Deep Tissue Injury Research Articles

INTRINSIC INCREASED ACE2 EXPRESSION PROTECTS SPINY MOUSE ACOMYS CAHIRINUS AGAINST ISCHEMIC‐INDUCED CARDIAC DYSFUNCTION

Angiotensin converting enzyme 2 (ACE2), a key component of the renin angiotensin system (RAS), is a potential therapeutic target for ischemic heart disease as it protects cardiovascular function. Recently, extensive evidence points to a significant role of ACE2 in regulation of hematopoiesis and vasculogenesis via correction of endothelial progenitor cell dysfunction and increases in the number of cardiac and endothelial progenitor cells after ischemic injury. Spiny mice (Acomys cahirinus, SM) possess lizard‐like abilities when a large portion of skin is “torn away” the deep tissue injury heals rapidly by regenerating complete hair follicles, dermis, epidermis, sebaceous glands, adipose tissue, microvessels, smooth muscle and skeletal muscle of the panniculus carnosus without scaring (Nature 2013). This skin auto to my provides an effective defense against predators. We tested the cardiac regenerative capacity of SM using a myocardial infarction (MI) model. Following ligation of left anterior descending coronary artery, the SM exhibited smaller infarct size (SM‐MI 20% of left ventricular free wall vs CD1‐MI 50%, p<0.05) with preserved ejection fraction vs CD1 mice (SM‐MI 62 ± 2% vs CD1‐MI 32± 7%, p<0.05). At baseline ACE2 activity in SM sham was elevated 12% in myocardial tissue and 23% in plasma vs CDl sham (both, p<0.05). MI resulted in a 37% decrease in ACE2 activity in CD1 mice (p<0.05 vs baseline and vs SM‐MI). Interestingly, SM exhibited further elevation of ACE2 activity (7%) in myocardial tissue following MI, while plasma ACE2 activity remained unchanged after MI. Collectively, our findings suggest that ACE2 is likely to be modulating, at least in part, the myocardial preservation/regeneration process in the SM.Support or Funding Information2 UM1 HL087366‐06, R01 HL056921, HL033610, and UL1 TR000064 from the National Institutes of Health

Risk Factors for Pressure Ulcers Including Suspected Deep Tissue Injury in Nursing Home Facility Residents: Analysis of National Minimum Data Set 3.0.

To provide information on risk factors associated with pressure ulcers (PrUs), including suspected deep tissue injury (sDTI), in nursing home residents in the United States. This continuing education activity is intended for physicians and nurses with an interest in skin and wound care. After participating in this educational activity, the participant should be better able to:1. Examine the literature related to risk factors for the development of PrUs.2. Compare risk factors associated with the prevalence of PrUs and sDTI from the revised Minimum Data Set 3.0 2012 using a modified Defloor's conceptual model of PrUs as a theoretical framework. This study aims to characterize and compare risk factors associated with pressure ulcers (PrUs), including suspected deep tissue injury (sDTI), in nursing home (NH) residents in the United States. Secondary analysis of the 2012 Minimum Data Set (MDS 3.0). Medicare- or Medicaid-certified NHs in the United States. Nursing home residents (n = 2,936,146) 18 years or older with complete PrU data, who received comprehensive assessments from January to December 2012. Pressure ulcer by stage was the outcome variable. Explanatory variables (age, gender, race and ethnicity, body mass index, skin integrity, system failure, disease, infection, mobility, and cognition) from the MDS 3.0 were aligned with the 4 elements of Defloor's conceptual model: compressive forces, shearing forces, tissue tolerance for pressure, and tissue tolerance for oxygen. Of 2,936,146 NH residents who had complete data for PrU, 89.9% had no PrU; 8.4% had a Stage 2, 3, or 4 or unstagable PrU; and 1.7% had an sDTI. The MDS variables corresponding to the 4 elements of Defloor's model were significantly predictive of both PrU and sDTI. Black residents had the highest risk of any-stage PrU, and Hispanic residents had the highest risk of sDTI. Skin integrity, system failure, infection, and disease risk factors had larger effect sizes for sDTI than for other PrU stages. The MDS data support Defloor's model and inform clinicians, educators, researchers, and policymakers on risk factors associated with PrUs and sDTI in NH residents in the United States participating in Medicare and Medicaid.

Risk Factors for Pressure Ulcers Including Suspected Deep Tissue Injury in Nursing Home Facility Residents

Risk Factors for Pressure Ulcers Including Suspected Deep Tissue Injury in Nursing Home Facility Residents

Change in viability of C2C12 myoblasts under compression, shear and oxidative challenges

Skeletal and epidermal loadings can damage muscle cells and contribute to the development of deep tissue injury (DTI) – a severe kind of pressure ulcers affecting many people with disability. Important predisposing factors include the multiaxial stress and strain fields in the internal tissues, particularly the vulnerable muscles around bony prominences. A careful study of the mechanical damage thresholds for muscle cell death is critical not only to the understanding of the formation of DTI, but also to the design of various body support surfaces for prevention. In this paper, we measured the mechanical damage thresholds of C2C12 myoblasts under prescribed compressive strains (15% and 30%) and shear strains (from 0% to 100%), and studied how oxidative stress, as caused potentially by reperfusion or inflammation, may affect such damage thresholds. A flat plate was used to apply a uniform compressive strain and a radially increasing shear strain on disks of Gelatin–methacrylate (GelMA) hydrogel with myoblasts encapsulated within. The percentages of cell death were estimated with propidium iodide (PI) and calcein AM staining. Results suggested that cell death depended on both the level and duration of the applied strain. There seemed to be a non-linear coupling between compression and shear. Muscle cells often need to function biomechanically in challenging oxidative environments. To study how oxidative stress may affect the mechanical damage thresholds of myoblasts, cell viability under compressive and shear strains was also studied after the cells were pre-treated for different durations (1h and 20h) with different concentrations (0.1mM and 0.5mM) of hydrogen peroxide (H2O2). Oxidative stress can either compromise or enhance the cellular resistance to shear damage, depending on the level and duration of the oxidative exposure.

Expression and significance of tumor necrosis factor alpha, matrix metalloproteinase 2 and collagen in skin tissue of pressure ulcer of rats

Objective To observe the expressions of tumor necrosis factor alpha (TNF-α), matrix metalloproteinase 2 (MMP-2) and collagen in local skin tissue of pressure ulcer of rats, and to explore the possible mechanism of the pathogenesis of pressure ulcer. Methods Forty male SD rats were divided into normal control group, 3 d compression group, 5 d compression group, 7 d compression group, and 9 d compression group according to the random number table, with 8 rats in each group. The rats in normal control group did not receive any treatment, whereas the rats in the latter 4 groups were established the deep tissue injury model (3 d compression group) and pressure ulcer model (the other 3 groups) on the gracilis muscle on both hind limbs using a way of cycle compression of ischemia-reperfusion magnet. The rats in 3 d compression group received only three cycles of compression, while the compressed skin of the rats in 5 d compression group, 7 d compression group, and 9 d compression group were cut through and received pressure to 5, 7 and 9 cycles after three cycles of compression, respectively. The rats in 3 d compression group were sacrificed immediately after receiving compression for 3 d (the rats in normal control group were sacrificed at the same time), and the rats in the other 3 groups were respectively sacrificed after receiving compression for 5, 7, and 9 d, and the skin tissue on the central part of gracilis muscle on both hind limbs were harvested. The morphology of the skin tissue was observed with HE staining. The expression of collagen fiber was observed with Masson staining. The expressions of collagen type Ⅳ and MMP-2 were detected by immunohistochemical method. The expressions of TNF-α and phosphorylated NF kappa B (NF-κB) were determined by Western blotting. Data were processed with one-way analysis of variance and LSD test. Results (1) In normal control group, the skin tissue of rats was stratified squamous epithelium, with the clear skin structure, and there was no obvious infiltration of inflammatory cells. In 3 d compression group, the skin layers of rats were clear, with quite a few fibroblasts, and the inflammatory cells began to infiltrate. In 5 d compression group, 7 d compression group, and 9 d compression group, the epidermis of rats thickened, with the number of fibroblasts reduced, and the infiltration of inflammatory cells enhanced with the compressed time prolonging. (2) In normal control group, the collagen fibers in skin tissue of rats were arranged in order, with rich content. In 3 d compression group, the collagen fibers in skin tissue of rats were arranged orderly, with high expression level, which was similar to that in normal control group (P>0.05). In 5 d compression group and 7 d compression group, the collagen fibers in skin tissue of rats were arranged in disorder, with the expression level gradually reduced, which were significantly lower than that in normal control group (with P values below 0.01). In 9 d compression group, the expression of collagen fiber in skin tissue of rats was a little higher than that in 7 d compression group, but it was still significantly lower than that in normal control group (P 0.05). The expressions of collagen type Ⅳ in skin tissue of rats in 5 d compression group, 7 d compression group, and 9 d compression group were significantly lower than that in normal control group (P 0.05). The expressions of MMP-2 in skin tissue of rats in 5 d compression group, 7 d compression group, and 9 d compression group were significantly higher than that in normal control group (P<0.05 or P<0.01). (4) The expression of TNF-α in skin tissue of rats in normal control group was 0.48±0.11, and the expressions of TNF-α in skin tissue of rats in 3 d compression group, 5 d compression group, 7 d compression group, and 9 d compression group were respectively 0.84±0.08, 1.13±0.19, 1.34±0.16, and 1.52±0.23, which were all significantly higher than that in normal control group (with P values below 0.01). The expressions of phosphorylated NF-κB in skin tissue of rats in 3 d compression group and 9 d compression group were similar to that in normal control group (with P values above 0.05), and the expressions of phosphorylated NF-κB in skin tissue of rats in 5 d compression group and 7 d compression group were significantly higher than that in normal control group (P<0.05 or P<0.01). Conclusions The high expression of MMP-2 and reduction of collagen induced by inflammatory reaction mediated by the high expression of TNF-α in local skin tissue of pressure ulcer of rats may be one of the important reasons for the formation of pressure ulcer. Key words: Pressure ulcer; Tumor necrosis factor-alpha; Matrix metalloproteinase 2; Collagen type Ⅳ

Pressure Combined with Ischemia/Reperfusion Injury Induces Deep Tissue Injury via Endoplasmic Reticulum Stress in a Rat Pressure Ulcer Model.

Pressure ulcer is a complex and significant health problem in long-term bedridden patients, and there is currently no effective treatment or efficient prevention method. Furthermore, the molecular mechanisms and pathogenesis contributing to the deep injury of pressure ulcers are unclear. The aim of the study was to explore the role of endoplasmic reticulum (ER) stress and Akt/GSK3β signaling in pressure ulcers. A model of pressure-induced deep tissue injury in adult Sprague-Dawley rats was established. Rats were treated with 2-h compression and subsequent 0.5-h release for various cycles. After recovery, the tissue in the compressed regions was collected for further analysis. The compressed muscle tissues showed clear cellular degenerative features. First, the expression levels of ER stress proteins GRP78, CHOP, and caspase-12 were generally increased compared to those in the control. Phosphorylated Akt and phosphorylated GSK3β were upregulated in the beginning of muscle compression, and immediately significantly decreased at the initiation of ischemia-reperfusion injury in compressed muscles tissue. These data show that ER stress may be involved in the underlying mechanisms of cell degeneration after pressure ulcers and that the Akt/GSK3β signal pathway may play an important role in deep tissue injury induced by pressure and ischemia/reperfusion.

Cell death induced by mechanical compression on engineered muscle results from a gradual physiological mechanism

Deep tissue injury (DTI), a type of pressure ulcer, arises in the muscle layers adjacent to bony prominences due to sustained mechanical loading. DTI presents a serious problem in the clinic, as it is often not visible until reaching an advanced stage. One of the causes can be direct mechanical deformation of the muscle tissue and cell. The mechanism of cell death induced by mechanical compression was studied using bio-artificial skeletal muscle tissues. Compression was applied by placing weights on top of the constructs. The morphological changes of the cytoskeleton and the phosphorylation of mitogen-activated protein kinases (MAPK) under compression were investigated. Moreover, inhibitors for each of the three major MAPK groups, p38, ERK, and JNK, were applied separately to look at their roles in the compression caused apoptosis and necrosis. The present study for the first time showed that direct mechanical compression activates MAPK phosphorylation. Compression also leads to a gradual destruction of the cytoskeleton. The percentage apoptosis is strongly reduced by p38 and JNK inhibitors down to the level of the unloaded group. This phenomenon could be observed up to 24h after initiation of compression. Therefore, cell death in bio-artificial muscle tissue caused by mechanical compression is primarily caused by a physiological mechanism, rather than through a physical mechanism which kills the cell directly. These findings reveal insight of muscle cell death under mechanical compression. Moreover, the result indicates a potential clinical solution to prevent DTI by pre-treating with p38 or/and JNK inhibitors.

Effects of pressure ulcer classification system education programme on knowledge and visual differential diagnostic ability of pressure ulcer classification and incontinence-associated dermatitis for clinical nurses in Korea.

The objective of this study was to evaluate the effect of pressure ulcer classification system education on clinical nurses' knowledge and visual differential diagnostic ability of pressure ulcer (PU) classification and incontinence-associated dermatitis (IAD). One group pre and post-test was used. A convenience sample of 407 nurses, participating in PU classification education programme of continuing education, were enrolled. The education programme was composed of a 50-minute lecture on PU classification and case-studies. The PU Classification system and IAD knowledge test (PUCS-KT) and visual differential diagnostic ability tool (VDDAT), consisting of 21 photographs including clinical information were used. Paired t-test was performed using SPSS/WIN 20.0. The overall mean difference of PUCS-KT (t = -11·437, P<0·001) and VDDAT (t = -21·113, P<0·001) was significantly increased after PU classification education. Overall understanding of six PU classification and IAD after education programme was increased, but lacked visual differential diagnostic ability regarding Stage III PU, suspected deep tissue injury (SDTI), and Unstageable. Continuous differentiated education based on clinical practice is needed to improve knowledge and visual differential diagnostic ability for PU classification, and comparison experiment study is required to examine effects of education programmes.

Repositioning for pressure ulcer prevention in adults--A Cochrane review.

The provision of good pressure area care is a core responsibility for nurses in all healthcare settings, particularly when patients are immobile, frail or elderly. Pressure area care involves assessment of the patient’s skin and regular repositioning to prevent pressure injury/ulcers (PU; also known as pressure sores, bed sores or decubitus ulcers). These preventable complications occur when the soft tissues over a bony prominence are compressed by an external surface, reducing oxygen flow over a prolonged period of time. The severity and level of tissue injury is commonly graded by classifying the injury as stage 1 to 4, unstageable or suspected deep tissue injury (six stages in all). Despite being largely preventable, PUs are one of the top five adverse events reported in hospitalized patients with a reported incidence ranging between 3% and 30%...

Building a Biopsychosocial Conceptual Framework to Explore Pressure Ulcer Pain for Hospitalized Patients.

Although pressure ulcers are a prevalent condition, pain associated with pressure ulcers is not fully understood. Indeed, previous studies do not shed light on the association between pressure ulcer stages and the experience of pain. Especially, pain characteristics of suspected deep tissue injury, which is a new category that was recently added by the National Pressure Ulcer Advisory Panel, are yet unknown. This is concerning because the incidence of pressure ulcers in hospitalized patients has increased exponentially over the last two decades, and health care providers are struggling to ensure providing adequate care. Thus, in order to facilitate the development of effective interventions, this paper presents a conceptual framework to explore pressure ulcer pain in hospitalized patients. The concepts were derived from a biopsychosocial model of pain, and the relationships among each concept were identified through a literature review. Major propositions are presented based on the proposed conceptual framework, which integrates previous research on pressure ulcer pain, to ultimately improve understanding of pain in hospitalized patients with pressure ulcers.

The Use of the Physical Stress Theory to Guide the Rehabilitation of a Patient With Bilateral Suspected Deep Tissue Injuries and Hip Repair

Background: The physical stress theory states that changes in the amount of physical stress applied to tissue cause an expected response in all biological tissues. Tissue Responds to Physical Stress in 5 Typical Ways: Decreased tolerance to stress (atrophy), maintenance of tolerance to stress, increased tolerance to stress (hypertrophy), tissue injury, and tissue death. The purpose of this case report was to describe a simple and inexpensive device that enables the application of the physical stress theory for a patient who needs both decreased stress to facilitate wound healing and increased stress to facilitate improved strength and function. Case Description: The patient was a 93-year-old man, status-post open-reduction internal fixation of the left hip to resolve an intertrochanteric hip fracture after a fall. The patient had existing suspected deep tissue injury pressure sores on the posterior aspects of both heels. Outcomes: After completion of the 16-day stay in inpatient rehabilitation, the patient was able to improve his level of function by using the device compared to initial evaluation. The patient was able to perform all functional activities with modified independence. Conclusion: The off-loading mechanism that was created and implemented into the patient's intervention strategy was essential to enable the performance of strengthening exercises without further damaging the already-injured tissue.

Effects of exogenous recombinant human basic fibroblast growth factor on the healing of muscles in rats after deep tissue injury of pressure ulcers

Objective To investigate the effect of exogenous recombinant human basic fibroblast growth factor (rhbFGF) on the healing of muscles in rats after deep tissue injury of pressure ulcers. Methods Forty-eight SD rats were randomly divided into normal control group, injury control group, post injury day (PID) 4 group, PID 7 group, PID 14 group, PID 21 group according to the random number table, with 8 rats in each group. The rats in normal control group did not receive any treatment, whereas the rats in the latter 5 groups were established the deep tissue injury of pressure ulcer model on both sides of the gracilis muscle on the hind limb. The rats in injury control group did not receive any treatment after injury, while the rats in the latter 4 groups were given subcutaneous injection of 0.1 mL rhbFGF to the left gracilis in a dosage of 100 μg/mL immediately after injury, and an equal volume of normal saline (NS) was injected to right gracilis, once every other day. The rats in injury control group were sacrificed immediately after injury, and the rats in normal control group were sacrificed at the same time point. The rats in the other 4 groups were sacrificed on PID 4, 7, 14, 21, and the gracilis muscles on both sides were harvested respectively. The morphology of the gracilis muscle was examined after HE staining. The expression of myogenin in the tissues was detected by immunofluorescence method. The levels of muscle structural proteins myosin heavy chain (MyHC), phosphorylated protein kinase B (Akt), and phosphorylated mammalian target of rapamycin (mTOR) were determined by Western blotting. Data were processed with one-way analysis of variance and LSD test. Results (1) In normal control group, the nuclei of graciles cells were in uniform size, and they were closely arranged with clear structure, and there were no significant infiltration of inflammatory cells. In injury control group, the nuclei of graciles cells showed signs of pyknosis, dissolution, fracture and structural disorder. Swelling of muscle cells, inflammation infiltration, structural disorder and other pathological signs of injury phenomena in graciles of PID 4 group, PID 7 group, PID 14 group, PID 21 group after rhbFGF treatment were milder compared with those after NS treatment. In addition, the numbers of regenerated myocytes in graciles of PID 4 group, PID 7 group, PID 14 group, PID 21 group after rhbFGF treatment were higher than those after NS treatment. (2) The numbers of graciles myogenin positive cells in normal control group and injury control group were respectively 28±17 and 42±28. The numbers of graciles myogenin positive cells in PID 4 group, PID 7 group, PID 14 group after NS treatment were 100±50, 196±87, 460±110 respectively, while the numbers of graciles myogenin positive cells in PID 4 group, PID 7 group, PID 14 group after rhbFGF treatment were 174±34, 717±182, 613±122 respectively, and the numbers of graciles myogenin positive cells after rhbFGF treatment were significantly higher than those after NS treatment in each group(P 0.05). The expressions of phosphorylated Akt and phosphorylated mTOR in graciles of normal control group were low, and the expression of phosphorylated Akt in graciles increased in injury control group, while the expression of phosphorylated mTOR in graciles decreased in injury control group. The expressions of phosphorylated Akt and phosphorylated mTOR in graciles of PID 4 group, PID 7 group, PID 14 group, PID 21 group after treatment with rhbFGF showed a trend of elevation in the beginning but declined afterwards. The expressions of phosphorylated Akt and phosphorylated mTOR in graciles of PID 4 group after rhbFGF treatment were significantly lower than those after NS treatment (P<0.05 or P<0.01). The expressions of phosphorylated Akt and phosphorylated mTOR in graciles of PID 7 group, PID 14 group, PID 21 group after rhbFGF treatment were significantly higher than those after NS treatment (P<0.05 or P<0.01). Conclusions Exogenous rhbFGF may effectively facilitate the healing of muscle structure and accelerate the regeneration of muscles in rats after deep tissue injury of pressure ulcers, and its mechanism may be related to the improvement of the expression of myogenin and enhancement of the expression of protein of muscle growth-related signaling pathways. Key words: Muscle development; Fibroblast growth factor 2; Myosin heavy chains; Pressure ulcer; Deep tissue injury; Protein kinase B; Mammalian target of rapamycin

Pressure ulcer and wounds reporting in NHS hospitals in England part 2: Survey of monitoring systems

This is the second of a two related papers describing work undertaken to compare and contrast Pressure Ulcer (PU) monitoring systems across NHS in-patient facilities in England. The work comprised 1) a PU/Wound Audit (PUWA) and 2) a survey of PU monitoring systems.This second paper focusses on the survey which explores differences in the implementation of PU adverse event monitoring systems in 24 NHS hospital Trusts in England. The survey questionnaire comprised 41 items incorporating single and multiple response options and free-text items and was completed by the PUWA Trust lead in liaison with key people in the organisation. All 24 (100%) Trusts returned the questionnaire, with high levels of data completeness (99.1%).The questionnaire results showed variation between Trusts in relation to the recording of PUs and their reporting as part of NHS prevalence and incident monitoring systems and to Trust boards and healthcare commissioners including the inclusion (or not) of device ulcers, unstageable ulcers, Deep Tissue Injury, combined PUs/Incontinence Associated Dermatitis, category ≥ 1 ulcers or category ≥ 2 ulcers, inherited ulcers, acquired ulcers, avoidable and unavoidable ulcers and the definition of Present On Admission. These fundamental differences in reporting preclude Trust to Trust comparisons of PU prevalence and incident reporting and monitoring systems due to variation in local application and data collection methods. The results of this work and the PUWA led to the development of recommendations for PU monitoring practice, many of which are internationally relevant.

Documentation Defines Clinical Conditions for Pressure Ulcers

Documentation Defines Clinical Conditions for Pressure Ulcers

TAT-Mediated Acidic Fibroblast Growth Factor Delivery to the Dermis Improves Wound Healing of Deep Skin Tissue in Rat.

BackgroundThe definition of deep tissue injury was derived from multiple clinical cases as “A purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear”. Acidic fibroblast growth factor (aFGF) significantly improves wound healing under diabetic conditions. However, to date, the therapeutic application of aFGF has been limited, due to its low delivery efficiency and short half-life.Methodology/Principal FindingsUsing an animal model of magnet-induced pressure ulcers, transactivator of transcription protein (TAT)-aFGF was evaluated for transdermal delivery and wound healing. Immunohistochemistry and Western blotting were also performed to determine the expression of transforming growth factor (TGF)-β1, α-smooth muscle actin (α-SMA), CD68, proliferating cell nuclear antigen (PCNA) and TGF-β-receptor II (TGF- βRII) in cultured human dermal fibroblasts. We found that that mice treated with TAT-aFGF had higher accumulation of aFGF in both dermis and subcutaneous tissues compared with mice treated with aFGF alone. In the remodeling phase, TAT-aFGF treatment decreased the expression of α-SMA to normal levels, thereby facilitating normal wound healing processes and abrogating hypertrophic scarring. In human dermal fibroblasts, TAT-aFGF reversed the suppressive effect of TNF-α on α-SMA expression and restored TGF-βRII and TGF-β1 expression.Conclusions/SignificanceOur results demonstrate that TAT-aFGF has a favorable therapeutic effect on the healing of subcutaneous deep tissue injury.

No Harm, No Foul, and No Hospital Readmissions

No Harm, No Foul, and No Hospital Readmissions

Contoured Foam Cushions Cannot Provide Long-term Protection Against Pressure-Ulcers for Individuals with a Spinal Cord Injury

To determine changes in internal soft-tissue loads in the buttocks of individuals with a spinal cord injury (SCI), who undergo pathoanatomical changes during the first months and years following the occurrence of the SCI, while sitting on a contoured foam cushion (CFC) that has been fitted close to the time of the injury but has not been replaced in subsequent years. Internal tissue loads in variant buttocks anatomies on a CFC were analyzed by means of finite element computer simulations. The pathoanatomical changes that are characteristic to SCI and were simulated here are: increase in fat tissue mass, intramuscular fat infiltration, muscle atrophy, and combinations of these conditions. Computational biomechanical modeling. Simulating the aforementioned pathoanatomical changes consistently resulted in greater mechanical strain and stress magnitudes and more inhomogeneity in the loading state of muscle and fat tissues, with a more profound effect in fat. The simulations further indicated a clear trend of exacerbation in tissue exposure to loads as the pathoanatomical changes progress chronologically and the CFC is not replaced. A CFC that has been fitted at a time close to the SCI, but has not been replaced in subsequent years, substantially loses its efficacy in protecting patients from developing pressure ulcers and deep tissue injury in particular.

Differential diagnosis of suspected deep tissue injury.

Deep tissue injury (DTI) can be difficult to diagnose because many other skin and wound problems can appear as purple skin or rapidly appearing eschar. The diagnosis of DTI begins with a thorough history to account for times of exposure to pressure, such as 'time down' at the scene or time during which the patient was flat and could not respond. Patients with light skin tones present with classic skin discolouration of purple or maroon tissue, a defined border around the area of injury, and often surrounding erythema is evident. Persistent erythema and hyperpigmentation, rather than blanching, should be used to determine pressure injury in dark skin tone patients. Differential diagnosis includes stage 2 pressure ulcers, incontinence-associated dermatitis, skin tears, bruising, haematoma, venous engorgement, arterial insufficiency, necrotising fasciitis and terminal skin ulcers. Many skin problems can also have a purple hue or rapidly developing eschar, and a working knowledge of dermatology is needed.

Factors Associated With Occipital Pressure Ulcers in Hospitalized Infants and Children.

The occiput is a common location for development of pressure ulcers in hospitalized infants and young children. However, risk factors associated with occurrence of the ulcers have not been fully described. To identify factors associated with development of occipital pressure ulcers in acutely ill infants and children. Charts of all patients with occipital pressure ulcers reported in a computerized safety event reporting system since its implementation in 2005 and of any patients with such ulcers recalled by members of the skin care special interest group were reviewed retrospectively. During a 4-year period, 60 cases of occipital pressure ulcers were identified: 40% stage I, 12% stage II, 30% unstageable, and 18% deep tissue Injury. The median age of the sample was 12 months. Among the patients, 86% were in the intensive care unit with cardiovascular or pulmonary problems. A total of 68% had comorbid conditions. Most of the patients were less than 1 year old; were critically ill, requiring high-risk therapies; and had multiple medical devices in place. Patients with the ulcers were commonly treated with mechanical ventilation (83%) and sedation (74%) and were described as agitated (42%). Many of these patients were receiving vasoactive medications (50%) and had vascular access devices in the neck that restricted head movement (45%). When documented, the median Braden Q score was 16. Infants and children at risk for occipital pressure ulcers can be prospectively identified, allowing implementation of nursing interventions to prevent these ulcers.

PTU-002 The use of plasmajet as a novel technique for tissue dissection in complex abdominal surgery: Abstract PTU-002 Table 1

<h3>Introduction</h3> The PlasmaJet system is a unique novel technology that utilises argon gas that is electrically excited into a plasma state. This argon plasma energy is highly focused in a beam that disperses rapidly with distance therefore causing minimal deep thermal tissue injury, unlike all other electrical devices such as diathermy, argon plasma coagulator or harmonic scalpel. <h3>Method</h3> The plasma stream that leaves the tip of the device releases kinetic, light and thermal energy that changes with distance and angulation to the tissue. These last two variables influence the dissection properties of the PlasmaJet. The closer the tip of device is to the tissue and the more acute the angulation, the greater is the kinetic and thermal energy stream, which produces to greater tissue separation and dissection. <h3>Results</h3> Plasmajet subjectively allows for easier and more efficient division of routine but also fibrotic “hostile” adhesions which would otherwise have been extremely difficult even with scalpel dissection. PlasmaJet appears to cause less bleeding compared to conventional dissection techniques, but needs formal evaluation. Plasmajet can be used across the spectrum of coloproctology (see Table 1). Inadvertent tissue injury can occur, and was noted in 1/97 major complex colorectal procedures. The complication was an enterotomy identified intra-operatively and repaired with no post-operative sequelae. No post-operative mortality was seen. A small number of collections (≥3 cm fluid diameter) were noted but were not significantly higher than unit data. <h3>Conclusion</h3> PlasmaJet represents a new surgical modality for efficient precise tissue dissection. It should be considered for any re-operative abdominal case where dense adhesions maybe encountered. It has minimal thermal penetration and is therefore very safe. It provides the surgeon with another valuable tool to aid difficult dissection of tenacious adhesions under very challenging conditions thereby improving patient outcomes. <h3>Disclosure of interest</h3> None Declared.