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PubMed1992

[Intramuscular meperidine for the prevention of shivering in spinal anesthesia].

Intravenous meperidine 25mg has been employed effectively to treat shivering following regional anesthesia and general anesthesia. The study was designed to evaluate the effectiveness of intramuscular meperidine for the prevention of shivering in spinal anesthesia. The series consisted of 60 patients who were divided into 2 groups with 30 patients in each, undergoing lower abdominal or lower extremity surgery. All patients were given diazepam 0.1mg/kg i.v. for anxiolysis when they came to the operating room. In a double blind and randomized fashion, patients in the study (meperidine) group received meperidine 25mg IM (= 0.5ml). In the control group 0.9% N/S 0.5ml IM was given instead. All patients received spinal anesthesia 15 minutes later. Measurement of the levels of sensory loss to pinprick was made. The ambient temperature and the rectal temperature were continuously monitored to evaluate the effect of the change in body temperature on shivering during operation. The degree and the occurrence of shivering were carefully evaluated and recorded by a blind-trust observer. There was no significant difference in maximal analgesic level, ambient temperature and change of rectal temperature during operation between the groups. Shivering occurred in 17 patients (56.7%) in the saline group with an onset time of 7.9 +/- 2.5min following spinal anesthesia. In the meperidine group, shivering occurred only in 3 patients (10%) with an onset time of 54 +/- 29.5min after spinal anesthesia. There was a significantly lower incidence of shivering in the meperidine group than in the saline group (p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed2005

[Effects of clonidine and midazolam on postoperative shivering, nausea, and vomiting].

BACKGROUND: Postoperative shivering, nausea, and vomiting are common problems after general anesthesia. We compared the effects of clonidine and those of midazolam on postoperative shivering, nausea and vomiting in elderly patients. METHODS: We studied 40 elderly patients (age > 60 yr) undergoing elective surgery under general anesthesia combined with epidural anesthesia. Patients were allocated randomly to receive oral clonidine 3-4 microg x kg(-1) (clonidine group) or intramuscular midazolam 0.04-0.05 mg x kg(-1) (midazolam group). Anesthesia was maintained with sevoflurane in a nitrous oxide and oxygen mixture, and fentanyl as needed, combined with epidural anesthesia with mepivacaine. Shivering, nausea, and vomiting were recorded at recovery from anesthesia, 3 h after the transference to the ward, and the next morning. Shivering was graded by using a three-point rating scale, whereas nausea and vomiting were assessed by means of a four-point rating. RESULTS: The incidence of shivering was lower at recovery from anesthesia in the clonidine group (P < 0.05). Likewise, the incidence of nausea was lower at recovery from anesthesia in the clonidine group (P < 0.05). There were no differences in shivering and nausea at other recording points. One patient in each group had vomiting. CONCLUSIONS: Clonidine premedication is effective for preventing shivering and nausea after general anesthesia combined with epidural anesthesia.

Administration, Oral↗
PubMedDate not supplied

Treatment of shivering after epidural lidocaine.

The effectiveness of intravenous meperidine and warm local anesthetic for prevention of postanesthetic shivering was evaluated in urology patients undergoing epidural blockade for extracorporeal shockwave lithotripsy. When administered before the blockade, meperidine, 12.5 mg or 25 mg, was not significantly better than saline placebo for preventing postepidural shivering. Changes in the concentrations of catecholamines or lidocaine did not result in differences between patients who shivered and those who did not shiver. In a second experiment, patients receiving body-temperature or room-temperature epidural lidocaine did not differ with respect to the incidence of postanesthetic shivering, onset of sensory blockade, or core temperature during a 30-minute observation period. The authors concluded that neither meperidine, in doses employed, nor body-temperature lidocaine prevents shivering after epidural blockade. This shivering appears to be different from that observed during emergence from general anesthesia.

Anesthesia, Epidural↗
PubMed1988

Contribution of exercise and shivering to recovery from induced hypothermia (31.2 degrees C) in one subject.

The ability of a modestly hypothermic victim to exercise, and indeed shiver, and thereby generate sufficient heat to rewarm has been questioned. One fit healthy subject was cooled in stirred water (7.7 degrees C) to a core temperature (Tc) of 32 degrees C. Tc by esophageal probe, cardiac rhythm, blood pressure (BP) and oxygen consumption (VO2) were monitored pre-, intra-, and postcooling (exercise). The subject rewarmed spontaneously as well as by exercising on a treadmill at speeds from 0.7 to 3.5 mph. Amount of Tc afterdrop (AD) was measured and rate of Tc increase (RI) and exercise and shivering contributions to heat production were calculated. The AD was 0.8 degrees C and the RI was 5.2 degrees C.h-1. VO2 values at the onset of hypothermic exercise indicated an approximate 4-fold increase in heat production from the normothermic resting value. A small portion of this heat production resulted from exercise while the majority was from shivering. Maximal heat production occurred at the lowest Tc (31.2 degrees C.). This represented an approximate 5-fold increase over the resting normothermic value. Shivering continued to provide the majority of the heat. As Tc increased, however, although heat production remained relatively constant, the contribution of exercise increased and that of shivering decreased. It was possible for this man to do a slight exercise at a Tc as low as 31.2 degrees C and the rewarming rate from shivering was substantial. Significant heat production is initially primarily by shivering thermogenesis, but soon, at a higher Tc, by exercise as well.

Adult↗
PubMed1998

Pre-anesthetic oral clonidine is effective to prevent post-spinal shivering.

BACKGROUND: Shivering is a common event during spinal anesthesia. Customarily we just treat it rather than prevent it. This study was designed to evaluate the efficacy of oral clonidine as a premedication to prevent post-spinal shivering. METHODS: One hundred males of ASA physical status I-III, aged above 40, scheduled for elective urological surgery under spinal anesthesia, were included in this study. All participants were randomly divided into the clonidine and control groups. They received either oral clonidine 150 micrograms (n = 48) or placebo (n = 52) 90 min before spinal anesthesia in a double-blind fashion. Spinal blockade was induced with heavy bupivacaine to a dermatomal level near T10. The shivering was graded as: none, no perceptible tension of muscles observed; mild, slight muscle tonus (masseter muscle); moderate, real shivering (proximal muscles); and severe, generalized shivering (whole body). The tympanic membrane temperature was recorded 30 min after spinal anesthesia. Data were expressed as mean +/- standard deviation. Chi-square and Student's t-test were used. A p value less than 0.05 was considered statistically significant. RESULTS: The incidence of post-spinal shivering, which was graded as none, mild, moderate, and severe, showed statistically significant differences (p < 0.05) between clonidine 150 micrograms and placebo (83% vs. 42%, 10% vs. 6%, 10% vs. 19%, 0% vs. 33%, respectively) during the 30 min immediately after spinal anesthesia. The respective mean tympanic temperature in oral clonidine and placebo groups showed no difference (clonidine vs. control = 35.9 +/- 0.8 degrees C vs. 35.9 +/- 0.7 degrees C). CONCLUSIONS: Pre-anesthetic medication with oral clonidine 150 micrograms is effective to prevent post-spinal shivering in patients undergoing elective urological surgery.

Administration, Oral↗
PubMed1990

The dysmyelinating mouse mutations shiverer (shi) and myelin deficient (shimld).

Shiverer (shi/shi) is an autosomal recessive mouse mutation that produces a shivering phenotype in affected mice. A shivering gait can be seen from a few weeks after birth until their early death, which occurs between 50 and 100 days. The central nervous system of the mutant mouse is hypomyelinated but the peripheral nervous system appears normal. The myelin of the CNS, wherever present, is not well compacted and lacks the major dense line. Myelin basic protein (MBP), which is associated with the major dense line, is absent, and this is due to a deletion of the major part of the gene encoding MBP. Transgenic shiverer mice that have integrated and express the wild-type mouse MBP transgene no longer shiver and have normal life spans. Conversely, normal mice that have integrated an antisense MBP transgene, shiver. Myelin deficient shimld/shimld is allelic to shiverer (shi/shi) but the mutant mouse is less severely affected. Although MBP is present in the CNS, it is low in quantity and is not developmentally regulated. The gene encoding MBP has been both duplicated and inverted. Transgenic shimld/shimld mice with the wild-type MBP transgene have normal phenotypes.

Animals↗
PubMed1987

Expression of a myelin basic protein gene in transgenic shiverer mice: correction of the dysmyelinating phenotype.

Mice homozygous for the autosomal recessive mutation shiverer (shi) lack myelin basic protein (MBP) and exhibit a distinct behavioral pattern including tremors (shivering), convulsions, and early death. We have previously demonstrated that shiverer mice have a partial deletion in the gene encoding MBP. We now have introduced the wild-type MBP gene into the germ line of shiverer mice by microinjection into fertilized eggs. Transgenic shiverer mice homozygous for the introduced gene have MBP mRNA and protein levels that are approximately 25% of normal, and produce compacted myelin with major dense lines. Correct temporal and spatial expression of the MBP gene is achieved with a genomic MBP cosmid clone containing 4 kb of 5' flanking sequence and 1 kb of 3' flanking sequence. Moreover, the four different forms of MBP produced by alternative patterns of RNA splicing are present. These homozygous transgenic shiverer mice no longer shiver nor die prematurely.

Alleles↗
PubMed1982

Shiverer peripheral myelin contains P2.

Myelin-deficient mutant mice, such as shiverer, can provide information about the normal mechanisms involved in myelination. The shiverer mouse carries a recessive, autosomal mutation resulting in an extreme deficiency in central myelin, and the small amount of myelin present is poorly compacted; the peripheral myelin, however, appears essentially normal. As the amount of myelin basic protein (P1) in both central and peripheral nervous system myelin is extremely low in shiverer, it is possible that P1 is essential for the normal formation and compaction of central myelin, but not of peripheral myelin. Some other protein would then be responsible for the formation of compact peripheral myelin in shiverer. Peripheral myelin contains another basic protein, designated P2, which could be a possible candidate for this role. Kirschner and Ganser, however, using SDS-polyacrylamide gel electrophoresis, reported that P2, as well as P1, is absent from shiverer sciatic nerve. This is an important observation if correct, because it not only excludes the possibility that P2 is required for compaction but also makes it less likely that the deficiency in P1 is the primary defect in shiverer. As P2 in rat and mouse has frequently been confused with another small basic protein (related to P1) in SDS-polyacrylamide gels, it seemed worthwhile to reassess this aspect of the Kirschner and Ganser observations. Immunohistochemistry and immunoblotting have been used here to show unambiguously that P2 is present in shiverer peripheral myelin.

Animals↗
PubMed1984

Normal basal laminas are realized on dystrophic Schwann cells in dystrophic in equilibrium shiverer chimera nerves.

Multiple discontinuities are observed in the basal laminas of Schwann cells in mature dystrophic mice. To explore the pathogenesis of this abnormality we have exploited a dystrophic in equilibrium shiverer mouse chimera preparation in which both the basal lamina phenotype and the genotype of myelin-forming Schwann cells can be determined. If the basal lamina abnormality were to arise from an intrinsic deficiency of the dystrophic Schwann cell itself, only those Schwann cells of dystrophic genotype could express the mutant phenotype, whereas the coexisting population of shiverer Schwann cells should express typically normal basal laminas. No such distinction was observed; rather both dystrophic and shiverer Schwann cells were found to express relatively normal basal laminas and two pathogenetic mechanisms remain theoretical possibilities. The dystrophic Schwann cell population may be intrinsically defective but also may be rescued by obtaining the normal product of the dy locus synthesized by the coexisting shiverer cells. Alternatively, an extra Schwann cell deficiency existing within dystrophic mice may be normalized by shiverer cells and the normal intrinsic potential of both dystrophic and shiverer Schwann cells can then be realized. Regardless of the exact mechanism underlying these findings, some extracellularly mediated influence, emanating in vivo from shiverer cells, is capable of ameliorating the basal lamina deficiency typically expressed by dystrophic Schwann cells.

Animals↗
PubMed1985

Shiverer and normal peripheral myelin compared: basic protein localization, membrane interactions, and lipid composition.

We have correlated membrane structure and interactions in shiverer sciatic nerve myelin with its biochemical composition. Analysis of x-ray diffraction data from shiverer myelin swollen in water substantiates our previous localization of an electron density deficit in the cytoplasmic half of the membrane. The density loss correlates with the absence of the major myelin basic proteins and indicates that in normal myelin, the basic protein is localized to the cytoplasmic apposition. As in normal peripheral myelin, hypotonic swelling in the shiverer membrane arrays occurs in the extracellular space between membranes; the cytoplasmic surfaces remain closely apposed notwithstanding the absence of basic protein from this region. Surprisingly, we found that the interaction at the extracellular apposition of shiverer membranes is altered. The extracellular space swells to a greater extent than normal when nerves are incubated in distilled water, treated at a reduced ionic strength of 0.06 in the range of pH 4-9, or treated at constant pH (4 or 7) in the range of ionic strengths 0.02-0.20. To examine the biochemical basis of this difference in swelling, we compared the lipid composition of shiverer and normal myelin. We find that sulfatides, hydroxycerebroside, and phosphatidylcholine are 20-30% higher than normal; nonhydroxycerebroside and sphingomyelin are 15-20% lower than normal; and ethanolamine phosphatides, phosphatidylserine, and cholesterol show little or no change. A higher concentration of negatively charged sulfatides at the extracellular surface likely contributes to an increased electrostatic repulsion and greater swelling in shiverer. The cytoplasmic surfaces of the apposed membranes of normal and shiverer myelins did not swell apart appreciably in the pH and ionic strength ranges expected to produce electrostatic repulsion. This stability, then, clearly does not depend on basic protein. We propose that P0 glycoprotein molecules form the stable link between apposed cytoplasmic membrane surfaces in peripheral myelin.

Animals↗
PubMed1992

Comparison of meperidine and pancuronium for the treatment of shivering after cardiac surgery.

Shivering after cardiac surgery can produce adverse haemodynamic and metabolic sequelae. In this study, the metabolic effects of shivering and the efficacy of treatment with meperidine or pancuronium were studied, using a metabolic cart, in 61 patients who had undergone cardiac surgery. The patients received premedication with morphine, perphenazine and diazepam or lorazepam, and were anaesthetised with fentanyl or sufentanil and diazepam. Muscle relaxation was achieved with pancuronium. Patients were monitored with a radial arterial line, pulmonary artery catheter and oesophageal and urinary bladder temperature probes. Rewarming to an oesophageal temperature of 38 degrees C was achieved before the termination of CPB and was maintained for a minimum of 15 min reperfusion time. Every 15 min after surgery, the patients' temperature at three sites (pulmonary artery, oesophagus, bladder) and shivering scores were monitored. Hourly measurements were made of haemodynamic variables (MAP, PAOP, CVP, SVR, PVR, CI), carbon dioxide production, oxygen consumption and respiratory quotient. If the patient shivered, the measurements were recorded prior to drug treatment and repeated 30 min later following randomization to either: meperidine 0.25 mg.kg-1 (Group 1), meperidine 0.5 mg.kg-1 (Group 2) or pancuronium 0.06 mg.kg-1 intravenously (Group 3). Thirty-two patients shivered and mean VO2 and VCO2 values were greater in the shivering group than in the nonshivering patients (VO2 334.8 +/- 17.6 vs. 240.5 +/- 8.8 ml.min-1; VCO2 238.8 +/- 17.2 vs 199.2 +/- 8.4 ml.min-1, P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1988

Shivering following retrobulbar block.

A case of a severe but brief period of shivering following a retrobulbar block (RBB) is presented. The shivering occurred within two minutes after completion of the RBB and subsided gradually within five minutes, without specific treatment. The patient remained conscious during the episode of shivering. The shivering was so abrupt and severe as to be misjudged as a seizure, but its onset appeared to be slower than a seizure. The mechanism of shivering appeared to be the central spread of local anaesthetic solution into the brain stem, along the optic nerve. Shivering may be a warning sign of brain stem anaesthesia and demands special care to anticipate life-threatening complications.

Anesthetics, Local↗
PubMed1995

Inhibition of shivering thermogenesis by centrally applied glucagon in muscovy ducklings.

Glucagon has marked thermogenic and lipolytic effects in birds but could also be involved in the central modulation of neural activity on the basis of the recently discovered glucagon receptors in several areas of the brain in ducklings. The aim of this work was to investigate the possible role of these receptors in the modulation of thermogenic processes. Glucagon was infused into the lateral ventricle of the brain in ducklings after an acute cold exposure (4 degrees C, 2 h) or at thermoneutrality (25 degrees C). Electromyographic (EMG) data were simultaneously recorded with electrodes implanted in the gastrocnemius muscle. Glucagon (10(-4) M) was infused at a rate of 8 microliters/min. When acutely exposed to cold, ducklings increased their metabolic rate by shivering thermogenesis. A significant decrease in shivering activity was elicited after 5 min of glucagon infusion. After 16 +/- 2 min of glucagon infusion, shivering was completely inhibited, corresponding to a total dose of 36 +/- 4 micrograms/kg. The suppression of shivering was accompanied by a diminution of metabolic rate (5.3 +/- 0.3 vs. 8.5 +/- 0.2 W/kg, P < 0.05). The values of metabolic rate obtained at 4 degrees C after glucagon infusion were not significantly different from those measured at 25 degrees C before glucagon infusion (6.4 +/- 0.3 W/kg, P > 0.05). The infusion of the same dose of glucagon did not induce any change in EMG activity and resting metabolic rate at 25 degrees C. These findings suggest that glucagon infused into the brain has no thermogenic effect but could be involved in the central control of somatic motricity. Although the origin and the mechanisms of action of the endogenous peptide still remain unknown, glucagon might have a role in the development of non shivering thermogenesis during prolonged cold exposure via an inhibition of shivering in birds.

Animals↗
PubMed1996

Effects of diabetes and food deprivation on shivering activity during progressive hypothermia in the rat.

Diabetes mellitus and food deprivation are two conditions known to significantly reduce the ability to generate body heat during periods of acute cold stress. The purpose of this study was to determine if shivering is attenuated in the urethane-anesthetized (1.5 g/kg; i.p.), streptozotocin-induced diabetic (STZ; n = 10) and food-deprived (12-hour nocturnal fast) rat (FD; n = 11) as colonic temperature (Tcol) declined from baseline (36 degrees C) to 28 degrees C. Shivering was assessed using the mean rectified electromyographic (EMG) signal obtained from indwelling bipolar electrodes placed in the gluteus superficialis muscle. Although the mean rectified EMG progressively increased (P < or = 0.05) between Tcol of 33 degrees C to 28 degrees C and achieved peak activity (7.89 +/- 1.80 microV) at 29 degrees C in non-diabetic rats, shivering activity was virtually absent in the STZ group throughout cooling (e.g. peak EMG = 0.49 +/- 0.09 microV). The lack of shivering activity in STZ could partially explain the shorter time to reach 28 degrees C (STZ, 48.5 +/- 1.5 vs CON, 136.5 +/- 23.0 min; P < or = 0.05) and the divergent trends in oxygen consumption (delta VO2) between STZ and non-diabetic rats. In the FD group, the mean peak rectified EMG activity (3.09 +/- 1.35 microV) was significantly lower (P < or = 0.05) than the fed group. The peak delta VO2 from baseline (FD, +2.11 +/- 0.36 vs. CON, +4.51 +/- 0.50 mlO2/min) and the time taken to reach 28 degrees C (FD, 73.4 +/- 4.2 vs CON, 136.5 +/- 23.0 min) were statistically different (P < or = 0.05) between groups. The results indicate that: 1) shivering thermogenesis is severely depressed and hypothermia accelerated in experimental diabetic animals as evidenced by the attenuation in mean rectified EMG and delta VO2, and 2) FD rats experienced a faster decline in colonic temperature than the fed group due, in part, to the relatively greater decline in shivering activity and oxygen consumption.

Animals↗
PubMed1996

A randomized, double-blind, placebo-controlled trial comparing pethidine to metamizol for treatment of post-anaesthetic shivering.

1. Shivering is frequent during the post-anaesthetic recovery period, and there is no clear consensus about the best strategy for its treatment. We tested the efficacy of two commonly used analgesic drugs, pethidine and metamizol. 2. A randomized, double-blind, placebo-controlled clinical trial was performed, including 104 adult patients who presented with post-anaesthetic shivering during the recovery from general anaesthesia. They were randomized to receive placebo (n = 32), metamizol 25 mg kg-1 (n = 37), or pethidine 0.4 mg kg-1 (n = 35). The response to treatment was assessed 5, 15 and 45 min after drug administration, and the main outcome variable was complete suppression of shivering. 3. The efficacy at 5, 15 and 45 min was as follows: placebo 6%, 16% and 37%; metamizol 13.5%, 32% and 76%, and pethidine 89%, 91% and 89%. With both active drugs the efficacy at all three time intervals was significantly higher than that with placebo (P < 0.05). The differences (at 5 and 15, but not at 45 min) between pethidine and metamizol were statistically significant (P < 0.05). Both drugs were well tolerated. 4. The persistence of shivering at 45 min in two thirds of placebo-treated patients indicates that drug treatment is worthwhile; metamizol produces a better postanaesthetic shivering response than placebo, especially 15 and 45 min after drug administration; the efficacy of pethidine was the highest and the response to it appeared more quickly; however, at 45 min it was similar to that observed with metamizol. 5. Both metamizol and pethidine suppress postanaesthetic shivering, but the latter induces a quicker and more reliable response.

Adult↗
PubMed1993

Double-blind comparison between doxapram and pethidine in the treatment of postanaesthetic shivering.

Sixty patients who shivered after routine surgery under general anaesthesia were allocated randomly to receive normal saline (n = 20), doxapram 1.5 mg kg-1 (n = 20) or pethidine 0.33 mg kg-1 (n = 20). Both doxapram and pethidine were effective in treating postoperative shivering 2-3 min after i.v. administration. In the group who received normal saline, 15 patients were still shivering 10 min after treatment, whilst in the doxapram group only three patients were shivering at that time. In the pethidine group, all patients had stopped shivering by 7 min after treatment. We conclude that both doxapram and pethidine were effective in the treatment of postoperative shivering.

Adolescent↗
PubMed1998

Epidural fentanyl reduces the shivering threshold during epidural lidocaine anesthesia.

UNLABELLED: Epidural local anesthetics and IV opioids both decrease the core temperature that triggers shivering. However, the effect of epidural opioids on shivering thresholds has not been assessed. In this study, we tested the hypothesis that adding epidural fentanyl to epidural lidocaine decreases the shivering threshold compared with epidural lidocaine alone. Fourteen healthy male patients undergoing extracorporeal shockwave lithotripsy under epidural anesthesia were randomly assigned to receive either epidural lidocaine or epidural lidocaine plus epidural fentanyl. Ice-cold lactated Ringer's solution was given IV before epidural blockade, and the core temperature that triggers shivering was established. Then epidural anesthesia was induced, and the shivering threshold was established again after lithotripsy. Results were analyzed using paired or unpaired t-tests. Reduction in the shivering threshold by epidural anesthesia was significantly greater when fentanyl was added to lidocaine than when lidocaine was used alone (mean +/- SD: -0.6+/-0.4 degrees C versus -0.1+/-0.4 degrees C; P < 0.02). We conclude that patients are at increased risk of hypothermia when fentanyl is added to epidural lidocaine. IMPLICATIONS: Fentanyl is often added to lidocaine to improve the quality of epidural blockade and to reduce side effects. However, this study shows that patients are at increased risk of hypothermia when fentanyl is added to lidocaine.

Adult↗
PubMed1999

A comparison among nalbuphine, meperidine, and placebo for treating postanesthetic shivering.

UNLABELLED: Postanesthetic shivering (PS) is distressing for patients and may induce a variety of complications. In this prospective, double-blinded, randomized study, we evaluated the value of nalbuphine, compared with meperidine and saline, for treating PS. Ninety adult patients were included in the study. Group 1 (n = 30) received i.v. nalbuphine 0.08 mg/kg, Group 2 (n = 30) received i.v. meperidine 0.4 mg/kg, and Group 3 (n = 30) received i.v. saline. Treatment that stopped shivering was considered to have been successful. The results demonstrated that, 5 min after treatment, both nalbuphine and meperidine provided a rapid and potent anti-shivering effect on PS, with high response rates of 80% and 83%, compared with those of saline (0%) (P < 0.01). Thirty minutes after injection, the response rates of nalbuphine and meperidine were 90% and 93%, respectively, compared with 17% in the saline group (P < 0.01). The differences between nalbuphine and meperidine were not significant. We conclude that nalbuphine may be an alternative to meperidine for treating PS. IMPLICATIONS: We evaluated nalbuphine versus meperidine and saline for treating postanesthetic shivering. Our results demonstrate that both nalbuphine and meperidine provide a similar rapid and potent anti-shivering effect. Nalbuphine may be an alternative to meperidine for treating postanesthetic shivering.

Adult↗