In Vivo Muscle Stiffening Under Bone Compression Promotes Deep Pressure Sores

Abstract

Pressure sores (PS) in deep muscles are potentially fatal and are considered one of the most costly complications in spinal cord injury patients. We hypothesize that continuous compression of the longissimus and gluteus muscles by the sacral and ischial bones during wheelchair sitting increases muscle stiffness around the bone-muscle interface over time, thereby causing muscles to bear intensified stresses in relentlessly widening regions, in a positive-feedback injury spiral. In this study, we measured long-term shear moduli of muscle tissue in vivo in rats after applying compression (35 KPa or 70 KPa for 1/4-2 h, N = 32), and evaluated tissue viability in matched groups (using phosphotungstic acid hematoxylin histology, N = 10). We found significant (1.8-fold to 3.3-fold, p < 0.05) stiffening of muscle tissue in vivo in muscles subjected to 35 KPa for 30 min or over, and in muscles subjected to 70 KPa for 15 min or over. By incorporating this effect into a finite element (FE) model of the buttocks of a wheelchair user we identified a mechanical stress wave which spreads from the bone-muscle interface outward through longissimus muscle tissue. After 4 h of FE simulated motionlessness, 50%-60% of the cross section of the longissimus was exposed to compressive stresses of 35 KPa or over (shown to induce cell death in rat muscle within 15 min). During these 4 h, the mean compressive stress across the transverse cross section of the longissimus increased by 30%-40%. The identification of the stiffening-stress-cell-death injury spiral developing during the initial 30 min of motionless sitting provides new mechanistic insight into deep PS formation and calls for reevaluation of the 1 h repositioning cycle recommended by the U.S. Department of Health.

Toward real-time detection of deep tissue injury risk in wheelchair users using Hertz contact theory

“…Needless to say, the IT is not a perfect half-sphere and does not have the same mechanical properties in all subjects; it is a unique living structure that has a distinctive elastic modulus depending on its location and physical history and should be evaluated on an individual basis [65]. Similarly, the tissue underneath is not a flat infinite half-space, and characteristics such as viscoelasticity and stiffening over time according to physical circumstances [14] should be considered.…”

“…A positive feedback mechanism was observed, in which the damaged area continues to expand under prolonged compression [14,38]. It is hypothesized that damage first occurs under the IT, where compression stress concentrations can be as high as 32 ± 9 kPa (mean ± standard deviation [SD]) according to a recent integrated magnetic resonance imaging (MRI) and FE study of sitting (nondisabled) subjects [39].…”

“…Hence, DTI owing to excessive tissue deformation, ischemia, and hypoxia may develop unnoticed under the IT until advanced stages. Indeed, between one-third and slightly less than half of all people with SCI will develop pressure ulcers during the years immediately following their trauma [12][13][14]. About 5 to 7 percent of these will eventually require hospitalization, and 7 to 8 percent of those who require hospitalization will die of consequent complications [1,15].…”

Dynamic sitting to prevent pressure ulcers in spinal cord injured

“…It appears that an unbalance between the loads exerted on the tissue and the ability of the tissue to withstand the load, causes ischemia and tissue deformation, eventually resulting in tissue necrosis. Recently, the distinction has been made between superficial pressure ulcers and deep pressure ulcers [28].…”

The NPUAP Meeting – This was No Consensus Conference

“…Dr. Gregory Bohn stated there is research demonstrating damage occurs from within and not from the surface. [4][5][6] Dr. Caroline Fife noted the staging system does not include the pathophysiology of how pressure ulcers form. She added ''Plaintiffs are anxious to link the development of pressure ulcers to elder abuse in order to avoid the cap on punitive damages.…”