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CONTRIBUTION OF EXTRADURAL TEMPERATURE TO SHIVERING DURING EXTRADURAL ANAESTHESIA
Br.J. Anaesth. (1986), 58, 1130-1134
CONTRIBUTION OF EXTRADURAL TEMPERATURE TO SHIVERING DURING EXTRADURAL ANAESTHESIA A. J. WALMSLEY, A. H. GIESECKE AND J. M. LIPTON
A. J. WALMSLEY,* M.B.B.S., F.FJ^.R.CJ., A. H. GIESECXE, JR,
MJJ. (Department of Anerthesiology); J. M. LIPTON, PHJJ.
(Department of Physiology); University of Texas Southwestern Medical School, 5323 Harry Hines Boulevard, Dallas, T X 75235, U.S.A. *Present address for correspondence: Department of Anaesthesia, King's College Hospital, Denmark Hill, London SE5.
SUMMARY Thirty patients having postpartum tuba/ ligation under extradural anaesthesia were studied. All received bupivacaine at 4 °C initially and the incidence of shivering (47%), and the extradural temperatures measured with a small thermistor threaded into the extradural catheter, were recorded. To eight patients in whom the resultant shivering was marked, further bupivacaine warmed to 41 °C was injected. In four of these patients, shivering was stopped. The results suggest that thermosensitive tissue within the spinal canal contributes to the shivering observed in association with extradural anaesthesia. Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
Shivering is a recognized complication of extradural anaesthesia (Downing, 1969; Waters, Rosen and Perkins, 1970), and various mechanisms have been suggested: a decrease in core temperature as a result of the peripheral vasodilatation caused by the sympathetic blockade; an effect of the anaesthetic after absorption into the systemic circulation; a differential inhibition of afferent thermoreceptor fibres within the spinal cord that causes an erroneous indication of a decrease in peripheral temperature (Fruhstorter, Nolte and Hensel, 1974), and a direct effect of cold anaesthetic solution on thermosensitive neurones within the spinal cord. Although peripheral vasodilatation does occur, there is no evidence that it is accompanied by the decrease in core temperature necessary to initiate shivering. Cutaneous vasodilatation also occurs in association with subarachnoid analgesia but, since shivering has not been reported, that hypothesis is unlikely. Toxic effects of bupivacaine on hypothalamic centres are unlikely, since similar quantities of the drug injected elsewhere in the body (for example, brachial plexus blockade or i.v. regional analgesia) rarely induce shivering, even in the presence of other signs of central toxicity. Subarachnoid blockade would be expected to affect thermoreceptor fibres but, as stated above, intrathecal analgesia does not result in shivering. Furthermore, evidence for a differential effect on thermal afferent inputs has only been reported for ulnar nerve blockade with mepivacaine (Fruhstorter, Nolte and Hensel, 1974) and not in association with extradural anaesthesia. On the other hand,
there is abundant evidence that thermosensitive structures exist within the spinal cord of various mammalian species (Kosaka, Simon and Thauer, 1966; Jessen and Mayer, 1971; Fuller, Horowitz and Horowitz, 1977), and it has been suggested that shivering can be activated by local cooling of the spinal canal in man (Ponte, Collett and Walmsley, 1986). The aims of the present study were: to determine the incidence of shivering when cold bupivacaine was injected to the extradural space; to correlate shivering with the temperature changes within the extradural space caused by these injections; and to determine whether shivering induced by the injection of cold anaesthetic solution could be reversed by the subsequent administration of warmed anaesthetic solution. PATIENTS AND METHODS
Following approval by the Institutional Review Board, 30 patients (mean age 27.2 yr± SEM 0.82, range 21—36 yr) who were scheduled to undergo tubal ligation under extradural anaesthesia 24—48 h postpartum gave informed consent to
SHIVERING AND EXTRADURAL ANAESTHESIA
MST = 0.3 (chest + deltoid)+ 0.2 (thigh + leg) All measurements were taken before the insertion of the extradural catheter, before the injection of the test dose of anaesthetic, and at 5-min intervals throughout the study. All patients received, via the extradural catheter, a test dose of 0.5 % plain bupivacaine 4 ml, cooled to 4 °C in a water bath maintained at this temperature, followed by doses of 7 and 5 ml at
the same temperature. If shivering did not occur after any of the first three injections, an additional 5 ml of cold anaesthetic was given. Extradural temperature was monitored continuously after each injection until it returned to baseline. The extradural temperature was allowed to return to 37 °C before a subsequent dose was given. Shivering was recorded by electromyography with electrodes placed over the muscles of the anterior shoulder girdle. In certain patients, bupivacaine 5 ml warmed to 41 °C was given in an attempt to reverse shivering induced by the administration of the cold solution. The electrocardiogram was monitored throughout the study, and arterial pressure was recorded (Dinamap) at the same time intervals as air, core, and skin temperatures. The dermatome levels to which neural blockade extended were noted at 15-min intervals. If necessary, additional lactated Ringer's solution (no more than 500 ml) at 37 °C was infused i.v. to counteract systemic arterial hypotension. Once blockade to the T6 sensory level or higher had been achieved and surgery could commence, the study was terminated. RESULTS
Fourteen of the 30 patients (47%) shivered after one or more of the injections of cold anaesthetic solution. There were no significant differences between those patients who shivered and those who did not, with respect to any of the variables in table I. The mean temperatures were calculated by averaging measurements taken at 5-min intervals from immediately before the placement of the extradural catheter until the end of the study. Likewise, although there were increases in mean skin and axillary temperatures from the insertion of the catheter to the last reading in both the shivering and non-shivering groups (table II),
TABLE I. Comparison of data of shivering and non-shivering patients. Mean valuues ± standard error of the mean (SEM)
Age (yr) Shivering (n = 14)
Non-shivering (n = 16) P (t test)
Weight (k«)
Volume of anaesthetic solution (ml)
Level of block (thoracic segment)
Ambient temperature (°C)
Mean skin temperature
Axillary temperature
CO
(°Q
28.69
66.12
21.86
5.36
20.74
32.21
36.91
±1.55
±3.63
±0.91
±0.37
±0.21
±0.21
±0.22
32.16
36.60
±0.20
±0.10
26.00
61.20
21.93
6.31
20.90
±0.71
±2.70
±0.93
±0.53
±0.22
0.132
0.282
0.951
0.162
0.608
0.883
0.217
Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
participate in the study. No patient was febrile nor had any received medication in the preoperative period. All were clinically nonnovolaemic with a normal haemoglobin concentration. An i.v. cannula was inserted under local anaesthesia, and an infusion of lactated Ringer's solution 1 litre warmed to 37 °C commenced. The patient was placed in the lateral position, and the lumbar region was cleaned with iodine solution. The extradural space was located with a 16-gauge Tuohy needle and an air-filled syringe, using the loss of resistance technique. An 18-gauge Concord extradural catheter with a thermistor probe (Yellow Springs Instruments (YSI) Series 511 sterilized with ethylene oxide) threaded to its tip was inserted. To reduce heat exchange, the extradural catheter was shortened to 40 cm before the insertion of the thermistor and was not taped to the patient's back (Walmsley, Ponte and Wright, 1984). The temperature of the ambient air was recorded throughout the procedure, and a record of core temperature was obtained by placing a thermistor probe (YSI 409) over the axillary artery. Measurements of skin temperature were recorded by means of thermistor probes at four sites: the outer aspect of the lower leg; the thigh; the deltoid muscle; and the chest. Mean skin temperature (MST) was calculated using the formula described by Ramanathan (1964):
1131
BRITISH JOURNAL OF ANAESTHESIA
1132
TABLE II. Pre-extradural and final values of mean skin and axillary temperatures in shivering and non-shivering patients (mean values ±SBAf). t = difference between means ±SED (standard error of the difference) Mean skin temperature (°C) 1st Shivering (n = 14) P Non-shivering (n = 16) P
Last
t
Core temperature C Q Last
1st
t
31.86
32.27
0.41
36.75
36.94
0.19
±0.20
±0.28
±0.28
±0.18
±0.25
±0.14
31.70
0.167 32.08
0.38
36.24
0.206 36.64
0.40
±0.24
±0.25
±0.22
±0.21
±0.14
±0.23
0.102
0.097
Dose 1 (4 ml) Injection to return to 37 °C (min) Injection to start of shivering (min)
7.36
±0.43
(n = 30)
neither these increases nor the differences in increase between the two groups were significant. Injections of cold anaesthetic solution caused extradural temperatures to decrease to less than 20 °C and to remain below 37 °C for several minutes. The larger the volume given, the longer the extradural temperature remained less than 37 °C. When shivering occurred (denned as an episode which lasted for longer than 30 s), it began within an average of 3.5-4.4 min after injection (table III). No patient shivered after the first dose alone, but the number of patients that shivered increased with each subsequent dose of cold solution. In each instance, shivering was noted by the patient as well as recorded on the electromyogram. Episodes of shivering lasted 1—22 min and in five patients shivering was still present when surgery commenced. Bupivacaine warmed to above body temperature was administered 11 times to eight patients in whom shivering had been present for longer than 5 min. In four of these patients in whom the temperature of the solution was 39-40 °C, shivering stopped within 0.5-2 min and did not resume for 7 or 8 min. Cessation of shivering corresponded well with the periods in which the extradural temperature had increased. The extradural temp-
Dose 2 (7 ml)
Dose3 (5 ml)
Dose4 (5 ml)
13.3
11.0
11.1
±0.51
±0.49
±0.50
(» = 30) 3.46
(n = 30) 4.36
(n = 9) 4.2
±2.05
±0.52
±0.79
(» = 5)
(" = 6)
(n = 7)
Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
TABLE III. Time (mm) (mean ± SEAT) from extradural injection to return of extradural space temperature to 37 "C and time from injection to start of shivering for first four cold doses given
erature returned to baseline in 7.5-10.7 min. Figure 1 shows two successful tests in one of these patients. Six attempts to decrease shivering in the other four patients were unsuccessful. (Four of these failures occurred early in the study when the bupivacaine solution was heated insufficiently to prevent its cooling to less than body temperature by the time it had entered the extradural space.) DISCUSSION
Although the injection of local anaesthetic solution at 4 °C to the extradural space is not usual clinically, it was considered justified to enhance the physiological response which has previously been noted with solutions at room temperature. The overall incidence of shivering in this series was comparable to those reported previously (Downing, 1969; Waters, Rosen and Perkins, 1970; Ponte, Collett and Walmsley, 1986). Evidence that cooling the spinal cord in man produces shivering has been reported only recently (Ponte, Collett and Walmsley, 1986). Studies in rabbits have shown that, in this species, it takes several minutes for the temperature of the extradural space to return to normal after injections of cold fluid (Ponte and Simpson,
SHIVERING AND EXTRADURAL ANAESTHESIA
1133
1 min
Extradural temp. (°C) 37.0
Injection of bupivacaine 5ml
39.0
38.0
37.3
37.5
Extradural temp. (°C) 39.5
38.5
37.5
37.3
FIG. 1. Electromyographic evidence of cessation of shivering episodes, and extradural temperature, in a single patient receiving warmed bupivacaine on two occasions. Large amplitude spikes represent ECG artefact.
1985). Our study has shown that even small volumes of cold anaesthetic solution can decrease extradural temperature for prolonged periods. In all patients in whom shivering occurred, it started during this period. However it is not known why the shivering did not begin immediately—when the decrease in temperature was greatest, rather than on average about 4 min later. Assuming the presence of temperature receptors in the spinal cord, one would expect that, having evoked shivering by cooling the cord, one would be able to stop it by warming the cord. In five of seven attempts in which the extradural temperature was increased, shivering stopped. The timing and duration of the cessation of shivering were remarkably consistent in the five instances and correlated well with the increase in extradural temperature. Shivering resumed in all cases as the extradural temperature approached baseline. Shivering is a physiological mechanism to increase heat production. Its initiation depends on the interaction of three factors: input from peripheral cold receptors, input from nonhypothalamic thermosensitive neurones (e.g., spinal cord), and the temperature of the hypothalamus. The hypothalamus acts as the integrating centre for such thermal inputs. Hypothalamic temperature may decrease as a result of heat loss consequent on cutaneous
Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
Injection of bupivacaine 5ml
vasodilatation or of the infusion of cold i.v. fluids. In this study, central temperature did not decrease in any of our patients. Rapid i.v. infusion of solutions kept at room temperature may decrease central temperature, but in this study this variable was eliminated by warming all i.v. fluids to 37 °C. Apart from the hypothalamus, the existence of other deep body temperature receptors has been suggested. Receptors in other parts of the central nervous system, namely, the midbrain reticular formation and the spinal cord, have been shown to initiate shivering. In several mammalian species, local cooling of the spinal cord produces shivering and vasoconstriction, and shivering as a result of peripheral cooling can be enhanced by direct cooling of the spinal cord. Selective warming of the spinal cord, on the other hand, suppresses ongoing shivering and induces cutaneous vasodilatation (Hemingway, 1963; Kosaka, Simon and Thauer, 1966; Jessen and Mayer, 1971; Fuller, Horowitz and Horowitz, 1977). Evidence for temperature sensors in the large veins and in the gut is inconclusive. It is unclear why some subjects shivered and others did not, despite low temperatures in the extradural space. One possible explanation could be in the height of sensory block achieved. The mean height of blockade in the shivering group
1134
ACKNOWLEDGEMENTS The authors thank Ms B. Rice, C.R.N.A. and Dr F. Birdsell for their assistance during the study and Dr W. G. Clark for his
editorial assistance. We also wish to thank Mrs W. Beard for her secretarial assistance.
REFERENCES Downing, J. W. (1969). Bupivacaine: a clinical assessment in lumbar extradural block. Br. J. Anaeith., 41, 427. Fruhstorfer, H. M., Nolte, H., and Hensel, H. (1974). Dissociated loss of cold and warm sensibility during regional anaesthesia. Pflugert Arch., 349, 73. Fuller, C. A., Horowitz, J. W., and Horowitz, B. A. (1977). Spinal cord thermosensitivity and sorting of neural signals in cold exposed rats. J. Appl. Phytiol., 42, 154. Hemingway, A. (1963). Shivering. Physiol. Rev., 43, 397. Jessen, C , and Mayer, E. T. (1971). Spinal cord and hypothalamus as core sensors of temperature in the conscious dog. Pflugers Arch., 324, 189. Kosaka, M., Simon, E., and Thauer, R. (1966). Shivering in intact and spinal rabbits during spinal cooling. Experienta, 23, 385. Ponte, J. C , Collett, B. J., and Walmsley, A. J. (1986). Effect of local anaesthetic temperature on the incidence of shivering during epidural anaesthesia. Acta Anaesthtsiol. Scand., (in press). Simpson, D. (1985). Measurement of extradural blood flow in the rabbit. A preliminary study. Br. J. Aruusth., 57, 815. Ramanathan, N. L. (1964). A new weighting system for mean surface temperature of the human body. J. Appl. Physiol., 19, 531. Walmsley, A. J., Ponte, J. C , and Wright, D. (1984). Temperature changes along an extradural catheter: experimental and theoretical calculation. Br. J. Anaesth., 56, 803. Waters, H. R., Rosen, N., and Perkins, D. H. (1970). Extradural blockade with bupivacaine. Anaesthesia, 25, 184. Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
was one thoracic segment higher than in the non-shivering group. Although this difference is small, this could affect the incidence of shivering in one of two ways. First, when a higher segment is reached, more of the spinal cord is exposed to the cold sensory stimuli providing, perhaps, a greater neuronal input to the hypothalamus. Alternatively, there may be a higher density of thermosensitive neurones in the spinal canal nearer the brain. It is possible, however, that there are many unknown mechanisms subserving the shivering and that the injection of cold local anaesthetic solutions is only one of these. The same theory would also explain why solution at 41 CC did not stop shivering in all patients. Although recent work has suggested that spinal canal thermosensitive tissue exists (Ponte, Collett and Walmsley, 1986), our observations that temperature changes within the extradural space can be marked and that shivering can be stopped by increasing the temperature in the extradural space provide further evidence of the importance of thermosensitive tissue outside the hypothalamus in the maintenance of body temperature. From a practical point of view, warming of i.v. fluids and local anaesthetic solutions to 37 °C before injection should reduce the incidence of shivering associated with extradural anaesthesia.
BRITISH JOURNAL OF ANAESTHESIA
CONTRIBUTION OF EXTRADURAL TEMPERATURE TO SHIVERING DURING EXTRADURAL ANAESTHESIA A. J. WALMSLEY, A. H. GIESECKE AND J. M. LIPTON
A. J. WALMSLEY,* M.B.B.S., F.FJ^.R.CJ., A. H. GIESECXE, JR,
MJJ. (Department of Anerthesiology); J. M. LIPTON, PHJJ.
(Department of Physiology); University of Texas Southwestern Medical School, 5323 Harry Hines Boulevard, Dallas, T X 75235, U.S.A. *Present address for correspondence: Department of Anaesthesia, King's College Hospital, Denmark Hill, London SE5.
SUMMARY Thirty patients having postpartum tuba/ ligation under extradural anaesthesia were studied. All received bupivacaine at 4 °C initially and the incidence of shivering (47%), and the extradural temperatures measured with a small thermistor threaded into the extradural catheter, were recorded. To eight patients in whom the resultant shivering was marked, further bupivacaine warmed to 41 °C was injected. In four of these patients, shivering was stopped. The results suggest that thermosensitive tissue within the spinal canal contributes to the shivering observed in association with extradural anaesthesia. Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
Shivering is a recognized complication of extradural anaesthesia (Downing, 1969; Waters, Rosen and Perkins, 1970), and various mechanisms have been suggested: a decrease in core temperature as a result of the peripheral vasodilatation caused by the sympathetic blockade; an effect of the anaesthetic after absorption into the systemic circulation; a differential inhibition of afferent thermoreceptor fibres within the spinal cord that causes an erroneous indication of a decrease in peripheral temperature (Fruhstorter, Nolte and Hensel, 1974), and a direct effect of cold anaesthetic solution on thermosensitive neurones within the spinal cord. Although peripheral vasodilatation does occur, there is no evidence that it is accompanied by the decrease in core temperature necessary to initiate shivering. Cutaneous vasodilatation also occurs in association with subarachnoid analgesia but, since shivering has not been reported, that hypothesis is unlikely. Toxic effects of bupivacaine on hypothalamic centres are unlikely, since similar quantities of the drug injected elsewhere in the body (for example, brachial plexus blockade or i.v. regional analgesia) rarely induce shivering, even in the presence of other signs of central toxicity. Subarachnoid blockade would be expected to affect thermoreceptor fibres but, as stated above, intrathecal analgesia does not result in shivering. Furthermore, evidence for a differential effect on thermal afferent inputs has only been reported for ulnar nerve blockade with mepivacaine (Fruhstorter, Nolte and Hensel, 1974) and not in association with extradural anaesthesia. On the other hand,
there is abundant evidence that thermosensitive structures exist within the spinal cord of various mammalian species (Kosaka, Simon and Thauer, 1966; Jessen and Mayer, 1971; Fuller, Horowitz and Horowitz, 1977), and it has been suggested that shivering can be activated by local cooling of the spinal canal in man (Ponte, Collett and Walmsley, 1986). The aims of the present study were: to determine the incidence of shivering when cold bupivacaine was injected to the extradural space; to correlate shivering with the temperature changes within the extradural space caused by these injections; and to determine whether shivering induced by the injection of cold anaesthetic solution could be reversed by the subsequent administration of warmed anaesthetic solution. PATIENTS AND METHODS
Following approval by the Institutional Review Board, 30 patients (mean age 27.2 yr± SEM 0.82, range 21—36 yr) who were scheduled to undergo tubal ligation under extradural anaesthesia 24—48 h postpartum gave informed consent to
SHIVERING AND EXTRADURAL ANAESTHESIA
MST = 0.3 (chest + deltoid)+ 0.2 (thigh + leg) All measurements were taken before the insertion of the extradural catheter, before the injection of the test dose of anaesthetic, and at 5-min intervals throughout the study. All patients received, via the extradural catheter, a test dose of 0.5 % plain bupivacaine 4 ml, cooled to 4 °C in a water bath maintained at this temperature, followed by doses of 7 and 5 ml at
the same temperature. If shivering did not occur after any of the first three injections, an additional 5 ml of cold anaesthetic was given. Extradural temperature was monitored continuously after each injection until it returned to baseline. The extradural temperature was allowed to return to 37 °C before a subsequent dose was given. Shivering was recorded by electromyography with electrodes placed over the muscles of the anterior shoulder girdle. In certain patients, bupivacaine 5 ml warmed to 41 °C was given in an attempt to reverse shivering induced by the administration of the cold solution. The electrocardiogram was monitored throughout the study, and arterial pressure was recorded (Dinamap) at the same time intervals as air, core, and skin temperatures. The dermatome levels to which neural blockade extended were noted at 15-min intervals. If necessary, additional lactated Ringer's solution (no more than 500 ml) at 37 °C was infused i.v. to counteract systemic arterial hypotension. Once blockade to the T6 sensory level or higher had been achieved and surgery could commence, the study was terminated. RESULTS
Fourteen of the 30 patients (47%) shivered after one or more of the injections of cold anaesthetic solution. There were no significant differences between those patients who shivered and those who did not, with respect to any of the variables in table I. The mean temperatures were calculated by averaging measurements taken at 5-min intervals from immediately before the placement of the extradural catheter until the end of the study. Likewise, although there were increases in mean skin and axillary temperatures from the insertion of the catheter to the last reading in both the shivering and non-shivering groups (table II),
TABLE I. Comparison of data of shivering and non-shivering patients. Mean valuues ± standard error of the mean (SEM)
Age (yr) Shivering (n = 14)
Non-shivering (n = 16) P (t test)
Weight (k«)
Volume of anaesthetic solution (ml)
Level of block (thoracic segment)
Ambient temperature (°C)
Mean skin temperature
Axillary temperature
CO
(°Q
28.69
66.12
21.86
5.36
20.74
32.21
36.91
±1.55
±3.63
±0.91
±0.37
±0.21
±0.21
±0.22
32.16
36.60
±0.20
±0.10
26.00
61.20
21.93
6.31
20.90
±0.71
±2.70
±0.93
±0.53
±0.22
0.132
0.282
0.951
0.162
0.608
0.883
0.217
Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
participate in the study. No patient was febrile nor had any received medication in the preoperative period. All were clinically nonnovolaemic with a normal haemoglobin concentration. An i.v. cannula was inserted under local anaesthesia, and an infusion of lactated Ringer's solution 1 litre warmed to 37 °C commenced. The patient was placed in the lateral position, and the lumbar region was cleaned with iodine solution. The extradural space was located with a 16-gauge Tuohy needle and an air-filled syringe, using the loss of resistance technique. An 18-gauge Concord extradural catheter with a thermistor probe (Yellow Springs Instruments (YSI) Series 511 sterilized with ethylene oxide) threaded to its tip was inserted. To reduce heat exchange, the extradural catheter was shortened to 40 cm before the insertion of the thermistor and was not taped to the patient's back (Walmsley, Ponte and Wright, 1984). The temperature of the ambient air was recorded throughout the procedure, and a record of core temperature was obtained by placing a thermistor probe (YSI 409) over the axillary artery. Measurements of skin temperature were recorded by means of thermistor probes at four sites: the outer aspect of the lower leg; the thigh; the deltoid muscle; and the chest. Mean skin temperature (MST) was calculated using the formula described by Ramanathan (1964):
1131
BRITISH JOURNAL OF ANAESTHESIA
1132
TABLE II. Pre-extradural and final values of mean skin and axillary temperatures in shivering and non-shivering patients (mean values ±SBAf). t = difference between means ±SED (standard error of the difference) Mean skin temperature (°C) 1st Shivering (n = 14) P Non-shivering (n = 16) P
Last
t
Core temperature C Q Last
1st
t
31.86
32.27
0.41
36.75
36.94
0.19
±0.20
±0.28
±0.28
±0.18
±0.25
±0.14
31.70
0.167 32.08
0.38
36.24
0.206 36.64
0.40
±0.24
±0.25
±0.22
±0.21
±0.14
±0.23
0.102
0.097
Dose 1 (4 ml) Injection to return to 37 °C (min) Injection to start of shivering (min)
7.36
±0.43
(n = 30)
neither these increases nor the differences in increase between the two groups were significant. Injections of cold anaesthetic solution caused extradural temperatures to decrease to less than 20 °C and to remain below 37 °C for several minutes. The larger the volume given, the longer the extradural temperature remained less than 37 °C. When shivering occurred (denned as an episode which lasted for longer than 30 s), it began within an average of 3.5-4.4 min after injection (table III). No patient shivered after the first dose alone, but the number of patients that shivered increased with each subsequent dose of cold solution. In each instance, shivering was noted by the patient as well as recorded on the electromyogram. Episodes of shivering lasted 1—22 min and in five patients shivering was still present when surgery commenced. Bupivacaine warmed to above body temperature was administered 11 times to eight patients in whom shivering had been present for longer than 5 min. In four of these patients in whom the temperature of the solution was 39-40 °C, shivering stopped within 0.5-2 min and did not resume for 7 or 8 min. Cessation of shivering corresponded well with the periods in which the extradural temperature had increased. The extradural temp-
Dose 2 (7 ml)
Dose3 (5 ml)
Dose4 (5 ml)
13.3
11.0
11.1
±0.51
±0.49
±0.50
(» = 30) 3.46
(n = 30) 4.36
(n = 9) 4.2
±2.05
±0.52
±0.79
(» = 5)
(" = 6)
(n = 7)
Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
TABLE III. Time (mm) (mean ± SEAT) from extradural injection to return of extradural space temperature to 37 "C and time from injection to start of shivering for first four cold doses given
erature returned to baseline in 7.5-10.7 min. Figure 1 shows two successful tests in one of these patients. Six attempts to decrease shivering in the other four patients were unsuccessful. (Four of these failures occurred early in the study when the bupivacaine solution was heated insufficiently to prevent its cooling to less than body temperature by the time it had entered the extradural space.) DISCUSSION
Although the injection of local anaesthetic solution at 4 °C to the extradural space is not usual clinically, it was considered justified to enhance the physiological response which has previously been noted with solutions at room temperature. The overall incidence of shivering in this series was comparable to those reported previously (Downing, 1969; Waters, Rosen and Perkins, 1970; Ponte, Collett and Walmsley, 1986). Evidence that cooling the spinal cord in man produces shivering has been reported only recently (Ponte, Collett and Walmsley, 1986). Studies in rabbits have shown that, in this species, it takes several minutes for the temperature of the extradural space to return to normal after injections of cold fluid (Ponte and Simpson,
SHIVERING AND EXTRADURAL ANAESTHESIA
1133
1 min
Extradural temp. (°C) 37.0
Injection of bupivacaine 5ml
39.0
38.0
37.3
37.5
Extradural temp. (°C) 39.5
38.5
37.5
37.3
FIG. 1. Electromyographic evidence of cessation of shivering episodes, and extradural temperature, in a single patient receiving warmed bupivacaine on two occasions. Large amplitude spikes represent ECG artefact.
1985). Our study has shown that even small volumes of cold anaesthetic solution can decrease extradural temperature for prolonged periods. In all patients in whom shivering occurred, it started during this period. However it is not known why the shivering did not begin immediately—when the decrease in temperature was greatest, rather than on average about 4 min later. Assuming the presence of temperature receptors in the spinal cord, one would expect that, having evoked shivering by cooling the cord, one would be able to stop it by warming the cord. In five of seven attempts in which the extradural temperature was increased, shivering stopped. The timing and duration of the cessation of shivering were remarkably consistent in the five instances and correlated well with the increase in extradural temperature. Shivering resumed in all cases as the extradural temperature approached baseline. Shivering is a physiological mechanism to increase heat production. Its initiation depends on the interaction of three factors: input from peripheral cold receptors, input from nonhypothalamic thermosensitive neurones (e.g., spinal cord), and the temperature of the hypothalamus. The hypothalamus acts as the integrating centre for such thermal inputs. Hypothalamic temperature may decrease as a result of heat loss consequent on cutaneous
Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
Injection of bupivacaine 5ml
vasodilatation or of the infusion of cold i.v. fluids. In this study, central temperature did not decrease in any of our patients. Rapid i.v. infusion of solutions kept at room temperature may decrease central temperature, but in this study this variable was eliminated by warming all i.v. fluids to 37 °C. Apart from the hypothalamus, the existence of other deep body temperature receptors has been suggested. Receptors in other parts of the central nervous system, namely, the midbrain reticular formation and the spinal cord, have been shown to initiate shivering. In several mammalian species, local cooling of the spinal cord produces shivering and vasoconstriction, and shivering as a result of peripheral cooling can be enhanced by direct cooling of the spinal cord. Selective warming of the spinal cord, on the other hand, suppresses ongoing shivering and induces cutaneous vasodilatation (Hemingway, 1963; Kosaka, Simon and Thauer, 1966; Jessen and Mayer, 1971; Fuller, Horowitz and Horowitz, 1977). Evidence for temperature sensors in the large veins and in the gut is inconclusive. It is unclear why some subjects shivered and others did not, despite low temperatures in the extradural space. One possible explanation could be in the height of sensory block achieved. The mean height of blockade in the shivering group
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ACKNOWLEDGEMENTS The authors thank Ms B. Rice, C.R.N.A. and Dr F. Birdsell for their assistance during the study and Dr W. G. Clark for his
editorial assistance. We also wish to thank Mrs W. Beard for her secretarial assistance.
REFERENCES Downing, J. W. (1969). Bupivacaine: a clinical assessment in lumbar extradural block. Br. J. Anaeith., 41, 427. Fruhstorfer, H. M., Nolte, H., and Hensel, H. (1974). Dissociated loss of cold and warm sensibility during regional anaesthesia. Pflugert Arch., 349, 73. Fuller, C. A., Horowitz, J. W., and Horowitz, B. A. (1977). Spinal cord thermosensitivity and sorting of neural signals in cold exposed rats. J. Appl. Phytiol., 42, 154. Hemingway, A. (1963). Shivering. Physiol. Rev., 43, 397. Jessen, C , and Mayer, E. T. (1971). Spinal cord and hypothalamus as core sensors of temperature in the conscious dog. Pflugers Arch., 324, 189. Kosaka, M., Simon, E., and Thauer, R. (1966). Shivering in intact and spinal rabbits during spinal cooling. Experienta, 23, 385. Ponte, J. C , Collett, B. J., and Walmsley, A. J. (1986). Effect of local anaesthetic temperature on the incidence of shivering during epidural anaesthesia. Acta Anaesthtsiol. Scand., (in press). Simpson, D. (1985). Measurement of extradural blood flow in the rabbit. A preliminary study. Br. J. Aruusth., 57, 815. Ramanathan, N. L. (1964). A new weighting system for mean surface temperature of the human body. J. Appl. Physiol., 19, 531. Walmsley, A. J., Ponte, J. C , and Wright, D. (1984). Temperature changes along an extradural catheter: experimental and theoretical calculation. Br. J. Anaesth., 56, 803. Waters, H. R., Rosen, N., and Perkins, D. H. (1970). Extradural blockade with bupivacaine. Anaesthesia, 25, 184. Downloaded from http://bja.oxfordjournals.org/ at Emory University on August 10, 2015
was one thoracic segment higher than in the non-shivering group. Although this difference is small, this could affect the incidence of shivering in one of two ways. First, when a higher segment is reached, more of the spinal cord is exposed to the cold sensory stimuli providing, perhaps, a greater neuronal input to the hypothalamus. Alternatively, there may be a higher density of thermosensitive neurones in the spinal canal nearer the brain. It is possible, however, that there are many unknown mechanisms subserving the shivering and that the injection of cold local anaesthetic solutions is only one of these. The same theory would also explain why solution at 41 CC did not stop shivering in all patients. Although recent work has suggested that spinal canal thermosensitive tissue exists (Ponte, Collett and Walmsley, 1986), our observations that temperature changes within the extradural space can be marked and that shivering can be stopped by increasing the temperature in the extradural space provide further evidence of the importance of thermosensitive tissue outside the hypothalamus in the maintenance of body temperature. From a practical point of view, warming of i.v. fluids and local anaesthetic solutions to 37 °C before injection should reduce the incidence of shivering associated with extradural anaesthesia.
BRITISH JOURNAL OF ANAESTHESIA