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PubMed1980

Brain uptake of meperidine in the fetal lamb.

The uptake of meperidine by the brain of the fetal lamb was investigated by determining the concentration of meperidine in the fetal brachiocephalic artery and sagittal vein after intravenous and intramuscular administration to the mother. A positive arteriovenous gradient across the fetal brain existed for 10 minutes after intravenous administration, and for 20 to 25 minutes after intramuscular administration, thus indicating the uptake of meperidine by the fetal brain. The peak concentration of unbound meperidine in the fetal brain, as estimated from the plasma concentration of free meperidine at equilibrium, was three to four times greater after intravenous administration than after intramuscular administration. The findings suggest that, during labor, the route of administration of meperidine will determine the time course of meperidine in the fetal brain and, consequently, the time action of effects seen in the neonate. The lag time required for plasma-brain equilibration may explain the lack of correlation between the incidence of neonatal respiratory depression and the levels of meperidine in the cord after intramuscular administration.

Animals↗
PubMedDate not supplied

[Continuous epidural perfusion with meperidine on demand for the treatment of postoperative pain].

OBJECTIVE: To determine whether epidural administration of meperidine through a system affording patient-controlled analgesia (PCA) is appropriate for postoperative pain. PATIENTS AND METHODS: A prospective double-blind study of 30 patients undergoing high abdominal surgery randomly into two groups. After surgery with the same type of general anesthesia for both groups, group A received epidural meperidine through a PCA pump (initial boluses of 50 mg + infusion of 10 mg/h with additional doses of 25 mg upon patient demand and closure time of 90 min). Control group B received 0.9% saline serum through an epidural PCA system with identical perfusion characteristics. All patients had access to additional analgesia with subcutaneous meperidine (1 mg/kg weight). RESULTS: There was a wide interindividual variation in meperidine consumption in group A, with a mean total dose of 301.4 +/- 73 mg in 24 hours and no patient requiring additional subcutaneous meperidine. Subcutaneous meperidine required in group B reached 273 +/- 65.8 mg in 24 hours, with no significant differences between groups A and B for total dose given. No side effects inherent to the technique were found. Sufficient control of pain was achieved for all patients receiving epidural meperidine. CONCLUSIONS: Epidurally administered PCA with meperidine affords better pain relief with greater patient satisfaction than the same amount of drug given subcutaneously in successive doses upon patient request.

Abdomen↗
PubMedDate not supplied

A comparison between lidocaine alone and lidocaine with meperidine for continuous spinal anesthesia.

BACKGROUND AND OBJECTIVES: Experimental investigations have demonstrated a synergistic interaction between opioids and local anesthetics. This study aims to assess the effective benefit-risk ratio of continuous spinal anesthesia (CSA) induced with either 1.6% lidocaine alone or in combination with 1% meperidine. METHODS: Thirty-four elderly patients (80.7 +/- 7.3 years) operated on for fracture of the neck of the femur were randomly allocated to two groups. In the first group (n = 15), CSA was induced with lidocaine 1.6% plain, whereas in the second group (n = 19) 1% meperidine was added. Reinjections were performed in both groups using lidocaine 1.6% alone. RESULTS: In the lidocaine group, 43 +/- 13 mg was used for induction whereas in the other group the addition of 18 +/- 5 mg of meperidine significantly reduced the dose of lidocaine required to 28 +/- 8 mg (p < 0.001). Delay between two reinjections was increased to 51 +/- 7 minutes in the lidocaine plus meperidine group, compared to 35 +/- 6 minutes in the lidocaine group (p < 0.001). Ephedrine was required for 9 out of the 19 patients in the lidocaine plus meperidine group, whereas it was required for only two patients in the other group (p = 0.05). Mean plasma concentrations of meperidine 1 hour and 3 hours after induction was 45.5 +/- 12 ng/ml and 59 +/- 22 ng/ml, respectively, and drowsiness was observed in 95% of the patients in the second group. Delay before requirement for pain medication was 2.2 +/- 2 hours in the lidocaine group and 14.1 +/- 8 hours in the lidocaine plus meperidine group (p < 0.001). CONCLUSIONS: The association of 1% meperidine with 1.6% lidocaine during the induction of CSA decreases the initial induction dose, prolongs analgesia, produces initial drowsiness, and provides long-lasting pain relief. However, such benefits are offset by some impairment of hemodynamic stability that is likely to make this combination of drugs unacceptable as an enhanced analgesic technique.

Aged↗
PubMed1993

Effect of hydroxyzine and meperidine on arterial blood gases in patients with chronic obstructive pulmonary disease.

Hydroxyzine is frequently used to tranquilize chronic obstructive pulmonary disease patients, who may be concomitantly receiving narcotic analgesics. Therefore, its effect alone and in combination with meperidine on arterial blood gases and ventilation at rest were evaluated in 44 patient volunteers, who gave informed consent. Hydroxyzine, 1.5 mg/kg i.v. caused no significant decrease in PaO2 and pH, no increase in PaCO2 at 5, 10, 20, 30 and 60 min post-infusion (n = 13, mean age = 63.4 years). Meperidine, 1.5 mg/kg i.v. caused a significant (p < 0.001) reduction in PaO2 for 20 min with concomitant increase in PaCO2 (n = 14; mean age = 49.4 years). The combination of the same doses of hydroxyzine with meperidine i.v. caused no greater decrease in PaO2 or in pH or increase in PaCO2 than did meperidine alone (n = 17; mean age = 52.6 years), indicating no greater ventilatory depression with the combination than with meperidine alone. The lack of significant pH decreases at 30 and 60 min further corroborates no potentiation of meperidine by hydroxyzine. In conclusion, hydroxyzine, even when given through the i.v. route in excess of the maximum i.m. therapeutic dose, caused no changes in PaO2, PaCO2 or pH in chronic obstructive pulmonary disease patients. Therefore, its i.m. administration resulting in lower blood levels than i.v., is not likely to cause ventilatory depression. Furthermore, hydroxyzine caused no potentiation of the ventilatory depression induced by meperidine, hence hydroxyzine may be safely employed in combination with meperidine.

Aged↗
PubMed1977

Meperidine effects on schedule-controlled responding.

The effect of meperidine were studied on responding by pigeons under a multiple fixed-ratio, fixed-interval schedule of food presentation. Low doses of meperidine (0.3-3 mg/kg) generally increased and higher doses decreased responding under the fixed-interval component of the multiple schedule. The responding under the fixed-ratio component was usually unaffected by low doses and decreased by doses greater than 3 mg/kg of meperidine. Naloxone (1 mg/kg) antagonized the rate increases in the fixed-interval component; however, no dose of naloxone (1-56 mg/kg) or cyclazocine (0.1-3 mg/kg) antagonized the rate decreases produced by meperidine under either schedule component. The effects of morphine and meperidine were compared in two birds treated daily with methadone. In a bird maintained on a daily dose of 120 mg/kg (p.o.) of methadone, there was a 10-fold shift of the dose-effect curve for morphine but no shift of the meperidine dose-effect curve. In a bird maintained on a daily dose of 30 mg/kg (p.o.) of methadone, there was a 3- to 5-fold shift of the morphine dose-effect curve, but again no shift of the meperidine dose-effect curve. Thus, the rate-decreasing effects of meperidine were not antagonized by narcotic antagonists, nor did they show cross-tolerance to methadone.

Animals↗
PubMed1996

Ketorolac versus meperidine for pain relief after orthopaedic surgery.

In this double-blind, randomized, multicenter study, 244 patients with at least moderate pain after major orthopaedic surgery received intramuscular Ketorolac (60 mg followed by 30 mg) or intramuscular meperidine (100 mg or placebo) every 2 to 6 hours as needed for as many as 5 days. Analgesic response was evaluated for 6 hours after initial study drug administration and thereafter each night at bedtime. Both active treatment groups had similar 3-hour summed pain intensity difference and 3-hour total pain relief scores after the first dose that were superior to placebo. The 6-hour summed pain intensity difference and total pain relief scores were significantly higher with Ketorolac than with meperidine or placebo. The mean daily categorical pain intensity scores were comparable with Ketorolac and meperidine, and both were significantly superior to placebo. Patient ratings of overall medication efficacy were significantly better with Ketorolac than with meperidine. In both patient and observer evaluations, Ketorolac was significantly better tolerated than meperidine, and the number of patients reporting adverse events was lower with Ketorolac than with meperidine. Following major orthopaedic surgery, Ketorolac provided effective analgesia that was superior to placebo and at least comparable with meperidine. Ketorolac was better tolerated than meperidine.

Adolescent↗
PubMed1978

Clinical effects of meperidine in hospitalized medical patients.

Of 26,294 hospitalized medical patients monitored in a drug surveillance program, 366 (1.4%) received meperidine orally and 3268 (12.4%) received meperidine parenterally during one or more admissions. Neoplastic disease was the most common category of primary diagnosis (43%) among oral recipients; among parenteral recipients cardiovascular and neoplastic diseases (23% each) were most common. Oral meperidine was prescribed almost exclusively (93%) for pain relief, whereas the parenteral drug also had substantial use (41%) as a diagnostic and preoperative adjunct. Oral meperidine was judged by attending physicians to have provided unsatisfactory pain relief in 22% of recipients, while parenteral meperidine was rated unsatisfactory in 11%. The drug was less effective in patients with a primary diagnosis of neoplastic disease than in patients with other primary diagnoses. Minor gastrointestinal disturbances were the most commonly reported adverse reactions among oral meperidine recipients (2.7%); among parenteral recipients central nervous system effects were most common (1.2%). Seven recipients had life-threatening adverse reactions. However, only two of these were judged definitely related to meperidine, and in both instances other drugs were also definitely implicated. Adverse reactions were dose related.

Administration, Oral↗
PubMed1992

Comparison of the efficacy and safety of ketorolac and meperidine in the relief of dental pain.

A single-dose, randomized, double-blind study of parallel design was conducted to determine the analgesic efficacy and safety of ketorolac tromethamine in patients who experience moderate or severe pain after the surgical removal of three or more third molars, one of which was a bony-impacted mandibular molar. Meperidine hydrochloride was used as the control analgesic. In this 8-hour study, assessments were made of pain intensity, pain relief, and overall rating of the medication in 145 patients, each of whom had received an intramuscular injection of 10 mg, 30 mg, or 90 mg of ketorolac, or 50 mg or 100 mg of meperidine. The summed pain intensity and total pain relief scores showed that, at 3 and 8 hours, the effectiveness of 30 mg of ketorolac was similar to that of 90 mg ketorolac and that both of these doses were significantly more efficacious than 10-mg ketorolac, 50-mg meperidine, or 100-mg meperidine. Patients who received 30 mg or 90 mg of ketorolac gave the study medication significantly higher ratings overall than did patients who received 50 mg or 100 mg of meperidine. Significantly fewer patients treated with ketorolac reported adverse events in comparison with those treated with meperidine (17% and 59%, respectively), which suggests that it possesses a better therapeutic index than meperidine. Thus, ketorolac appears to represent an important advance in analgesic therapy.

Analgesics↗
PubMed1981

TLC identification adn GLC determination of meperidine and its metabolites in biological fluids.

Procedures were developed for TLC identification and GLC determination of meperidine and its metabolites, i.e., p-hydroxymeperidine, normeperidine, and meperidinic and normeperidinic acids. Meperidine, p-hydroxymeperidine, and normeperidine were extracted with ether from biological fluids at pH 10, whereas meperidinic and normeperidinic acids and conjugated metabolites remained in the aqueous phase. The residue, upon evaporation of the extract to dryness, was derivatized with trifluoroacetic anhydride and gas chromatographed. Total (free and conjugated) meperidinic and normeperidinic acids in the aqueous phase were converted and determined as meperidine and normeperidine, respectively. A preliminary result of urinary disposition of meperidine and its metabolites in the rat is presented. The identity of these metabolites was confirmed with GLC-mass spectrometry.

Animals↗
PubMed1976

Determination of therapeutic serum concentrations of oral and parenteral meperidine by liquid chromatography.

A sensitive and specific method for estimation of serum meperidine by gas-liquid chromatography and its application in a clinical study are described. Patients were given, under double-blind conditions, either oral (75 or 150 mg) or intramuscular (50 or 100 mg) doses of meperidine for postoperative analgesia. Serum meperidine levels were measured 0.5, 1, 2, 3, and 4 hours post-dose. Although wide variations of serum meperidine levels were observed among individuals within each group for each time period, the intramuscular route produced and sustained significantly higher serum levels than did the oral route. The mean concentration of meperidine (mug/100 ml +/- S.E.) for 100 mg i.m. was 37.7 +/- 3.8 at one hour and 23.4 +/-5.7 at three hours; for 150 mg orally it was 11.9 +/- 1.6 at one hour and 11.8 +/- 3.2 at three hours. A correlation observed between the intramuscular dose (in mg/kg body weight) and serum meperidine concentration attained at one hour indicated that 1 mg/kg meperidine i.m. will achieve a one-hour serum level of approximately 20 mug/100 ml, an apparent minimally effective level for analesia in most patients.

Administration, Oral↗
PubMed1990

Comparison of intrathecal meperidine and lidocaine in endoscopic urological procedures.

The purpose of this study was to determine if a small dose of intrathecal meperidine would achieve adequate spinal anaesthesia while minimizing complications and to compare its effectiveness with lidocaine. The spinal anaesthetic effects of five per cent lidocaine 0.5 mg.kg-1 in 7.5 percent glucose (n = 20) or five per cent meperidine 0.5 mg.kg-1 (n = 22) were evaluated in 42 ASA physical status II or III patients. Intrathecal injection of the anaesthetic agent was given with the patient in the sitting position in which he remained for ten minutes before being placed in the lithotomy position. The onset time for sensory blockade was seven minutes in the lidocaine group and ten minutes in the meperidine group. Final sensory levels were identical in both groups. Mean arterial blood pressure decreased significantly in the lidocaine group but not in the meperidine group. Motor block was absent in ten patients in the meperidine group but was present in all the patients in the lidocaine group. Duration of postoperative analgesia was 968 min in the meperidine group and 681 min in the lidocaine group (NS). Complications such as nausea, vomiting, itching, drowsiness and respiratory depression were similar in the two groups. It is concluded that low-dose meperidine, 0.5 mg.kg-1, is effective as a spinal anaesthetic agent and has few complications.

Aged↗
PubMed1978

A double-blind comparison of butorphanol and meperidine in labour: maternal pain relief and effect on the newborn.

Butorphanol tartrate 1 mg and 2 mg were compared in 80 normal mothers at term in a double-blind study with meperidine hydrochloride 40 mg and 80 mg for the relief of pain in labour. Butorphanol was found to be as effective as meperidine in relieving pain in labour. The foetal condition, as measured by ECG monitoring, Apgar scores, time to sustained respiration, umbilical venous H+ (pH) and PCO2, and a general nursery survey were comparable for meperidine and butorphanol. No psychomimetic phenomena were seen. Assays indicated that both butorphanol and meperidine crossed the placenta. The mean concentration of butorphanol in neonatal serum was 0.84 times maternal serum at 1.5 to 3.5 hours after intramuscular administration of a single or two successive doses of butorphanol 1 mg or 2 mg to the mother. The mean concentrations for meperidine in neonatal serum was 0.89 times maternal serum at 0.85 to 3.6 hours after intramuscular administration of meperidine 40 mg or 80 mg to the mother. Neither analgesic caused severe depression of the infant except for one meperidine-treated case.

Anesthesia, Obstetrical↗
PubMed1997

Bupivacaine decreases epidural meperidine requirements after abdominal surgery.

PURPOSE: The purpose of this study was to determine the optimal of three concentrations of bupivacaine (0.0%, 0.05%, 0.10%) to add to an epidural infusion of meperidine (1 mg.ml-1) for postoperative pain relief. METHODS: In this prospective, double blind study, 60 patients undergoing abdominal surgery with general anaesthesia were randomized into three groups to receive for postoperative epidural analgesia: 1) 1 mg.ml-1 meperidine (0% group), 2) bupivacaine 0.05% and 1 mg.ml-1 meperidine (0.05% group), 3) bupivacaine 0.10% and 1 mg.ml-1 meperidine (0.10% group). Postoperatively, the epidural infusion rate was titrated to produce adequate analgesia and pain was assessed at rest and on movement. RESULTS: There were no differences in demographic data, average pain scores or side effects among the three groups. However, there was improvement of pain relief at rest over time in the three groups (P < 0.05). Postoperative epidural analgesic infusion rates increased over time for the three groups (P < 0.05) and were lower in the 0.10% group (mean of 10.0 ml.hr-1) than in the 0% group (mean of 12.6 ml.hr-1) (P < 0.05). More than half of the 0% group had serum meperidine concentrations > 400 g.L-1 to control moderate postoperative pain. CONCLUSION: Although analgesia was identical among groups, the lower serum concentrations of meperidine support the addition of bupivacaine 0.10% to meperidine when administered as a continuous infusion following abdominal surgery.

Abdomen↗
PubMed1988

Species differences in the hydrolysis of meperidine and its inhibition by organophosphate compounds.

The hydrolysis of meperidine was assayed in washed, unfortified liver microsomal fractions of guinea pig, rat, mouse, dog, and human, by following substrate disappearance as quantitated by high-performance liquid chromatography. Using the method of Lineweaver-Burk plots, the velocity of the meperidine hydrolysis reaction was not detectable in guinea pig, very low in human, and extremely high in dog. Hydrolysis of p-nitrophenyl acetate was also monitored in liver microsomal preparations from the same animal species, with guinea pig showing greatest hydrolytic activity and rat showing least hydrolytic activity for this substrate. The data in the above two assays suggested that meperidine hydrolysis is mediated by a unique esterase not present in guinea pig and very low in human, but present with high activity in dog liver microsomes. From these comparative studies we concluded that liver microsomes from different species may contain different carboxylesterases having different affinities for meperidine. To further characterize meperidine carboxylesterase of dog and rat liver microsomes, inhibitory studies in vitro with two organophosphate compounds--paraoxon (diethyl-p-nitrophenyl phosphate) and soman (pinacolyl methylphosphonofluoridate)--indicated a varied pattern of enzyme inhibition. These results suggested that liver microsomal carboxylesterases are involved in the metabolism of meperidine and that interference with these enzymes by organophosphate compounds may alter pharmacologic and toxicologic effects of meperidine.

Animals↗
PubMed1994

Investigation of meperidine and its metabolites in urine of an addict by gas chromatography-flame ionization detection and gas chromatography-mass spectrometry.

A gas chromatographic method with flame ionization detection (FID) for the quantitative analysis of meperidine and mass spectrometry (MS) for the qualitative analyses of meperidine and its metabolites in urine was established. Meperidine, normeperidine and acetyl normeperidine in urine were extracted with ether. Free and conjugated meperidinic and normeperidinic acids in urine, which are hydrophillic, were hydrolyzed by acid, esterified with methanol and derivatized with acetic anhydride. Meperidine and its four metabolites were identified by GC-MS. Meperidine was measured by GC-FID during 72 h after intramuscular administration of meperidine to an addict.

Biotransformation↗
PubMedDate not supplied

Meperidine need not be proscribed during sphincter of Oddi manometry.

Meperidine is routinely proscribed during sphincter of Oddi manometry because narcotics have been associated with spasm of the sphincter of Oddi. We have performed a prospective study of the effect of meperidine on sphincter of Oddi manometry in 18 patients undergoing manometry for suspected sphincter dysfunction. After diagnostic manometry using only intravenous diazepam sedation, the endoscope remained in the duodenum while 1 mg/kg intravenous meperidine was given. Five minutes later sphincter manometry was repeated. There was no difference in the baseline sphincter pressure before and after meperidine in all patients. The frequency of phasic contractions increased after meperidine (p = 0.001). Baseline sphincter pressure is generally the only manometric criteria used to diagnose sphincter dysfunction and this did not change after meperidine. We conclude that meperidine may be used for additional analgesia during sphincter manometry. This may improve patient tolerance and the success rate of this procedure.

Adult↗
PubMedDate not supplied

Failure of meperidine to anesthetize human median nerve. A blinded comparison with lidocaine and saline.

BACKGROUND AND OBJECTIVES: Although meperidine safely produces clinical spinal anesthesia, the responsible mechanism is unknown. This study was undertaken to test the possibility that this drug acts as a local anesthetic by investigating its ability to inhibit conduction in a human peripheral nerve. METHODS: In a blinded fashion, the abilities of 5-mL injections of meperidine (0.5% and 1.5%), lidocaine (0.25%), and saline to produce median nerve block were tested in eight volunteer subjects, and these four solutions were compared with standard local anesthetic solutions that had been tested in previous studies. The extent of local anesthesia was measured objectively by electrodiagnostic tests, namely, compound motor action potentials (CMAPs) and sensory nerve action potentials (SNAPs), as well as by qualitative tests of sensation. RESULTS: Lidocaine (0.25%) prolonged median SNAP latency from 3.1 ms to 3.3 ms (P < .015) and prolonged mean CMAP latency from 4.1 ms to 4.7 ms (P < .002). The SNAP amplitude trended downward after lidocaine (0.25%), but the decrease did not reach statistical significance (35 microV to 25 microV, P < .19). Neither meperidine solution (0.5% or 1.5%) nor saline inhibited SNAP or CMAP amplitudes or prolonged SNAP or CMAP latencies. Also, in contrast to previous findings with more potent local anesthetic solutions (eg, lidocaine 1%, mepivacaine 1%, and bupivacaine 0.33%), none of the four solutions tested in this study altered subjective sensations of hot, cold, or pinprick. Meperidine 1.5% produced systemic side effects, including vertigo, nausea, and flushing, in all subjects. CONCLUSIONS: Meperidine produced no signs of local anesthesia, even when given at a dose (75 mg) and concentration (1.5%) that consistently produced systemic side effects. Thus, the coequivalent ability of meperidine and lidocaine to produce spinal anesthesia contrasts with their discordant ability to produce local anesthesia. This disparity suggests that meperidine may produce spinal anesthesia through mechanisms other than inhibition of sodium channel function.

Action Potentials↗
PubMed2002

Removing meperidine from the health-system formulary--frequently asked questions.

Meperidine is FDA-approved for relieving moderate to severe pain and has been widely used since its introduction in the 1930s. However, the drug is no longer considered a first-line analgesic. Many clinicians recommend that meperidine be removed from health-systems or that its use be restricted, due to concerns about adverse reactions, drug interactions, and normeperidine neurotoxicity. In addition, clinical evidence shows that meperidine has no advantage over other opioids for biliary colic or pancreatitis. The formulary status of meperidine has been extensively discussed at University of Utah Hospitals and Clinics. The Pharmacy and Therapeutics Committee has been working with hospital staff to assess the impact of either removing meperidine from the formulary, or limiting its use. The Drug Information Service developed this document to help pharmacists respond to prescribers' questions and to alleviate the prescribers' concerns about these changes. Information is provided comparing meperidine with other opioids, including dosage equivalency, pharmacodynamics, pharmacokinetics, cost, adverse effects, and drug interactions. Where available, alternatives to meperidine are suggested for various indications.

Analgesics, Opioid↗