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EXTRADURAL PRESSURE FOLLOWING THE INJECTION OF TWO VOLUMES OF BUPIVACAINE
Br. J. Anaesth. (1989), 62, 368-372
EXTRADURAL PRESSURE FOLLOWING THE INJECTION OF TWO VOLUMES OF BUPIVACAINE D. L. PAUL AND J. A. W. WILDSMITH
SUMMARY We investigated the influence of the pressure generated by low lumbar extradural injection of bupivacaine on the development of block in a randomized double-blind study. Thirty patients (aged 17-66 yr) received one of two volumes of 0.75% bupivacaine. Group I (n = 15) received 10 ml (75 mg) and group II (n = 15) 15 ml (112.5 mg). Injection of the larger volume resulted in a greater pressure at the end of injection, but within 1 min this decayed to the same plateau pressure that was produced by the smaller volume. Mean maximum cephalad spread of block was the same in each group (group I, 19.5; group II, T8.4) and there was no correlation between individual level of block and maximum or plateau extradural pressure, or with patient characteristics.
PATIENTS AND METHODS
Thirty healthy patients who were to undergo elective varicose vein surgery under extradural blockade gave informed consent to the study, which had been approved by the Hospital Ethics Committee. Each patient was premedicated with temazepam 10 mg by mouth 1 h before arrival in the operating theatre. A venous cannula was inserted in the dorsum of a hand, but no fluids or drugs were administered. The patient was placed in the right lateral position on a horizontal operating table. The extradural space was identified using an 18gauge Tuohy needle and the loss of resistance technique with as small a volume (1-2 ml) of saline as possible. The third lumbar space was D. L. PAUL*, M.B., CH.B., F.F.A.R.C.S., J. A. W. WILDSMITH,
M.D., F.F.A.R.C.S.; Department of Anaesthetics, Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW. Accepted for Publication: September 26, 1988. •Present address: Department of Anaesthesia, Western Infirmary, Glasgow.
used on each occasion and all the blocks were performed by the same anaesthetist. The needle was inserted with the bevel facing cephalad. After identification of the extradural space the hub was connected, via a three-way tap, to a standard pressure transducer (Sensonor S40), amplifier (S&W 8041) and chart recorder (Elcomatic EM852). Zero was set with the system and extradural space open to atmosphere and calibration was with a 40-cm water column. A syringe was attached and 0.75% bupivacaine injected at 0.5 ml s"1. At the end of the injection the three-way tap was turned to form a closed system between the extradural space and the transducer. Pressure was recorded from the start of the injection until 90 s after its completion. The patient was turned supine with a slightly headdown tilt to maintain venous return. The patients were randomly allocated to receive either 0.75% bupivacaine 10 ml (group I,
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
The factors which determine accurately the spread of local anaesthetic in the extradural space have not been fully elucidated. The dose of drug injected [1], patient age [2], arteriosclerosis [3] and pregnancy [2, 4] have been suggested as dominant factors, with lesser contributions from speed of injection [5], direction of needle bevel [6] and patient position [2, 7]. However, the first three of these factors have been disputed [8, 9]. A recent study [10] showed that height of block was independent of dose and volume of solution and unrelated to patient height, weight and age. Another factor said to influence extradural spread, and also to be related to patient age, is the pressure generated by the injection [11]. This led us to re-examine the relationship between the pressure generated by the extradural injection of local anaesthetic solution and the spread of block.
EXTRADURAL PRESSURES
369
TABLE I. Demographic data (mean (SD)) for two groups of patients who received extradural block with 0.75% bupivacaine 10 ml (group I) or 15 ml (group II)
Group I (n = 15)
Group II (n = 15)
42.3 (13.3) 4/11 1.70(0.10) 67.4 (16.3) 23.5 (5.8)
49.3(11.5) 5/10 1.70(0.10) 66.0 (9.5) 22.8 (2.7)
Age (yr) Sex (M/F) Height (m) Weight (kg) Body mass index (wt ht~2)
Pressure Maximum (end of injection) Plateau (1 min) Oscillation (circulatory impulse)
Group II (n = 15)
Group I (n = 15) 40.3 (14.5) [21.0-67.3] 17.9 (7.8) [7.6-34.2] 6.3 (3.7) [1.7-14.6]
*
**
52.9 (14.2) [30.5-75.9] 18.1(5.4) [11.4-27.0] 13.4(8.6) [3.8-34.9]
Time (s) FIG. 1. Sample recording of extradural pressure during and after injection of 0.75% bupivacaine 10 ml. A = Calibration; B = injection artefact; C = end of injection; D = oscillation pressure; E = respiratory artefact; F = plateau pressure.
n= 15) or 0.75% bupivacaine 15ml (group II, n = 15). The resulting block was assessed by a single observer who did not know which volume had been injected. The level of sensory block (analgesia to pinprick with a short-bevel 26-gauge needle) and degree of motor block (Bromage score) were assessed at 10-min intervals for 30 min. The patients were sedated lightly (i.v. midazolam) during surgery, for which conditions were adequate in all.
Association of upper level of sensory block with individual patient variables was evaluated by Spearman rank correlation. Comparisons between the two were assessed by the Mann-Whitney test. RESULTS
There were no significant differences between demographic data for the two groups (table I). Mean extradural pressure (table II) at the end
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
TABLE II. Extradural pressure data (cm H2O) (mean (SD) [range]) for two groups of patients who received extradural block with 0.75% bupivacaine 10 ml (group I) or 15 ml (group II). *P < 0.05; **P < 0.001
BRITISH JOURNAL OF ANAESTHESIA
370
TABLE III. Distribution of block {mean (SD)) in two groups oftowards the plateau value. The degree of circupatients who received extradural block with 0.75% bupwacainelatory oscillation was measured immediately after 10 ml (group I) or 15 ml (group //)
the injection and the mean value was twice as high in group II (13.4 cm H2O) as in group I (6.3 cm H2O). Sensory (dermatome) The mean height of block was the same in each 10 min L2.8 (5.3) L2.9 (3.4) group (table III). Full analgesia of the sacral 20min Tl 1.7 (4.5) T9.2 (3.5) segments was obtained, there were no "missed 30 min T9.5(3.1) T8.4 (3.6) segments" and all blocks were suitable for the Motor (Bromage) 0.6 0.8 30 min proposed surgery. The degree of motor block was similar in the two groups, most patients being unable to straight-leg raise, but able to extend the of the injection was greater in group II (52.9 cm knees. There was no significant correlation between H2O) than in group 1 (40.3 cm H2O). The range of end injection pressure was wide in both groups cephalad spread of block and extradural pressure (group I, 21.0-67.3cm H 2 O; group II, 30.5-75.9 at any time (fig. 2), and no relationship between cm H2O). Extradural pressure decreased rapidly extent of block and patient age, height, weight or in both groups and plateaued in every patient body mass index. within 1 min of the end of injection. There was no difference in mean plateau pressure between the DISCUSSION groups. A trace of a sample recording is shown in figure 1. In all patients it was possible to see These results conflict with the work of Usubiaga respiratory and circulatory oscillations super- [11] who found that the extent of block did relate imposed on the extradural pressure trace. These to generated extradural pressure. Usubiaga inbecame less marked as the pressure decreased jected 2% lignocaine 10 ml through a needle, but Mean block
Group I
Group II
234CD O
ro E CD
567 8910-
o !• o
11-
•
o
o
o
T12
a.
Q. 3
LV
C CD
2
0)
o •
o
34L5-
35 10 15 20 25 30 Plateau extradural pressure (cm H2O) FIG. 2. Relationship between plateau extradural pressure and maximum upper level of block in 30 patients. O = 0.75% bupivacaine 10 ml; • = 0.75% bupivacaine 15 ml. 0
5
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
T1-
EXTRADURAL PRESSURES
sumably, the volume at which the pressure starts to increase depends on the characteristics of the individual spinal canal which, in turn, depend on the degree of hydration, venous engorgement, CSF pressure and ligamentous calcification. The pressure generated during injection causes the local anaesthetic solution to spread out along those tissue planes that offer least resistance. At this stage, there might be some relationship between pressure and spread, but for the potential "leakiness" of the spinal canal. Local anaesthetic might leave the extradural space by absorption into the circulation, diffusion into tissues and escape through the intervertebral foramina, or even along the needle track. The higher the pressure, the quicker this may occur, so leaving proportionately less anaesthetic in the space. It is interesting that, regardless of the pressure at the end of injection, mean plateau pressure was the same in both groups. This implies that there is a pressure-limiting feature in the extradural space and traditional thinking would probably ascribe this to resistance to fluid escaping through the intervertebral foramina. However, it should be noted that the plateau pressure was at the upper limit of normal for CSF pressure in the lateral position. It may be that displacement of CSF is in fact the main "safety valve" limiting extradural pressure, because recent anatomical studies in cadavers have suggested that solution cannot escape through the foramina [13]. Such a view is supported by a report [14] of sustained increases in ICP after lumbar extradural injection in patients with intracranial space-occupying lesions. Both the cadaver and the patient with intracranial hypertension may be irrelevant to the clinical situation, and further investigation is needed. The measurement of extradural pressure for a longer period of time might have been helpful, but would have required the use of a catheter, which we wished to avoid. The catheter might modify the direction in which the fluid spreads immediately after injection, or prevent solution leaking along the needle track as could have happened in our subjects. This analysis might explain why it is impossible to predict height of block from any of a range of readily made measurements and explain our inability, under the conditions of this study, to find any correlation between cephalad spread of block and patient age, height, weight, body mass index or maximum or plateau extradural pressure.
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
a catheter was inserted after measurement of pressure and the block was assessed for only 10 min. It is recognized today that a considerably longer period is needed to establish the maximum height of block, although we found no correlation between pressure and block height at any time. It is possible that lignocaine and bupivacaine behave differently or that catheter insertion has some unrecognized influence. The mean height of block was virtually the same in our two groups, despite a difference of 50% in both volume and dose of bupivacaine injected. This confirms the results of a recent study which also used a "single-shot" technique and examined the independent effects of concentration, volume and dose [10]. The reasons for this further conflict with traditional views are not clear, but also may relate to the use of a catheter in most earlier work. The pressures measured in the extradural space were very variable, but were significantly greater at the end of the injection of the larger volume. Despite this, the pressures in both groups decreased to the same value in less than 1 min. The oscillation pressures associated with circulatory events were also initially greater after injection of the larger volume. This indicates that the extradural pressure was on a steeper part of the compliance curve than after the smaller injection. An analogy may be made with an oedematous brain within a rigid skull [12], although the "rigidity" of the extradural space would depend as much on the softer tissues as on the bony components of the spinal canal. Bearing this rigidity in mind, it is possible to relate the results of this study to the sequence of events that occurs after injection. The contents of the canal are to some extent compressible and there are a number of avenues (in theory at least) through which the solution may escape. As local anaesthetic is injected into the extradural space, the volume that it occupies is created by displacement of blood from the venous plexuses and movement of CSF headwards. There may also be some "slack" in the ligaments between vertebrae. Thus the injection of small volumes is likely to produce little or no change in pressure. With the injection of larger volumes, the pressure starts to increase as the capacitance remaining within the system diminishes. This implies that the pressure-volume relationship was not linear, as did the differences between our groups in their initial oscillation pressures. Pre-
371
BRITISH JOURNAL OF ANAESTHESIA
372
9. 10.
11.
12. 13. 14.
AP. Extradural analgesia revisited: A statistical study. British Journal of Anaesthesia 1978; 50: 805-809. Park WY, Hagins FM, Rivat EL, Macnamara TE. Age and epidural response in adult men. Anesthesiology 1982; 56: 318-320. Duggan J, Bowler GMR, McClure JH, Wildsmith JAW. Extradural block with bupivacaine: The influence of dose, volume, concentration and patient characteristics. British Journal of Anaesthesia 1988; 61: 324-331. Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and its relation to spread of anesthetic solution in the epidural space. Anesthesia and Analgesia 1967; 46: 440-^46. Miller JD. Intracranial pressure—volume relationships in pathological conditions. Journal of Neurological Science 1976; 20: 203. Covino BG, Scott DB. Handbook of Epidural Anaesthesia and Analgesia. Copenhagen: Schultz, 1985. Hilt H, Gramm H—J, Link J. Changes in intracranial pressure associated with anaesthesia. British Journal of Anaesthesia 1986; 58: 676-680.
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
REFERENCES 1 Bromage PR. Mechanism of action of extradural anaesthesia. British Journal of Anaesthesia 1975; 47: 199-211. 2. Bromage PR. Spread of analgesic solutions in the epidural space and their site of action: A statistical study. British Journal of Anaesthesia 1962; 34: 161-178. 3. Bromage PR. Exaggerated spread of epidural analgesia in arteriosclerotic patients. British Medical Journal 1962; 2: 1634-1638. 4. Bromage PR. Physiology and pharmacology of epidural analgesia. Anesthesiology 1967; 28: 592-622. 5. Erdemir HA, Sopper LE, Sweet RB. Studies of factors affecting peridural anesthesia. Anesthesia and Analgesia 1965; 44: 400-404. 6. Park WY, Poon KC, Massengale MD, Macnamara TE. Direction of the needle bevel and epidural anesthetic spread. Anesthesiology 1982; 57: 327-328. 7. Grundy EM, Rao LN, Winnie AP. Epidural anesthesia and the lateral position. Anesthesia and Analgesia 1978; 57: 95-97. 8. Grundy EM, Ramamurthy S, Patel KP, Mani M, Winnie
EXTRADURAL PRESSURE FOLLOWING THE INJECTION OF TWO VOLUMES OF BUPIVACAINE D. L. PAUL AND J. A. W. WILDSMITH
SUMMARY We investigated the influence of the pressure generated by low lumbar extradural injection of bupivacaine on the development of block in a randomized double-blind study. Thirty patients (aged 17-66 yr) received one of two volumes of 0.75% bupivacaine. Group I (n = 15) received 10 ml (75 mg) and group II (n = 15) 15 ml (112.5 mg). Injection of the larger volume resulted in a greater pressure at the end of injection, but within 1 min this decayed to the same plateau pressure that was produced by the smaller volume. Mean maximum cephalad spread of block was the same in each group (group I, 19.5; group II, T8.4) and there was no correlation between individual level of block and maximum or plateau extradural pressure, or with patient characteristics.
PATIENTS AND METHODS
Thirty healthy patients who were to undergo elective varicose vein surgery under extradural blockade gave informed consent to the study, which had been approved by the Hospital Ethics Committee. Each patient was premedicated with temazepam 10 mg by mouth 1 h before arrival in the operating theatre. A venous cannula was inserted in the dorsum of a hand, but no fluids or drugs were administered. The patient was placed in the right lateral position on a horizontal operating table. The extradural space was identified using an 18gauge Tuohy needle and the loss of resistance technique with as small a volume (1-2 ml) of saline as possible. The third lumbar space was D. L. PAUL*, M.B., CH.B., F.F.A.R.C.S., J. A. W. WILDSMITH,
M.D., F.F.A.R.C.S.; Department of Anaesthetics, Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW. Accepted for Publication: September 26, 1988. •Present address: Department of Anaesthesia, Western Infirmary, Glasgow.
used on each occasion and all the blocks were performed by the same anaesthetist. The needle was inserted with the bevel facing cephalad. After identification of the extradural space the hub was connected, via a three-way tap, to a standard pressure transducer (Sensonor S40), amplifier (S&W 8041) and chart recorder (Elcomatic EM852). Zero was set with the system and extradural space open to atmosphere and calibration was with a 40-cm water column. A syringe was attached and 0.75% bupivacaine injected at 0.5 ml s"1. At the end of the injection the three-way tap was turned to form a closed system between the extradural space and the transducer. Pressure was recorded from the start of the injection until 90 s after its completion. The patient was turned supine with a slightly headdown tilt to maintain venous return. The patients were randomly allocated to receive either 0.75% bupivacaine 10 ml (group I,
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
The factors which determine accurately the spread of local anaesthetic in the extradural space have not been fully elucidated. The dose of drug injected [1], patient age [2], arteriosclerosis [3] and pregnancy [2, 4] have been suggested as dominant factors, with lesser contributions from speed of injection [5], direction of needle bevel [6] and patient position [2, 7]. However, the first three of these factors have been disputed [8, 9]. A recent study [10] showed that height of block was independent of dose and volume of solution and unrelated to patient height, weight and age. Another factor said to influence extradural spread, and also to be related to patient age, is the pressure generated by the injection [11]. This led us to re-examine the relationship between the pressure generated by the extradural injection of local anaesthetic solution and the spread of block.
EXTRADURAL PRESSURES
369
TABLE I. Demographic data (mean (SD)) for two groups of patients who received extradural block with 0.75% bupivacaine 10 ml (group I) or 15 ml (group II)
Group I (n = 15)
Group II (n = 15)
42.3 (13.3) 4/11 1.70(0.10) 67.4 (16.3) 23.5 (5.8)
49.3(11.5) 5/10 1.70(0.10) 66.0 (9.5) 22.8 (2.7)
Age (yr) Sex (M/F) Height (m) Weight (kg) Body mass index (wt ht~2)
Pressure Maximum (end of injection) Plateau (1 min) Oscillation (circulatory impulse)
Group II (n = 15)
Group I (n = 15) 40.3 (14.5) [21.0-67.3] 17.9 (7.8) [7.6-34.2] 6.3 (3.7) [1.7-14.6]
*
**
52.9 (14.2) [30.5-75.9] 18.1(5.4) [11.4-27.0] 13.4(8.6) [3.8-34.9]
Time (s) FIG. 1. Sample recording of extradural pressure during and after injection of 0.75% bupivacaine 10 ml. A = Calibration; B = injection artefact; C = end of injection; D = oscillation pressure; E = respiratory artefact; F = plateau pressure.
n= 15) or 0.75% bupivacaine 15ml (group II, n = 15). The resulting block was assessed by a single observer who did not know which volume had been injected. The level of sensory block (analgesia to pinprick with a short-bevel 26-gauge needle) and degree of motor block (Bromage score) were assessed at 10-min intervals for 30 min. The patients were sedated lightly (i.v. midazolam) during surgery, for which conditions were adequate in all.
Association of upper level of sensory block with individual patient variables was evaluated by Spearman rank correlation. Comparisons between the two were assessed by the Mann-Whitney test. RESULTS
There were no significant differences between demographic data for the two groups (table I). Mean extradural pressure (table II) at the end
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
TABLE II. Extradural pressure data (cm H2O) (mean (SD) [range]) for two groups of patients who received extradural block with 0.75% bupivacaine 10 ml (group I) or 15 ml (group II). *P < 0.05; **P < 0.001
BRITISH JOURNAL OF ANAESTHESIA
370
TABLE III. Distribution of block {mean (SD)) in two groups oftowards the plateau value. The degree of circupatients who received extradural block with 0.75% bupwacainelatory oscillation was measured immediately after 10 ml (group I) or 15 ml (group //)
the injection and the mean value was twice as high in group II (13.4 cm H2O) as in group I (6.3 cm H2O). Sensory (dermatome) The mean height of block was the same in each 10 min L2.8 (5.3) L2.9 (3.4) group (table III). Full analgesia of the sacral 20min Tl 1.7 (4.5) T9.2 (3.5) segments was obtained, there were no "missed 30 min T9.5(3.1) T8.4 (3.6) segments" and all blocks were suitable for the Motor (Bromage) 0.6 0.8 30 min proposed surgery. The degree of motor block was similar in the two groups, most patients being unable to straight-leg raise, but able to extend the of the injection was greater in group II (52.9 cm knees. There was no significant correlation between H2O) than in group 1 (40.3 cm H2O). The range of end injection pressure was wide in both groups cephalad spread of block and extradural pressure (group I, 21.0-67.3cm H 2 O; group II, 30.5-75.9 at any time (fig. 2), and no relationship between cm H2O). Extradural pressure decreased rapidly extent of block and patient age, height, weight or in both groups and plateaued in every patient body mass index. within 1 min of the end of injection. There was no difference in mean plateau pressure between the DISCUSSION groups. A trace of a sample recording is shown in figure 1. In all patients it was possible to see These results conflict with the work of Usubiaga respiratory and circulatory oscillations super- [11] who found that the extent of block did relate imposed on the extradural pressure trace. These to generated extradural pressure. Usubiaga inbecame less marked as the pressure decreased jected 2% lignocaine 10 ml through a needle, but Mean block
Group I
Group II
234CD O
ro E CD
567 8910-
o !• o
11-
•
o
o
o
T12
a.
Q. 3
LV
C CD
2
0)
o •
o
34L5-
35 10 15 20 25 30 Plateau extradural pressure (cm H2O) FIG. 2. Relationship between plateau extradural pressure and maximum upper level of block in 30 patients. O = 0.75% bupivacaine 10 ml; • = 0.75% bupivacaine 15 ml. 0
5
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
T1-
EXTRADURAL PRESSURES
sumably, the volume at which the pressure starts to increase depends on the characteristics of the individual spinal canal which, in turn, depend on the degree of hydration, venous engorgement, CSF pressure and ligamentous calcification. The pressure generated during injection causes the local anaesthetic solution to spread out along those tissue planes that offer least resistance. At this stage, there might be some relationship between pressure and spread, but for the potential "leakiness" of the spinal canal. Local anaesthetic might leave the extradural space by absorption into the circulation, diffusion into tissues and escape through the intervertebral foramina, or even along the needle track. The higher the pressure, the quicker this may occur, so leaving proportionately less anaesthetic in the space. It is interesting that, regardless of the pressure at the end of injection, mean plateau pressure was the same in both groups. This implies that there is a pressure-limiting feature in the extradural space and traditional thinking would probably ascribe this to resistance to fluid escaping through the intervertebral foramina. However, it should be noted that the plateau pressure was at the upper limit of normal for CSF pressure in the lateral position. It may be that displacement of CSF is in fact the main "safety valve" limiting extradural pressure, because recent anatomical studies in cadavers have suggested that solution cannot escape through the foramina [13]. Such a view is supported by a report [14] of sustained increases in ICP after lumbar extradural injection in patients with intracranial space-occupying lesions. Both the cadaver and the patient with intracranial hypertension may be irrelevant to the clinical situation, and further investigation is needed. The measurement of extradural pressure for a longer period of time might have been helpful, but would have required the use of a catheter, which we wished to avoid. The catheter might modify the direction in which the fluid spreads immediately after injection, or prevent solution leaking along the needle track as could have happened in our subjects. This analysis might explain why it is impossible to predict height of block from any of a range of readily made measurements and explain our inability, under the conditions of this study, to find any correlation between cephalad spread of block and patient age, height, weight, body mass index or maximum or plateau extradural pressure.
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
a catheter was inserted after measurement of pressure and the block was assessed for only 10 min. It is recognized today that a considerably longer period is needed to establish the maximum height of block, although we found no correlation between pressure and block height at any time. It is possible that lignocaine and bupivacaine behave differently or that catheter insertion has some unrecognized influence. The mean height of block was virtually the same in our two groups, despite a difference of 50% in both volume and dose of bupivacaine injected. This confirms the results of a recent study which also used a "single-shot" technique and examined the independent effects of concentration, volume and dose [10]. The reasons for this further conflict with traditional views are not clear, but also may relate to the use of a catheter in most earlier work. The pressures measured in the extradural space were very variable, but were significantly greater at the end of the injection of the larger volume. Despite this, the pressures in both groups decreased to the same value in less than 1 min. The oscillation pressures associated with circulatory events were also initially greater after injection of the larger volume. This indicates that the extradural pressure was on a steeper part of the compliance curve than after the smaller injection. An analogy may be made with an oedematous brain within a rigid skull [12], although the "rigidity" of the extradural space would depend as much on the softer tissues as on the bony components of the spinal canal. Bearing this rigidity in mind, it is possible to relate the results of this study to the sequence of events that occurs after injection. The contents of the canal are to some extent compressible and there are a number of avenues (in theory at least) through which the solution may escape. As local anaesthetic is injected into the extradural space, the volume that it occupies is created by displacement of blood from the venous plexuses and movement of CSF headwards. There may also be some "slack" in the ligaments between vertebrae. Thus the injection of small volumes is likely to produce little or no change in pressure. With the injection of larger volumes, the pressure starts to increase as the capacitance remaining within the system diminishes. This implies that the pressure-volume relationship was not linear, as did the differences between our groups in their initial oscillation pressures. Pre-
371
BRITISH JOURNAL OF ANAESTHESIA
372
9. 10.
11.
12. 13. 14.
AP. Extradural analgesia revisited: A statistical study. British Journal of Anaesthesia 1978; 50: 805-809. Park WY, Hagins FM, Rivat EL, Macnamara TE. Age and epidural response in adult men. Anesthesiology 1982; 56: 318-320. Duggan J, Bowler GMR, McClure JH, Wildsmith JAW. Extradural block with bupivacaine: The influence of dose, volume, concentration and patient characteristics. British Journal of Anaesthesia 1988; 61: 324-331. Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and its relation to spread of anesthetic solution in the epidural space. Anesthesia and Analgesia 1967; 46: 440-^46. Miller JD. Intracranial pressure—volume relationships in pathological conditions. Journal of Neurological Science 1976; 20: 203. Covino BG, Scott DB. Handbook of Epidural Anaesthesia and Analgesia. Copenhagen: Schultz, 1985. Hilt H, Gramm H—J, Link J. Changes in intracranial pressure associated with anaesthesia. British Journal of Anaesthesia 1986; 58: 676-680.
Downloaded from http://bja.oxfordjournals.org/ at Cornell University Library on August 2, 2015
REFERENCES 1 Bromage PR. Mechanism of action of extradural anaesthesia. British Journal of Anaesthesia 1975; 47: 199-211. 2. Bromage PR. Spread of analgesic solutions in the epidural space and their site of action: A statistical study. British Journal of Anaesthesia 1962; 34: 161-178. 3. Bromage PR. Exaggerated spread of epidural analgesia in arteriosclerotic patients. British Medical Journal 1962; 2: 1634-1638. 4. Bromage PR. Physiology and pharmacology of epidural analgesia. Anesthesiology 1967; 28: 592-622. 5. Erdemir HA, Sopper LE, Sweet RB. Studies of factors affecting peridural anesthesia. Anesthesia and Analgesia 1965; 44: 400-404. 6. Park WY, Poon KC, Massengale MD, Macnamara TE. Direction of the needle bevel and epidural anesthetic spread. Anesthesiology 1982; 57: 327-328. 7. Grundy EM, Rao LN, Winnie AP. Epidural anesthesia and the lateral position. Anesthesia and Analgesia 1978; 57: 95-97. 8. Grundy EM, Ramamurthy S, Patel KP, Mani M, Winnie