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PubMed2002

Use of meperidine in patient-controlled analgesia and the development of a normeperidine toxic reaction.

HYPOTHESIS: Intravenous patient-controlled analgesia (IV PCA) meperidine hydrochloride can be used with a reasonable margin of safety. DESIGN: A retrospective review was performed of 355 medical records of patients receiving IV PCA meperidine treatment. Four groups of patients were defined, based on daily meperidine dose and the presence or absence of central nervous system excitation adverse effects. Use of more than 600 mg/d of meperidine hydrochloride was considered a high dose. SETTING: University tertiary care hospital. PARTICIPANTS: Postoperative patients from general, orthopedic, neurosurgical, gynecological, and urologic procedures receiving IV PCA. INTERVENTIONS: If patients were judged to have consumed significant amounts of meperidine, the analgesic regimen was modified to (1) discontinue meperidine therapy, (2) substitute hydromorphone hydrochloride, or (3) decrease the use of meperidine by adding oral methadone hydrochloride or transdermal fentanyl citrate to the regimen. MAIN OUTCOME MEASURES: Patients who received less than 10 mg/kg per day of IV PCA meperidine hydrochloride therapy were unlikely to experience central nervous system excitatory adverse effects and maintain adequate analgesia. RESULTS: The mean meperidine hydrochloride consumption for those patients classified as high dose, asymptomatic was 13.3 mg/kg per day (95% confidence interval, 12.1-14.4 mg/kg per day). This differed statistically significantly (P<.05) from the mean meperidine hydrochloride dose in patients classified as high dose, symptomatic, which was 16.9 mg/kg per day (95% confidence interval, 14.7-19.2 mg/kg per day). The duration of meperidine use did not differ among the 4 patient groups. The incidence of a central nervous system toxic reaction associated with IV PCA meperidine therapy was 2%. CONCLUSIONS: We recommend 10 mg/kg per day as a maximum safe meperidine hydrochloride dose by an IV PCA device for no longer than 3 days. Daily patient evaluation is mandatory. Care must also be taken when using this dose to ensure the absence of renal dysfunction or enhanced hepatic metabolism of meperidine.

Adult↗
PubMed1995

Postthoracotomy pulmonary function: a comparison of epidural versus intravenous meperidine infusions.

It has remained unclear whether epidural opioid analgesia permits better recovery of postthoracotomy pulmonary function than an optimal method of systemic opioid administration. Lumbar epidural meperidine infusions were compared with intravenous patient-controlled analgesic (PCA) meperidine infusions in a prospective randomized unblinded study for 72 hours postthoracotomy. Before induction of general anesthesia, patients received a bolus of meperidine, 1 mg/kg, and an infusion of meperidine, 0.33 mg/kg/hr, was started via either a lumbar epidural or intravenous catheter. Postoperatively, the meperidine infusion rates were titrated as needed for analgesia. In addition, the intravenous group received meperidine, 10 mg per dose, as required, from a patient-controlled analgesia pump. No other opioid was administered during the study period. Patients were studied for recovery of spirometric tests of pulmonary function, visual analog pain scores, sedation, arterial blood gases, meperidine dose requirements, radiographic pulmonary complications, and neurologic signs and symptoms. A subgroup of 10 patients (5 from each group) had venous blood samples drawn every 24 hours for 96 hours and assayed for serum meperidine and normeperidine concentrations. Epidural meperidine analgesia was associated with improved postthoracotomy pulmonary function, better analgesia scores, and lower meperidine dose requirements than intravenous PCA meperidine. There were no differences between the epidural versus intravenous PCA subgroups with respect to serum meperidine or normeperidine levels. Normeperidine levels greater than 300 ng/mL were associated with an increased incidence of shakiness and/or tremors. Meperidine provides satisfactory postthoracotomy analgesia via a lumbar epidural infusion. This analgesia is associated with improved recovery of postoperative pulmonary function when compared with an intravenous PCA meperidine infusion.

Aged↗
PubMed1999

Meperidine utilization and compliance with Agency for Health Care Policy and Research guidelines in a tertiary care hospital.

The Agency for Health Care Policy and Research (AHCPR) established guidelines for the use of meperidine (demerol), a common inpatient analgesic. These guidelines define standards of care for acute and chronic cancer pain management and address many of the problems with meperidine and its metabolite, normeperidine. The purpose of this study was to determine whether meperidine was prescribed in compliance with AHCPR guidelines, whether patients exhibited any adverse reactions to meperidine, and to determine the analgesic efficacy of meperidine. Three hundred inpatient charts were reviewed and identified meperidine as the primary analgesic in 157 nonobstetric inpatients. Age, sex, weight, dosing interval, route of administration, duration of meperidine use, serum chemistry values, primary diagnosis, associated medical conditions, and medications concurrently being taken with meperidine were the parameters analyzed. An interview was conducted to ascertain medical and drug history, chronicity of pain syndromes, analgesic drug history, and analgesic efficacy. A visual analog scale for pain (range = 0 to 10) and an analgesic satisfaction survey (range = 1 to 5) were used. Of 157 patients, 124 (79.8%) were in conflict with AHCPR guidelines. The most frequent conflict was found to be suboptimal dosing regimen and treatment of chronic pain. Often concurrent analgesics were given with the meperidine to achieve adequate analgesia. Higher analgesic satisfaction scores were noted when meperidine was given with concurrent analgesics. Meperidine also was administered to patients in renal failure or with medications contraindicated with meperidine use. No significant adverse effects were noted with meperidine use in this sample population other than an increased incidence of confusion in the elderly population.

Academic Medical Centers↗
PubMed2002

Meperidine exerts agonist activity at the alpha(2B)-adrenoceptor subtype.

BACKGROUND: The opioid agonist meperidine has actions, such as antishivering, that are more pronounced than those of other opioid agonists and that are not blocked with nonselective opioid antagonists. Agonists at the alpha(2) adrenoceptors, such as clonidine, are very effective antishivering drugs. Preliminary evidence also indicates that meperidine interacts with alpha(2) adrenoceptors. The authors therefore studied the ability of meperidine to bind and activate each of the alpha(2)-adrenoceptor subtypes in a transfected cell system. METHODS: The ability of meperidine to bind to and inhibit forskolin-stimulated cyclic adenosine monophosphate formation as mediated by the three alpha(2)-adrenoceptor subtypes transiently transfected into COS-7 cells has been tested. The ability of the opioid antagonist naloxone and the alpha(2)-adrenoceptor antagonists yohimbine and RX821002 to block the analgesic action of meperidine in the hot-plate test was also assessed. The ability of meperidine to fit into the alpha(2B) adrenoceptor was assessed using molecular modeling techniques. RESULTS: Meperidine bound to all alpha2-adrenoceptor subtypes, with alpha(2B) having the highest affinity (alpha(2B), 8.6 +/- 0.3 microm; alpha(2C), 13.6 +/- 1.5 microm, P < 0.05; alpha(2A), 38.6 +/- 0.7 microm). Morphine was ineffective at binding to any of the receptor subtypes. Meperidine inhibited the production of forskolin-stimulated cyclic adenosine monophosphate mediated by all receptor subtypes but was most effective at the alpha(2B) adrenoceptor (alpha(2B), 0.6 microm; alpha(2A), 1.3 mm; alpha(2C), 0.3 mm), reaching the same level of inhibition (approximately 70%) as achieved with the alpha2-adrenoceptor agonist dexmedetomidine. The analgesic action of meperidine was blocked by naloxone but not by the alpha 2-adrenoceptor antagonists yohimbine and RX821002. The modeling studies demonstrated that meperidine can fit into the alpha(2B)-adrenoceptor subtype. CONCLUSION: Meperidine is a potent agonist at the alpha2 adrenoceptors at its clinically relevant concentrations, especially at the alpha(2B)-adrenoceptor subtype. Activation of the alpha(2B) receptor does not contribute significantly to the analgesic action of meperidine. This raises the possibility that some of its actions, such as antishivering, are transduced by this mechanism.

Adenylyl Cyclase Inhibitors↗
PubMed1975

Two mechanisms for the meperidine block of action potential production in frog's skeletal muscle; non-specific and opiate drug receptor mediated blockade.

The effects of meperidine and naloxone, and their interaction effects on action potential production in frog's sartorius muscle fibres, were studied with intracellular micro-electrode techniques. 1. Meperidine, a narcotic analgesic drug, depressed the rate of rise, the rate of fall and the amplitude of the action potentials. 2. At a meperidine concentration of 0-35 mM, the depression in the action potential maximum rate of rise followed a diphasic time course. At first there was a rapid reduction in the maximum rate of rise which was levelling off at about 60% of control 60-90 min after drug application. This was followed by the second phase during which there was an initial rapid decrease in the maximum rate of rise and all surface fibres were inexcitable by 180 min. 3. The addition of naloxone, a narcotic antagonist, in low concentrations (3 X 10(-5) to 3 X 10(-4) mM) at 70-90 min blocked the second phase of the meperidine-induced depression. 4. With lower concentrations of meperidine (0-18 and 0-07 mM) the depression usually developed more slowly (up to 6 hr with the latter dose) and the addition of low naloxone concentrations partially antagonized the effects of meperidine. However, under no conditions was it possible to completely antagonize the effects of meperidine by the addition of naloxone. 5. A linear relation was found between action potential amplitude and the action potential maximum rate of fall. 6. Meperidine caused a shift in the relation of rate of fall against amplitude to higher action potential amplitudes, indicating that the drug inhibited the increase in potassium conductivity (gK) associated with the falling phase of the action potential. 7. When low naloxone concentrations antagonized the effects of meperidine on the rate of rise and restored action potential amplitudes to control levels, the effect of meperidine on the maximum rate of fall was not antagonized. 8. Larger naloxone concentrations (1-5 X 10(-2) mM or more) depressed the action potential rate of rise but did not alter the relation between action potential amplitude and the maximum rate of fall. 9. It is proposed that meperidine blocks action potential production by two mechanisms: (i) a non-specific mechanism in which the increases in both gNa and gK ar depressed and (ii) an opiate drug receptor mediated mechanism causing a specific depression of gNa. 10. The impression gained from the results is that there are opiate drug receptors located on the inner surface of the muscle membrane associated with the 'sodium channels' and that drug activation of these receptors by either meperidine or high naloxone concentrations interferes with the opening of the 'sodium channels' normally produced by membrane depolarization.

Action Potentials↗
PubMed1981

Drug interaction: meperidine and chlorpromazine, a toxic combination.

To determine the effect of chlorpromazine on the serum concentration-time curve and metabolism of meperidine, 10 healthy volunteers were injected on two separate days in a two-way crossover design with 26 mg/m2 meperidine hydrochloride combined with either 30 mg/m2 chlorpromazine or a placebo. The subjects demonstrated the same serum meperidine concentration-time curves after meperidine plus placebo and meperidine plus chlorpromazine. The excretion of the metabolites normeperidine and normeperidinic acid, however, showed a significant increase with the meperidine-chlorpromazine combination. A marked lethargy was observed after the administration of the meperidine-chlorpromazine combinations in most subjects, which was quite debilitating and may have resulted from the alteration of meperidine metabolism by chlorpromazine. The meperidine-chlorpromazine combination also caused a greater mean depression of the systolic and diastolic pressures than the meperidine-placebo combination. The differences in the blood pressure and symptomatology were significant and represent a potential toxicity that may result from the use of the chlorpromazine-meperidine combination.

Adult↗
PubMed1996

Comparison of intravenous ketorolac, meperidine, and both (balanced analgesia) for renal colic.

STUDY OBJECTIVE: To compare the analgesic efficacy and safety of IV ketorolac, the only nonsteroidal antiinflammatory drug indicated for parenteral use in acute pain in the United States, with IV meperidine and with a combination of the two agents in renal colic. METHODS: We carried out a double-blind, randomized, multicenter clinical trial in the emergency departments of four urban tertiary care teaching hospitals. Our study subjects were 154 patients with suspected renal colic. Each subject received an initial IV dose of ketorolac 60 mg, meperidine 50 mg, or both supplemented as needed beyond 30 minutes with additional doses of meperidine. RESULTS: The main outcome measures were changes in pain-intensity and pain-relief scores, amount of supplemental meperidine required, end-of-study drug tolerability, and adverse events. Analyses of 106 subjects with confirmed renal colic indicated that ketorolac and the combination were significantly better than meperidine alone by all efficacy measures, including pain relief and time elapsed before the need for supplemental meperidine. By 30 minutes, 75% of the ketorolac group and 74% of the combination group had a 50% reduction in pain scores, compared with 23% of the meperidine group (P < .001). The ketorolac and combination groups did not differ significantly in any of the efficacy measures. CONCLUSION: IV ketorolac, alone or in combination with meperidine, was superior to IV meperidine alone in moderate and severe renal colic. Because many subjects in all three treatment groups received supplemental meperidine and because response to ketorolac alone cannot be predicted, clinicians may choose to initiate treatment with a ketorolac-meperidine combination.

Adult↗
PubMed2002

Intravenous single-dose tramadol versus meperidine for pain relief in renal colic.

BACKGROUND AND OBJECTIVE: Comparison of the effectiveness of tramadol with meperidine given intravenously to emergency patients with suspected renal colic. METHODS: A double-blind, randomized clinical trial was performed in the Emergency Department of a tertiary-care university hospital. Consecutive patients with suspected renal colic (n = 47) were randomized to receive intravenously an initial dose of tramadol 50 mg (n = 23) or meperidine 50 mg (n = 24). After 30 min, additional doses of meperidine 50 mg were given intravenously as a rescue medication in an open fashion. Pain relief was assessed using a 10 cm visual analogue scale, the primary outcomes being pain relief at 15 and 30 min after the analgesics. Secondary outcomes were the frequency of rescue meperidine use and the development of side-effects. RESULTS: Visual analogue scale pain scores after 15 and 30 min decreased in both tramadol and meperidine groups (P < 0.05). However, pain relief was better in the meperidine group at the 15 and 30 min evaluations (P < 0.05). Only 11 patients (48%), initially receiving meperidine, needed more meperidine compared with 16 patients (67%) initially receiving tramadol. Both drugs were well tolerated with no adverse effects occurring in either group. CONCLUSIONS: Meperidine 50 mg was superior to tramadol 50 mg for acute pain relief in patients with suspected renal colic when given intravenously. Because many patients in both groups received supplemental meperidine and the response to tramadol alone cannot be predicted, clinicians may want to choose higher doses of meperidine alone or other alternative combinations.

Adult↗
PubMed2000

N-methyl-D-aspartate receptor channel block by meperidine is dependent on extracellular pH.

UNLABELLED: Large concentrations of meperidine inhibit N-methyl-D-aspartate-(NMDA) receptor channels by channel block mechanisms. Extracellular pH regulates the activity and drug sensitivity of NMDA-receptor channels. We examined the influence of extracellular pH on sensitivity to meperidine of epsilon/zeta heteromeric NMDA-receptor channels expressed in Xenopus oocytes. Inhibition of epsilon1/zeta1, epsilon2/zeta1, epsilon3/zeta1, and epsilon4/zeta1 channels by meperidine was dependent on pH, with more inhibition at acidic pH and less inhibition at alkaline pH. The degree of voltage-dependence of meperidine block was only slightly affected by changes in pH, whereas affinity for meperidine was greatly reduced at alkaline pH. Furthermore, interaction of meperidine with Mg(2+) block was reduced at alkaline pH. Because the percentage of the protonated form of meperidine is only slightly affected by pH, changes in properties of the meperidine binding site may be involved in mechanisms of alteration of meperidine potency by pH. IMPLICATIONS: At acidic pH the potency of meperidine for N-methyl-D-aspartate-receptor channels was increased. Any antinociceptive and neuroprotective benefit from the N-methyl-D-aspartate-receptor antagonist property of meperidine may be pH dependent.

Analgesics, Opioid↗
PubMed1987

Pharmacokinetics of epidural morphine and meperidine in humans.

Five groups of surgical patients, each comprising six individuals, received epidural doses of morphine or meperidine, and the plasma and CSF kinetics were studied. Three groups received epidural doses of morphine 3 mg in 1 or 10 ml or meperidine 30 mg in 1 ml. Cerebrospinal fluid (CSF) and central venous blood opioid concentrations were measured intermittently for 6 h after injection. Two groups received epidural doses of morphine 3 mg in 1 ml or meperidine 30 mg in 1 ml, and opioid CSF concentrations were determined over a 24-h period. Morphine appeared rapidly in plasma, and maximum plasma concentrations were usually detected 5 min after injection and averaged 33 ng.ml-1 in the 1-ml volume group and 40 ng.ml-1 in the 10-ml volume group. The terminal plasma half-life averaged 91 +/- 34 min and 87 +/- 27 min, respectively (mean +/- SEM). Maximal plasma concentrations of meperidine were usually detected 10 or 15 min post-injection and averaged 196 +/- 29 ng.ml-1. The terminal plasma half-life averaged 124 +/- 26 min. Morphine crossed the dura relatively slowly, and the absorption half-life across the dura averaged 22 min. Maximal CSF concentrations were usually seen 60-90 min post-injection. In contrast, meperidine crossed the dura quickly, with an absorption half-life averaging 7.6 +/- 2.0 min. Maximal CSF concentrations were seen 15 or 30 min post-injection. Morphine and meperidine concentrations remained several times higher in the CSF than in the plasma. The fraction of the opioid dose crossing the dura was calculated to be 3.6% for morphine and 3.7% for meperidine. There were no significant differences in the kinetics of morphine administered in 1 or in 10 ml when CSF was sampled close to the site of lumbar epidural injection. The CSF concentration-time curves of both drugs decreased biexponentially after the initial rise due to diffusion across the dura. The early half-life in CSF averaged 73.3 +/- 11.5 min for morphine and 71.3 +/- 3.1 min for meperidine, and the late half-life averaged 369 +/- 113 min for morphine and 982 +/- 449 min for meperidine. Dose-normalized morphine and meperidine CSF concentrations after epidural administration showed that meperidine concentrations were down to one-fourth the corresponding morphine concentrations from the 2nd to the 15th h after administration, which may partly explain the longer duration of analgesia from morphine.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

Naloxone, meperidine, and shivering.

BACKGROUND: Meperidine, which binds both mu and kappa opioid receptors, is reportedly more effective in treating shivering than are equianalgesic doses of morphine (a nearly pure mu-receptor agonist). Furthermore, butorphanol, a kappa-receptor agonist/antagonist, treats shivering better than does fentanyl, which mostly binds mu receptors. These data indicate that much of meperidine's special antishivering activity may be mediated by its kappa activity. Accordingly, the authors tested the hypothesis that the antishivering activity of meperidine will be minimally impaired by low-dose naloxone (blocking most mu-receptors), but largely prevented by high-dose naloxone (blocking all mu and most kappa receptors). METHODS: Twelve volunteers each participated on 2 days. On both days, shivering was induced by central venous infusion of cold fluid. Twenty minutes later, six volunteers were given a placebo infusion of saline on one day, or an infusion of 0.5 microgram.kg-1.min-1 naloxone hydrochloride ("low-dose," designed to block mu receptors) on the other. The second group of six volunteers was given a saline bolus and infusion on one day, or a bolus of 11.5 micrograms/kg naloxone hydrochloride followed by an infusion of naloxone at 5 micrograms.kg-1.min-1 ("high-dose," designed to block both mu and kappa receptors) on the other day. The infusions were continued for the duration of the study. The order of the treatment days (saline vs. naloxone) was randomly assigned, and the study was double blinded. Fifteen minutes after the test infusion was started, all 12 volunteers were given an intravenous bolus of 1 mg/kg meperidine hydrochloride. Pupillary diameter and light reflex amplitude were used to quantify opioid-receptor agonist activity; shivering intensity was evaluated using oxygen consumption. RESULTS: Administration of naloxone alone did not alter oxygen consumption, pupil size, or the pupillary light reflex. No pupillary constriction was detected in either group when naloxone and meperidine were combined; in contrast, meperidine alone decreased pupil size and amplitude of the light reflex 30%. The meperidine bolus decreased oxygen consumption nearly to control values when the volunteers were given saline placebo. Combined administration of meperidine and low-dose naloxone also significantly reduced oxygen consumption, but the reduction and the duration of the reduction was less than during saline. When the volunteers were given high-dose naloxone, meperidine only slightly reduced oxygen consumption, and the values rapidly returned to premeperidine levels. CONCLUSIONS: These data indicate that the antishivering property of meperidine is not fully mediated by mu-receptors. Although meperidine has well-known nonopioid actions, stimulation of kappa receptors seems a likely alternative explanation for much of the drug's antishivering action.

Adult↗
PubMedDate not supplied

Comparison of methotrimeprazine and meperidine as components of balanced anesthesia.

Methotrimeprazine (MTM) (0.5 mg/kg) and meperidine (1.5 mg/kg) was administered to four groups of 10 patients each. Two of these groups (I and II) received MTM or meperidine 12 minutes before, two other groups (III and IV), 3 minutes after, induction of thiopental anesthesia. N2O-O2 was administered after thiopental induction, and fractional doses of meperidine and muscle relaxants were used as required for maintenance of anesthesia. The preliminary administration of MTM or meperidine decreased the induction dose of thiopental by about 60 percent. When administered before thiopental, both had similar effects on heart rate, but whereas MTM moderately decreased, meperidine moderately increased systolic and diastolic blood pressure MTM had little or no effect on respiratory rate, which was significantly depressed by meperidine. When given after an induction dose of thiopental, the circulatory effects of MTM and meperidine were similar. Respiratory measurements were little affected by MTM but were markedly depressed by meperidine. The mug/kg/min maintenance doses of meperidine were about the same in the four groups. Postanesthetic recovery of consciousness was delayed in the two MTM groups. The incidence of postoperative nausea and vomiting was less in the MTM than in the meperidine groups. MTM appears to have several advantages over meperidine as a component of balanced anesthesia, but is not desirable if rapid postanesthetic recovery or early ambulation is important. Its use is indicated in patients in whom even transient respiratory depression is undesirable and in those in whom prolonged postoperative sedation is desired.

Adolescent↗
PubMed2003

Meperidine misuse in a patient with sphincter of Oddi dysfunction.

OBJECTIVE: To report a seizure occurring secondary to meperidine treatment despite normal renal and central nervous system (CNS) function, and to provide a review of meperidine's role in pain management, including its use in pancreatitis and sphincter of Oddi dysfunction. CASE SUMMARY: A 55-year-old white woman with a history of sphincter of Oddi dysfunction presented to the emergency department with severe abdominal pain. On admission to the hospital, the serum creatinine level was 0.6 mg/dL with slightly elevated aspartate aminotransferase of 56 U/L (normal range 0-31) and alanine aminotransferase of 34 U/L (0-31). The patient received repeated and escalating doses of intravenous meperidine, resulting in a generalized seizure on day 4 of hospitalization. The accumulated meperidine dose was 2125 mg. Buprenorphine was substituted in place of meperidine, and the patient had no further reported complications. She was then transferred to a tertiary-care facility for sphincter of Oddi reevaluation. An objective causality assessment revealed the adverse drug event as probable. DISCUSSION: Despite alternative opioids, meperidine continues to be used in pain management. Meperidine is different from other opioids because its active metabolite, normeperidine, is neurotoxic. Patients with renal insufficiency, liver failure, or CNS dysfunction are at increased risk for adverse drug reactions related to normeperidine accumulation. Due to normeperidine's extended half-life, however, accumulation of normeperidine can occur in any patient receiving repeated doses of meperidine. CONCLUSIONS: This case demonstrates the potential hazards that exist when using meperidine in any patient. Meperidine's inherent risks of both undertreating pain and causing adverse drug reactions should prompt clinicians and health organizations to restrict its use in pain management. This restriction should not make exceptions to meperidine's traditional use in pancreatitis or sphincter of Oddi dysfunction.

Analgesics, Opioid↗
PubMedDate not supplied

[Administration of lysine acetylsalicylate and meperidine in acute postoperative pain].

INTRODUCTION: Postoperative analgesia is insufficiently done due, among others, to the undesirable effects of analgesic agents. OBJECTIVE: The aim of this study was to analyze the effects of the simultaneous administration of opiates (meperidine) and AINES (lysine acetylsalicylate, ASL). MATERIAL AND METHODS: We studied 160 patients during the immediate postoperative phase. All of them underwent programmed surgery with the same general anesthetic technique. Patients were allocated into 8 groups of treatment: A) ASL 900 mg and 1.800 mg/8 h, B) ASL 900 mg and 3.600 mg/8 h, C) ASL 900 mg and meperidine 100 mg/8 h, D) ASL 900 mg and 1.800 mg/8 h together with meperidine 100 mg/8 h, E) meperidine 50 mg and ASL 1.800 mg/8 h, F) meperidine 50 mg and ASL 3.600 mg/8 h, G) meperidine 50 mg and 100 mg/8 h, and H) meperidine 50 mg and 100 mg/8 h together with ASL 1.800 mg/8 h. The effects of analgesic agents were evaluated on the basis of patient's appreciation of the degree of pain and relief and on the basis of an observer who did not know the therapeutic regime administered. Results were compared according to the analysis of variance in a graded factorial design. A p value less than 0.05 was considered significant. RESULTS: The degree of pain was significantly lower in groups C, D, G and H (specially in G and H) than in the remaining groups, but there were no significant differences between them. The lowest pain relief was observed in groups A, B, E and F. The highest attenuation of pain was achieved in groups G and H. The highest attenuation of pain was achieved in groups G and H. The observer considered that the two latter groups were those with the highest pain relief, followed by groups C and D. The remaining patients failed to show appreciable improvement. Nausea and vomiting only occurred in some patients after administration of a bolus of meperidine. There were no other secondary effects. CONCLUSIONS: The best degree of postoperative analgesia is achieved after administration of continuous infusion of meperidine 100 mg/8 h. Simultaneous infusion of ASL 1.800 mg/8 h did not improve the analgesia obtained with a bolus of 900 mg of ASL nor with a bolus of 50 mg of meperidine. Secondary effects were only nausea and vomiting and coincided with the administration of a bolus of meperidine.

Adult↗
PubMed2004

Determinants of prescribing meperidine compared to morphine in hospitalized patients.

Morphine is a preferred narcotic since meperidine forms toxic metabolites. Determinants of meperidine use have been poorly described. The objective of this study is to explore factors associated with the ordering of meperidine versus morphine. Retrospective chart review of adult patients, randomly selected based on orders for morphine or meperidine. 1552 orders were written for 670 patients. Of these, 36% were for meperidine. In multivariable analysis, the ordering of meperidine was associated with the following variables in decreasing order of importance: physician specialty, total doses received, hospital location, patient race, age and insurance, and physician gender. More orders for meperidine were written for those receiving fewer doses. Though meperidine has little role in the routine management of hospital pain, we found it continues to be used frequently. Importantly, meperidine is ordered more frequently for patients who receive shorter courses of narcotics. Our study suggests that interventions targeted at more appropriate use of meperidine rather than complete elimination might be more acceptable to physicians while minimizing the risk of toxicity.

Adult↗
PubMedDate not supplied

Subarachnoid meperidine-morphine combination. An effective perioperative analgesic adjunct for cesarean delivery.

BACKGROUND AND OBJECTIVES: Low-dose subarachnoid morphine provides effective perioperative analgesia but may be associated with a transient period of inadequate pain relief between the regression of local anesthetic block and the onset of morphine's analgesic effect. We hypothesized that this period of suboptimal analgesia could be avoided by adding meperidine, a rapid-acting, intermediate-duration opioid. METHODS: In a double-blind, randomized trial, 49 patients scheduled for elective cesarean delivery received subarachnoid 0.75% bupivacaine, 12 mg in 8.25% dextrose, with either meperidine 10 mg, morphine 0.15 mg, or meperidine 10 mg plus morphine 0.15 mg. Visual analog scale scores for pain and satisfaction were obtained at skin incision, delivery, uterine exteriorization, on arrival in the postanesthesia care unit, and 2, 4, 6, 12, and 24 hours after drug administration. Neonatal Apgar scores and adverse effects were also noted. Postoperative intravenous patient-controlled analgesia (PCA) requirements were recorded for 24 hours. The data were analyzed by chi-square analysis Fisher's exact test, the Wilcoxon rank sum test, and analysis of variance with Tukey's adjustment for multiple comparisons. RESULTS: There were no significant differences in the incidence and severity of side effects, including nausea, vomiting, pruritus, and sedation. Respiratory depression was not observed. Patients treated with morphine alone were least comfortable (P < .006), expressed the lowest satisfaction scores at early observations (P < .002), and required more PCA meperidine (P < .001) than any other group. Patients treated with meperidine alone were comfortable at early observations but required the greatest total amount of PCA meperidine over the first 24 hours (P < .05). Patients in the meperidine-morphine combination group reported the lowest pain scores and highest satisfaction scores at 4-hour and 6-hour observations (P < .03) and required the least total amount of PCA meperidine. CONCLUSION: The subarachnoid combination of meperidine-morphine provided more uniform analgesia, higher satisfaction, and a lower requirement for intravenous narcotic supplementation than either morphine or meperidine alone in patients recovering from cesarean delivery.

Adult↗
PubMed1999

A dose-response study of intravenous regional anesthesia with meperidine.

UNLABELLED: Intravenous regional anesthesia (IVRA) with meperidine in doses > or = 100 mg provides effective postoperative analgesia. However, this technique is associated with excessive opioid-related side effects, which limit its clinical usefulness. The minimal dose of meperidine that is effective for IVRA has yet to be established. We added 0, 10, 20, 30, 40, or 50 mg of meperidine to 0.5% lidocaine IVRA for either carpal tunnel or tenolysis surgery. Pain and sedation scores and the incidence of side effects were assessed in the postanesthesia care unit. The duration of analgesia, defined as the time to first request for pain medications, and use of acetaminophen/codeine (T3) tablets were measured. The duration of analgesia increased, in a dose-dependent manner, in the groups that received 0, 10, 20, and 30 mg of meperidine. There was no significant difference in the duration of analgesia for patients receiving > or = 30 mg of meperidine. T3 use was similar in the groups that received 0, 10, and 20 mg of meperidine and in the groups that received 30, 40, and 50 mg. T3 use was significantly lower in the larger dose groups. The incidence of sedation and of all other side effects was significantly higher in the groups that received 30-50 mg of meperidine compared with those that received smaller doses. We conclude that doses of meperidine large enough to produce the most effective postoperative analgesia with IVRA lidocaine causes a significant incidence of side effects, thus limiting its clinical usefulness. IMPLICATIONS: Meperidine may be a useful addition to 0.5% lidocaine for i.v. regional anesthesia. We showed that 30 mg is the optimal dose of meperidine with respect to postoperative analgesia. However, this dose caused a significant incidence of sedation, dizziness, and postoperative nausea and vomiting.

Adult↗
PubMed1998

Meperidine and alfentanil do not reduce the gain or maximum intensity of shivering.

BACKGROUND: Thermoregulatory shivering can be characterized by its threshold (triggering core temperature), gain (incremental intensity increase with further core temperature deviation), and maximum intensity. Meperidine (a combined mu- and kappa-agonist) treats shivering better than equianalgesic doses of pure mu-opioid agonists. Meperidine's special antishivering action is mediated, at least in part, by a disproportionate decrease in the shivering threshold. That is, meperidine decreases the shivering threshold twice as much as the vasoconstriction threshold, whereas alfentanil (a pure mu-agonist) decreases the vasoconstriction and shivering thresholds comparably. However, reductions in the gain or maximum shivering intensity might also contribute to the clinical efficacy of meperidine. Accordingly, we tested the hypothesis that meperidine reduces the gain and maximum intensity of shivering much more than alfentanil does. METHODS: Ten volunteers were each studied on three separate days: (1) control (no drug); (2) a target total plasma meperidine concentration of 1.2 microg/ml; and (3) a target plasma alfentanil concentration of 0.2 microg/ml. Skin temperatures were maintained near 31 degrees C, and core temperatures were decreased by central-venous infusion of cold lactated Ringer's solution until maximum shivering intensity was observed. Shivering was evaluated using oxygen consumption and electromyography. A sustained increase in oxygen consumption identified the shivering threshold. The gain of shivering was calculated as the slope of the oxygen consumption versus core temperature regression, and as the slope of electromyographic intensity versus core temperature regression. RESULTS: Meperidine and alfentanil administration significantly decreased the shivering thresholds. However, neither meperidine nor alfentanil reduced the gain of shivering, as determined by either oxygen consumption or electromyography. Opioid administration also failed to significantly decrease the maximum intensity of shivering. CONCLUSIONS: The authors could not confirm the hypothesis that meperidine reduces the gain or maximum intensity of shivering more than alfentanil does. These results suggest that meperidine's special antishivering effect is primarily mediated by a disproportionate reduction in the shivering threshold.

Adjuvants, Anesthesia↗