In Vivo Muscle Stiffening Under Bone Compression Promotes Deep Pressure Sores

[+] Author and Article Information
A. Gefen, N. Gefen, E. Linder-Ganz

Department of Biomedical Engineering, Faculty of Engineering,  Tel Aviv University, Tel Aviv, Israelgefen@eng.tau.ac.il

S. S. Margulies

Department of Bioengineering,  University of Pennsylvania, Philadelphia, Pennsylvania

J Biomech Eng 127(3), 512-524 (Jan 31, 2005) (13 pages) doi:10.1115/1.1894386 History: Received August 12, 2004; Revised December 23, 2004; Accepted January 31, 2005

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 14–2 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.

Copyright © 2005 by American Society of Mechanical Engineers
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Figure 6

Representative phosphotungstic acid hematoxylin (PTAH) staining of (a) control rat gracilis muscle tissue (not subjected to pressure), showing a clear cross-striation structure stained blue by PTAH, and of (b) muscle tissue which was subjected to compression of 35 KPa for 15 min. Injuries in (b) are dispersed, with dead muscle fascicles (not stained, and no cross striation) being adjacent to viable fascicles (stained blue, and cross-striation maintained). Within the frame shown in (b), ∼88% of the area of muscle tissue contained dead cells. Magnification was set as X300.

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Figure 7

Model predictions of distributions of principal compressive stresses in the buttocks during wheelchair sitting with the backrest of the wheelchair inclined (a) 70 deg and (b) 80 deg with respect to the horizon. Arrowheads indicate locations of peak principal compressive stress (in the right longissimus muscle, adjacent to the sacrum).

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Figure 8

Finite element model predictions of the time-dependent distribution of principal compression stresses in the longissimus muscle during wheelchair sitting. Based on our animal studies, muscle tissue elements subjected to compressive stresses σc in the range 35KPa⩽σc<70KPa stiffen (by factors specified in Table 3) after 1∕2h of immobilized sitting. Stiffening of muscle tissue at sites subjected to σc⩾70KPa occurs after just 15 min of immobilized sitting (Table 3). For simulation case (a), where the backrest inclination is 70 deg, 28% of the cross-sectional area of the longissimus is subjected to potentially injuring stresses (⩾35KPa) after 15 minutes of immobilized sitting. For simulation case (b), where the backrest inclination is 80 deg, 35% of the cross-sectional area of muscle tissue is susceptible to injury after 15 min of immobilization. The dotted line in each time frame of the stress analysis shows the propagation and widening of the 70 KPa stress wave within the right longissimus.

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Figure 1

Scheme of the computer-controlled indentation system for measuring long-term shear modulus G∞ of rat muscle tissue

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Figure 2

Scheme of the compression apparatus used to induce pressure injury on the exposed rat muscle tissue

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Figure 3

Computational modeling of the buttocks during wheelchair sitting: (a) three-dimensional solid model, (b) free-body-diagram showing the system of skeletal forces (F1,F2), skin-cushion friction force and skeletal moments (M1,M2) acting on the model, and (c) finite element meshing with magnification of the abdominal cavity region subjected to abdominal pressure

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Figure 4

Nonpreconditioned (NPC) and preconditioned (PC) long-term shear moduli G∞ of gracilis muscle of surgical control rats over time (N=4), from time of skin reflection (baseline). No pressure was applied on muscles of this group.

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Figure 5

Nonpreconditioned (NPC) and preconditioned (PC) long-term shear moduli G∞ of gracilis muscle of rats subjected to pressure of 35 KPa for (a) 15 min, (b) 30 min, (c) 60 minutes, and (d) 120 min, and of rats subjected to 70 KPa for (e) 15 min, (f) 30 min and (g) 120 min. Bars indicate means and vertical lines indicate standard deviations. For each group (N=4 in each) the baseline shear modulus (immediately after skin reflection), post-compression modulus, and modulus after 30 mins of reperfusion are depicted.



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