Abstract
Edema of the vocal folds (VFs) is the result of an inflammatory response to injury (phonotrauma), or other deleterious stimuli, causing fluid build-up in the VF tissue. Although a mild level of edema has been postulated to be prophylactic, excessive edema has been identified as a pathway in the development of vocal hyperfunction. Herein we present a multi-time scale finite element model to examine the progression of VF edema in response to phonotrauma. Phonotraumatic damage was assessed by two measures: viscous dissipation and positive strain energy rate. Time-averaged phonotrauma over short time scales was assumed to drive swelling over longer time scales in proportion to the damage measure via a damage sensitivity gain. Healing was assumed to continuously act to reduce swelling. Growth rate analysis indicated that edema depends on a balance between healing, compensatory adjustments to maintain desired voice output measures, and altered VF vibration due to edema. For high damage sensitivity relative to healing, peak edema resulted in roughly 25% local peak swelling at 0.15 h, whereas low damage sensitivity led to swelling trending toward a steady condition requiring little compensation to maintain voice outputs. In general, fluid accumulation was distributed non-uniformly across the VFs with concentrations near the VF medial surface and the superior end of the body. Results from this first-ever model connecting phonotrauma at the short time scale and swelling at the longer time scale exhibited rapid edema progression under certain conditions, aligned with the "vicious cycle" hypothesis of hyperfunction, wherein localized edema initiated a positive feedback loop that led to even greater localized swelling.