Compression of Subcutaneous Blood Vessels as a
Cause of Pressure Sores: Analysis of Risk Factors
and Protective Means

Amit Gefen, Ph.D.
The Dept of Cardiology, Tel Aviv Medical Center;
Department of Biomedical Engineering,
Faculty of Engineering, Tel-Aviv University

Summary of Research Activities:
Pressure sores (PS) are caused by extensive and prolonged loading of vascularized soft tissues. Elevated local mechanical stresses obstruct blood vessels, thereby depriving required tissue nutrients and inhibiting waste clearance. PS are considered one of the most severe complications in geriatric and paralyzed patients. We developed realistic, anatomically accurate three-dimensional (3D) computational (finite element) models of the body regions vulnerable to PS during immobilized recumbency (e.g. Fig. 1). These models indicated that elevated stresses, which can potentially lead to ulceration, are found at deep muscle tissue underlying bony prominences (Linder-Ganz and Gefen, 2002). The deep focal muscle stresses are greater by two orders of magnitude with respect to contact stresses at the body-support interface, which strongly supports the hypothesis that the more severe and difficult to treat PS necroses initiate deep in the body. Accordingly, we utilized our models to characterize the etiology of deep PS.

Exposure of muscle tissue to intensive and prolonged compression may affect its microstructure and thereby, the muscle's constitutive law is also expected to change. We therefore measured changes in stiffness of muscle tissue in vitro as a result of prolonged compression applied to rat models of PS (Protocol #11-02-41 approved by Tel Aviv University's Animal Care and Use Committee), and used the modified properties of injured muscles in our 3D numerical models to characterize the etiology of PS. A pre-calibrated rigid indentor was used to apply constant compression to the gracillis (hind limb) muscle of anesthetized rats. Comparable pressure doses (product of applied compression and exposure time) were delivered to the gracillis of 43 animals: 11.5, 35 and 70 KPa for 2, 4, and 6 hours, based on our preliminary 3D model simulations of internal muscle tissue stresses. After hind limb compression, animals were sacrificed and muscles were harvested. Uninjured (control) and injured muscles were tested in uniaxial tension (Instron 5544) at a saline container kept at the rat’s body temperature (330C), and tangent moduli of elasticity were calculated from the stress-strain relations. Tangent moduli Et (5% strain) of rat muscles injured by exposure of 2-6 hours to compression of 70 KPa (Et = 172 ± 39 KPa) were shown to be 43% higher (p<0.05 using a Tukey-Kramer test) compared with uninjured muscles (Et = 120 ± 19 KPa). Considering this muscle stiffening effect in our 3D models, internal stress distributions in deep muscles during recumbency were shown to evolve with time due to changes in the injured muscle’s constitutive law, as demonstrated in regions A, B of the longissimus muscles under the sacrum (Fig. 1). This suggests a mechanism of deterioration in which soft tissues that were not directly affected by the intensified internal stresses could be gradually damaged due to induction of elevated stress by adjacent stiffening injured muscle tissue.

Integrating our numerical models of the stress evolution in deep muscles with thresholds for muscle injury that are currently being determined from animal studies, it was possible to start developing a monitoring system that recommends a relief of pressure at the common sites for PS injury (head, scapula, sacrum, buttocks, and heels) based on stress levels in deep muscles (Yemal et al., 2002). Comprising 20 flexible ultra-thin contact pressure and 8 temperature sensors placed under the patient’s body, the system converts measured contact stress to deep muscle stress using transformations determined using our set of biomechanical models. It calculates pressure/temperature doses in real time, and compares them with injury thresholds obtained from animal models.

Fig. 1. Pelvis model and evolution of stresses in muscles underlying the sacrum with PS injury

The PS prevention monitor is able to provide anatomically-specific alerts, based on weighted values of local pressure/temperature doses (patent pending via RAMOT of Tel Aviv University). It now awaits completion of characterization of injury thresholds and interface-to-internal stress transformations, which will allow a pre-clinical study.

Publications (8/2001-12/2002)
Linder-Ganz, E. and Gefen, A., 2002, "Biomechanical interactions of the pelvis girdles and surrounding soft tissues: toward understanding the mechanism of pressure sore onset," IV World Congress of Biomechanics, Calgary, Canada. Yemal, E., Portnoy, S., and Gefen, A., 2002, “Monitoring the risk for pressure sore onset,” 22nd Convention of IEEE Israel Section, Tel Aviv University, Israel.