European Pressure Ulcer Advisory Panel

What Are the Effects of Pressure and Shear on Tissue?

Laura E. Edsberg, Ph.D.

Natural & Health Sciences Research Center, Center for Wound Healing Research, Daemen College, Amherst, NY 14226, USA

Pressure and shear contribute to pressure ulcers, but the study of the tissue’s response to these forces is a challenge. Once a pressure ulcer is present the tissue surrounding the ulcer or the tissue in the bed of the wound is all that remains to study. The changes initiated with pressure and shear in the microstructure and mechanical properties of the tissue are difficult to assess when in fact we are looking at the end result of the loading applied to the tissue in the form of a pressure ulcer, and the tissue present during the development of the ulcer is now absent.

Both in vitro and in vivo studies have been conducted to examine the effects of pressure and shear on tissue. The findings in our laboratory, as well as those of other researchers, have shown that relatively small loads can result in significant changes to the tissue’s structure and properties. The changes in the tissue’s fiber bundle alignment may be indicative of changes leading to the tissue’s inability to tolerate loads and thus tissue breakdown. It may well be that tissue remodeling is a necessary part of the response to the tissue loading, but in some cases this remodeling is ineffective and leads to pressure ulcer formation.

Biochemical factors are also integral to both pressure ulcer formation, as well as pressure ulcer healing. The biochemical response to loading may play a pivotal role in pressure ulcer development versus effective remodeling. Some of the potential biomarkers associated with tissue breakdown have been described in the literature, but the biomarkers associated with changes in the wound’s status are relatively unknown. In our laboratory we are seeking to identify specific biochemical changes seen in healing versus non-healing wounds. The correlation between the biochemical factors and the tissue’s response to loading is critical to better understanding pressure ulcer development and healing.

The Combined Effect of Pressure and Shear on Capillary Closure in the Microscale of Skeletal Muscle Tissue

Amit Gefen, PhD

Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv 69978, Israel

Deep tissue injury (DTI) is a serious and potentially deadly type of pressure ulcers, which initiate in deep muscle tissue under bony prominences of immobilized patients, and progress outwards towards the skin with no clear visual indications of the injury at the surface of the body. It had been suggested that DTI appear in muscle tissue first due to the dense capillary vasculature in skeletal muscles which is susceptible to obstruction and occlusion by mechanical forces, particularly shearing forces. Though mechanical forces may cause capillaries to collapse and thus induce ischemic conditions in dependent muscle cells, some investigators stipulated that ischemia alone cannot explain the etiology of DTI, and so, other mechanisms, particularly excessive cellular deformations must be involved (Stekelenburg, Ph.D. Thesis, Technische Universiteit Eindhoven, 2005; Gawlitta et al., Ann. Biomed. Eng., 2007). We hypothesize that physiological levels of stresses and strains in muscle tissue under bony prominences - even when muscles are highly loaded as in paraplegic patients during sitting - do not cause complete capillary closure, and therefore, do not cause total ischemia in muscles. If this is indeed the case, then ischemia cannot be the only factor contributing to DTI onset. In order to test our hypothesis, we developed (i) a coupled MRI-finite element method to determine shear and compression strains and stresses in gluteal muscles of sitting normal and paraplegic subjects at the macroscopic scale, (ii) finite element model of the microstructure of skeletal muscle, at the level of muscle fascicles, which was loaded based on the macroscopic mechanical conditions, to predict capillary closure at the microscale of muscle tissue. (iii) rat models of muscle ischemia to validate the computational results by means of infrared thermography measurements of muscle perfusion under mechanical loading. Taken together,results from these integrated studies indicate that shear strains and stresses are indeed very likely to promote ischemia and hypoxia, as commonly believed. However, it appears that the ischemic conditions alone are insufficient to cause DTI. This later finding supports recently published animal and cell culture studies where it was concluded that excessive cellular deformation, not just ischemia, must be involved in the onset of DTI (Stekelenburg, Gawlitta).

Can we define a damage threshold for soft tissues under sustained mechanical loading?

Cees Oomens¹, Karlien Ceelen¹, Anke Stekelenburg¹ & Dan Bader^1,2

1. Biomedical Engineering Department, Eindhoven University of Technology
2. Queen Mary, University of London

A vast majority of papers on aetiology of pressure ulcers have attempted to identify the level of sustained mechanical loading on skin and soft tissue, beyond which they will break down. This has led to a number of qualitative observations like:

• There is a relationship between time and magnitude of externally applied load and the risk of acquiring a pressure ulcer. It is generally accepted that a high magnitude requires less time to cause an ulcer. Low loads can also lead to an ulcer but require a longer time.
• In certain cases, muscle is more susceptible to breakdown than skin or adipose tissue.
• Externally applied shear forces are more damaging than normal forces.
• The highest stresses and strains can be found internally (i.e. adjacent to bony prominences), leading to deep tissue injury. This is extremely dangerous to paraplegic patients, who are insensate.

The above observations have been confirmed by experimental studies. Less documented, but often stated in the literature is the notion that pathology reduces tissue susceptibility.

One of the problems with defining a quantitative damage threshold for tissues is, to determine the effects of an externally applied load at the interface between skin and supporting surface. Techniques to measure this external load are available in the form of interface pressure monitors. Furthermore, techniques to measure shear forces at the interface are being introduced. However how this external load is transferred to within the tissue is a more complex issue. What is the effect of the external loading on the internal mechanical stresses and strains of skin, fat, muscle and other connective tissues? Such a relationship will depend on the geometry of the bone and tissue layers involved and the mechanical properties of the different tissues, both factors being specific for each individual patient. In the last decennium experimental (MRI, Ultrasound) as well as theoretical (Finite Element Method) tools have become available to interrogate the internal mechanical state, even if that has to be done for an individual patient.

In the presentation examples will be given on how the first indicators of tissue damage can be measured with T2-weighted MRI and compared to a dedicated Finite Element Model to estimate the internal mechanical state of the loaded tissues. Accordingly, a damage threshold will be proposed.