Reswick and Rogers pressure-time curve for pressure ulcer risk.part 2

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1 art & science tissue viability Reswick and Rogers pressure-time curve for pressure ulcer risk.part 2 Gefen A (2009) Reswick and Rogers pressure-time curve for pressure ulcer risk. Part 2. Nursing Standard. 23, 46, Date of acceptance: February Summary In part one of this article, the concepts of an injury threshold were explained and it was shown that the Reswick and Rogers pressure-time curve is inaccurate at the extremes of the timescale. It was also shown that their curve cannot be used for studying deep tissue injuries, and that it is likely to be irrelevant for studying most pressure ulcers. The second part of this article describes recent research work focusing on tissue injury thresholds as related to pressure ulcers, with particular emphasis on thresholds that are specific for deep tissue injuries. Clinical implications are also discussed, with particular reference to patients who are obese and those with muscle atrophy. Author Amit Gefen is associate professor, Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv, Israel. gefen@eng.tau.ac.il Keywords Deep tissue injury; Obesity; Pressure ulcers; Risk assessment; Wound management These keywords are based on the subject headings from the British Nursing Index. This article has been subject to double-blind review. For author and research article guidelines visit the Nursing Standard home page at nursingstandard.rcnpublishing.co.uk. For related articles visit our online archive and search using the keywords. PART ONE OF THIS ARTICLE highlighted some fundamental problems in using the Reswick and Rogers (1976) pressure-time curve to understand the conditions under which pressure ulcers occur, or for developing guidelines and technologies to prevent pressure ulcers. It was indicated that extrapolations of the Reswick and Rogers (1976) data to short and long periods of exposure to body loads are incorrect, and that interface pressures are not a standardised measure of internal tissue loads (Gefen and Levine 2007). Formulation of a standardised tissue injury threshold Recently, intensive research work has been carried out (Peeters et al 2005, Linder-Ganz et al 2006, Stekelenburg et al 2007, Gefen et al 2008), including some collaborative studies, to propose a more accurate and standardised tissue injury threshold as related to pressure ulcers. The studies focus was on muscle tissue, which is more susceptible to damage than fat and skin (Daniel et al 1981, Salcido et al 1994), and is also the site for the onset of deep tissue injury (Ohura et al 2007). The purpose of the studies (Peeters et al 2005, Linder-Ganz et al 2006, Stekelenburg et al 2007, Gefen et al 2008) was to determine the load tolerance of muscle tissue as an inherent property of the muscle material, as opposed to the Reswick and Rogers (1976) approach of using external (interface) pressures, which may have different internal effects for different anatomies (Gefen 2009). Determining an injury threshold that is specific for muscle tissue requires contemporary bioengineering research methods that can determine internal mechanical conditions (for example, distribution of deformations) in loaded muscle tissue in vivo, cell and tissue culture models, animal models and living humans. Such methods include small animal magnetic resonance imaging (MRI), open MRI and computational modelling, the use of which in pressure ulcer research is described elsewhere (Gefen 2008). The availability of these methods has opened up new opportunities in pressure ulcer research, and has boosted the efforts to characterise the injury tolerance of muscle tissue to mechanical loads. The key outcomes from these recent studies are reviewed later on in this article. Stekelenburg et al (2007) attempted to distinguish between the contributions of tissue deformation and ischaemia to muscle tissue damage. They studied the separate and combined effects of the deformation and ischaemia factors, by loading the hind limb of the anaesthetised rats for two hours, during which the loaded muscles were examined internally by means of small animal MRI. Tissue deformations were induced to the tibialis anterior muscle of the animals using an indenter, a rigid 3mm diameter rod, curved at the edges, that is pressed against the skin; ischaemia 40 july 22 :: vol 23 no 46 :: 2009 NURSING STANDARD

2 was produced with an inflatable tourniquet. The muscles were also analysed histologically post-euthanasia. One of the most important results from this study was that two hours of sustained deformation inflicted substantial and irreversible damage to muscle tissue, which indicated that high enough deformations can induce serious tissue damage in a relatively short period of time, or even immediately (Stekelenburg et al 2008), as explained in part one of this article (Gefen 2009). This finding in the animal studies of Stekelenburg et al (2007) reconfirmed at the scale of observing an entire living muscle previous results obtained from observing single cells (Peeters et al 2005). Specifically, Peeters et al (2005) used muscle (myoblast) cell cultures to measure the maximal deformations that can be sustained by individual cells attached to the surface of a culture dish. A device was developed that was able to compress the cells at controlled deformations, while measuring the forces applied to deform the cells. The entire process of deforming the muscle cells was visualised by means of a confocal laser scanning microscope. The confocal images showed that at large deformations, the cell membranes begin to bulge, and if deformation is increased further, the membrane tears completely. Deformations exceeding about 80% consistently ruptured the cell membranes, thereby indicating that cells subjected to such elevated deformations would be damaged instantaneously and irreversibly. The Stekelenburg et al (2007) and Peeters et al (2005) studies reveal that even for short exposures to mechanical loads, living cells and tissues do have a finite tolerance, which can be viewed as their failure strength. This statement might be considered almost trivial in the context of traumatic injury to soft or hard tissues, from bruises to bone fractures, because all physical structures, including biological tissues, have an inherent failure strength which is constituted by their internal geometrical arrangement and mechanical properties. However, the failure strength characteristic of soft tissues is not reflected in the Reswick and Rogers (1976) pressure-time curve. An alternative to the Reswick and Rogers (1976) pressure-time curve was first suggested by Linder-Ganz et al (2006). With a specific focus on deep tissue injury, Linder-Ganz et al (2006) analysed muscle histopathology from models of pressure ulcers in albino rats. Muscle tissue in the rats hind limbs was subjected to pressures of 86mmHg to 578mmHg for 15 minutes to six hours, by means of a rigid indenter that locally compressed the tissue. The histopathology from each animal in the experiment was used to determine whether muscle tissue was able to FIGURE 1 The Reswick and Rogers (1976) pressure-time curve compared with the sigmoid injury threshold Pressure (mmhg) Key Sigmoid injury threshold Reswick and Rogers (1976) injury threshold Failure 300 Muscle 90 strength of is likely to withstand 2 muscle loads under this level for several hours Intolerable levels Tolerable levels Time (hours) Left vertical axis = direct pressure on muscle tissue (Linder-Ganz et al 2006) Right vertical axis = relative deformations in the tissue (Gefen et al 2008) tolerate the applied pressure and time exposure, and remain viable. Data from these experiments were superimposed on data from a meta-analysis of all the previous histopathology reported for albino rat muscles subjected to pressure (refer to Linder-Ganz et al (2006) for relevant references to the literature). The pooled data enabled a new mathematical characterisation of the pressure-time threshold for muscle tissue damage. This took the form of a sigmoid pressure-time function, which corrects the previously discussed inaccuracies in the Reswick and Rogers (1976) hyperbola function for short and long time periods. A sigmoid function is a mathematical function that produces an s-shaped curve. The sigmoid function of Linder-Ganz et al s (2006) study is shown in Figure 1 (solid line), together with the Reswick and Rogers (1976) curve (dashed line) for comparison. The sigmoid data of Linder-Ganz et al (2006) refer to pressures applied directly to muscle tissue, whereas the Reswick and Rogers (1976) data refers to interface pressures. However, the sigmoid and the Reswick and Rogers (1976) curves show similarity at the time frame between one and a half and five and a half hours. However, the curves become substantially dissimilar at the shorter and longer times because of the inaccuracies in the Reswick and Rogers (1976) pressure-time curve at these time domains (see Figure 1, Gefen 2009). The most important advantage of the sigmoid curve is that it defines a finite failure strength for muscle tissue at short times that is consistent with experimental data Relative deformation (%) NURSING STANDARD july 22 :: vol 23 no 46 ::

3 art & science tissue viability (Peeters et al 2005, Linder-Ganz et al 2006, Stekelenburg et al 2007). It also defines finite load levels that the tissue can bear without damage, over long periods (Figure 1). Compared with the Reswick and Rogers (1976) pressure-time curve, the sigmoid curve allows more pressure on the tissue at long times but lower pressures for short times (Figure 1). Overall, the sigmoid injury threshold provides more accurate limits on the pressure levels and exposure times (Figure 1). It is no surprise that a sigmoid curve (Figure 1) describes the tissue injury threshold better than the hyperbola of Reswick and Rogers (1976) pressure-time curve, because sigmoid functions were previously shown to be useful for a wide range of biological and medical applications, including, for example, the modelling of bacterial or tumour growth (Buchwald 2007). Researchers collaborated to fine-tune the sigmoid tissue injury threshold, and also to find the tissue deformations (in addition to pressures) that induce irreversible damage to muscle cells (Gefen et al 2008). They used tissue-engineered, bioartificial muscles (approximately 10mm long and 5mm wide) that were grown from muscle cell (myoblast) cultures (Gefen et al 2008). The bioartificial muscles were deformed by an indenter with a round tip, which induced non-uniform distributions of tissue deformations, thereby causing more cell death in the highly deformed areas and less cell death in the less deformed areas (Gefen et al 2008). The tissue cultures were stained with propidium iodide, which is a fluorescent dye that only marks dead cells. Following staining, cell death was monitored over time under a confocal laser scanning microscope, and the cell death patterns were correlated with the intensity of local tissue deformations in the bioartificial muscle specimens. Cell death occurrences versus load magnitudes and exposure times were in agreement with the sigmoid law from the animal studies of Linder- Ganz et al (2006) thereby reconfirming the sigmoidal form of the injury threshold. The data also provided the extreme deformations that produce immediate cell damage, or no cell damage, in muscle tissue (Figure 1, right vertical axis). Specifically, analysis of the parameters of this sigmoid injury threshold indicated a 95% likelihood that muscle cells could tolerate compressive deformations below 65% over time periods of less than one hour. After four hours and 45 minutes, they were only able to tolerate much lower deformations, below 40% (Gefen et al 2008). The steepest decrease in endurance of the cells to deformations occurred between one and three hours post-loading (Gefen et al 2008), which was consistent with the findings of Reswick and Rogers (1976). Overall, the sigmoid curve in Figure 1 provides a complete description of how much internal pressure or how much deformation is allowed in muscle tissue, and for how much time, to avoid tissue damage. This is a necessary piece of information for understanding the aetiology of pressure ulcers and deep tissue injury. Moreover, when methods are available to measure internal mechanical loads in deep soft tissues in vivo (for example, deformations in muscle tissue next to a bony prominence), this tissue injury threshold could be used to assess the risk of an individual developing a deep tissue injury. Clinical implications The sigmoid tissue injury threshold in Figure 1 can be interpreted in practice to indicate risk factors and perhaps interventions that are needed to protect patients from developing serious pressure ulcers and deep tissue injury. One such risk factor, as implied by analysis of the sigmoid threshold, is obesity. Paraplegia and quadriplegia are often accompanied by a significant gain in body weight (Gupta et al 2006, Weaver et al 2007). Accordingly, other than the impaired motor-sensory capacities that these patients have, the weight of the trunk increases the load on their load-bearing soft tissues, particularly on muscle tissue in contact with bony prominences. For example, let us assume that one ischium transfers 10% of the body weight during sitting, and that the effective contact radius of the ischium with overlying gluteal muscle tissue is approximately 4cm. A seated male with a recent spinal cord injury and a non-obese body weight of 55kg would then apply a pressure of about 80mmHg on gluteal muscle tissue under the ischia (pressure calculated as body weight per contact area (Figure 2, bottom left)). Let us assume that in the years following spinal cord injury, that person becomes obese so that his body weight increases to 120kg. The individual s increased trunk load would now apply pressures of 180mmHg on the gluteal muscle next to the ischia (Figure 2, top left). Using the sigmoid tissue injury threshold, the obese patient is expected to develop a deep tissue injury in the gluteal muscle tissue within one and a half hours if internal tissue loads are not relieved during that time, whereas with the patient s previous 55kg body weight, the muscle tissue was likely to sustain loads for three hours. 42 july 22 :: vol 23 no 46 :: 2009 NURSING STANDARD

4 FIGURE 2 Clinical implications of using the sigmoid injury threshold Internal pressure (mmhg) Relative disinformation (%) Obese patient Non-obese patient Bony prominence Atrophied muscle 1 Intolerable levels Tolerable levels Non-atrophied 0 40 muscle Time (hours) Key Top left = an example of an obese male patient whose ischial tuberosities apply pressures of 180mmHg on the overlying gluteus muscles, while sitting in a wheelchair. Bottom left = an example of a non-obese male patient whose ischial tuberosities apply pressures of 80mmHg on the overlying gluteus muscle, while sitting in a wheelchair. The risk of developing pressure ulcers and deep tissue injury is therefore expected to be much higher for obese patients, as observed in clinical reports (Gallagher 1997, Kramer 2004, Hahler 2006, Baugh et al 2007). It should be emphasised that the risk for deep tissue injury intensifies only if obesity is combined with complete immobilisation so that no internal load relief occurs in the tissues, since ambulant patients who are obese do not seem to be at a higher risk of pressure ulcers or deep tissue injury (Compher et al 2007). This means that maintaining a normal body weight is important for patients with impaired motor-sensory capacities to avoid pressure ulcers and deep tissue injury. Efforts should therefore be made to engage such patients in regular physical exercise programmes, whenever this is possible. Another example of why physical exercise, if feasible, can lower the risk of pressure ulcers and deep tissue injury relates to the muscle mass of patients. Let us assume again a hypothetical male patient, in whom thickness of the gluteal muscle tissue is 23mm, which is normal according to MRI studies of the buttocks (Linder-Ganz et al 2008). Given that the ischial tuberosities sag into the overlying gluteal muscle tissue about 12mm during sitting (Linder-Ganz et al 2008), the mean compressive deformation of gluteal tissue under the ischial tuberosities would be approximately 52% (12mm/23mm). Using the right vertical axis in Figure 2, this will allow the patient a three-hour safe time during which injury can be avoided, NURSING STANDARD which is similar to the case of the non-obese patient from the previous example. Now let us assume that in the years following spinal cord injury, the patient loses gluteal muscle mass, so that the thickness of his atrophied gluteus muscles reduces to 17mm. While sitting, the patient now deforms his muscle tissue to about 71% (12mm/17mm), which gives him a much shorter safe time of only one and a half hours before injury is likely to occur (Figure 2). It is interesting to note that in recent MRI studies of the buttock anatomy in patients with spinal cord injury, the only patient who did not develop muscle atrophy was an athlete (Linder-Ganz et al 2008). Accordingly, the benefit of maintaining muscle mass is another reason why physical activity is desirable in avoiding pressure ulcers and deep tissue injury in patients with impaired motor-sensory capacities. However, although because of individual limitations and lifestyle, it cannot be considered an overall solution. To summarise, patients who use a wheelchair as a result of neurological injury or disease tend to gain body weight and lose muscle mass, which both contribute to substantially increased internal muscle loads (increased pressures from the bones, or higher tissue deformations). The present sigmoid tissue injury threshold (Figure 2) suggests that obesity and muscle atrophy each shorten the time for tissue damage, and therefore these factors increase the risk of the individual to pressure ulcers and deep tissue injury. july 22 :: vol 23 no 46 ::

5 art & science tissue viability Conclusion This article has outlined some fundamental flaws in the commonly used hyperbola pressure-time curve of Reswick and Rogers (1976) for predicting the risk of developing pressure ulcers. It was shown that the Reswick and Rogers (1976) hyperbola is inaccurate at the extremes of the timescale. Moreover, the Reswick and Rogers (1976) pressure-time curve is not applicable for predicting deep tissue injury, or any pressure ulcer that chronologically appears first in deep tissues, because it was developed based on interface pressure measurements, which cannot be associated with a unique loading condition in deep tissues. An alternative injury threshold was presented, in the form of a sigmoid mathematical function, which provides more accurate limits on the pressure levels and exposure times. Clinical implications of the sigmoid curve were discussed, as related to patients who use a wheelchair as a result of neurological injury or disease. The literature indicates that such patients tend to gain body weight and lose muscle mass owing to denervation, physical limitations and sedentary lifestyle. Obesity and muscle atrophy each contribute to a substantially increased internal muscle load. As a consequence of either obesity or muscle atrophy, the time for tissue damage shortens, which increases the risk of the individual to experience pressure ulcers and deep tissue injury. Therefore, the healthcare team should actively encourage patients confined to a wheelchair to be physically active, and to practise sports, if possible, so that patients will maintain a normal body weight, and retain muscle mass. For overweight wheelchair-bound patients, involvement of a dietician or a nutrition consultant is important to help achieve and maintain a normal body weight NS References Baugh N, Zuelzer H, Meador J, Blankenship J (2007) Wound wise: wounds in surgical patients who are obese. American Journal of Nursing. 107, 6, 40-. Buchwald P (2007) A general bilinear model to describe growth or decline time profiles. Mathematical Biosciences. 205, 1, Compher C, Kinosian BP, Ratcliffe SJ, Baumgarten M (2007) Obesity reduces the risk of pressure ulcers in elderly hospitalized patients. Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 62, 11, Daniel RK, Priest DL, Wheatley DC (1981) Etiologic factors in pressure sores: an experimental model. Archives of Physical Medicine and Rehabilitation. 62, 10, Gallagher SM (1997) Morbid obesity: a chronic disease with an impact on wounds and related problems. Ostomy/ Wound Management. 43, 5, Gefen A (2008) Bioengineering models of deep tissue injury. Advances in Skin & Wound Care. 21, 1, Gefen A (2009) Reswick and Rogers pressure-time curve for pressure ulcer risk. Part 1. Nursing Standard. 23, 45, Gefen A, Levine J (2007) The false premise in measuring body-support interface pressures for preventing serious pressure ulcers. Journal of Medical Engineering and Technology. 31, 5, Gefen A, van Nierop B, Bader DL, Oomens CW (2008) Strain-time cell-death threshold for skeletal muscle in a tissue-engineered model system for deep tissue injury. Journal of Biomechanics. 41, 9, Gupta N, White KT, Sandford PR (2006) Body mass index in spinal cord injury: a retrospective study. Spinal Cord. 44, 2, Hahler B (2006) An overview of dermatological conditions commonly associated with the obese patient. Ostomy/ Wound Management. 52, 6, Kramer KL (2004) WOC nurses as advocates for patients who are morbidly obese: a case study promoting the use of bariatric beds. Journal of Wound, Ostomy, and Continence Nursing. 31, 6, Linder-Ganz E, Engelberg S, Scheinowitz M, Gefen A (2006) Pressure-time cell death threshold for albino rat skeletal muscles as related to pressure sore biomechanics. Journal of Biomechanics. 39, 14, Linder-Ganz E, Shabshin N, Itzchak Y, Yizhar Z, Siev-Ner I, Gefen A (2008) Strains and stresses in sub-dermal tissues of the buttocks are greater in paraplegics than in healthy during sitting. Journal of Biomechanics. 41, 3, Ohura T, Ohura N, Oka H (2007) Incidence and clinical symptoms of hourglass and sandwich-shaped tissue necrosis in stage IV pressure ulcers. Wounds. 19, 11, Peeters EA, Oomens CW, Bouten CV, Bader DL, Baaijens FP (2005) Mechanical and failure properties of single attached cells under compression. Journal of Biomechanics. 38, 8, Reswick J, Rogers JE (1976) Experience at Rancho Los Amigos Hospital with devices and techniques to prevent pressure ulcers. In Kenedi RM, Cowden JM, Scales JT (Eds) Bedsore Biomechanics. Macmillan Press, London, Salcido R, Donofrio JC, Fisher SB et al (1994) Histopathology of pressure ulcers as a result of sequential computer-controlled pressure sessions in a fuzzy rat model. Advances in Wound Care. 7, 5, Stekelenburg A, Strijkers GJ, Parusel H, Bader DL, Nicolay K, Oomens CW (2007) Role of ischemia and deformation in the onset of compression-induced deep tissue injury: MRI-based studies in a rat model. Journal of Applied Physiology. 102, 5, Stekelenburg A, Gawlitta D, Bader DL, Oomens CW (2008) Deep tissue injury: how deep is our understanding? Archives of Physical Medicine and Rehabilitation. 89, 7, Weaver FM, Collins EG, Kurichi J et al (2007) Prevalence of obesity and high blood pressure in veterans with spinal cord injuries and disorders: a retrospective review. American Journal of Physical Medicine and Rehabilitation. 86, 1, july 22 :: vol 23 no 46 :: 2009 NURSING STANDARD

Reswick and Rogers pressure-time curve for pressure ulcer risk.part 1

Reswick and Rogers pressure-time curve for pressure ulcer risk.part 1 Gefen A (2009) Reswick and Rogers pressure-time curve for pressure ulcer risk. Part 1. Nursing Standard. 23, 45, 64-74. Date of acceptance: