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PubMed1999

Regular use of analgesics is a risk factor for renal cell carcinoma.

Phenacetin-based analgesics have been linked to the development of renal pelvis cancer and renal cell carcinoma (RCC). The relationship between non-phenacetin types of analgesics and kidney cancer is less clear, although laboratory evidence suggests that these drugs possess carcinogenic potential. A population-based case-control study involving 1204 non-Asian RCC patients aged 25-74 and an equal number of sex-, age- and race-matched neighbourhood controls was conducted in Los Angeles, California, to investigate the relationship between sustained use of analgesics and risk of RCC according to major formulation categories. Detailed information on medical and medication histories, and other lifestyle factors was collected through in-person interviews. Regular use of analgesics was a significant risk factor for RCC in both men and women (odds ratio (OR) = 1.6, 95% confidence interval (CI) = 1.4-1.9 for both sexes combined). Risks were elevated across all four major classes of analgesics (aspirin, non-steroidal anti-inflammatory agents other than aspirin, acetaminophen and phenacetin). Within each class of analgesics, there was statistically significant increasing risk with increasing level of exposure. Although there was some minor variability by major class of formulation, in general individuals in the highest exposure categories exhibited approximately 2.5-fold increase in risk relative to non- or irregular users of analgesics. Subjects who took one regular-strength (i.e. 325 mg) aspirin a day or less for cardiovascular disease prevention were not at an increased risk of RCC (OR = 0.9, 95% CI = 0.6-1.4).

Acetaminophen↗
PubMed2001

Long-term follow-up of patients treated for chronic headache with analgesic overuse.

The study aim is to describe the long-term clinical outcome of 102 chronic headache patients with analgesic daily use. They were assessed for daily drug intake (DDI), headache index (HI) and quality of life (QoL) and compared with a parallel group of patients with active chronic daily headache but no analgesic overuse. For the primary study group, baseline 1995 DDI was 1.80 +/- 1.87 and did not differ significantly in 1999. Patients who daily continued to use analgesics had a higher 1995 baseline DDI (t = 2.275, P = 0.025), a longer drug abuse history (t = 2.282, P = 0.025) and a higher DDI (t = 4.042, P < 0.001) 4 years later. At 4 years of follow-up, only one-third of patients initially treated for chronic daily headache and analgesic overuse are successful in refraining from chronic overuse. Those subjects appear to have a persistence for combination analgesic agents; however, their QoL is slightly better than that of patients who revert to episodic headache or continue with chronic daily headache but do not overuse analgesic agents. Persistent analgesic overuse seems to be linked to the length of abuse and to the number of drugs ingested.

Adult↗
PubMed2003

Caffeine as a promoter of analgesic-associated nephropathy--where is the evidence?

Individual groups of nephrologists - in their responsibility for their patients - initiated a most controversial discussion whether or not caffeine - coformulated to analgesics - might initiate or sustain analgesic overdosing. The original sources (data) of such suspicion have got lost during the debate of the last two decades. Therefore, it seemed to be appropriate to investigate the original data background and the reasons why nephrologists started to suspect caffeine as a stimulant of analgesic overdosing by employing a systematic and exhaustive review of primary nephrological publications. Their selection followed a precise selection plan, including all epidemiological studies on analgesic-associated nephropathy, the original papers of all groups having been involved in those studies, further originals from the mainly involved countries (academically, politically), and any literature thereof cited as a proof. The following results emerged from the investigation: (i) The epidemiological studies warranted no conclusion about a role of caffeine in prompting excessive analgesic use. (ii) The identified groups of nephrologists provided not substantial data to advocate the said suspicion, except for the observation of a preferential choice of phenacetin-containing combinations, especially powder preparations. (iii) Only two cited original data sources revealed drug-seeking behaviour with phenacetin-containing preparations which subsided, after phenacetin was banned from the respective markets. Conclusively, it appears that there is no substantial data to support a pivotal role of caffeine in initiating or sustaining analgesic overdosing. However, there is strong data that phenacetin, by its psychotropic properties, may have caused drug-seeking behaviour and thus led to analgesic overdosing. This conclusion is convincingly supported by thorough pharmacokinetic investigations. Note: All caffeine-related statements within the reviewed literature have been collected in tables (referred to as Table SX) which are provided in full text for check on the following website: http://www.blackwellpublishing.com/products/journals/suppmat/FCP/FCP174/FCP174sm.htm

Analgesics↗
PubMed2002

Triptans versus analgesics.

OBJECTIVES: To retrospectively assess patient preferences between triptans and analgesics in treating migraine headache. METHODS: The study assessed patient preferences for triptans versus commonly used migraine analgesic preparations. Over a 3-month period, 663 patients with migraine between the ages of 17 and 62 years completed an office-based survey. RESULTS: Most patients preferred a treatment regimen that included either a triptan alone (52%) or a triptan with an analgesic medication within 1 hour (18%). Overall, 70% of patients who had been given triptans in the past chose to continue to use them, either alone or with an analgesic. Patients who preferred analgesics alone comprised 21% of the total. Nine percent preferred not to take either triptans or analgesic medications. Among the patients who preferred triptans, 62% stated that increased efficacy was the primary reason for their preference. Thirty percent cited both efficacy and decreased adverse events. The remaining 8% believed that decreased adverse events was the basis for their preference. CONCLUSIONS: Despite cost and other limitations of triptans, most patients prefer them over nontriptan medications. Enhanced efficacy was the main reason for choosing triptans over analgesics.

Adolescent↗
PubMed2002

Patterns of analgesic use in trauma patients in the ED.

The objective was to describe patterns of analgesic use for trauma patients treated in our emergency department (ED). We reviewed analgesic use in consecutive patients meeting American College of Surgeons (ACS) Trauma Center Guidelines. A comprehensive database was abstracted from this institution's Trauma Registry and medical records of each patient. A total of 38% (95% CI: 31-46%) of patients received analgesics. Time to administration of first dose of analgesia was 109 minutes (95% CI: 85-133). Women, patients with long bone and pelvic fractures, and those with a longer ED stay were most likely to receive analgesics. Patients with head trauma and those admitted to the intensive care unit were least likely to receive analgesics. Morphine was the most frequent analgesic used with an average total dose of 14 milligrams. A majority of patients meeting ACS Trauma Center Guidelines did not receive analgesics in the ED.

Adolescent↗
PubMed2001

Interindividual differences in the analgesic response to ketamine in chronic orofacial pain.

The analgesic effect of the N-methyl-D-aspartate (NMDA) receptor blocker ketamine in 17 patients (13 females and four males, age 32-88 years) who had suffered neuropathic orofacial pain for time periods ranging from 6 months to 28 years was examined. The patients were given an i.m. test-dose of 0.4 mg/kg ketamine combined with 0.05 mg/kg midazolam. Four patients did not experience any analgesic effect of the i.m. test dose. The remaining 13 patients experienced an analgesic effect which lasted for less than 1 h (transient effect) in seven and for several hours (long-term effect) in six. One week later they were given 4 mg/kg ketamine to be taken orally in combination with a hypnotic drug for three consecutive nights. All patients who reported a long-term analgesic effect after i.m. ketamine also reported reduced pain intensity on days after taking ketamine at night. The findings of this open study are in accord with the results from a previous double-blind randomized investigation. In order to evaluate the role of age and pain duration for the analgesic effect of ketamine, we pooled the data from the two studies and performed a correlation analysis of 43 patients. We found a positive correlation between a long pain-history and lack of analgesic effect and also between a short pain-history and a long-term analgesic effect of low-dose ketamine. The apparent relationship between patient age and ketamine response was, however, not statistically significant. Further, patients with pain following a nerve lesion and patients without a known lesion of peripheral nerves were equally distributed between the three response groups. These results indicate that pain mechanisms are subject to alterations with time and that these alterations involve transition from NMDA to non-NMDA receptor mediated transmission in central pain pathways.

Adjuvants, Anesthesia↗
PubMed2000

Do caffeine-containing analgesics promote dependence? A review and evaluation.

OBJECTIVE: Debates about the suspected association between kidney disease and use of analgesics have led to concern about whether caffeine could stimulate an undesirable overuse of phenacetin-free combined analgesics. A committee was asked to critically review the pertinent literature and to suggest guides for clinical practice and for consideration of international regulatory authorities. PARTICIPANTS: A group of international scientists, jointly selected by the regulatory authorities of Germany, Switzerland, and Austria and the pharmaceutical industry. EVIDENCE: All invited experts evaluated relevant literature and reports and added further information and comments. CONCLUSIONS: Caffeine has a synergistic effectiveness with analgesics. Although caffeine has a dependence potential, the potential is low. Experimental data regarding dependence potential for caffeine alone may not correspond to the conditions in patients with pain. Withdrawal is not likely to cause stimulation or sustainment of analgesic intake. For drug-induced headache, no single or combined analgesic was consistently identified as causative, and no evidence exists for a special role of caffeine. Strong dependence behavior was observed only in patients using phenacetin-containing preparations, coformulated with antipyretics/analgesics and caffeine. This finding may have led to the impression that caffeine stimulates overuse of analgesics. SUMMARY: Although more experimental and long-term data would be desirable to show possible mechanisms of dependence and to offer unequivocal proof of safety, the committee concluded that the available evidence does not support the claim that analgesics coformulated with caffeine, in the absence of phenacetin, stimulate or sustain overuse.

Analgesics↗
PubMed2004

Influence of anaesthetic and analgesic techniques on outcome after surgery.

Postoperative symptoms and complications can be prevented by a suitable choice of anaesthetic and analgesic technique for specific procedures. The aim of analgesic protocols is not only to reduce pain intensity but also to decrease the incidence of side-effects from analgesic agents and to improve patient comfort. Moreover, adequate pain control is a prerequisite for the use of rehabilitation programmes to accelerate recovery from surgery. Thus, combining opioid and/or non-opioid analgesics with regional analgesic techniques not only improves analgesic efficacy but also reduces opioid demand and side-effects such as nausea and vomiting, sedation, and prolongation of postoperative ileus. Although all attempts to demonstrate that regional anaesthesia and analgesia decrease postoperative mortality are unsuccessful, there is evidence supporting a reduction in pulmonary complications after major abdominal surgery, and an improvement in patient rehabilitation after orthopaedic surgery. When such techniques are used, cost-benefit analysis should be considered to determine suitable analgesic protocols for specific surgical procedures.

Abdomen↗
PubMed2006

Long-term effects of analgesics in a population of elderly nursing home residents with persistent nonmalignant pain.

BACKGROUND: Little is known about the long-term effects of analgesics on functional status and well-being of nursing home residents with chronic pain. METHODS: Using the Minimum Data Set, we performed a longitudinal study of nursing home residents (n = 10,372) with persistent pain. Using propensity score adjustment techniques, we compared the effect of different analgesics on changes in physical, cognitive, emotional, and social functioning, and examined rates of adverse events over a 6-month period. RESULTS: There was no change in the analgesic class for at least 6 months for 35.4% of residents, including 40% who received no analgesics during this time. Use of nonopioids was 37.9%, short-acting opioids was 18.9%, and long-acting opioids was 3.3%. We found improvement in functional status (adjusted hazard ratio = 1.85; 95% confidence interval [CI], 1.05-3.23) and social engagement (adjusted hazard ratio = 1.58; 95%, CI, 0.99-2.50) with long-acting opioids compared with short-acting opioids. There were no changes in cognitive status or mood status, or increased risk of depression with use of any analgesics, including opioids. There was a trend toward a lower risk of falls with use of any analgesics (adjusted odds ratio = 0.87; 95% CI, 0.70-1.06). Rates of other adverse events (i.e., constipation, delirium, dehydration, pneumonia) were not found to be higher among chronic opioid users compared to those taking no analgesics or nonopioids. CONCLUSIONS: The use of long-acting opioids may be a relatively safe option in the management of persistent nonmalignant pain in the nursing home population, yielding benefits in functional status and social engagement.

Affect↗
PubMed1999

Incidence of analgesic nephropathy in Berlin since 1983.

BACKGROUND: Phenacetin was removed from the German market in 1986 and was replaced mainly in analgesic compounds by acetaminophen. Our objective was to examine the effect of this measure on the incidence of analgesic nephropathy in light of the changes in other end-stage renal diseases. METHODS: We therefore compared the proportion of renal diseases in all patients starting dialysis treatment during three 18-month periods: 4/1982-9/1983 (n=57); 1/1991-6/1992 (n=81); and 10/1995-3/1997 (n=76). RESULTS: On the one hand, the proportion of end-stage analgesic nephropathy decreased significantly from 30% in 1981-1982 to 21% in 1991-1992 and 12% in 1995-1997 (P=0.01). On the other hand, type II diabetes increased significantly from 7% to 22% (P=0.01) and 29%, (P=0.001). Using the chi2 distribution test to analyze the frequencies of seven diseases at three different time intervals, however, showed that the changes in renal-disease proportions between 1982-1983, 1991-1992 and 1995-1997 were not significantly independent. There was a significant median age increase from 52 years (CI0.95 44-58) in 1982-1983 to 63 (CI0.95 55-67) in 1991-1992 and 63 (CI0.95 60-66) in 1995-1997 (P=0.003) for all patients starting dialysis but not for those with analgesic nephropathy [59 (55-71) vs 64 (53-67) and 61 (50-72); n.s.]. CONCLUSION: The decrease of end-stage analgesic nephropathy since 1983 may be partially due to the removal of phenacetin from the German market in 1986. However, considering the general increase in numbers of dialysis patients, their higher age and the increased incidence of type II diabetes, the decrease in analgesic nephropathy is not a statistically significant independent variable. Altered admittance policies for dialysis treatment have yielded a new pattern of renal-disease proportion which interferes with changes in the incidence of analgesic nephropathy.

Acetaminophen↗
PubMed1996

Hypnotic and analgesic effects of the alpha 2-adrenergic agonist dexmedetomidine in morphine-tolerant rats.

Combinations of alpha 2 agonists and opiates are used in the clinical management of pain to harness their potential synergistic interaction for analgesia while limiting their side-effects. To better predict the clinical consequences of this combination, we studied the behavioral effects of dexmedetomidine, a highly selective alpha 2 agonist with analgesic and hypnotic properties, during the development of, and recovery from, morphine tolerance. Rats were implanted with morphine pellets (or placebo), daily for 5 days. The analgesic response to morphine, dexmedetomidine, or the combination of the two drugs was assessed with the tail-flick latency response. The hypnotic response to dexmedetomidine, and to the combination of dexmedetomidine and morphine, was measured by the duration of the loss of righting reflex (sleep-time). One day after the last morphine pellet implantation, alpha 2 adrenoceptor binding was assessed in vitro in the locus coeruleus (LC) and the spinal cord (SC). Data were analyzed by analysis of variance (ANOVA), t-test, or Mann-Whitney test. The morphine tolerance was present after 1 day of morphine administration. At Days 1 and 3 of morphine administration, the hypnotic and analgesic responses to dexmedetomidine were significantly increased. After 5 days of morphine treatment, the analgesic response to dexmedetomidine was unaltered, while the hypnotic response to dexmedetomidine was now significantly decreased. The kd for the alpha 2 adrenoceptors was unaffected while the Bmax was significantly decreased only in the SC. Acutely administered morphine significantly enhanced the hypnotic and analgesic effects of dexmedetomidine in naive rats but not in morphine-tolerant rats. During morphine withdrawal, the hypnotic response to dexmedetomidine normalized; however, the analgesic response to dexmedetomidine was significantly decreased 5 days after withdrawal before returning to normal at Day 10 after withdrawal. We conclude that in the development of, and recovery from, the morphine-tolerant state, the hypnotic and analgesic responses to alpha 2 agonists are asynchronous.

Adrenergic alpha-Agonists↗
PubMed1998

The analgesic potency of dexmedetomidine is enhanced after nerve injury: a possible role for peripheral alpha2-adrenoceptors.

UNLABELLED: This study investigated the analgesic potency and site of action of systemic dexmedetomidine, a selective alpha2-adrenoceptor (alpha2AR) agonist, in normal and neuropathic rats. Ligation of the L5-6 spinal nerves produced a chronic mechanical and thermal neuropathic hyperalgesia in rats. von Frey fibers and a thermoelectric Peltier device were used to measure mechanical and heat withdrawal thresholds over the hindpaw. Systemic dexmedetomidine dose-dependently increased the mechanical and thermal thresholds in the control animals (50% effective dose [ED50] 144 and 180 microg/kg intraperitoneally [i.p.], respectively). Neuropathic animals responded to much smaller doses of dexmedetomidine with mechanical and thermal ED50 values of 52 and 29 microg/kg i.p., respectively. There was no difference between the control and neuropathic animals with respect to dexmedetomidine-evoked sedation, as determined by decreased grid crossings in an open-field activity chamber (ED50 12 and 9 microg/kg i.p., respectively). Atipamezole, a selective alpha2AR antagonist, blocked the analgesic and sedative actions of dexmedetomidine inboth the neuropathic and control animals. However, L-659,066, a peripherally restricted alpha2AR antagonist, could only block the analgesic actions of dexmedetomidine in the neuropathic rats, with no effect in control animals. In conclusion, nerve injury enhanced the analgesic but not the sedative potency of systemic dexmedetomidine and may have shifted the site of alpha2 analgesic action to outside the blood-brain barrier. IMPLICATIONS: We tested the analgesic efficacy of the alpha2 agonist dexmedetomidine in normal and nerve-injured rats. The analgesic potency of dexmedetomidine was enhanced after nerve injury with a site of action outside the central nervous system. Peripherally restricted alpha2 agonists may be useful in the management of neuropathic pain.

Adrenergic alpha-Agonists↗
PubMed1999

Clonidine administered as an axillary block does not affect postoperative pain when given as the sole analgesic.

UNLABELLED: Used as the sole analgesic, clonidine produces analgesia after epidural, intrathecal, and intraarticular administration. We conducted this double-blinded study to determine whether clonidine has analgesic effects when administered into the brachial plexus sheath. At the conclusion of hand or forearm surgery, performed under axillary brachial plexus block, 45 patients were randomly divided into three groups of 15 each to receive, through an axillary catheter, 15 mL of saline (Group Saline), clonidine 150 microg in 15 mL of saline (Group Clonidine), or bupivacaine 15 mL (Group Bupivacaine). The analgesic effects of the three solutions were evaluated for 6 h. Times to onset of pain and to first analgesic request were longer, and the total dose of pain medication was smaller in Group Bupivacaine compared with the other groups. Visual analog scores were significantly lower in Group Bupivacaine. There was no significant difference in time to onset of pain, time to first analgesic request, total dose of pain medication, and visual analog scores between Group Saline and Group Clonidine at any time. We conclude that the administration of clonidine 150 microg into the brachial plexus sheath does not prolong the onset of postoperative pain. IMPLICATIONS: Used as the sole analgesic, clonidine produces analgesia after epidural, intrathecal, and intraarticular administration. It also prolongs the analgesic effect of brachial plexus block when mixed with local anesthetics. In this study, the administration of clonidine 150 microg alone into the brachial plexus sheath did not produce postoperative analgesia.

Adult↗
PubMed1999

Relative analgesic potencies of ropivacaine and bupivacaine for epidural analgesia in labor: implications for therapeutic indexes.

BACKGROUND: The minimum local analgesic concentration (MLAC) has been defined as the median effective local analgesic concentration in a 20-ml volume for epidural analgesia in the first stage of labor. The aim of this study was to assess the relative analgesic potencies of epidural bupivacaine and ropivacaine by determining their respective minimum local analgesic concentrations. METHODS: Seventy-three parturients at < or = 7 cm cervical dilation who requested epidural analgesia were allocated to one of two groups in this double-blinded, randomized, prospective study. After a lumbar epidural catheter was placed, 20 ml of the test solution was given, either ropivacaine (n = 34) or bupivacaine (n = 39). The concentration of local anesthetic was determined by the response of the previous patient in that group to a higher or lower concentration using up-down sequential allocation. Analgesic efficacy was assessed using 100-mm visual analog pain scores with < or = 10 mm within 30 min defined as effective. An effective result directed a 0.01% wt/vol decrement for the next patient. An ineffective result directed a 0.01% wt/vol increment. RESULTS: The minimum local analgesic concentration of ropivacaine was 0.111% wt/vol (95% confidence interval, 0.100-0.122), and the minimum local analgesic concentration of bupivacaine was 0.067% wt/vol (95% confidence interval, 0.052-0.082). Ropivacaine was significantly less potent than bupivacaine, with a potency ratio of 0.6 (95% confidence interval, 0.49-0.74). No difference in motor effects was observed. CONCLUSION: Ropivacaine was significantly less potent than bupivacaine for epidural analgesia in the first stage of labor.

Adult↗
PubMed1999

The analgesic action of nitrous oxide is dependent on the release of norepinephrine in the dorsal horn of the spinal cord.

BACKGROUND: The authors and others have demonstrated that supraspinal opiate receptors and spinal alpha2 adrenoceptors are involved in the analgesic mechanism for nitrous oxide (N2O). The authors hypothesize that activation of opiate receptors in the periaqueductal gray results in the activation of a descending noradrenergic pathway that releases norepinephrine onto alpha2 adrenoceptors in the dorsal horn of the spinal cord. METHODS: The spinal cord was transected at the level of T3-T4 in rats and the analgesic response to 70% N2O in oxygen was determined by the tail flick latency test. In a separate experiment in rats a dialysis fiber was positioned transversely in the dorsal horn of the spinal cord at the T12 level. The following day, the dialysis fiber was infused with artificial cerebrospinal fluid at a rate of 1.3 microl/min, and the effluent was sampled at 30-min intervals. After a 60-min equilibration period, the animals were exposed to 70% N2O in oxygen. The dialysis experiment was repeated in animals that were pretreated with naltrexone (10 mg/kg, intraperitoneally) before N2O. In a third series, spinal norepinephrine was depleted with n-(2-chloroethyl)-n-ethyl-2-bromobenzylamine (DSP-4), and the analgesic response to 70% N2O in oxygen was determined. RESULTS: The analgesic effect of N2O was prevented by spinal cord transection. After exposure to N2O, there was a fourfold increase in norepinephrine released in the first 30-min period, and norepinephrine was still significantly elevated after 1 h of exposure. The increased norepinephrine release was prevented by previous administration of naltrexone. Depletion of norepinephrine in the spinal cord blocked the analgesic response to N2O. CONCLUSIONS: A descending noradrenergic pathway in the spinal cord links N2O-induced activation of opiate receptors in the periaqueductal gray, with activation of alpha2 adrenoceptors in the spinal cord. N2O-induced release of norepinephrine in the dorsal horn of the spinal cord is blocked by naltrexone, as is the analgesic response. Spinal norepinephrine is necessary for the analgesic response to the N2O.

Analgesics, Non-Narcotic↗
PubMed2001

Sedative but not analgesic alpha2 agonist tolerance is blocked by NMDA receptor and nitric oxide synthase inhibitors.

BACKGROUND: Studies show that the sedative and analgesic effects of alpha2 adrenergic agonists decrease over time, which is a form of synaptic plasticity referred to as tolerance. Because both the N-methyl-D-aspartate (NMDA) receptor complex and nitric oxide synthase are pivotal for some forms of synaptic plasticity, their role in tolerance to the hypnotic and analgesic effects of alpha2 agonists was investigated. METHODS: After institutional approval, rats were made tolerant to the hypnotic or analgesic action of an alpha2 agonist, dexmedetomidine. The hypnotic response to dexmedetomidine was assessed by the duration of loss of righting reflex, and the analgesic response to dexmedetomidine was assessed by the tail-flick assay. In separate cohorts, either the NMDA receptors or nitric oxide synthase was antagonized by coadministration of MK-801, ketamine, or NO2-arginine, respectively, during induction of tolerance. In a separate series of experiments, after tolerance was induced, the hypnotic and analgesic responses to dexmedetomidine were assessed in the presence of acutely administered MK-801 or NO2-arginine. RESULTS: Induction of tolerance to the hypnotic effect of dexmedetomidine is blocked by coadministration of MK-801, ketamine, and NO2-arginine. However, after tolerance developed, acute administration of MK-801, ketamine, or NO2-arginine did not prevent the expression of tolerance. Coadministration of MK-801 or NO2-arginine neither prevents the development nor reverses the expression of tolerance to the analgesic action of dexmedetomidine. CONCLUSION: The underlying processes responsible for the development of tolerance to the hypnotic and analgesic actions of systemically administered alpha2 agonists were different, with only the sedative tolerance involving the NMDA receptor and nitric oxide synthase system.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2004

Sub-Tenon infiltration or classical analgesic drugs to relieve postoperative pain.

BACKGROUND: In a prospective randomized double-blind study, the analgesic effect produced by sub-Tenon infiltration was compared with classic analgesic drugs in patients scheduled for posterior segment surgery under general anaesthesia. METHODS: One hundred patients were randomized into two groups of 50. One group received sub-Tenon infiltration (group 1) with 3 mL of bupivacaine 0.50% by the surgeon before the end of the surgery and the other (group 2) received only classical analgesic drugs postoperatively. A visual analogue scale (VAS) (graded from 1 to 10) was used to assess pain. For both groups, when VAS was between 1 and 3 paracetamol (3 g/24 h) associated with ketoprofen (200 mg/24 h) was given; between 3 and 6 nalbuphine (0.2 mg/kg slowly intravenously repeated every 4 h if necessary) was given; and over 6 morphine was given. Morphine 1 mg was injected every 2 min until VAS below 3 was obtained. RESULTS: All patients in group 2 (control) experienced pain in the recovery room period; however, no patient in group 1 required analgesic drugs in the first 6 h after the sub-Tenon infiltration. In the recovery room period, the VAS pain score in patients who received sub-Tenon infiltration (group 1) was 0.6 +/- 1.3 (mean +/- SD) compared to 3.4 +/- 2.2 in group 2. The difference was statistically significant (P = 0.000001). All patients in group 2 asked for analgesic drugs in the recovery room, some of whom required morphine. Despite the administration of drugs the pain score was statistically higher in group 2. Between the end of the recovery room period and the 6th hour, the VAS pain score in group 1 was statistically lower. From the 6th until the 24th hour, the pain score was not statistically significantly different between the groups. Regarding consumption of analgesic drugs from the recovery room until the 24th hour, the consumption of level 1 analgesic drugs (paracetamol, ketoprofen) and level 3 (morphine) was statistically lower in group 1 (P = 0.0009). The difference was not significant for level 2, probably because the number of patients was not sufficient. CONCLUSION: Sub-Tenon infiltration with 3 mL of bupivacaine 0.50% offers excellent postoperative analgesia for about 6 h and is an excellent alternative to classical drugs. Furthermore, it is highly reliable and safe.

Adult↗
PubMed1976

Analgesic abuse and kidney disease.

The analgesic syndrome, comprising renal disease, hypertension, peptic ulcer, anaemia and recurrent headache, accounts for wide-spread morbidity and mortality especially in Queensland and New South Wales. Epidemiological and clinical evidence gathered from many Western societies implicates unsupervised consumption of compound analgesic preparations, particularly those containing phenacetin, in the causation of the majority of cases. Laboratory experiments so far have failed to produce an entirely satisfactory model of clinical analgesic nephropathy. In small animals, papillary necrosis results from prolonged feeding with large doses of aspirin and a number of other anti-inflammatory agents more readily than when phenacetin, paracetamol or phenazone is given alone. The apparently conflicting deductive and experimental data may be reconciled if, as indicated by preliminary observations, salicylates enhance the toxicity of phenacetin derivatives. In planning a programme of prevention for the analgesic syndrome, the central aetiological role of non-narcotic drug dependency must be recognized. As the analgesics to which addiction commonly occurs are the compound powders and tablets, or those containing a stimulant, these preparations should be available only in circumstances where their use can be monitored. Suspected unsupervised and unwarranted consumption of analgesics should be checked by urinary testing for drug metabolites. Because the underlying problem of analgesic dependency is behavioural and environmental in origin rather than medical, the physician must combine forces with the social engineer to devise a definitive solution for this condition.

Analgesics↗