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From the *Department of Anesthesiology, Intensive Care and Pain Management, Amphia Hospital, 4800 RL Breda, The Netherlands; and Department of Anesthesiology, University Medical Center Nijmegen, 6500 HB Nijmegen, The Netherlands.
Address correspondence to W. Anton Visser, MD, Department of Anesthesiology, Intensive Care and Pain Management, Amphia Hospital, PO Box 90157, 4800 RL Breda, The Netherlands. Address e-mail to avisser{at}amphia.nl.
Abstract
BACKGROUND: Differences in epidural pressure (EP) may influence the spread of blockade in thoracic epidural anesthesia. We evaluated if EP and the incidence of subatmospheric EP differ between the mid- and low-thoracic epidural space.
METHODS: Patients received an epidural catheter at the T3-5 (MID group, n = 20) or T7-10 (LOW group, n = 20) intervertebral space, respectively. The epidural space was identified using a Tuohy needle connected to a pressure transducer, after which EP was measured.
RESULTS: The epidural space could not be identified in three patients who were excluded from the study. EP data are presented as median value (interquartile range). Median EP was 1 mm Hg (–1 to 4.5) in the MID group, and 4 mm Hg (2-7.8) in the LOW group (P = 0.04). The incidence of an EP 
0 mm Hg was 8 of 17 patients in the MID group and 2 of 20 patients in the LOW group (P = 0.02).
CONCLUSIONS: We conclude that EP is lower, and the incidence of subatmospheric EP is higher in the mid-thoracic epidural space when compared with that in the low-thoracic epidural space. However, median EP was positive in both groups. It remains to be investigated whether this pressure gradient is sufficient to influence the spread of thoracic epidural blockade.
It is not clear which factors affect the distribution of sensory blockade after epidural injection of local anesthetics (LAs). In an earlier study, we (1) reported several clinically relevant patterns of extension of thoracic epidural blockade after a test dose of lidocaine: Spread of sensory blockade was primarily caudad after high thoracic administration of LAs (C7-T2), cephalad after low thoracic administration (T7-9), and equally caudad and cephalad after mid-thoracic administration (T3-5). We hypothesized that differences in epidural pressure (EP) may cause LAs to spread toward the mid-thoracic region, as this region is closest to the intrathoracic space and thus may harbor a lower EP than the high- and low-thoracic regions. Previous publications on EP(2–8), have not systematically compared EPs between two thoracic epidural regions. Also, debate continues as to whether there is a true subatmospheric pressure in the thoracic epidural space (2–5). We designed this study to evaluate if there is a difference in EP between the mid-thoracic (T3-5) and low-thoracic (T7-10) epidural space, and if there is a difference in the incidence of true subatmospheric EP between these sites.
METHODS
After local medical ethical committee approval and informed patient consent, we included 20 patients scheduled for elective thoracotomy (MID group) and 20 patients for elective laparotomy (LOW group), ASA class I-III, aged 25-75 yr, height 160-200 cm, and weight 55-100 kg, in the study. Exclusion criteria consisted of general contraindications for epidural anesthesia (blood clotting disorders, infection at the proposed insertion site, language barrier, patient refusal), pregnancy, large abdominal mass, history of back surgery, thoracotomy, or sternotomy, obstructive lung disease with a forced expiratory volume1/vital capacity ratio <60%, or a body mass index (weight in kg divided by the square of height in m) >35 kg/m2.
All patients were placed in the left lateral position, with the spine flexed and parallel to the ground. A pressure transducer (Edwards Lifesciences, Irvine, CA) was taped to the patient’s back, no more than 10 cm away from the intended epidural puncture site, and with the side port at the level of the midline of the spine, as determined by palpation. Correct placement of the transducer was verified by an anesthesiologist or nurse anesthetist not involved in the study. The transducer was connected to a pressure monitor (Hewlett Packard, Amstelveen, The Netherlands) and a thermal array recorder and zeroed.
In the MID group, the T3-4 or T4-5 intervertebral space was identified by counting down from C7. In the LOW group, the line connecting the inferior angles of the scapulae, with the arms adducted, was assumed to represent the level of the seventh thoracic vertebra or the T7-8 intervertebral space, and the T8-9 or T9-10 intervertebral space was counted down from there.
Identification of the epidural space and measurement of EP was performed as outlined by Okutomi et al. (2). In brief, an 18G Perican Tuohy needle (B.Braun AG, Melsungen, Germany) was placed in the supraspinous ligament or ligamentum flavum, using the paramedian approach on the patient’s nondependent side. The stylet was then removed, and the needle was filled with saline and connected to the pressure transducer via a 60-cm long polyvinyl chloride tube, also filled with saline. After flushing the transducer system, the pressure bag holding the saline reservoir was deflated and the reservoir was placed at the level of the patient’s spine. The Tuohy needle was slowly advanced until a tactile sensation of give was noted. The needle was then held immobile. The bevel of the needle was considered to have entered the epidural space when a concurrent sudden deflection in the pressure recording was seen, with the appearance of a typical pressure waveform, consisting of small oscillations, representing arterial pulsations, superimposed on greater oscillations, representing breathing (Fig. 1). In the absence of these typical pressure changes, the needle was further advanced and the procedure described above repeated. After identification of the epidural space, the needle was held immobile for at least 120 s, to allow the EP to stabilize. At this time, the mean pressure displayed on the monitor was recorded.
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After successful identification of the epidural space, a 20G Perifix multihole epidural catheter (B.Braun AG, Melsungen, Germany) was inserted 4 cm beyond the needle tip. All patients were then positioned supine with the head of the bed raised to 45°, and 3 mL of lidocaine 2% was injected by hand with a speed of 1 mL/10 s. Twenty minutes after completion of the epidural injection, the borders of sensory blockade were assessed by an anesthesiologist not involved in the study, using a small ice pack.
Statistical Analysis
We performed a power analysis using the data from Okutomi et al. (2). They found a mean EP at the T7-8 level of 3.7 mm Hg (sd, 3.2). Therefore, a true negative pressure in the mid-thoracic epidural space would require a pressure difference of almost 4 mm Hg. To demonstrate a difference of 4 mm Hg, with 
= 0.05 and ß = 0.1, would require a minimal sample size of 10 patients per group. However, since we were unaware of the range of pressures at the mid-thoracic epidural space, we included 20 patients per group.
Demographic data were analyzed using Student’s t-test, except the distribution of males versus females, which was analyzed using Fisher’s exact test. Primary end-points were the EPs, which were analyzed using the Mann-Whitney U-test. Incidences of true negative EP (0 mm Hg) were compared using Fisher’s exact test. Secondary end-points were the total number of segments blocked, and the number of segments blocked cranial and caudad to the site of injection. These data were analyzed using Student’s t-test. P values <0.05 were considered statistically significant.
RESULTS
With the exception of three patients, the epidural space was successfully identified in all patients using the method described above, as demonstrated by the development of a typical sensory block after injection of lidocaine. Three patients in the MID group failed to develop sensory blockade. In two of these three patients, an evident deflection was noted in the pressure tracing, with subsequent oscillations smaller than that expected. One patient in the MID group showed an evident EP trace as described above; however, we were unable to advance a catheter through the Tuohy needle. These three patients successfully received another epidural catheter using the hanging drop method and were excluded from the study.
Demographic data are displayed in Table 1. There were no differences in demographic data. EP and sensory blockade data are displayed in Table 2.
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DISCUSSION
Our study is the first to demonstrate a lower EP in the mid-thoracic epidural space compared with the low-thoracic epidural space, using a closed pressure transducer system with the Tuohy needle held immobile, and with the patient in the lateral position. Also, we have demonstrated that the incidence of zero or true subatmospheric EP is higher in the mid-thoracic epidural space compared with the low-thoracic epidural space. However, the EP gradient and the magnitudes of the negative EPs measured were small: In most patients exhibiting a negative EP, pressures ranged from 0 to -3 mm Hg, with only two patients in the MID group demonstrating an EP of -15 and -16 mm Hg, respectively. Indeed, median EPs in both groups were positive. Furthermore, we have confirmed the different patterns of sensory blockade after mid- versus low-thoracic epidural injection found in our earlier study (1): The total number of segments blocked was similar in both groups, but spread of sensory blockade was more cranial in the LOW group compared with that in the MID group.
Whether the thoracic epidural space exhibits negative pressure has been the subject of debate. Bulging of the dura by the Tuohy needle (9), retraction of the ligamentum flavum (2,3), and the balance of forces defined in Starling’s equation in the minute space between the epidural fat and the ligamentum flavum (10) have been implicated as causes for such a negative EP, and may account for the entry of a hanging fluid drop into the needle hub when the needle tip is advanced into the epidural space. Although the studies by Usubiaga et al. (4,5) are often quoted to support the idea that EP is mostly subatmospheric and varies in different regions of the epidural space, the lack of homogeneity in subjects and measurements precluded statistical treatment of most data. In contrast, Okutomi et al. (2) concluded that the subatmospheric pressures found at the moment of epidural puncture at the T7-8 level are probably artifacts and the subsequent equilibration to positive pressures was due to adaptation of the surrounding tissue. Lumbar EP has been found to be positive by some authors (7,8), but slightly negative by others (3–5). Comparison of these studies is hindered by the many different study designs. In particular, methods of pressure measurements, patient positioning, and demographics vary widely. Also, most of these studies provide different answers to the question of what constitutes true EP. We agree with Okutomi et al. (2) and believe that true EP is best measured with a closed system (preventing equilibration of EP with ambient pressure, and evacuation of fluid or air from the measuring device into the epidural space) and the Tuohy needle held immobile until the EP trace stabilizes after the initial pressure decreases. We assume that, in this way, the disturbance of anatomic structures is minimized.
Our findings support the idea that LAs may preferentially spread toward the epidural region that exhibits the lowest EP (1). However, our study does not supply evidence for a causal relationship between EP differences and patterns of spread of sensory blockade. Further studies are needed to demonstrate such a relationship.
Our study may be criticized for the following reasons. First, differences in EPs between different epidural regions may be better documented by comparing them in individual patients rather than between patient groups. However, performing multiple epidural punctures in a single patient or volunteer without a clinical indication would raise ethical concerns. Second, since the results were dependent on correct placement of the pressure transducer, small errors may have occurred in the EP measurements. We have tried to minimize this possible error by having a second person, not involved in the study, verify correct placement.
In conclusion, we have demonstrated a small significant EP difference between the low- and mid-thoracic epidural spaces, indicating that EP is not homogenous among different sites in the thoracic epidural space. Also, we have demonstrated a greater incidence of zero or true subatmospheric EP, in the mid-thoracic epidural space compared with the low-thoracic epidural space. However, median EP was positive in both the low-thoracic and mid-thoracic epidural space. The significance of these findings is, at present, unclear. In particular, it remains to be investigated whether this pressure gradient is sufficient to influence the spread of thoracic epidural blockade.
ACKNOWLEDGMENTS
The authors thank the recovery room nursing staff at the Amphia Hospital, Langendijk site, in particular, Piet van den Berg, RNA, for their assistance in performing the study, Wim Kleinhans for technical support, and Dr. Eric Robertson for reviewing the manuscript.
Footnotes
Accepted for publication July 18, 2006.
Reprints will not be available from the authors.
REFERENCES
This article has been cited by other articles:
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  W. A. Visser, R. A. Lee, and M. J. M. Gielen Factors Affecting the Distribution of Neural Blockade by Local Anesthetics in Epidural Anesthesia and a Comparison of Lumbar Versus Thoracic Epidural Anesthesia Anesth. Analg., August 1, 2008; 107(2): 708 - 721. [Abstract] [Full Text] [PDF]
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W. A. Visser, M. J. P. G. van Eerd, R. van Seventer, M. J. M. Gielen, J. L. P. Giele, and G. J. Scheffer Continuous Positive Airway Pressure Breathing Increases Cranial Spread of Sensory Blockade After Cervicothoracic Epidural Injection of Lidocaine Anesth. Analg., September 1, 2007; 105(3): 868 - 871. [Abstract] [Full Text] [PDF]
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