Factors affecting the distribution of sensory blockade after epidural injection of local anesthetics remain incompletely clarified. On the basis of earlier studies (1,2), we have suggested that differences in epidural pressure may cause local anesthetic injected into the high-thoracic (C7–T2) or low-thoracic (T7–9) epidural spaces to spread toward the midthoracic (T3–5) region. This region is closest to the intrathoracic space, and thus may harbor a lower epidural pressure compared with the high- and low-thoracic regions. Epidural pressure has been shown to be lower in the midthoracic compared with the low-thoracic epidural region (3). We previously demonstrated that continuous positive airway pressure (CPAP) increases the spread of sensory blockade after low-thoracic epidural injection of lidocaine by 57%, primarily by a more caudad extension of sensory blockade (4). We hypothesized that CPAP will also increase spread of sensory blockade after cervicothoracic epidural injection of local anesthetic, but by a more cranial extension of blockade. This study was designed to test this hypothesis and to evaluate whether a more cranial extension of epidural blockade by the application of CPAP may affect pulmonary function.
After local medical ethical committee approval and written informed consent from the patient, we included 20 patients diagnosed with cervicobrachialgia or cervical radicular pain and scheduled for an epidural injection with local anesthetic and steroid. Inclusion criteria were ASA class I–III, aged 25–75 years, height 160–200 cm, and weight 60–105 kg. Exclusion criteria consisted of general contraindications for epidural anesthesia (blood clotting disorders, infection at the proposed insertion site, language barrier, patient refusal), pregnancy, history of back surgery, obstructive lung disease with a forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) ratio <70%, claustrophobia, body mass index >35, or sensory deficiency in the cervicothoracic dermatomes that could preclude sensory testing (e.g., carpal tunnel syndrome). All patients had undergone computed tomography or magnetic resonance imaging of the cervical spine. None of these investigations showed disk protrusions or significant narrowing of the spinal canal.
A 20-gauge multiorifice epidural catheter (B. Braun AG, Melsungen, Germany) was advanced 3–4 cm beyond the Tuohy needle tip through the C6–7 or C7–T1 intervertebral space. The median approach and loss-of-resistance technique with ≤0.5 mL of saline were used, with the patient in the sitting position. Up to 0.5 mL of Iohexol 3 mg I/mL (Omnipaque 300, Amersham Health, Eindhoven, The Netherlands) was used to verify epidural placement of the catheter using real time fluoroscopy. Patients were then randomized by closed envelope to either the CPAP group (n = 10) or the control group (n = 10) and positioned in the supine position with the head of the bed raised to 45°. A Whisperflow CPAP facemask (Caradyne Ltd., Galway, Ireland) was firmly attached to the patient’s face and 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 3 mL of lidocaine 2% with 1 mL methylprednisolone 40 mg/mL (DepoMedrol, Pharmacia-Upjohn, Kalamazoo, MI) was started using a 10-mL syringe in an Orchestra Module DPS syringe pump (Fresenius Vial SA, Brezins, France), set at 60 mL/h (1 mL/min). The epidural solution was freshly mixed, and the syringe pump with syringe was gently agitated halfway during the injection. Fifteen minutes after completion of the epidural injection, CPAP was discontinued, and the borders of sensory blockade were assessed by application of a small ice pack, by an anesthesiologist blinded to the mode of breathing. In case of asymmetrical blockade, the larger extension of blockade was recorded.
Immediately before the experiment and after completion of the epidural injection, FEV1 and FVC were recorded using a Jaeger SpiroPro hand-held spirometer (Viasys Healthcare, Hoechberg, Germany), and the FEV1/FVC ratio was calculated by the spirometer software. Three attempts were made by each patient. The set of data with the highest FVC was recorded.
Noninvasive arterial blood pressure, percutaneous arterial oxygen saturation (SaO2), and heart rate were recorded before epidural injection, and at 5 and 15 min after completion of the injection.
In a previous study, the mean caudal border of sensory blockade after high-thoracic epidural injection of 60 mg lidocaine was located at T1 ± 1.5 segments (1). To demonstrate a change in the cranial border of sensory blockade of two segments, with α = 0.05, a power of 80%, and two-sided testing, we calculated a sample size of 10 patients per group.
Our end-points were the total number of segments blocked, the cranial and caudal border of sensory blockade, and the number of segments blocked cranial and caudal to the site of injection. Dermatomes were numbered from 2 (C2) to 30 (S5). Since cervical root dermatomes are usually numbered C2–8, while there are only seven cervical vertebrae, cervical epidural spread was assessed using the following rule: The C2–7 cervical nerve roots exit from the cervical vertebrae through a gutter in the transverse process (5). The C8 nerve root exits just cranially from the C7–T1 intervertebral space, joining the C7 root in its course (5). Therefore, cranial spread of blockade relative to the insertion site was considered to be C8 and up in patients with the epidural catheter at the C7–T1 interspace, and C6 and up in patients with the epidural catheter at the C6–7 interspace. Differences in borders of sensory blockade and numbers of segments blocked were analyzed using the Mann–Whitney U-test. Incidences of maximal cranial spread of sensory blockade (up to C2) were analyzed using Fisher’s exact test. Demographic data were analyzed using Student’s t-test, except the distribution of men versus women, which was analyzed using the χ2 test. Spirometry data were analyzed using Student’s t-test. P < 0.05 was considered statistically significant.
All patients tolerated breathing through the CPAP mask well and finished the study. All spirometric data measured before the experiment were within 10% of the predicted values calculated for each patient by the spirometer software. Vital signs remained stable in all patients. There were no significant differences in demographic data (Table 1). With fluoroscopy, all epidural catheter tips were found to be positioned not more than one segment away from the intended insertion site. Bilateral sensory blockade developed in all patients, with left–right differences of up to three dermatomes. There were statistically significant differences in the median cranial border of sensory blockade, the number of segments blocked cranial to the insertion site, and the incidence of maximal cranial spread of sensory blockade (up to C2) (Table 2). There were no differences in spirometry between groups; however, in both groups, there was a small but significant decrease in spirometry values after epidural injection (Table 3).
We reported that breathing with CPAP during and for 15 min after cervicothoracic epidural injection of local anesthetic alters the spread of sensory blockade. This is similar to our previous study on low-thoracic epidural spread (4), where we demonstrated a more caudad spread of sensory blockade when subjects breathed with CPAP, whereas cephalad spread of blockade did not differ significantly between groups. This suggests that, in awake patients breathing at ambient pressure, local anesthetic preferentially spreads toward the midthoracic epidural space after both high-thoracic and low-thoracic epidural injection (1,2). However, when airway pressure is increased by CPAP, the distal border of sensory blockade extends further away from the thorax, i.e., more cranially after cervicothoracic injection (this study), and more caudad after low-thoracic injection (4).
Although we did not measure epidural pressure during this experiment, we believe a possible explanation for our findings is that the increased airway pressure is transmitted to the epidural space, thereby inhibiting spread of local anesthetic toward the midthoracic epidural space. Indeed, it has been shown that epidural pressure increases significantly when increasing levels of positive end-expiratory pressure are applied during mechanical ventilation (6). Likewise, pressure may be transmitted from the pleural cavity to the epidural space via communication with the paravertebral space (7,8). Alternatively, diminished compliance of the epidural space by the application of CPAP may have played a role. Our findings warrant further investigation to evaluate the influence of increased airway pressure on epidural pressure.
Spirometry values did not differ between groups; however, in both groups there was a small but statistically significant decrease in spirometry values after epidural injection compared to baseline values. This is in accordance with other studies in which cervicothoracic epidural anesthesia has been shown to cause phrenic nerve motor block (9,10) and a decrease in spirometry values in a dose and concentration-dependent manner (9–11). The larger extension of sensory block after injection of the same dose of local anesthetic did not alter pulmonary function to a greater degree in the CPAP group compared with the control group. Although the decreases in spirometry values were statistically significant, it is unlikely the changes are clinically relevant in healthy patients. Indeed, SaO2 remained stable in all patients. However, in patients with a compromised respiratory system, such an effect might be significant.
The difference between groups in the total number of segments blocked and number of segments blocked distal from the thorax was smaller than in our previous study with low-thoracic epidural anesthesia (TEA). This may be explained by the fact that the cervical epidural space ends at the foramen magnum. Therefore, the potential upward spread of local anesthetic from the thorax is limited to only 6–7 segments in cervico-TEA, whereas it may spread 14–15 segments downwards from the thorax in low TEA. Also, the mixing of local anesthetic with a particulate steroid may have changed the physicochemical properties of the epidural solution compared with the one used in our other studies.
Our study may be criticized for several reasons. First, sensory blockade at the C8 dermatome was considered to be located caudal to the injection site in patients with the epidural catheter at C6–7, whereas it would be considered cranial to the injection site in patients with the epidural catheter at C7–T1. This could have influenced our results. Second, although spirometry has been used in other studies to evaluate the effects of cervical epidural anesthesia on pulmonary function (9–11), this method may not be adequate to detect subtle changes or differentiate between partial paralysis of abdominal, scalene, and intercostal muscles versus impaired diaphragmatic function. Future studies should use methods such as ultrasonography, maximal inspiratory pressure, and forceful sniff maneuvers to specifically evaluate phrenic nerve function. Since we included only patients without signs of obstructive lung disease (documented with spirometry), and since the FEV1/FVC ratio remained unchanged, it is unlikely that small airway caliber has contributed to the decrease in FEV1 after epidural injection. Third, since patients were breathing spontaneously, inspiratory–expiratory ratios were not controlled, which may have induced differences in intrinsic positive end-expiratory pressure. However, all patients tolerated CPAP well and showed normal breathing patterns.
In conclusion, we report that applying CPAP during and for 15 min after cervicothoracic epidural injection of lidocaine results in a more cranial extension of sensory blockade when compared with breathing at ambient pressure. Increases in airway pressure by intermittent positive pressure ventilation may have similar effects (4). Although other factors may play a role in anesthetized patients, administering high-thoracic epidural bolus doses of local anesthetic during intermittent positive pressure ventilation may result in a more cranial extension of blockade compared with administration in awake patients.
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, and Dr. Eric Robertson for reviewing the manuscript.
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