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REGIONAL ANESTHESIA

Continuous Positive Airway Pressure Breathing Increases the Spread of Sensory Blockade After Low-Thoracic Epidural Injection of Lidocaine

W. Anton Visser, MD^*, Mathieu J. M. Gielen, MD, PhD, and Janneke L. P. Giele, MSci

*Department of Anesthesiology, Intensive Care and Pain Management, Amphia Hospital, Breda, The Netherlands; Department of Anesthesiology, University Medical Center Nijmegen, Nijmegen, The Netherlands; and Department of Anesthesiology, University Medical Center Nijmegen, 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. Reprints will not be available from the authors.

	Abstract

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Factors affecting the distribution of sensory blockade after epidural injection of local anesthetics remain incompletely clarified. To evaluate if increasing intrathoracic pressure affects the spread of thoracic epidural anesthesia, we randomized 20 patients who received an epidural catheter at the T7-8 or T8-9 intervertebral space into 2 groups. The control group (n = 10) received an epidural test dose of 4 mL lidocaine 2% during spontaneous breathing at ambient pressure. The continuous positive airway pressure (n = 10) group received the same epidural test dose but during spontaneous respiration with 7.5 cm H₂O continuous positive airway pressure. The groups were comparable with respect to demographic variables. Fifteen minutes after the conclusion of the epidural injection, the sensory block ranged from from T4 [median, interquartile range 2.75 segments] to T11 (interquartile range 3.5 segments) in the control group and from T5 (interquartile range 2.25 segments) to L2 (IQR 2.25 segments) in the continuous positive airway pressure group (P = 0.005 for the caudal border). The total number of segments blocked was 7 (median, interquartile range 2.25) in the control group and 11 (interquartile range 3.5) in the continuous positive airway pressure group (P = 0.004). The number of segments blocked caudad to the injection site was 3 (median, interquartile range 3.5) in the control group and 6 (interquartile range 2.25) in the continuous positive airway pressure group (P = 0.005). We conclude that continuous positive airway pressure increases the spread of sensory blockade in thoracic epidural anesthesia, primarily by a more caudad extension of sensory blockade.

	Introduction

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Factors affecting the distribution of sensory blockade after epidural injection of local anesthetics (LA) remain incompletely clarified. In an earlier study, we reported several clinically relevant patterns of extension of thoracic epidural blockade: spread of sensory blockade was primarily caudad after high thoracic administration of LA (C7-T2), cephalad after low thoracic administration (T7-9) and equally caudad and cephalad after midthoracic administration (T3-5) (1). These findings have been confirmed by others (2). We suggested that differences in epidural pressure (EP) may cause LA to spread toward the midthoracic region, as this region is closest to the intrathoracic space and thus may harbor a lower EP compared to the high and low thoracic regions. Also, it has been suggested that thoracic EP may be increased by increased intrathoracic pressure (3).

In our earlier study, distribution of sensory blockade after low thoracic epidural injection was almost completely unidirectional in relation to the injection site, i.e., cephalad towards the midthoracic level (1). We hypothesized that increasing intrathoracic pressure may alter the spread of sensory blockade after low thoracic epidural injection of LA. To investigate this, we designed a double-blind study comparing the distribution of low thoracic epidural blockade in patients breathing with continuous positive airway pressure (CPAP) to patients breathing at ambient pressure.

	Methods

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After local medical ethical committee approval and written informed consent from the patient, we included 20 patients scheduled for elective laparotomy, ASA physical status I–III, aged 25 to 75 yr, height 160–200 cm, and weight 60 to 100 kg. Exclusion criteria were 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, obstructive lung disease with a forced expiratory volume in 1 s/vital capacity ratio < 70%, claustrophobia or a body mass index (weight in kg divided by the square of height in m) > 35.

After the insertion of an 18-gauge multi-orifice epidural catheter (B. Braun AG, Melsungen, Germany) through the T7-8 or T8-9 intervertebral space, with the patient in the sitting position, using the paramedian approach and hanging drop technique, patients were randomized by closed envelope to either the CPAP group (n = 10) or the control group (n = 10). 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. All epidural catheters were filled with saline before insertion, advanced 4 cm beyond the Tuohy needle tip, and inserted by the first author. All patients were then positioned in the supine position with the head of the bed raised to 45°, and a Whisperflow CPAP facemask (Caradyne Ltd., Galway, Ireland) was firmly attached. The mask was connected to a CF 800 CPAP apparatus (Dräger Medical AG, Lübeck, Germany). In the control group, the port of the mask designed for the pressure valve was left open. In the CPAP group, a valve delivering CPAP of 7.5 cm H₂O was attached to the facemask. All patients were instructed that they might experience some resistance to exhalation. Correct application of CPAP was confirmed by the manometer on the CPAP apparatus. When patients were comfortably breathing through the CPAP mask, an epidural injection of 4 mL of lidocaine 2% was initiated using a 20 mL syringe in a syringe pump (Graseby Medical Ltd., Watford, UK), set at 60 mL/h (1 mL/min). Fifteen minutes after completion of the epidural injection, the borders of sensory blockade were assessed by application of a small ice pack by an anesthesiologist not involved in the study and blinded as to the mode of breathing.

EPs were measured before applying the CPAP mask, immediately after applying CPAP, at the conclusion of epidural injection, and immediately before discontinuing CPAP. The proximal end of the epidural catheter was connected to a 3-way stopcock, which in turn was connected to the syringe with lidocaine 2% and a pressure transducer (Edwards Lifesciences, Irvine, CA). The pressure transducer was attached to the patient in the mid-axillary line at the level of the fourth rib. During and after injection, the stopcock was set to connect the epidural catheter with the syringe. When measuring EP, the stopcock was set to connect the catheter with the pressure monitoring set. The EP was recorded using a pressure monitor (Hewlett Packard, Amstelveen, The Netherlands) and a thermal array recorder. The pressures were only recorded when a typical waveform (Fig. 1), consisting of small oscillations, representing arterial pulsations, super-imposed on greater oscillations, representing breathing, was noted (4–12). The mean pressure displayed on the monitor was recorded (Fig. 2).

View larger version (36K): [in this window] [in a new window]   Figure 1. Sample waveform of epidural pressure, consisting of small oscillations, representing arterial pulsations, superimposed on greater oscillations, representing breathing, after low thoracic epidural injection of 4 mL of lidocaine in a patient in the control group. Recording speed 50 mm/min.

View larger version (19K): [in this window] [in a new window]   Figure 2. Sample waveforms of epidural pressure, consisting of small oscillations, representing arterial pulsations, superimposed on greater oscillations, representing breathing. Recordings made after application of continuous positive airway pressure (CPAP), after low thoracic epidural injection of 4 mL of lidocaine and 15 min after the conclusion of the epidural injection, in a patient in the CPAP group. Pressure data expressed as mm Hg, recording speed 50 mm/min. A reliable baseline recording could not be made in this patient.

In a previous study, the mean caudal border of blockade was located at T9 ± 1.5 segments (1). To demonstrate a change in the caudal border of sensory blockade of 2 segments, with = 0.05, a power of 80%, and two-sided testing, we calculated a sample size of 10 patients per group.

Primary end-points were the total number of segments blocked, the cranial and caudal border of sensory blockade, and the number of segments blocked caudal to the site of injection. Dermatomes were numbered from 1 (C1) to 30 (S5). Differences in borders of sensory blockade and numbers of segments blocked were analyzed using the Mann-Whitney U-test. Secondary end-points were the EPs before application of CPAP, immediately after applying CPAP, immediately after epidural injection, and just before discontinuing CPAP. Pressure data were analyzed using the Mann-Whitney U-test. Demographic data were analyzed using the Mann-Whitney U-test, except the distribution of males versus females, which was analyzed using the ² test. P < 0.05 was considered statistically significant.

	Results

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All patients tolerated breathing through the CPAP mask well and finished the study. Data are presented as median with interquartile range (IQR) in brackets. There were no significant differences in demographic data (Table 1). The median cranial border of sensory blockade was T4 (2.75 segments) in the control group and T5 (2.25 segments) in the CPAP group (P > 0.05). The median caudal borders of sensory blockade were T11 (3.5 segments) in the control group and L2 (2.25 segments) in the CPAP group (P = 0.005). The total number of segments blocked was 7 (2.25) in the control group and 11 (3.5) in the CPAP group (P = 0.004). The number of segments blocked caudal to the insertion site was 3 (3.5) in the control group and 6 (IQR) in the CPAP group (P = 0.005).

Tracings of EP with evident oscillation patterns were recorded in only 10 patients before epidural injection and in 16 patients after injection (Table 2). There were no statistically significant differences in EPs between groups.

	Discussion

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Our study is the first to demonstrate the influence of increased airway pressure on the distribution of low thoracic epidural anesthesia. There was a 57% increase in the number of segments blocked when applying CPAP during epidural injection of lidocaine and for 15 min thereafter, primarily through increased caudad spread of LA while the cephalad spread remained unchanged compared to patients breathing at ambient pressure.

We were unable to reliably document EP changes over time in all patients. It proved particularly difficult to obtain the typical pressure oscillations through the epidural catheter in awake patients before epidural injection. In other studies, EPs were successfully measured through the Tuohy needle (4–11). It has been suggested that a continuous epidural fluid infusion would be required to allow for stable long-term monitoring of EP through an epidural catheter (12). This would turn the epidural space, which is normally filled with tissue, into a fluid-filled space. Indeed, we acquired more acceptable pressure tracings after epidural injection than before injection.

Effects of positive end-expiratory pressure (PEEP) on EP have both been confirmed (12) and unconfirmed (13). Unfortunately, the number of acceptable EP tracings in our study was not sufficient to make any statements about the effects of CPAP on EP and the spread of LA in the epidural space. Factors that may have caused the larger and more caudad spread of sensory blockade include diminished compliance of the epidural space by the application of CPAP and changes in cerebrospinal fluid pressure.

The speed of injection may have influenced our results. Peak EPs after epidural injection correlate with the injection speed (11). For this experiment, we therefore chose a relatively slow speed of injection to avoid disturbing the physiologic pressure relationships within the epidural space. This speed may be slower than the typical speed of injection of a bolus dose of LA but is much faster than that of a continuous epidural infusion in daily practice. We chose to inject a volume of 4 mL of LA because this would be effective in establishing a demonstrable block (1) and still be safe for use as a test dose (14).

Because our conclusions are based on the relationship between sensory blockade and the injection site, our study may also be criticized for not radiographically confirming the position of the epidural catheter tip. However, it has been shown that the actual insertion site is usually not more than one segment away from the insertion site as determined by external landmarks when the catheter is advanced 3 cm beyond the Tuohy needle tip (1).

Regardless of the mechanism, we have demonstrated a statistically and clinically significant alteration in the distribution of low thoracic epidural block when a continuously positive airway pressure is present. In a typical healthy subject, intermittent positive pressure ventilation (IPPV) with a peak inspiratory pressure of 15 cm H₂O and 3 cm H₂O of PEEP will result in a mean airway pressure of approximately 10 cm H₂O. Mean airway pressure may be even higher in patients with obstructive lung disease. Although other factors may play a role in anesthetized patients, this suggests that administering bolus doses of LA during IPPV may result in a larger and more caudad extension of blockade than expected.

In conclusion, we report that applying CPAP during low thoracic epidural injection of lidocaine results in an increased number of segments blocked, primarily by a more caudad extension of sensory blockade.

The authors thank the recovery room nursing staff at the Amphia Hospital, in particular Piet van den Berg, RNA, for their assistance in performing the study, Wim Kleinhans for technical support, Dr. Jan Kluytmans for performing the power analysis, and Dr. Eric Robertson for reviewing the manuscript.

	Footnotes

 
Accepted for publication August 16, 2005.

	References

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1. Visser WA, Liem TH,van Egmond J, Gielen MJM. Extension of sensory blockade after thoracic administration of a test dose of lidocaine at three different levels. Anesth Analg 1998;86:332–5.[Abstract]
2. Yokoyama M, Hanazaki M, Fujii H et al. Correlation between the distribution of contrast medium and the extent of blockade during epidural anesthesia. Anesthesiology 2004;100:1504–10.[Web of Science][Medline]
3. Armitage EN. Lumbar and thoracic epidural block. In: Wildsmith, JAW, Armitage EN, McClure JH, eds. Principles and practice of regional anesthesia. London: Churchill Livingstone, 2003: 139–68.
4. Usubiaga JE, Wikinski JA, Usubiaga LE. Epidural pressure and its relation to spread of anesthetic solutions in the epidural space. Anesth Analg 1967;46:440–6.[Free Full Text]
5. Usubiaga JE, Moya F, Usubiaga LE. Effect of thoracic and abdominal pressure changes on the epidural space pressure. Br J Anaesth 1967;39:612–8.[Abstract/Free Full Text]
6. Zarzur E. Genesis of the ‘true' negative pressure in the lumbar epidural space. Anaesthesia 1984;39:1101–4.[Web of Science][Medline]
7. Paul DL, Wildsmith JAW. Extradural pressure following the injection of two volumes of bupivacaine. Br J Anaesth 1989;62:368–72.[Abstract/Free Full Text]
8. Hirabayashi Y, Shimizu R, Matsuda I, Inoue S. Effect of extradural compliance and resistance on spread of extradural analgesia. Br J Anaesth 1990;65:508–13.[Abstract/Free Full Text]
9. Telford RJ, Hollway TE. Observations on deliberate dural puncture with a Tuohy needle: pressure measurements. Anaesthesia 1991;46:725–7.[Web of Science][Medline]
10. Okutomi T, Watanabe S, Goto F. Time course in thoracic epidural pressure measurement. Can J Anaesth 1993;40:1044–8.[Web of Science][Medline]
11. Cardoso MM, Carvalho JC. Epidural pressures and spread of 2% lidocaine in the epidural space: influence of volume and speed of injection of the local anesthetic solution. Reg Anesth Pain Med 1998;23:14–9.[Web of Science][Medline]
12. Iwama H, Ohmori S. Continuous monitoring of lower thoracic epidural pressure. J Crit Care 2000;15:60–3.[Web of Science][Medline]
13. Nystrom EUM, Blomberg SG, Buffington CW. Transmural pressure of epidural veins in the thoracic and lumbar spine of pigs. Anesthesiology 1998;89:449–55.[Web of Science][Medline]
14. Holman SJ, Bosco RR, Kao TC et al. What constitutes an effective but safe initial dose of lidocaine to test a thoracic epidural catheter? Anesth Analg 2001;93:749–54.[Abstract/Free Full Text]

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