As opposed to previously reported cadaveric studies,9,10,11,12,13 this was an in vivo MRI study of injectate spread of the ESP block in living patients. We showed that there was consistent spread of injectate into the intercostal space, neural foramina, and the erector spinae muscles, thus contributing to the sensory findings in the ventral and dorsal thoracic and abdominal walls. Nevertheless, the extent of the cephalocaudal spread and the sensory block to the anterior abdominal and thoracic walls were highly variable (Figs 2 and 3).
Since it was first published, ESP block had been one of the most popular regional anesthesia techniques described in the literature.2,17 Multiple randomized-controlled trials have also confirmed the analgesic efficacy of this block.2,3 Despite its popularity, the mechanism of ESP block action is unclear. The popular belief is that the ESP block leads to LA injectate crossing the superior costotransverse ligament and spreading into the paravertebral space.11 This anterior spread is the basis for the blockade of the ventral rami resulting in thoracic (or abdominal) analgesic effects. Five studies, all in cadavers, examined the spread, but the results were conflicting. Spread to the paravertebral space was minimal to none in two studies,12,13 with no spread to the intercostal nerves in three studies.10,12,13 Four studies used anatomical dissection to examine the spread,9,10,12,13 one assessed the spread with three-dimensional computed tomography scan,13 and another one with MRI.11 The volume of injectate was 20 mL in all but one study (where 30 mL of injectate was used).13 Nevertheless, the authors of those studies agreed that correlating spread in cadaver models with spread in live human subjects is limited. The ESP is an interfascial plane block with the target between the tip of the transverse process and erector spinae muscles. In live human subjects, the spread can be potentially enhanced by the contraction of the erector spinae muscles and the negative intrathoracic pressure during inspiration (Fig. 5). These mechanisms potentially enhance spread towards the paravertebral and intercostal spaces.8,14 Thus, examining the injectate spread in live human subjects can further enhance our understanding of the mechanism of ESP block in clinical settings.
In the present study, consistent sensory block in the posterior (dorsal) thoracic and abdominal wall was evident, and was supported by the extensive spread of injectate in the erector spinae muscles through which the posterior rami transit. Nevertheless, the cephalocaudal extent of the sensory block to the anterior (ventral) thoracic and abdominal walls was much more variable although it was present in all patients. Though it is not feasible to perform a correlation analysis with such a small number of patients, the spread patterns seen with MRI (i.e., with spread to neural foramina and intercostal nerve distributions) were consistent with the sensory block. The pattern of spread showed that the larger the extent of spread to both the intercostal nerve and neural foramina (e.g., comparing patients 1 and 2 with patients 4 and 5), the more extensive were the sensory levels shown. In two patients (patients 1 and 2), injectate spread to the epidural space, but the significance of this epidural spread was uncertain; it may have been a consequence of extensive injectate spread into the paravertebral space and neural foramina. Thus, the mechanism of sensory blockade of the anterior thoracoabdominal wall by the ESP block appears to be related to spread to the neural foramina and intercostal space. Spread to the epidural space is an unlikely mechanism with 30–35 mL injectate.
Compared with previous cadaver studies on injectate spread following ESP block, our model in live human subjects offers a few advantages. First, it simulates a real-life situation, including the theoretical effects of respiration and muscle contraction on the extent of injectate spread in the erector spinae muscle plane. It also avoids biochemical change of hyaluronic acid, a key substance controlling the viscosity of connective tissue and thus injectate spread. Even in fresh embalmed cadavers, a slight drop in the temperature will increase the viscosity of hyaluronic acid in the extracellular matrix and affect connective tissue in the fascial plane. This could be relevant to the spread of injectate to the intercostal nerves,18,19 and may account for the negative spread to the intercostal space observed in three previous cadaver studies (while our study consistently showed extensive spread to the intercostal nerve).
A second difference in our study compared with those published previously is that we added gadolinium to the injectate. Nevertheless, using MRI to track the LA fluid spread following the injection can be challenging.20 The fluid signal is usually hypointense in the T1-weighted sequence. To accentuate the visualization of water content, a T2-weighted sequence is usually used, but it can be difficult to differentiate the fluid content from cerebrospinal fluid, blood vessels, and soft tissue. Gadolinium has an odd number of electrons, which confers it considerable paramagnetic power and renders it hyperintense by increasing the intensity of the magnetic field around it. Thus, by mixing gadolinium with LA, the signal of the mixture is accentuated and can be tracked with just a T1 sequence; this can differentiate it from cerebrospinal fluid in the spinal canal.21
We also correlated MRI findings with sensory evaluations and pain relief. Spreading of the contrast in MRI studies (or dye in cadavers) to any nerves may not be clinically significant because of the concentration effect. On the other hand, when intact nerves are exposed to LA with a high pKa (e.g., ropivacaine and bupivacaine) at lower concentrations, the C fibres are consistently blocked ahead of the myelinated A fibres. Therefore, the spread may not be detected by the usual sensory test, which in turn may underestimate the clinical analgesic effects.22 By correlating with sensory assessment and pain relief in live subjects, the clinician can better appreciate the clinical significance of the spread.
A limitation of this study was the sample size. Even with a single physician performing all blocks at the same level on the same side, the extent of spread and the sensory effects were quite variable. A larger sample size might allow for a better appreciation of the relationship between the sensory effects and injectate spread. Nevertheless, the recruitment of patients was very difficult, especially because an extra MRI procedure was required.
In summary, our novel study examining injectate spread in live patients following the ESP block showed that the LA injectate consistently spread to the dorsal rami among the erector spinae muscle resulting in posterior thoracic and abdominal wall blockade. We also showed that the LA injectate consistently spread to the neural foramina and into the intercostal space, contributing to a clinically meaningful sensory change and pain relief in the anterior (ventral) thoracic and abdominal walls. Nevertheless, the extent of spread to the neural foramina and intercostal space was highly variable. Lastly, although the full clinical impact is not known, the LA injectate spread to the epidural space in some patients, so clinicians need to exercise caution when using high volumes of LA during ESP blockade.