Mechanical compression-induced pressure sores in rat hindlimb: muscle stiffness, histology, and computational models

Abstract

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%) and strain energy densities were 1.4-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.

Evaluation of a new sitting concept designed for prevention of pressure ulcer on the buttock using finite element analysis

“…These studies suggested an optimal method to reduce interface pressure and stress/strain on the skin and in the deep tissue of the buttock. Using a rat model, Linder-Ganz and Gefen [13] reported the compressive strain between 3 and 9% within the muscles beneath the ischial tuberosity, which was supported by our data of 6.9% (for the Normal sitting posture) within the muscle in the same area. However, in a later human subject study of Linder-Ganz et al [14], a substantially higher compressive strain (70-84%) was reported for the gluteus muscle, which deviated from our findings and their previous data on rats.…”

“…Although it still is uncertain what mechanical parameters are the most relevant to tissue damage [19], evidence supports that living cells are more vulnerable to deformation than to a high hydrostatic pressure [4]. Therefore, the von Mises stress, which is related to the deformational energy stored in the material [13,19,23], was analyzed in this study to identify the risk of possible tissue damage by sitting load [19,23].…”

Assessing evidence supporting redistribution of pressure for pressure ulcer prevention: A review

“…Linder-Ganz and Gefen exposed rat hind limbs to pressure magnitudes of 86, 262, and 525 mmHg for 2, 4, and 6 hours, respectively [5]. They used finite ele ment modeling to calculate internal stresses and concluded that tissue damage occurred with 13 kPa o f internal stress applied for 6 hours and 40 kPa of interna l stress applied for 2 ho urs.…”

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

“…Evidence for susceptibility of muscle to compression injury was found in several studies [21][22][23][24][25][26][27], while in comparison, skin and subcutaneous tissues appear more resistant to pressure [21][22][23]. However, because of obvious limitations, experiments in this line have only been carried out on animal models or tissue-engineered constructs [5].…”