 2

BACKGROUND: Nonsteroidal antiinflammatory drugs have been associated with exacerbation of hypertension. Differing effects on blood pressure (BP) have been reported in studies comparing celecoxib and rofecoxib. Concern regarding the cardiovascular safety of the cyclooxygenase-2 (COX-2) inhibitor class has intensified since the removal of rofecoxib from the market. OBJECTIVE: To evaluate the effect of a formulary change from celecoxib to rofecoxib on the BP of Native American patients at an Indian Health Service medical center. METHODS: Medical records of patients switched from celecoxib to rofecoxib were retrospectively reviewed. BP during the respective treatments was compared as follows: measurements recorded while taking celecoxib within 6 months before the index date and while taking rofecoxib from 1 week after the index date through 6 months of treatment were averaged. Differences in systolic and diastolic BP before and after the therapy change were evaluated using a paired Student's t-test. Subgroup analysis was performed for patients with preexisting hypertension. RESULTS: During rofecoxib therapy, the mean systolic BP was 2.9 mm Hg higher (p = 0.015) and the mean diastolic BP was 1.5 mm Hg higher (p = 0.042) than during celecoxib therapy. Among hypertensive patients, the respective mean systolic and diastolic BPs were 4.8 mm Hg (p = 0.009) and 2.0 mm Hg (p = 0.063) higher while taking rofecoxib. CONCLUSIONS: Switching patients from celecoxib to rofecoxib resulted in an increase in BP, with a larger difference observed in patients with hypertension. Future studies assessing the cardiovascular safety of currently marketed and investigational COX-2 inhibitors should evaluate the possible contribution of BP effects of these agents to overall risk.

Effects of ketorolac tromethamine on erythropoietin levels in Sprague Dawley rats

1994 ◽  
Vol 17 (12) ◽  
pp. 629-634 ◽  
Author(s):  
K.K. Hoff ◽  
E.T. Zawada ◽  
F.K. Alavi ◽  
J.W. Leyse ◽  
R.N. Santella
Keyword(s):  
Repeated Administration ◽  
Nonsteroidal Antiinflammatory Drugs ◽  
Ketorolac Tromethamine ◽  
Sprague Dawley ◽  
Antiinflammatory Drugs ◽  
Tail Vein ◽  
Sd Rats ◽  
Sprague Dawley Rats ◽  
Normal Controls ◽  
Injectable Form

Ketorolac tromethamine (KT) is a potent analgesic, most often used in its injectable form postoperatively. Similar to other nonsteroidal antiinflammatory drugs (NSAIDs), it inhibits prostaglandin (PG) synthesis. Prostaglandins have been shown to be involved in the regulation of renal function as well as erythropoietin (Ep) production. The intent of this study was to determine the effect of KT on plasma Ep levels in Sprague Dawley (SD) rats. Twenty rats received either 15 mg/kg/d or the KT vehicle IM for 5d. Blood samples (1 ml) were collected via tail vein each day of treatment. Plasma Ep levels were significantly higher in the KT rats than normal controls with the greatest difference occurring on d4 of treatment (70.1 ± 10.8 vs 30.9 ± 10.84 mU/ml, p < 0.01). This change in Ep corresponded with a significant reduction in hematocrit (KT, 29.5 ± 2.2 vs C, 40.8 ± 2.2%, p< 0.01). Presence of fecal blood was noted in the KT treated rats. A similar second experiment was designed to determine if blood loss was the cause of altered Ep production. In this experiment controls (HC) were bled via tail vein, to match the hematocrits of KT treated animals. Repeated administration of KT led to a steady reduction in hematocrit. When compared, hematocrit matched animals showed no difference in plasma Ep levels on all days of treatment (KT, 48.0 ± 4.9 vs HC, 44.6 ± 3.1 mU/ml, N.S.). In conclusion, repeated administration of KT showed no impairment of Ep production and release in response to reduced hematocrit, suggesting that in this instance, prostaglandin inhibition plays a minimal role in Ep production or release.

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