Fluid dynamics of local anesthetic spread: a hypothesis-generating review

Background Fascial plane blocks (FPBs) have gained popularity for perioperative analgesia due to their simplicity and low complication rates, yet the anatomical and fluid-dynamic determinants of their injectate spread remain incompletely understood. A possible reason, so far largely unexamined, is that the biomechanics of fascial tissue and the fluid dynamics of injected solutions are poorly understood. Objective To introduce a theoretical, hypothesis-generating biophysical framework describing how fascial geometry, the viscoelastic properties of hyaluronan (HA)-rich fascial extracellular matrix, and injection parameters might influence spread of local anesthetics (LAs). None of the mechanisms discussed has been studied in patients receiving FPB, and the framework is offered as a research agenda rather than guidance for practice. Evidence review PubMed/MEDLINE and Google Scholar were searched from inception to May 2026 for work on fascial geometry, HA, LA spread, and fluid mechanics of narrow and porous media. Because the mechanisms of interest have not been investigated in regional anesthesia, evidence was also drawn from biomechanics, tissue engineering, porous-media flow, Hele-Shaw cell research, and ophthalmic anesthesia (sub-Tenon block). Sources were selected for conceptual relevance with no formal assessment of study quality or risk of bias. Findings Two conventional modes of fluid propagation are distinguished: pressure-driven bulk-flow hydrodissection, initiating the initial anatomical distribution, and concentration-driven diffusion, acting later over a shorter distance. Hydrodynamic interfascial pattern-forming instabilities—of which viscous fingering is the best characterized—are proposed as a hypothesis, not as a third transport mechanism but as a pattern the advancing front may adopt during pressure-driven flow. In laboratory Hele-Shaw systems, a branched, fingering front fills a compartment with less work than a blunt front, but whether this occurs in living fascia is unknown. HA behaves as a non-Newtonian viscoelastic matrix whose rheology could modulate spread. Its postmortem degradation may contribute to the discrepancy between cadaveric and in vivo injectate patterns. Conclusions Recognizing HA as a dynamic functional matrix rather than merely a passive conduit for LA provides a theoretical explanation for the variability of FPBs. A strategy incorporating slow injection, warmed LA solution, real-time pressure monitoring, and the adjunctive use of hyaluronidase may promote more homogeneous distribution in experimental settings, but requires clinical validation.