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Pressure sores affecting muscles are severe injuries associated with ischemia, impaired metabolic activity, excessive tissue deformation, and insufficient lymph drainage caused by prolonged and intensive mechanical loads. We hypothesize that mechanical properties of muscle tissue change as a result of exposure to prolonged and intensive loads. Such changes may affect the distribution of stresses in soft tissues under bony prominences and potentially expose additional uninjured regions of muscle tissue to intensified stresses. In this study, we characterized changes in tangent elastic moduli and strain energy densities of rat gracilis muscles exposed to pressure in vivo (11.5, 35, or 70 kPa for 2, 4, or 6 h) and incorporated the abnormal properties that were measured in finite element models of the head, shoulders, pelvis, and heels of a recumbent patient. Using in vitro uniaxial tension testing, we found that tangent elastic moduli of muscles exposed to 35 and 70 kPa were 1.6-fold those of controls (P < 0.05, for strains /=5%). Histological (phosphotungstic acid hematoxylin) evaluation showed that this stiffening accompanied extensive necrotic damage. Incorporating these effects into the finite element models, we were able to show that the increased muscle stiffness in widening regions results in elevated tissue stresses that exacerbate the potential for tissue necrosis. Interfacial pressures could not predict deep muscle (e.g., longissimus or gluteus) stresses and injuring conditions. We conclude that information on internal muscle stresses is required to establish new criteria for pressure sore prevention.

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.

Computational studies of deep pressure sores (DPS) in skeletal muscles require information on viscoelastic constitutive behavior of muscles, particularly when muscles are loaded transversally as during bone-muscle interaction in sitting and lying immobilized patients. In this study, we measured transient shear moduli G(t) of fresh porcine muscles in vitro using the indentation method. We employed a custom-made pneumatic device that allowed rapid (2000 mms) 4 mm indentations. We tested 8 gluteus muscles, harvested from 5 adult pigs. Each muscle was indented transversally (perpendicularly to the direction of fibers) at 3 different sites, 7 times per site, to obtain nonpreconditioned (NPC) and preconditioned (PC) G(t) data. Short-term (GS) and long-term (GL) shear moduli were obtained directly from experiments. We further fitted measured G(t) data to a biexponential equation G(t) = G1 x exp(-t/tau1)+ G2 x exp(-t/tau2) + Ginfinity, which provided good fit, visually and in terms of the correlation coefficients. Typically, plateau of the stress relaxation curves (defined as 10% difference from final GL) was evident approximately 20 s after indentation. Short-term shear moduli GS (mean NPC: 8509 Pa, PC: 5711 Pa) were greater than long-term moduli GL (NPC: 609 Pa, PC: 807 Pa) by about an order of magnitude. Statistical analysis of parameters showed that only G2 was affected by preconditioning, while GL, GS, Ginfinity, tau1, tau2, and G1 properties were unaffected. Since DPS develop over time scales of minutes to hours, but most stress relaxation occurs within approximately 20 s, the most relevant property for computational modeling is GL (mean approximately 700 Pa), which is, conveniently, unaffected by preconditioning.

Deep tissue injury (DTI) is a severe pressure ulcer, which initiates in muscle tissue under a bony prominence, and progresses outwards. It is associated with mechanical pressure and shear that may cause capillaries to collapse and thus, induce ischemic conditions. Recently, some investigators stipulated that ischemia alone cannot explain the etiology of DTI, and other mechanisms, particularly excessive cellular deformations may be involved. The goal of this study was to evaluate the functioning of capillaries in loaded muscle tissue, using animal and finite element (FE) models. Pressures of 12, 37, and 78 kPa were applied directly to one gracilis muscle of 11 rats for 2 h. Temperatures of the loaded and contralateral muscles were recorded with time using infrared thermography (IRT) as a measure of the ischemic level. In addition, a non-linear large deformation muscle-fascicle-level FE model was developed and subjected to pressures of 12-120 kPa without and with simultaneous shear strain of up to 8%. For each simulation case, the accumulative percentage of open capillary cross-sectional area and the number of completely closed capillaries were determined. After 2 h, temperature of the loaded muscles was 2.4 +/- 0.3 degrees C (mean +/- standard deviation) lower than that of the unloaded contralateral limbs (mean of plateau temperature values across all pressure groups). Temperature of the loaded muscles dropped within 10 min but then remained stable and significantly higher than room temperature for at least 30 additional minutes in all pressure groups, indicating that limbs were not completely ischemic within the first 40 min of the trials. Our FE model showed that in response to pressures of 12-120 kPa and no shear, the accumulative percentage of open capillary cross-sectional area decreased by up to 71%. When shear strains were added, the open capillary cross-sectional area decreased more rapidly, but even for maximal loading, only 46% of the capillaries were completely closed. Taken together, the animal and FE model results suggest that acute ischemia does not develop in skeletal muscles under physiological load levels within a timeframe of 40 min. Since there is evidence that DTI develops within a shorter time, ischemia is unlikely to be the only factor causing DTI.

current findings provide preliminary evidence for the ability of an artificial PCU meniscal implant to delay or prevent osteoarthritic changes in knee joint following complete medial meniscectomy.