Mechanisms of action of the erector spinae plane (ESP) block: a narrative review

The erector spinae plane (ESP) block is an emerging regional anesthetic technique with significant potential for clinical benefit. Nevertheless, its exact mechanism(s) of action has been much debated. We reviewed the available literature to explore the possible mechanisms of analgesia for the ESP block. These include neural blockade and central inhibition from direct spread of local anesthetic to the paravertebral or epidural space; analgesia mediated by elevated local anesthetic plasma concentrations due to systemic absorption; immunomodulatory effects of local anesthetics; and an effect mediated through the mechanosensory properties of thoracolumbar fascia. Based on evidence from clinical, human cadaveric, animal, and mechanistic laboratory studies, the most probable primary mechanism is a direct effect of local anesthetic via physical spread and diffusion to neural structures in the fascial plane deep to the erector spinae muscles and adjacent tissue compartments. Biological plausibility of this primary mechanism is confirmed by injectate spread to the ventral rami of spinal nerves (though quite variable) in most studies. There is consistent involvement of dorsal rami; epidural spread is a less commonly observed phenomenon. A systemic effect of local anesthetic is also plausible, but unlikely to be a major contributor to clinical analgesic efficacy. The evidence for significant analgesia due to other proposed mechanisms, such as fascia-mediated analgesia or lymphatic spread, are currently limited and thus remain speculative. Understanding the mechanisms of action could assist clinicians in further investigating and refining ESP block performance, with the ultimate goal of optimizing analgesic efficacy and improving postoperative patient outcomes.

Automated summary

The possible mechanisms of analgesia for the ESP block include neural blockade, central inhibition, direct spread of local anesthetic, elevated plasma concentrations, immunomodulatory effects, and mechanosensory properties. The primary mechanism is likely the direct effect of local anesthetic via physical spread to neural structures. Evidence for other proposed mechanisms is limited and speculative at present.