The Effects of Pressure and Shear on Capillary Closure in the Microstructure of Skeletal Muscles

Abstract

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.

Effects of dynamic sitting interventions on tissue oxygenation in individuals with spinal cord disorders

“…Friction and shear are associated with the development of superficial PUs. 21,22 Deformation of the tissue is an important factor in the development of deep tissue injury. 23,24 Individual factors that influence the ability of the tissue to withstand load, such as level of mobility, atrophy and vascularization, also have a function.…”

Preventing Ischial Pressure Ulcers: I. Review of Neuromuscular Electrical Stimulation

“…In addition to the capillary occlusion that results from both of these factors [25,45,68] many other etiological mechanisms contribute too, including lymphatic occlusion, reperfusion injury, and tissue deformation [1,3,26,64]. Finite element modeling of the latter, predicts that as dead cells accumulate, the resultant microstructural heterogeneity further deforms surviving cells, thereby aggravating the spread of tissue damage [1,13,14].…”

“…Several researchers have attempted to qualify and quantify the relative importance of increased shear [24,25,45,68]. Over the past decade groups such as Bouten's [10,24,25], Stekelenburg's [67,68], and Linder-Ganz & Geffen [45] have questioned one of the most basic assumptions about PU etiology: Do muscle cells under bony prominences die due to hypoxia and ischemia directly, or is tissue damage predominantly a consequence of the mechanical loading itself? Recently Linder-Ganz & Geffen employed animal (rat) and computer models to investigate the relative effects of pressure vs. shear on capillary patency in relation to DTI [45].…”

“…Over the past decade groups such as Bouten's [10,24,25], Stekelenburg's [67,68], and Linder-Ganz & Geffen [45] have questioned one of the most basic assumptions about PU etiology: Do muscle cells under bony prominences die due to hypoxia and ischemia directly, or is tissue damage predominantly a consequence of the mechanical loading itself? Recently Linder-Ganz & Geffen employed animal (rat) and computer models to investigate the relative effects of pressure vs. shear on capillary patency in relation to DTI [45]. Even relatively low shear strains (<10%) were found to decrease patent capillary cross-sectional area substantially (34-55%), so contributing to the effect of compressive stresses by increasing the extent of tissue ischemia.…”

Use of weight-bearing MRI for evaluating wheelchair cushions based on internal soft-tissue deformations under ischial tuberosities

“…Increasing evidence shows that DTI develops in deep tissues because of sustained mechanical deformations that damage cells directly as well as obstruct blood flow [16][17][18]; however, no quantitative noninvasive clinical method exists for measuring internal mechanical conditions in deep tissues. In a previous basic science study, we used magnetic resonance imaging (MRI) to demonstrate internal soft-tissue deformations in the buttocks during weight-bearing sitting [14][15].…”