Pressure Ulcer Formation Research Articles

Traumatic brain injury and palliative care: a retrospective analysis of 49 patients receiving palliative care during 2013-2016 in Turkey.

Traumatic brain injury (TBI), which is seen more in young adults, affects both patients and their families. The need for palliative care in TBI and the limits of the care requirement are not clear. The aim of this study was to investigate the length of stay in the palliative care center (PCC), Turkey, the status of patients at discharge, and the need for palliative care in patients with TBI. The medical records of 49 patients with TBI receiving palliative care in PCC during 2013–2016 were retrospectively collected, including age and gender of patients, the length of stay in PCC, the cause of TBI, diagnosis, Glasgow Coma Scale score, Glasgow Outcome Scale score, Karnofsky Performance Status score, mobilization status, nutrition route (oral, percutaneous endoscopic gastrostomy), pressure ulcers, and discharge status. These patients were aged 45.4 ± 20.2 years. The median length of stay in the PCC was 34.0 days. These included TBI patients had a Glasgow Coma Scale score ≤ 8, were not mobilized, received tracheostomy and percutaneous endoscopic gastrostomy nutrition, and had pressure ulcers. No difference was found between those who were discharged to their home or other places (rehabilitation centre, intensive care unit and death) in respect of mobilization, percutaneous endoscopic gastrostomy, tracheostomy and pressure ulcers. TBI patients who were followed up in PCC were determined to be relatively young patients (45.4 ± 20.2 years) with mobilization and nutrition problems and pressure ulcer formation. As TBI patients have complex health conditions that require palliative care from the time of admittance to intensive care unit, provision of palliative care services should be integrated with clinical applications.

Best Practices for Pressure Ulcer Prevention in the Burn Center.

The State of Pennsylvania Hospital Engagement Network, in collaboration with a hospital system in Southwestern Pennsylvania, established a goal of reducing hospital-acquired pressure ulcers by 20%. A 6-month unfavorable trend of nurse-sensitive clinical indicators called for immediate process improvement. A retrospective chart review resulted in identification of predominant risk factors placing the burn patient at high risk for pressure ulcer formation. Implementations of pressure ulcer prevention measures were inconsistent. Nurses demonstrated varied levels of knowledge about products used for prevention. It became imperative to examine processes within the unit and provide nursing with education, access to skin care supplies, and advanced skin/wound care products for maintaining skin integrity. Creation of evidence-based guidelines was necessary to improve patient outcomes. A collaborative team approach influenced nursing and physician awareness of pressure ulcer risk. Evidence-based prevention guidelines were developed, and consistency in early intervention was achieved, supporting our culture of safety. A change in interprofessional collaborative practice and positive trend in pressure ulcer incidence data supports the success of our program.

Pressure ulcers in palliative ward patients: hyponatremia and low blood pressure as indicators of risk.

BackgroundPrevention strategies for pressure ulcer formation remain critical in patients with an advanced illness. We analyzed factors associated with the development of pressure ulcers in patients hospitalized in a palliative care ward setting.Patients and methodsThis study was a retrospective analysis of 329 consecutive patients with a mean age (± standard deviation) of 70.4±11.8 years (range: 30–96 years, median 70.0 years; 55.3% women), who were admitted to the Palliative Care Department between July 2012 and May 2014.ResultsPatients were hospitalized for mean of 24.8±31.4 days (1–310 days, median 14 days). A total of 256 patients (77.8%) died in the ward and 73 patients (22.2%) were discharged. Two hundred and six patients (62.6%) did not develop pressure ulcers during their stay in the ward, 84 patients (25.5%) were admitted with pressure ulcers, and 39 patients (11.9%) developed pressure ulcers in the ward. Four factors assessed at admission appear to predict the development of pressure ulcers in the multivariate logistic regression model: Waterlow score (odds ratio [OR] =1.140, 95% confidence interval [CI] =1.057–1.229, P=0.001), transfer from other hospital wards (OR =2.938, 95% CI =1.339–6.448, P=0.007), hemoglobin level (OR =0.814, 95% CI =0.693–0.956, P=0.012), and systolic blood pressure (OR =0.976, 95% CI =0.955–0.997, P=0.023). Five other factors assessed during hospitalization appear to be associated with pressure ulcer development: mean evening body temperature (OR =3.830, 95% CI =1.729–8.486, P=0.001), mean Waterlow score (OR =1.194, 95% CI =1.092–1.306, P<0.001), the lowest recorded sodium concentration (OR =0.880, 95% CI =0.814–0.951, P=0.001), mean systolic blood pressure (OR =0.956, 95% CI =0.929–0.984, P=0.003), and the lowest recorded hemoglobin level (OR =0.803, 95% CI =0.672–0.960, P=0.016).ConclusionHyponatremia and low blood pressure may contribute to the formation of pressure ulcers in patients with an advanced illness.

Biomarkers Associated with Pressure Ulcer Formation in Traumatic Spinal Cord Individuals with Pneumonia

Biomarkers Associated with Pressure Ulcer Formation in Traumatic Spinal Cord Individuals with Pneumonia

INFLUÊNCIA DE FÁRMACOS SOBRE A FORMAÇÃO DE ÚLCERAS POR PRESSÃO: REVISÃO INTEGRATIVA

Objetivo: objetivou-se caracterizar a produção científica acerca da influência de fármacos sobre a formação de úlceras por pressão (UPP). Método: foi realizada uma revisão integrativa, de abordagem qualitativa, no SciELO, BDENF e LILACS. Utilizando-se os seguintes descritores: enfermagem, fármacos, úlceras por pressão, efeitos adversos, cuidados críticos. Foram incluídas as produções publicadas nos últimos 10 anos, artigos relacionados ao tema influência de fármacos sobre a úlcera por pressão e trabalhos completos. Resultados: a partir da análise dos 9 artigos foi encontrado que o uso de broncodilatadores, antidemenciais, ansiolíticos e antibióticos foram os medicamentos mais frequentes entre os indivíduos com UPP. Conclusão: é de suma importância relatar a influência negativa de fármacos sobre este complexo processo fisiopatológico para o surgimento das UPPs, para que o enfermeiro possa aprofundar seus conhecimentos sobre a farmacologia das substâncias que influenciam no desenvolvimento das úlceras por pressão.

Pressure Ulcer Prevention in the Hospital Setting Using Silicone Foam Dressings.

Patient care is of the utmost importance in the hospital setting. Bedrest and immobility during hospitalization, especially in the surgical and intensive care setting, place the patient at high risk for pressure ulcers. It is very important to prevent or notice a pressure ulcer forming due to the significant health care costs involved and patient health associated with them. Various measures are in place to prevent patients from getting pressure ulcers, but a newer material, silicone foam dressings, has been introduced as an alternative solution for the prevention of these ulcers. We review the current literature to examine whether the standard protocol or silicone material is superior to the prevention of pressure ulcer formation. We conclude that silicone foam dressings, when used as prophylactic treatment, seems very promising and may even be superior to the standard care of prevention. However, there were limitations to some studies and further research is needed to confirm the role of silicone foam dressings.

A non-invasive method to produce pressure ulcers of varying severity in a spinal cord-injured rat model

Experimental study. The objective of this study was to establish a non-invasive model to produce pressure ulcers of varying severity in animals with spinal cord injury (SCI). The study was conducted at the Johns Hopkins Hospital in Baltimore, Maryland, USA. A mid-thoracic (T7-T9) left hemisection was performed on Sprague-Dawley rats. At 7 days post SCI, rats received varying degrees of pressure on the left posterior thigh region. Laser Doppler Flowmetry was used to record blood flow. Animals were killed 12 days after SCI. A cardiac puncture was performed for blood chemistry, and full-thickness tissue was harvested for histology. Doppler blood flow after SCI prior to pressure application was 237.808±16.175 PFUs at day 7. Following pressure application, there was a statistically significant decrease in blood flow in all pressure-applied groups in comparison with controls with a mean perfusion of 118.361±18.223 (P<0.001). White blood cell counts and creatine kinase for each group were statistically significant from the control group (P=0.0107 and P=0.0028, respectively). We have created a novel animal model of pressure ulcer formation in the setting of a SCI. Histological analysis revealed different stages of injury corresponding to the amount of pressure the animals were exposed to with decreased blood flow immediately after the insult along with a subsequent marked increase in blood flow the next day, conducive to an ischemia-reperfusion injury (IRI) and a possible inflammatory response following tissue injury. Following ischemia and hypoxia secondary to microcirculation impairment, free radicals generate lipid peroxidation, leading to ischemic tissue damage. Future studies should be aimed at measuring free radicals during this period of increased blood flow, following tissue ischemia.

Topical betamethasone butyrate propionate exacerbates pressure ulcers after cutaneous ischemia-reperfusion injury.

Ischaemia-reperfusion (I/R) is involved in the development of various organ diseases. There has been increasing evidence that cutaneous I/R injury is associated with the pathogenesis of pressure ulcers (PUs), especially at the early stage presenting as non-blanchable erythema. However, there is no evidence-based treatment for early-stage PUs. Our objective was to assess the effects of topical steroid on the development of PUs after cutaneous I/R injury in mice. Cutaneous I/R was performed by trapping the dorsal skin between two magnetic plates for 12 h, followed by plate removal. Topical application of betamethasone butyrate propionate (BBP) in I/R areas significantly increased the size of PUs after I/R. The number of thromboses was increased, and CD31(+) vessels were decreased in the I/R area treated with topical BBP. The number of oxidative stress-associated DNA-damaged cells and apoptotic cells in the I/R area was increased by topical BBP treatment. In addition, the mRNA level of NADPH oxidase 4 (Nox4), the essential enzyme that produces reactive oxygen species, was significantly increased and that of NF-E2-related factor 2 (Nrf2), a transcription factor that regulates the expression of antioxidant proteins, was inhibited in the I/R area treated by BBP. The number of CD68(+) macrophages and the level of transforming growth factor-beta in lesional skin were also decreased by BBP. These results suggest that a topical steroid might accelerate the formation of PUs induced by cutaneous I/R injury by aggravating oxidative stress-induced tissue damage. Topical steroids might not be recommended for the treatment of acute-phase decubitus ulcers.

Elevated Levels of Protein Disulfide Isomerase and Binding Immunoglobulin Protein Implicated in Spinal Cord Injury Paraplegia Patients with Pressure Ulcers.

To explore the associations between two endoplasmic reticulum (ER) stress proteins, protein disulfide isomerase (PDI), binding immunoglobulin protein (BIP), and the development and progression of pressure ulcers (PUs) in spinal cord injury (SCI) paraplegia patients. ELISA kits were used to measure the levels of serum PDI and BIP in 67 SCI paraplegia patients with PUs and 61 SCI paraplegia patients without PUs. The associations between PDI and BIP, PU formation, PU staging, and pressure ulcer scale for healing (PUSH) score were analyzed. The patients in the PU group had higher levels of PDI and BIP than those in the non-PU group (both p < 0.05). Furthermore, the levels of PDI were positively correlated with those of BIP (r = 0.707, p < 0.0001). There were significant differences in the PDI and BIP levels among the different stages of PU (all p < 0.05). As the PU stages progressed, the levels of PDI and BIP first increased, then decreased, and finally peaked at stage III of the PUs. The PUSH scores significantly declined 7 days after debridement for the PU stage II (p < 0.01) but showed no significant difference between stages III and IV at 7 days after debridement (p > 0.05). The PUSH scores also decreased at 28 days after debridement for stages II, III, and IV (all p < 0.01). Higher PUSH scores indicated a longer time of debridement accompanied by a longer wound surface healing time (p < 0.05). ER stress proteins may be involved in the process of PU formation and healing; moreover, the levels of PDI and BIP were also associated with the severity of the PUs. Finally, we found that the PUSH scores can be used as a reference to evaluate PU severity and healing.

Association between presence of pneumonia and pressure ulcer formation following traumatic spinal cord injury

Objective: To determine if the presence of pneumonia and pressure ulcers are associated in individuals with an acute spinal cord injury during acute care and rehabilitation hospitalizations.Design: Retrospective, secondary analyses of data obtained from the Spinal Cord Injury Model Systems enrolled from 1993 until 2006Setting: Acute care hospitalization and inpatient rehabilitation facilitiesParticipants: A cohort of individuals hospitalized in acute care (n = 3,098) and inpatient rehabilitation (n = 1,768) was included in the analysis. Frequencies of pressure ulcer formation and episodes of pneumonia were noted in both settings.Interventions: Not applicable.Outcome Measures: Pressure ulcer formation and diagnosis of pneumoniaResults: The development of pressure ulcers, including stage I, was 20.3% acute care and 21.1% during in inpatient rehabilitation. Multivariate logistic regression analyses revealed a significant association of pneumonia with occurrence of pressure ulcers (P ≤ 0.001, OR = 2.3 and 2.2 respectively), the American Spinal Injury Association Impairment Scale grades (P < 0.001), and utilization of mechanical ventilation (P < 0.01) in both settings.Conclusion: A higher presence of pressure ulcers was found in individuals with pneumonia, after adjusting for injury severity, age, sex, and utilization of mechanical ventilation. Impaired inflammatory response and decreased mobility in individuals with pneumonia may predispose these individuals to develop pressure ulcers. Surveillance and preventive measures for pressure ulcers should be rigorous in individuals with SCI and pneumonia.

Risk Factors Associated With Pressure Ulcer Formation in Critically Ill Cardiac Surgery Patients: A Systematic Review.

Risk Factors Associated With Pressure Ulcer Formation in Critically Ill Cardiac Surgery Patients: A Systematic Review.

Risk Factors Associated With Pressure Ulcer Formation in Critically Ill Cardiac Surgery Patients: A Systematic Review.

Cardiac surgery patients are among those most at risk for developing pressure ulcers (PUs), with a reported incidence as high as 29.5%. Although numerous studies documenting PU risk factors and prevention strategies exist, the availability of literature examining risk factors specific to the cardiac surgery population is limited. A systematic review was completed that aimed to identify the risk factors associated with PU development in critically ill, adult, cardiac surgery patients. The MEDLINE, CINAHL, and Cochrane databases were searched. Studies that focused on PU risk factors in critical care, surgical intensive care, or cardiac surgery populations and used PU occurrences as an outcome variable were included in the review. Twelve high-quality studies were retrieved and included in the review; they revealed 30 potential PU risk factors. Current evidence is limited in 2 important ways. First, the impact of intraoperative factors, such as cardiopulmonary bypass time or body temperature, appears to be underexplored. Second, a substantive discussion of the risk factors associated specifically with deep tissue injuries, a unique PU category, is absent. The relatively high PU incidence among cardiac surgery patients suggests that typical PU prevention methods are insufficient for this population. Targeted prevention measures must be developed and implemented. Completion of this task required identification of risk factors unique to this population. Specific risk factors likely to increase risk among cardiac surgery patients include prolonged exposure to pressure during long surgical procedures, vascular disease, and/or vasopressor use postoperatively. Additional research concerning risk factors specific to this population is urgently needed.

Selective inhibition of COX-2 improves cutaneous wound healing of pressure ulcers in mice through reduction of iNOS expression

AimsCyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) are involved in chronic inflammation observed in chronic lesions. Nonetheless, neither study demonstrated if decreased COX-2 activation could promote the wound healing of pressure ulcers. Therefore, this study investigated the effect of the administration of celecoxib (a selective COX-2 inhibitor) in wound healing of pressure ulcers. Materials and methodsMale mice were treated daily with celecoxib until euthanasia. One day after the beginning of treatment, two cycles of ischemia–reperfusion by external application of two magnetic plates were performed in skin to induce pressure ulcer formation. Key findingsCelecoxib administration reduced the protein expression of inducible nitric oxide synthase (iNOS), COX-2 and PGE2. The hydroperoxide levels, neutrophil and macrophage number, and protein elastase and matrix metalloproteinase-1 levels were reduced in celecoxib-treated group when compared to control group. Celecoxib administration increased myofibroblastic differentiation, re-epithelialization and wound contraction, and decreased the skin necrosis and angiogenesis. Celecoxib administration also stimulated the formation of a more organized and mature scar increasing collagen deposition and reducing tenascin-C expression. SignificanceCelecoxib administration improves the wound healing of pressure ulcers through decreased expression of iNOS and COX-2, which reduces wound inflammation and promotes dermal reconstruction and scar formation.

Best Method for Securing an Endotracheal Tube.

Best Method for Securing an Endotracheal Tube.

Olive oil-induced reduction of oxidative damage and inflammation promotes wound healing of pressure ulcers in mice

BackgroundThe overproduction of reactive oxygen species (ROS) and exacerbated inflammatory response are the main events that impair healing of pressure ulcers. Therefore, olive oil may be a good alternative to improve the healing of these chronic lesions due to its anti-inflammatory and antioxidant properties. ObjectiveThis study investigated the effect of olive oil administration on wound healing of pressure ulcers in mice. MethodsMale Swiss mice were daily treated with olive oil or water until euthanasia. One day after the beginning of treatment, two cycles of ischemia-reperfusion by external application of two magnetic plates were performed in skin to induced pressure ulcer formation. ResultsThe olive oil administration accelerated ROS and nitric oxide (NO) synthesis and reduced oxidative damage in proteins and lipids when compared to water group. The inflammatory cell infiltration, gene tumor necrosis factor-α (TNF-α) expression and protein neutrophil elastase expression were reduced by olive oil administration when compared to water group. The re-epithelialization and blood vessel number were higher in the olive oil group than in the water group. The olive oil administration accelerated protein expression of TNF-α, active transforming growth factor-β1 and vascular endothelial growth factor-A when compared to water group. The collagen deposition, myofibroblastic differentiation and wound contraction were accelerated by olive oil administration when compared to water group. ConclusionOlive oil administration improves cutaneous wound healing of pressure ulcers in mice through the acceleration of the ROS and NO synthesis, which reduces oxidative damage and inflammation and promotes dermal reconstruction and wound closure.

Pressure Ulcer Prevention: Optimizing a Temporally Redistributing Support Interface

One of the most common complications from long-term wheelchair use or bed rest is pressure ulcers. Pressure ulcers have significant morbidity and are associated with high mortality. Prolonged sitting can cause high pressures in the skin and subcutaneous tissue which can lead to local ischemia and breakdown of skin. Rapid relief of pressure prevents ulcer formation. One prevention strategy is to change the temporal distribution of pressure at the interface between user and surface so that no one area is subjected to high pressures for long periods of time. While there are several dynamic interfaces in use currently, there is no definitive evidence of enhanced pressure ulcer prevention with their use. The purpose of this research was to parametrically evaluate interface array sizes, shapes and patterns for dynamic support surfaces to optimize pressure redistribution to prevent pressure ulcers. Finite element analyses, anatomical phantom deep tissue pressure measurements and interface pressure mapping were used to test various support geometries and sizes and different array spacing and patterns. Results indicate that modulating pressure in an array of supports that are equally spaced is not effective. Only interrupted pattern arrays resulted in sufficient pressure reduction. These data suggest that dynamic surface supports can be optimized based on the geometry and size of the individual supports and the pattern of the array to further reduce the likelihood of pressure ulcer formation.

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

Orthopedic shoe treatment: Inserts

The use of inserts and orthopedic shoe adjustment represents an essential component of the conservative therapy of degenerative diseases and deformities of the musculoskeletal system. Inserts can have supportive, bedding and corrective effects and are used in particular for complaints of the feet and ankles. The combination of diverse materials allows a high level of cushioning and supporting features and corresponding longevity to be accomplished. The production is carried out on an individual basis and if necessary computer-assisted in order to achieve an optimal fit. For severe and rigid deformities the formation of pressure ulcers can be prevented by orthopedic shoe adjustment and by the use of orthopedic tailor-made shoes.

Early Detection of Pressure Ulcer Development Following Traumatic Spinal Cord Injury Using Inflammatory Mediators

ObjectiveTo identify changes in concentrations of inflammatory mediators in plasma and urine after traumatic spinal cord injury (SCI) and before the occurrence of a first pressure ulcer. DesignRetrospective; secondary analysis of existing data. SettingAcute hospitalization and inpatient rehabilitation sites at a university medical center. ParticipantsIndividuals with a pressure ulcer and plasma samples (n=17) and individuals with a pressure ulcer and urine samples (n=15) were matched by age and plasma/urine sample days to individuals with SCI and no pressure ulcer (N=35). InterventionsNot applicable. Main Outcome MeasuresPlasma and urine samples were assayed in patients with SCI, capturing samples within 4 days after the SCI to a week before the formation of the first pressure ulcer. The Wilcoxon signed-rank test was performed to identify changes in the inflammatory mediators between the 2 time points. ResultsAn increase in concentration of the chemokine interferon-γ–induced protein of 10kd/CXCL10 in plasma (P<.01) and a decrease in concentration of the cytokine interferon-α in urine (P=.01) were observed before occurrence of a first pressure ulcer (∼4d) compared with matched controls. ConclusionsAltered levels of inflammatory mediators in plasma and urine may be associated with pressure ulcer development after traumatic SCI. These inflammatory mediators should be explored as possible biomarkers for identifying individuals at risk for pressure ulcer formation.

Posture Recognition to Prevent Bedsores for Multiple Patients Using Leaking Coaxial Cable

Leaky coaxial cable (LCX) has long been used to cover blind and semi-blind zones in wireless communication. In this paper, we propose a novel system using a LCX. The key idea is to deploy LCX and use wireless information obtained through PHY layer wireless channel state information (CSI).The core application involves identifying multiple patients’ postures in bed in order to reduce the formation of pressure ulcers or bedsores on the skin. The indoor installation and periodic recording of postures help monitor and prevent bedsores. The CSI registrations are collected using 802.11n Intel WLAN NICs. These CSI registration signatures are unique for particular posture. The amplitude variation is used for differentiating and classifying the postures for inference.